pituitrin and Kidney-Diseases

The kidneys, which regulate many homeostatic pathways, are also a major endocrinological target organ. Many genetic renal diseases can be classified according to the affected protein along such endocrinological pathways. In this review, we examine the hypothesis that a more severe phenotype is expected as the affected protein is located more distally along such pathways. Thus, the location of a defect along its endocrinological pathway should be taken into consideration, in addition to the mutation type, when assessing genetic renal disease severity.

Topics: Aldosterone; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Homeostasis; Humans; Kidney Diseases; Mutation; Phenotype; Renin-Angiotensin System; Vasopressins

The alteration of water balance and related disorders has emerged as being strictly linked to the state of activation of the vasopressin-aquaporin-2 (vasopressin-AQP2) pathway. The lack of responsiveness of the kidney to the vasopressin action impairs its ability to concentrate the urine, resulting in polyuria, polydipsia, and risk of severe dehydration for patients. Conversely, non-osmotic release of vasopressin is associated with an increase in water permeability in the renal collecting duct, producing water retention and increasing the circulatory blood volume. This review highlights some of the new insights and recent advances in therapeutic intervention targeting the dysfunctions in the vasopressin-AQP2 pathway causing diseases characterized by water balance disorders such as congenital nephrogenic diabetes insipidus, syndrome of inappropriate antidiuretic hormone secretion, nephrogenic syndrome of inappropriate antidiuresis, and autosomal dominant polycystic kidney disease. The recent clinical data suggest that targeting the vasopressin-AQP2 axis can provide therapeutic benefits in patients with water balance disorders.

Topics: Aquaporin 2; Diabetes Insipidus, Nephrogenic; Humans; Kidney; Kidney Diseases; Mutation; Vasopressins

ADH is a hormone secreted by neurohypophysis that plays different roles based on the target organ. At the renal level, this peptide is capable of causing electrolyte-free water absorption, thus playing a key role in the hydro-electrolytic balance. There are pathologies and disorders that jeopardize this balance and, in this field, ADH receptor inhibitors such as Vaptans could play a key role. By inhibiting the activation pathway of vasopressin, they are potentially useful in euvolemic and hypervolemic hypotonic hyponatremia. However, clinical trials in heart failure have not given favourable results on clinical outcomes. Even in SIADH, despite their wide use, there is no agreement by experts on their use. Since vaptans inhibit the cAMP pathway in tubular cells, their use has been proposed to inhibit cystogenesis. A clinical trial has shown favourable effects on ADPKD progression. Because vaptans have been shown to be effective in models of renal cysts disorders other than ADPKD, their use has been proposed in diseases such as nephronophthisis and recessive autosomal polycystic disease. Other possible uses of vaptans could be in kidney transplantation and cardiorenal syndrome. Due to the activity of ADH in coagulation and haemostasis, ADH's activation pathway by Desmopressin Acetate could be a useful strategy to reduce the risk of bleeding in biopsies in patients with haemorrhagic risk.

Topics: Antidiuretic Hormone Receptor Antagonists; Cadaver; Cyclic AMP; Forecasting; Humans; Hyponatremia; Kidney Diseases; Kidney Diseases, Cystic; Kidney Transplantation; Kidney Tubules, Collecting; Molecular Targeted Therapy; Neurophysins; Polycystic Kidney, Autosomal Dominant; Protein Precursors; Receptors, Vasopressin; Second Messenger Systems; Tissue Donors; Vasopressins; Water-Electrolyte Imbalance

People with chronic kidney disease (CKD) are at risk of severe outcomes, such as end-stage renal disease or cardiovascular disease, and CKD is a globally increasing health burden with a high personal and economic cost. Despite major progresses in prevention and therapeutics in last decades, research is still needed to reverse this epidemic trend. The regulation of water balance and the state of activation of the vasopressin system have emerged as factors tightly associated with kidney health, in the general population but also in specific conditions; among them, various stages of CKD, diabetes and autosomal dominant polycystic kidney disease (ADPKD). Basic science findings and also epidemiological evidence have justified important efforts towards interventional studies supporting causality, and opening therapeutic avenues. On the basis of recent clinical data, the blockade of V2 vasopressin receptors using tolvaptan in patients with rapidly progressing ADPKD has been granted in several countries, and a long-term randomized trial evaluating the effect of an increase in water intake in patients with CKD is on-going.

Topics: Antidiuretic Hormone Receptor Antagonists; Biomarkers; Diabetic Nephropathies; Fluid Therapy; Glycopeptides; Humans; Kidney; Kidney Diseases; Polycystic Kidney, Autosomal Dominant; Renal Insufficiency, Chronic; Vasopressins

We performed a comprehensive literature review to examine evidence on the effects of hydration on the kidney. By reducing vasopressin secretion, increasing water intake may have a beneficial effect on renal function in patients with all forms of chronic kidney disease (CKD) and in those at risk of CKD. This potential benefit may be greater when the kidney is still able to concentrate urine (high fluid intake is contraindicated in dialysis-dependent patients). Increasing water intake is a well-accepted method for preventing renal calculi, and current evidence suggests that recurrent dehydration and heat stress from extreme occupational conditions is the most probable cause of an ongoing CKD epidemic in Mesoamerica. In polycystic kidney disease (PKD), increased water intake has been shown to slow renal cyst growth in animals via direct vasopressin suppression, and pharmacologic blockade of renal vasopressin-V2 receptors has been shown to slow cyst growth in patients. However, larger clinical trials are needed to determine if supplemental water can safely slow the loss of kidney function in PKD patients.

Topics: Animals; Disease Progression; Humans; Kidney Diseases; Organism Hydration Status; Renal Insufficiency, Chronic; Vasopressins; Water

There has been considerable recent progress liver transplantation (LTX). The postreperfusion syndrome has clearly defined and typically responds to vasopressin and/or methylene blue when refractory to catecholamine therapy. Diastolic dysfunction and cirrhotic cardiomyopathy are prevalent and important in LTX recipients. The high cardiovascular risk and the increasing medical complexity of the current liver transplant recipient have stimulated the publication of guidelines for cardiovascular assessment before LTX. Cardiac surgery is increasingly more successful in patients with cirrhosis, including simultaneous heart-liver transplantation. Cardiopulmonary bypass in LTX is indicated for hemodynamic rescue and, at some centers, serves as the hemodynamic platform for liver implantation. Although acute renal injury is common after LTX, early diagnosis is now possible with novel biomarkers. Earlier detection of postoperative renal dysfunction may prompt intervention for renal rescue. The metabolic milieu in LTX remains critical. Regular insulin therapy may be more effective than infrequent large bolus therapy for potassium homeostasis. Careful titration of insulin therapy may improve freedom from severe hyperglycemia to decrease morbidity. Since the organization of dedicated anesthesia care teams for LTX improves perioperative outcome, this aspect of perioperative care is receiving systematic attention to optimize safety and quality. The specialty of LTX is likely to continue to flourish even more, given these pervasive advances.

Topics: Anesthesia; Cardiac Surgical Procedures; Humans; Kidney Diseases; Liver Transplantation; Methylene Blue; Postoperative Complications; Reperfusion Injury; Vasoconstrictor Agents; Vasoplegia; Vasopressins

Most patients with heart failure (HF) already have or develop renal dysfunction; this might contribute to their poor outcome. Current treatment for HF can also contribute to worsen renal function. High furosemide doses are traditionally associated with worsening renal function (WRF), but patients with fluid overload may benefit of aggressive fluid removal. Unfortunately, promising therapies like vasopressin antagonists and adenosine antagonists have not been demonstrated to improve outcomes. Likewise, correction of low renal blood flow through dopamine, inotropic agents, or vasodilators does not seem to be associated with a clear benefit. However, transient WRF associated with acute HF treatment may not necessarily portend a poor prognosis. In this review, we focus on the strategies to detect renal dysfunction in acute HF, the underlying pathophysiological mechanisms, and the potential treatments.

Topics: Acute Disease; Adenosine; Biomarkers; Cardiotonic Agents; Diuretics; Dopamine; Heart Failure; Humans; Kidney; Kidney Diseases; Mineralocorticoid Receptor Antagonists; Prognosis; Vasodilator Agents; Vasopressins

The association between fructose and increased blood pressure is still incompletely defined, because experimental studies have produced dissimilar conclusions. Amplified vasopressor responses to minimal stimuli and differing responses to fructose in peripheral versus central sites may explain the controversy. Fructose induces systemic hypertension through several mechanisms mainly associated with deleterious effects on target organs (kidney, endothelium, heart) exerted by the byproducts of its metabolism, such as uric acid. The kidney is particularly sensitive to the effects of fructose because high loads of this sugar reach renal tissue. In addition, fructose increases reabsorption of salt and water in the small intestine and kidney; thus the combination of salt and fructose has a synergistic effect in the development of hypertension. Clinical and epidemiologic studies have also linked fructose consumption with hypertension. Further studies are warranted in order to understand the role of fructose in the development of hypertension.

Topics: Animals; Blood Pressure; Disease Models, Animal; Endothelium, Vascular; Fructose; Humans; Hypertension; Kidney Diseases; Metabolic Syndrome; Oxidative Stress; Risk Factors; Sodium Chloride, Dietary; Sweetening Agents; United States; Uric Acid; Vasopressins

Hospitalization for heart failure is a major health problem with high in-hospital and postdischarge mortality and morbidity. Non-potassium-sparing diuretics (NPSDs) still remain the cornerstone of therapy for fluid management in heart failure despite the lack of large randomized trials evaluating their safety and optimal dosing regimens in both the acute and chronic setting. Recent retrospective data suggest increased mortality and re-hospitalization rates in a wide spectrum of heart failure patients receiving NPSDs, particularly at high doses. Electrolyte abnormalities, hypotension, activation of neurohormones, and worsening renal function may all be responsible for the observed poor outcomes. Although NPSD will continue to be important agents to promptly resolve signs and symptoms of heart failure, alternative therapies such as vasopressine antagonists and adenosine blocking agents or techniques like veno-venous ultrafiltration have been developed in an effort to reduce NPSD exposure and minimize their side effects. Until other new agents become available, it is probably prudent to combine NPSD with aldosterone blocking agents that are known to improve outcomes.

Topics: Adenosine; Cardiovascular Diseases; Heart Failure; Hemofiltration; Hormone Antagonists; Humans; Kidney Diseases; Risk Assessment; Risk Factors; Sodium Potassium Chloride Symporter Inhibitors; Time Factors; Treatment Outcome; Vasopressins; Water-Electrolyte Balance

Arginine vasopressin (AVP or antidiuretic hormone) is one of the key hormones in the human body responsible for a variety of cardiovascular and renal functions. It has so far escaped introduction into the routine clinical laboratory due to technical difficulties and preanalytical errors. Copeptin, the C-terminal part of the AVP precursor peptide, was found to be a stable and sensitive surrogate marker for AVP release. Copeptin behaves in a similar manner to mature AVP in the circulation, with respect to osmotic stimuli and hypotension. During the past years, copeptin measurement has been shown to be of interest in a variety of clinical indications, including cardiovascular diseases such as heart failure, myocardial infarction, and stroke. This review summarizes the recent progress on the diagnostic use of copeptin in cardiovascular and renal diseases and discusses the potential use of copeptin measurement in the context of therapeutic interventions with vasopressin receptor antagonists.

Topics: Arginine Vasopressin; Biomarkers; Blood Volume; Cardiovascular Diseases; Cardiovascular System; Glycopeptides; Heart Failure; Humans; Kidney; Kidney Diseases; Myocardial Infarction; Prognosis; ROC Curve; Shock, Cardiogenic; Stroke; Vasopressins

The pathogenesis of cardiac failure involves activation of the neurohumoral axis including stimulation of the sympathetic nervous system, the renin-angiotensin-aldosterone, and nonosmotic vasopressin systems. While these responses are critical in maintaining arterial pressure, they are associated with renal vasoconstriction, as well as sodium and water retention. In advanced circumstances, renal dysfunction and hyponatremia occur with cardiac failure. Even a modest rise in serum creatinine related to diminished renal function in heart failure patients is associated with increased risk for cardiovascular morbidity and mortality. Similarly, increased thirst and the nonosmotic stimulation of vasopressin in advanced cardiac failure leads to hyponatremia, which is also a major risk factor for mortality. Currently, V2 vasopressin receptor antagonists have been shown to correct hyponatremia in cardiac failure. One such agent, conivaptan, also is a V1 receptor antagonist which could theoretically benefit heart failure patients by decreasing cardiac afterload and remodeling. The effect of V2 receptor antagonists to correct hyponatremia in heart failure patients appears to be quite safe. However, to date no effect on mortality has been demonstrated.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Heart Failure; Humans; Hyponatremia; Kidney; Kidney Diseases; Vasopressins

Vasopressin analogues are increasingly used for haemodynamic support of catecholamine-refractory, hyperdynamic septic shock. Arginine vasopressin (AVP) and terlipressin (TP) effectively increase mean arterial pressure and reduce catecholamine requirements in this condition. However, the use of either of the drugs may be linked to relevant haemodynamic side effects, including reductions in cardiac output, oxygen delivery and mixed-venous oxygen saturation. These alterations may result in impaired tissue perfusion and foster the genesis of ischemic tissue injury. In addition, decreases in platelet count and increases in aminotransferases activity and bilirubin concentration have been reported with the use of V1 agonists. However, it remains unclear whether these changes are of clinical relevance. This review article summarizes the previous data on adverse effects related to the therapy with vasopressin analogues and discusses potential options to prevent such adverse events. In summary, continuous TP infusion appears to be superior to bolus infusion. Maximum doses of 0.03 (-0.067) U min(-1) of AVP or 2 microg kg(-1) h(-1) of TP, respectively, should not be exceeded. Aggressive fluid therapy may prevent adverse haemodynamic effects linked to infusion of either AVP or TP. Finally, platelet count, surrogate variables of hepatic dysfunction, electrolytes and osmolality should be strictly monitored in patients treated with vasopressin analogues.

Topics: Animals; Chemical and Drug Induced Liver Injury; Humans; Ischemia; Kidney Diseases; Lypressin; Shock; Skin; Terlipressin; Thrombosis; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Imbalance

To prevent dehydration, terrestrial animals and humans have developed a sensitive and versatile system to maintain their water homeostasis. In states of hypernatremia or hypovolemia, the antidiuretic hormone vasopressin (AVP) is released from the pituitary and binds its type-2 receptor in renal principal cells. This triggers an intracellular cAMP signaling cascade, which phosphorylates aquaporin-2 (AQP2) and targets the channel to the apical plasma membrane. Driven by an osmotic gradient, pro-urinary water then passes the membrane through AQP2 and leaves the cell on the basolateral side via AQP3 and AQP4 water channels. When water homeostasis is restored, AVP levels decline, and AQP2 is internalized from the plasma membrane, leaving the plasma membrane watertight again. The action of AVP is counterbalanced by several hormones like prostaglandin E2, bradykinin, dopamine, endothelin-1, acetylcholine, epidermal growth factor, and purines. Moreover, AQP2 is strongly involved in the pathophysiology of disorders characterized by renal concentrating defects, as well as conditions associated with severe water retention. This review focuses on our recent increase in understanding of the molecular mechanisms underlying AVP-regulated renal water transport in both health and disease.

Topics: Absorption; Animals; Aquaporin 2; Humans; Kidney; Kidney Diseases; Signal Transduction; Vasopressins; Water

Topics: Arteriosclerosis; Catecholamines; Chronic Disease; Endothelium, Vascular; Heart Diseases; Humans; Inflammation; Kidney Diseases; Oxidative Stress; Renin-Angiotensin System; Risk Factors; Vasopressins

Beyond polyuria following psychogenic polydipsia, in a more narrow sense, this condition may be classified into impaired water re-absorption (i) due to tubular injury or (ii) relative or absolute loss of function of antidiuretic hormone (ADH). Tubular injury may be caused by different toxins affecting the ascending Henle loop as hypercalciuria, drugs and antibiotics as tubular necrosis. ADH deficiency, either absolute or relative, occurs with central or peripheral diabetes insipidus, which is based on synthesis failure or loss of peripheral efficacy of ADH due to receptor malfunction. Diagnosis of polyuria rests upon a thirst challenge in conjunction with laboratory studies of osmolality in serum and urine, which discloses the non-function of the hypothalamic-renal axis. Administration of ADH may differentiate between central and peripheral diabetes insipidus.

Topics: Humans; Kidney Diseases; Polyuria; Practice Guidelines as Topic; Practice Patterns, Physicians'; Vasopressins

Nocturia is common in older people and it may be bothersome for both patients and carers. It is most commonly related to bladder storage difficulties and nocturnal polyuria. The former results most frequently from an uninhibited overactive bladder. The latter occurs as a consequence of age-associated changes in the circadian rhythm of urine excretion. The management of an overactive bladder includes both behavioural and drug treatment. The management options for nocturnal polyuria include an afternoon diuretic and desmopressin, but caution is required, particularly with the latter, as it can cause significant hyponatraemia.

Topics: Adult; Aged; Aged, 80 and over; Arginine Vasopressin; Atrial Natriuretic Factor; Circadian Rhythm; Humans; Kidney Diseases; Life Style; Male; Middle Aged; Sleep Wake Disorders; Sodium; Urinary Bladder Diseases; Urination Disorders; Vasopressins; Water-Electrolyte Imbalance

Topics: Angiotensin-Converting Enzyme Inhibitors; Aquaporin 2; Aquaporin 6; Aquaporins; Heart Failure; Humans; Kidney; Kidney Diseases; Natriuretic Peptide, Brain; Vasopressins

Water balance depends essentially on fluid intake and urine excretion. Mild dehydration and the consequent hypertonicity of the extracellular fluid induce an increase in vasopressin secretion, thus stimulating urine concentrating processes and the feeling of thirst. The osmotic threshold for the release of vasopressin is lower than that for thirst and also shows appreciable individual variation. Sustained high levels of vasopressin and low hydration induce morphological and functional changes in the kidney. However, they could also be risk factors in several renal disorders, such as chronic renal failure, diabetic nephropathy and salt-sensitive hypertension.

Topics: Animals; Dehydration; Humans; Kidney; Kidney Concentrating Ability; Kidney Diseases; Rats; Thirst; Urination; Vasopressins; Water-Electrolyte Balance

Cranial diabetes insipidus (DI) arises when release of arginine vasopressin (AVP, antidiuretic hormone) in response to osmotic stimuli is inadequate. The correct diagnosis and management of cranial DI is particularly important when it arises as an acute complication of surgery, trauma or in subjects who lack thirst sensation. Desmopressin (1-desamino-8-D-arginine-vasopressin, DDAVP) provides an effective and convenient replacement therapy when given by the intranasal route. However, nasal administration is difficult for some patients, and in the future oral or transcutaneous desmopressin formulations may prove to be satisfactory alternatives. By contrast, treatments for nephrogenic DI, where there is failure of the antidiuretic response to endogenous or exogenous vasopressin, have been disappointing and water replacement remains the mainstay of therapy. An understanding of the physiology and pathophysiology of water homeostasis and correct interpretation of water balance and electrolyte data are essential for correct diagnosis and management of all cases of DI.

Topics: Arginine Vasopressin; Diabetes Insipidus; Female; Humans; Hypernatremia; Kidney Diseases; Male; Pregnancy; Pregnancy Complications; Thirst; Vasopressins

Topics: Body Water; Diagnosis, Differential; Hepatorenal Syndrome; Humans; Kidney; Kidney Diseases; Prognosis; Sodium; Vasopressins

Normal osmoregulation is maintained by the proper function and interplay of factors influencing thirst, renal water metabolism, and vasopressin secretion. In pathophysiologic states, body water homeostasis is disrupted and hyponatremia ensures. Hyponatremia associated with cardiac failure, hepatic failure, respiratory failure, diabetes mellitus, the postoperative state, and other disorders is commonly found in the critical care setting. The pathophysiology, diagnosis, and treatment of hyponatremia are discussed.

Topics: Body Water; Humans; Hyponatremia; Kidney Diseases; Multiple Organ Failure; Osmolar Concentration; Thirst; Vasopressins

In the last decade, our knowledge of the renal kallikrein-kinin system has been advanced significantly. More specific and sensitive methods for assessing its activity have been developed. Further, it has been found that in the kidney this system is localized in the distal nephron, where it appears to be linked to processes that control water and electrolyte excretion. Data indicate that the kallikrein-kinin system interacts with other renal hormonal systems such as the prostaglandin and renin-angiotension-kinin system may participate in the control of renal function and the pathophysiology of renal diseases. An increase in kallikrein excretion has been observed after administration of antihypertensive drugs. The kallikrein-kinin system may therefore participate in their mechanism(s) of action. Our current knowledge suggests that the renal kallikrein-kinin system is an integral part of the intrarenal hormonal system that controls water and electrolyte excretion and participates in the regulation of blood pressure.

Topics: Animals; Dinoprostone; Humans; Hypertension, Renovascular; Kallikreins; Kidney; Kidney Diseases; Kinins; Nephrons; Peptidyl-Dipeptidase A; Prostaglandins E; Rats; Subcellular Fractions; Tissue Distribution; Vasopressins

Data from humans and experimental animals indicate that hypertensive diseases triggered by extracellular fluid volume expansion are characterized, in their chronic phases, by relatively normal blood volume (BV) and heightened pressure-volume relationship may be viewed as corresponding to a condition of "virtual hypervolemia," where BV is inappropriately "high" relative to blood pressure. The limited data available on the phasic relationship between these variables indicate that the BV expansion appears to be a prerequisite to alterations in vascular ion metabolism, that both of these changes precede the rise in blood pressure, and that structures within the central nervous system may be a critical link between the body fluid volumes and vascular functional changes. In contrast, hypertensive diseases triggered by secretion of pressor agents or their precursors appear to be characterized in their chronic phases by low BV. These relationships and the associated alterations in plasma aldosterone and renin levels are summarized for a variety of clinical syndromes, including essential hypertension and pregnancy-induced hypertension. Direct or indirect evidence of a primary or secondary defect in renal function is apparent as an underlying event in many of these diseases.

Topics: Animals; Blood Pressure; Extracellular Space; Female; Humans; Hypertension; Kidney; Kidney Diseases; Mineralocorticoids; Pregnancy; Pregnancy Complications, Cardiovascular; Sodium Chloride; Vasopressins

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.

Topics: Acid-Base Equilibrium; Adolescent; Adult; Aged; Aging; Animals; Glomerular Filtration Rate; Glomerulosclerosis, Focal Segmental; Humans; Kidney; Kidney Diseases; Middle Aged; Renal Circulation; Vasopressins

Topics: Animals; Arachidonic Acids; Hormones; Kidney; Kidney Diseases; Kinins; Prostaglandins; Rabbits; Rats; Renin-Angiotensin System; Vasopressins

Topics: Acid-Base Equilibrium; Glomerular Filtration Rate; Humans; Kidney; Kidney Diseases; Kidney Tubules; Kinetics; Lithium; Mental Disorders; Polyuria; Sodium; Vasopressins; Water-Electrolyte Balance

Vasodilatory renal prostaglandins, especially PGE2 and PGI2, maintain renal blood flow and glomerular filtration rate under certain circumstances, especially clinical and experimental conditions accompanied by renal vasoconstriction and increased plasma concentrations of catecholamines, angiotensin, and vasopressin. Inhibition of arachidonate cyclooxygenase by nonsteroidal antiinflammatory drugs reduces renal PGE2 and PGI2, exaggerates renal vasoconstriction, and thereby decreases renal blood flow and glomerular filtration rates. Reversible acute renal failure can accompany the clinical use of prostaglandin inhibitory drugs.

Topics: Angiotensins; Animals; Anti-Inflammatory Agents; Arachidonic Acids; Cyclooxygenase Inhibitors; Dinoprostone; Epoprostenol; Glomerular Filtration Rate; Humans; Kidney; Kidney Diseases; Norepinephrine; Prostaglandins; Prostaglandins E; Renal Circulation; Sulindac; Vasoconstriction; Vasodilation; Vasopressins

Glomeruli contain receptors for many hormones. Binding of angiotensin II (ANG II) or antidiuretic hormone (ADH) to glomerular mesangial cells elicits a contractile response. Other hormones induce synthesis of cyclic nucleotides (cAMP, cGMP). Glomeruli also synthesize several prostaglandins, renin, and ANG II. Micropuncture studies in Munich-Wistar rats have examined the effects of vasoactive drugs and hormones on the filtration process. Several vasodilators increase renal plasma flow in the dog and rat, but GFR remains relatively unchanged due to an offsetting fall in the ultrafiltration coefficient (Kf). Vasoconstrictor substances such as ANG II and norepinephrine cause declines in renal plasma flow and Kf, but GFR remains constant due to an increase in the transcapillary hydraulic pressure gradient. Antidiuretic peptides and parathyroid hormone also reduce Kf. Glomerular mesangial cells may regulate Kf by contracting and reducing glomerular capillary surface area. ANG II and ADH directly stimulate mesangial cell contraction in vitro. Other hormones appear to cause contraction by inducing local ANG II synthesis. These hormonal pathways are implicated in the pathogenesis of altered glomerular function in diverse forms of renal injury.

Topics: Animals; Cyclic AMP; Cyclic GMP; Disease Models, Animal; Glomerular Filtration Rate; Hormones; Kidney Diseases; Kidney Glomerulus; Parathyroid Hormone; Rats; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Topics: Absorption; Acetylglucosaminidase; beta 2-Microglobulin; Humans; Kidney Diseases; Kidney Glomerulus; Kidney Tubules; Kidney Tubules, Distal; Kidney Tubules, Proximal; Molecular Weight; Proteinuria; Vasopressins

A new approach to the classification of disorders of urinary concentration and dilution is recommended based on recent studies of how the kidney elaborates a urine of widely varying osmolality. The capacity to concentrate urine depends on ft, the fractional reabsorption of solute delivered to the loop of Henle; fu, the excretion of solute relative to the sum of solute excretion and solute delivery to Henle's loop; fw, the fraction of solute loss by vascular outflow from the medulla relative to that reabsorbed by the loop; and finally, collecting duct response to antidiuretic hormone (ADH). A decrease in ft or in increased fu or fw will diminish urinary concentrating ability, as will resistance of the tubule to ADH. Conversely, urinary dilution depends on the delivery of sodium and water to the ascending limb; NaCl reabsorption by the ascending limb; and the absence of ADH. A decrease in sodium and water delivery to the ascending limb or in NaCl reabsorption by the ascending limb will impair urinary diluting ability, as will the presence of ADH. The consequences of disorders in urinary concentrating and diluting ability vary widely. In an alert patient with an intact thirst center, there may be no consequence; in a patient unable to communicate thirst or whose thirst center is deranged, the results may be catastrophic. Keeping in mind the kidney's few basic requirements for formation of concentrated or dilute urine may help the physician avoid these potentially serious dislocations of water balance.

Topics: Absorption; Animals; Body Water; Diabetes Insipidus; Humans; Kidney Concentrating Ability; Kidney Diseases; Kidney Medulla; Loop of Henle; Osmolar Concentration; Potassium; Sodium; Vasopressins

Topics: Blood Coagulation; Blood Coagulation Disorders; Catecholamines; Contraceptives, Oral; Delivery, Obstetric; Factor VIII; Female; Humans; Immune System Diseases; Insulin; Kidney Diseases; Liver Diseases; Nicotinic Acids; Physical Exertion; Pregnancy; Pregnancy Complications; Surgical Procedures, Operative; Vasopressins

The effects of clonidine on renal hemodynamics and renal function make it a particularly useful antihypertensive agent. During treatment of hypertensive patients with clonidine, renal blood flow and glomerular filtration rate are well maintained, and renin secretion is reduced. Early in therapy, a slight tendency to retain salt and water may be seen as blood pressure is lowered. This effect on salt and water excretion is usually transient and may be avoided if a diuretic is used concomitantly. No deterioration of renal function was noted in patients with primary hypertension who were treated with clonidine for periods from 6 months to at least 5 years. The drug is effective in patients with renal hypertension with or without renal failure and well tolerated. Clonidine is also effective in hypertensive patients undergoing chronic hemodialysis, but doses may have to be reduced because the drug is excreted chiefly by the kidney.

Topics: Adrenal Gland Neoplasms; Aldosterone; Antihypertensive Agents; Catecholamines; Clonidine; Humans; Hypertension; Kidney; Kidney Diseases; Pheochromocytoma; Renal Artery Obstruction; Sympathetic Nervous System; Vasopressins; Water-Electrolyte Balance

The use of diagnostic and therapeutic angiography for postoperative bleeding which began with its application for bleeding following GI surgery can be ezpanded to almost all other areas of the body. Severe postoperative hemorrhage that previously required a second operation can now be successfully managed by the use of intraarterial or intravenous vasoconstrictors or transcatheter occlusion, thus significantly reducing patient morbidity and mortality. In those patients where a reexploration becomes necessary, diagnostic angiogarphy is a useful guide and helps to tailor the operative procedures.

Topics: Aged; Angiography; Catheterization; Embolization, Therapeutic; Esophageal Diseases; Gastrointestinal Hemorrhage; Gelatin; Hemorrhage; Hip; Humans; Intestine, Small; Kidney Diseases; Male; Pelvic Neoplasms; Postoperative Complications; Stomach Diseases; Tissue Adhesives; Vasopressins

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.

Topics: Acute Disease; Analgesics; Humans; Hypercalcemia; Immune System Diseases; Kidney Calculi; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubular Necrosis, Acute; Necrosis; Nephrosis; Nephrotic Syndrome; Potassium Deficiency; Proteins; Tetracyclines; Ureteral Diseases; Ureteral Obstruction; Urologic Neoplasms; Vascular Diseases; Vasopressins

Topics: Diabetes Insipidus; Endocrine System Diseases; Female; Humans; Kidney Diseases; Male; Neurophysins; Osmolar Concentration; Oxytocin; Pituitary Function Tests; Polyuria; Radioimmunoassay; Vasopressins

Topics: Acid-Base Equilibrium; Aldosterone; Angiotensin II; Animals; Blood Volume; Catecholamines; Diuresis; Dogs; Humans; Immersion; Kidney; Kidney Diseases; Liver Cirrhosis; Natriuresis; Parathyroid Hormone; Phosphates; Potassium; Primates; Prostaglandins; Renin; Temperature; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Cyclic AMP; Diabetes Insipidus; Humans; Kidney Diseases; Kidney Medulla; Lithium; Polyuria; Serous Membrane; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

This paper reviews the physiology of antidiuretic hormone, including the factors involving the formation, storage and release of the hormone, the metabolism of vasopressin and its physiologic and pharmacologic effects on water and electrolyte transport. The consequences of both deficiency and excess of the hormone are also discussed.

Topics: Blood Physiological Phenomena; Blood Pressure; Blood Volume; Body Fluids; Cyclic AMP; Female; Humans; Kidney; Kidney Diseases; Liver; Osmolar Concentration; Pregnancy; Secretory Rate; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Blood Proteins; Diabetic Coma; Diuresis; Female; Humans; Hypertonic Solutions; Hyponatremia; Kidney Diseases; Lipids; Male; Mannitol; Middle Aged; Osmolar Concentration; Peritoneal Dialysis; Renal Dialysis; Sodium Chloride; Vasopressins; Water Intoxication

Topics: Acute Kidney Injury; Alcoholism; Animals; Dogs; Ethanol; Glomerular Filtration Rate; Glomerulonephritis; Humans; Kidney; Kidney Diseases; Kidney Glomerulus; Pyelonephritis; Rats; Urinary Bladder; Vasopressins

Topics: Animals; Arginine; Carbamazepine; Chlorpropamide; Clofibrate; Cyclic AMP; Diabetes Insipidus; Hypothalamus; Kidney Diseases; Lithium; Methoxyflurane; Peptide Biosynthesis; Protein Biosynthesis; Rats; Rodent Diseases; Tetracycline; Vasopressins; Vermont

Topics: Adenylyl Cyclases; Animals; Chlorpropamide; Crosses, Genetic; Diabetes Insipidus; Disease Models, Animal; Drug Synergism; Genes; Genetic Diseases, Inborn; Humans; Hybridization, Genetic; Hypertrophy; Hypothalamus; Kidney Concentrating Ability; Kidney Diseases; Kidney Medulla; Loop of Henle; Mice; Pituitary Gland; Rats; Vasopressins

Topics: Acidosis; Acute Kidney Injury; Alkalosis; Amyloidosis; Hodgkin Disease; Humans; Hyperkalemia; Hypernatremia; Hypertension, Renal; Hypokalemia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Multiple Myeloma; Neoplasms; Nephritis; Nephrotic Syndrome; Osmolar Concentration; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Acute Kidney Injury; Alcoholism; Animals; Dogs; Ethanol; Glomerular Filtration Rate; Glomerulonephritis; Humans; Kidney; Kidney Diseases; Kidney Glomerulus; Pyelonephritis; Rats; Urinary Bladder; Vasopressins

Topics: Aldosterone; Angiotensin II; Edema; Extracellular Space; Female; Glomerular Filtration Rate; Humans; Hyperaldosteronism; Hypertension; Hypotension; Juxtaglomerular Apparatus; Kidney; Kidney Diseases; Kidney Failure, Chronic; Natriuresis; Potassium; Pregnancy; Pregnancy Complications; Pressoreceptors; Regional Blood Flow; Renal Artery Obstruction; Renin; Vasopressins

Topics: Aldosterone; Anesthesia, Inhalation; Anesthetics; Angiotensin II; Animals; Dose-Response Relationship, Drug; Epinephrine; Glomerular Filtration Rate; Homeostasis; Humans; Infusions, Parenteral; Kidney; Kidney Diseases; Methoxyflurane; Norepinephrine; Regional Blood Flow; Renin; Surgical Procedures, Operative; Vasopressins

Topics: Adrenal Gland Diseases; Diabetes Insipidus; Diabetic Nephropathies; Diagnosis, Differential; Diuresis; Glomerular Filtration Rate; Humans; Hypercalcemia; Hyponatremia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Natriuresis; Osmolar Concentration; Urologic Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Glands; Aldosterone; Feedback; Glomerular Filtration Rate; Humans; Hyponatremia; Kidney; Kidney Diseases; Kidney Neoplasms; Mixed Function Oxygenases; Natriuresis; Sodium; Vasopressins; Water Intoxication

Topics: Adrenal Cortex Hormones; Animals; Biopsy; Body Weight; Diet, Sodium-Restricted; Eclampsia; Edema; Female; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Kidney; Kidney Diseases; Nephritis; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pyelonephritis; Sodium; Uric Acid; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Glands; Aldosterone; Diagnosis, Differential; Edema; Extracellular Space; Female; Heart Diseases; Humans; Kidney; Kidney Diseases; Liver Cirrhosis; Male; Parasitic Diseases; Pituitary Gland; Posture; Pre-Eclampsia; Pregnancy; Pulmonary Edema; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aldosterone; Angiotensin II; Blood Coagulation Disorders; Catecholamines; Diagnosis, Differential; Estrogens; Female; Humans; Kidney Diseases; Placenta; Placenta Diseases; Pre-Eclampsia; Pregnancy; Renin; Serotonin; Uric Acid; Vasopressins; Water-Electrolyte Balance

Topics: Acidosis, Renal Tubular; Electrolytes; Humans; Kidney Diseases; Kidney Failure, Chronic; Magnesium; Muscular Diseases; Neurologic Manifestations; Vasopressins

Topics: Aldosterone; Angiotensin II; Blood Pressure; Chronic Disease; Female; Humans; Hypertension, Renal; Kidney; Kidney Diseases; Norepinephrine; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Complications, Cardiovascular; Renin; Time Factors; Vasopressins

Topics: Acute Kidney Injury; Glomerulonephritis; Humans; Hypertension, Renal; Kidney Diseases; Kidney Failure, Chronic; Kidney Transplantation; Kidneys, Artificial; Nephrotic Syndrome; Pyelonephritis; Transplantation, Homologous; Vasopressins

Topics: Alcoholism; Animals; Diuretics; Female; Humans; Infant, Newborn; Kidney Diseases; Lactation Disorders; Magnesium; Magnesium Deficiency; Porphyrias; Pregnancy; Vasopressins

Topics: Alcohols; Body Water; Central Nervous System Diseases; Child; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diuresis; Edema; Ethanol; Histiocytosis, Langerhans-Cell; Homeostasis; Humans; Hyponatremia; Infant; Infant, Newborn; Kidney Diseases; Nicotine; Physiology; Pituitary Gland; Pituitary Gland, Posterior; Potassium Deficiency; Prednisone; Pyloric Stenosis; Vasopressins; Water

Topics: Arginine Vasopressin; Humans; Hypokalemia; Kidney Diseases; Pathology; Physiology; Proteins; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Anesthetics; Blood Urea Nitrogen; Body Weight; Creatinine; Halothane; Humans; Hypernatremia; Kidney Concentrating Ability; Kidney Diseases; Male; Methoxyflurane; Middle Aged; Osmolar Concentration; Polyuria; Postoperative Care; Prospective Studies; Sodium; Surgical Procedures, Operative; Time Factors; Uric Acid; Vasopressins; Water-Electrolyte Balance

We examined the effects of rapid restriction of food and fluid intake on the pathways of water homeostasis, the vasopressinergic system (VPS), and the renin-angiotensin-aldosterone system (RAAS), in rats with or without regular exercise.. Sprague Dawley rats were divided into the following groups: no intervention, rapid restriction, regular exercise, and rapid restriction combined with regular exercise. Rats in the exercise group performed climbing exercise for 4 weeks. All rats consumed food ad libitum, and those in the rapid restriction group fasted for the last 3 days with no water on the last 1 day.. Despite no significant differences in body weight among the groups, the kidney weight was decreased when rapid restriction and regular exercise were combined. Rapid restriction reduced the urine volume and increased the urine osmolality, whereas regular exercise did not. Rapid restriction but not regular exercise increased the levels of circulating aldosterone and the renal expression levels of the ion channel SGK-1 compared to those without rapid restriction, indicating the stimulation of RAAS. Conversely, VPS showed no significant response to these interventions. Moreover, rapid restriction combined with regular exercise induced the renal expression levels of proinflammatory cytokines and increased the active forms of apoptotic effector caspase-3 compared with the no intervention group.. Functional significance may differ between VPS and RAAS in water homeostasis in response to rapid restriction. Moreover, the combination of rapid restriction and regular exercise has potentially deleterious effects on the kidney.

Topics: Animals; Dehydration; Fasting; Homeostasis; Kidney Diseases; Male; Models, Animal; Physical Conditioning, Animal; Rats; Rats, Sprague-Dawley; Renin-Angiotensin System; Vasopressins; Water

Retinoic acid (RA) activates RA receptors (RAR), resulting in RA response element (RARE)-dependent gene expression in renal collecting duct (CD). Emerging evidence supports a protective role for this activity in acute kidney injury (AKI) and chronic kidney disease (CKD). Herein, we examined this activity in RARE-LacZ transgenic mice and by RARE-Luciferase reporter assays in CD cells, and investigated how this activity responds to neurotransmitters and mediators of kidney injury. In RARE-LacZ mice, Adriamycin-induced heavy albuminuria was associated with reduced RA/RAR activity in CD cells. In cultured CD cells, RA/RAR activity was repressed by acetylcholine, albumin, aldosterone, angiotensin II, high glucose, cisplatin and lipopolysaccharide, but was induced by aristolochic acid I, calcitonin gene-related peptide, endothelin-1, gentamicin, norepinephrine and vasopressin. Compared with age-matched normal human CD cells, CD-derived renal cystic epithelial cells from patients with autosomal recessive polycystic kidney disease (ARPKD) had significantly lower RA/RAR activity. Synthetic RAR agonist RA-568 was more potent than RA in rescuing RA/RAR activity repressed by albumin, high glucose, angiotensin II, aldosterone, cisplatin and lipopolysaccharide. Hence, RA/RAR  in CD cells is a convergence point of regulation by neurotransmitters and mediators of kidney injury, and may be a novel therapeutic target.

Topics: Acetylcholine; Albumins; Aldosterone; Angiotensin II; Animals; Calcitonin Gene-Related Peptide; Cell Line; Cisplatin; Endothelin-1; Female; Glucose; Humans; Kidney Diseases; Kidney Tubules, Collecting; Lipopolysaccharides; Mice; Mice, Transgenic; Receptors, Retinoic Acid; Tretinoin; Vasopressins

Topics: Brain; Congresses as Topic; Dehydration; Drinking; Humans; Kidney Diseases; Neurophysins; Neurosecretory Systems; Protein Precursors; Urinary Tract Infections; Vasopressins; Water; Water-Electrolyte Balance

Topics: Antidiuretic Hormone Receptor Antagonists; Cardiovascular Diseases; Congresses as Topic; Glycopeptides; Humans; Kidney; Kidney Diseases; Liver; Metabolic Diseases; Vasopressins

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Topics: Adult; Algorithms; Blood Glucose; Brain Edema; Critical Care; Endocrinology; Evidence-Based Medicine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Kidney Diseases; Male; Nephrology; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Vasopressins

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Topics: Adult; Algorithms; Blood Glucose; Brain Edema; Critical Care; Endocrinology; Evidence-Based Medicine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Kidney Diseases; Male; Nephrology; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Vasopressins

Topics: Adult; Dehydration; Diuresis; Drinking; Humans; Kidney; Kidney Diseases; Vasopressins; Water-Electrolyte Balance

Although recent advances have led to a better understanding of the beneficial effects of vasopressin on haemodynamics in paediatric cardiac surgery, not much information is available on the adverse effects. The objective of this study was to assess the impact of intraoperative vasopressin infusion on postoperative liver, renal and haemostatic function and lactate levels in neonates undergoing cardiac surgery.. We reviewed data from 34 consecutive neonates who had undergone complex cardiac surgery. The cohort was divided into two groups according to the use of vasopressin. Seventeen patients received vasopressin [vasopressin (+) group], and 17 patients did not [vasopressin (-) group].. No differences between the groups in terms of age, weight, cardiopulmonary bypass time, Risk Adjustment for Congenital Heart Surgery-1 score or the comprehensive Aristotle score were seen. No differences in the systolic or diastolic arterial blood pressures, heart rate or inotropic score upon admission to the intensive care unit were observed between the groups. No adverse effects on the aminotransferase levels were seen. The vasopressin (+) group had higher urea and creatinine levels. All the patients except one received peritoneal dialysis on the day of surgery. Thirteen patients in the vasopressin (+) group and 7 patients in the vasopressin (-) group continued to require peritoneal dialysis on postoperative day 5 (POD 5) (P = 0.04). The platelet count had decreased to a significantly lower level in the vasopressin (+) group on POD 5 [97 x 10(3)/mm(3) (range: 40-132 x 10(3)/mm(3))]. A tendency toward a high lactate concentration was seen in the vasopressin (+) group. In comparison with the vasopressin (-) group, the number of patients whose lactate level remained above 2.0 mmol/l was higher in the vasopressin (+) group on PODs 2 and 3 (17 patients vs 8 patients, P < 0.01 and 15 patients vs 7 patients, P = 0.01, respectively).. These findings suggest that the intraoperative use of vasopressin extends the period of peritoneal dialysis, reduces platelet counts and delays the recovery of the lactate concentration. Intraoperative vasopressin infusion should not be used routinely, but only in catecholamine-refractory shock.

Topics: Alanine Transaminase; Aspartate Aminotransferases; Biomarkers; Blood Urea Nitrogen; Cardiac Surgical Procedures; Cardiopulmonary Bypass; Chi-Square Distribution; Creatinine; Drug Administration Schedule; Heart Defects, Congenital; Hemodynamics; Hemostasis; Humans; Hypotension; Infant; Infusions, Intravenous; International Normalized Ratio; Intraoperative Care; Kidney Diseases; Lactic Acid; Peritoneal Dialysis; Platelet Count; Platelet Transfusion; Retrospective Studies; Risk Factors; Time Factors; Treatment Outcome; Urea; Vasoconstrictor Agents; Vasopressins

A 74-year-old man was diagnosed with nephrotic syndrome due to focal segmental glomerulosclerosis, and steroid therapy was initiated. Subsequently, he was affected by deep mycosis, and hence, voriconazole (VRCZ) was administered. On the 16th day, he was transferred to our hospital because of somnolence and malaise. His systolic blood pressure was approximately 80 mmHg, and he showed decreased skin turgor, indicating volume depletion. Laboratory analysis revealed hyponatremia and liver dysfunction. Discontinuation of VRCZ and drip infusion of normal saline improved the consciousness disorder, hyponatremia, and liver dysfunction. The levels of antidiuretic hormone (ADH) and plasma renin activity were elevated. This patient showed high excreted urine sodium, despite volume depletion and low serum osmolality. Therefore, this patient was diagnosed with salt-losing nephropathy (SLN). SLN should be considered for treatment of VRCZ-associated hyponatremia, together with syndrome of inappropriate secretion of ADH.

Topics: Aged; Antifungal Agents; Biomarkers; Chemical and Drug Induced Liver Injury; Fluid Therapy; Humans; Hyponatremia; Kidney Diseases; Liver; Male; Neurophysins; Protein Precursors; Pyrimidines; Renin; Sodium; Sodium Chloride; Time Factors; Treatment Outcome; Triazoles; Vasopressins; Voriconazole; Water-Electrolyte Balance

Heart failure constitutes a significant source of morbidity and mortality in the United States, and its incidence and prevalence continue to grow, increasing its burden on the healthcare system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This interaction, termed the cardiorenal syndrome, is a complex phenomenon characterized by a pathophysiologic disequilibrium between the heart and the kidney, in which malfunction of 1 organ consequently promotes the impairment of the other. Multiple neurohumoral mechanisms are involved in this cardiorenal interaction, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with the cardiorenal syndrome can be challenging and should be individualized. Emerging therapies must address the function of both organs to secure better clinical outcomes. To this end, a multidisciplinary approach is recommended to achieve optimal results.

Topics: Adenosine; Heart Failure; Humans; Kidney Diseases; Natriuretic Agents; Ultrafiltration; Vasopressins

Topics: Aquaporins; Humans; Kidney; Kidney Diseases; Signal Transduction; Vasopressins

Kidney is thought to be a regenerative organ in terms of repair from acute tubular injury. It is unknown whether cell population contributes to repair disordered kidney. We attempted to identify and isolate highly proliferative cells from a single cell. We dissected a single nephron from adult rat kidney. Isolated nephrons were separated into segments and cultured. Outgrowing cells were replated after limiting dilution so that each well contained a single cell. One of cell line which was the most potent to grow was designated as rKS56. rKS56 cells showed cobblestone appearance and expressed immature cell markers relating to kidney development and mature tubular cell markers. rKS56 cells grew exponentially and could be maintained for 300 days without transformation. In different culture conditions, rKS56 cells differentiated into mature tubular cells defined by aquaporin-1, 2 expression, and responsiveness to parathyroid hormone or vasopressin. Engrafted to kidney in rat ischemic reperfusion model, rKS56 cells replaced in injured tubules in part after implantation and improved renal function. These results suggest rKS56 cells possess character such as self-renewal, multi-plasticity and capability of tissue repair. rKS56 may possibly contribute to the future development of cell therapy for renal regeneration.

Topics: Animals; Aquaporin 1; Aquaporin 2; Arginine Vasopressin; Cell Culture Techniques; Cell Differentiation; Cell Line; Cell Proliferation; Cells, Cultured; Cyclic AMP; Electrophoresis, Polyacrylamide Gel; Epithelial Cells; Immunoblotting; Karyotyping; Keratins; Kidney; Kidney Diseases; Kidney Tubules; Male; Microscopy, Fluorescence; Nephrons; Parathyroid Hormone; Phenotype; Rats; Rats, Sprague-Dawley; Regeneration; Renal Insufficiency; Reperfusion Injury; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Stem Cells; Time Factors; Vasopressins

Topics: Adult; Amphotericin B; Antifungal Agents; Humans; Kidney Diseases; Kidney Tubules; Leukemia, Monocytic, Acute; Liposomes; Male; Sodium; Vasopressins

The antimalaria drug chloroquine is often taken against a background of analgesic nephropathy caused by nonsteroidal anti-inflammatory drugs such as paracetamol (acetaminophen). Chloroquine has marked effects on the normal kidney and stimulates an increase in plasma vasopressin via nitric oxide. The aim of this study was to determine the renal action of chloroquine in a model of analgesic nephropathy. Sprague-Dawley rats (n = 6-8/group) were treated with paracetamol (500 mg kg(-1) day(-1)) for 30 days in drinking water to induce analgesic nephropathy; control rats received normal tap water. Under intraval anesthesia (100 mg kg(-1)) rats were infused with 2.5% dextrose for 3 h to equilibrate and after a control hour they received either vehicle, chloroquine (0.04 mg h(-1)), N(omega)-nitro-L-arginine methyl ester (L-NAME, nitric-oxide synthase inhibitor, 60 micro g kg(-1) h(-1)) or combined chloroquine and L-NAME over the next hour. Plasma was collected from a parallel group of animals for vasopressin radioimmunoassay. Long-term paracetamol treatment resulted in a decrease in glomerular filtration rate (p < 0.05), sodium excretion (p < 0.001), and urine osmolality (p < 0.001), but no change in urine flow rate compared with untreated animals. Chloroquine administration in paracetamol treated rats induced a significant reduction (p < 0.05) in urine flow rate and a significant increase in plasma vasopressin (p < 0.001). These effects were blocked by coadministration of L-NAME and thus seem to be mediated by a pathway involving nitric oxide. However, these responses contrast with the chloroquine-induced diuresis previously observed in untreated rats, possibly reflecting paracetamol inhibition of renal prostaglandin synthesis and consequent moderation of vasopressin's action.

Topics: Acetaminophen; Analgesia; Analgesics, Non-Narcotic; Analysis of Variance; Animals; Chloroquine; Disease Models, Animal; Glomerular Filtration Rate; Kidney Concentrating Ability; Kidney Diseases; Kidney Function Tests; Male; Rats; Rats, Sprague-Dawley; Sodium; Urination; Vasopressins

The effect of orally available, nonpeptide vasopressin V1 and V2 receptor antagonists on chronic progressive glomerular disease was investigated in Wistar rats with Adriamycin-induced nephropathy. At weeks 0 and 3, Adriamycin was injected twice, and at week 3 drugs started to be given as follows: groups 2 and 3 were treated with V1 and V2 antagonists, respectively, while the untreated group 1 served as control. To block the effects of vasopressin totally, both V1 and V2 antagonists were simultaneously administered (group 4). At weeks 8 and 10, V1 and V2 antagonists given either alone or combined significantly reduced the urinary protein excretion to the same levels. Urinary volume increased in groups 3 and 4 from week 4. Systolic blood pressure did not significantly increase in all groups during the study. Histological alterations in the kidney of groups 2, 3 and 4 were significantly attenuated compared to the control. These results suggest that both vasopressin V1 and V2 agonism plays a role in the pathophysiology of Adriamycin-induced nephropathy despite plasma levels of vasopressin within the normal range. These findings also lead to the notion that in some types of nephrotic patients these orally available V1 and/or V2 receptor antagonists may be effective for reduction of proteinuria and for retardation of progression of renal failure.

Topics: Animals; Antibiotics, Antineoplastic; Blood Pressure; Body Weight; Doxorubicin; Eating; Kidney; Kidney Diseases; Male; Proteinuria; Rats; Rats, Wistar; Receptors, Vasopressin; Vasopressins

Symptoms and other abnormalities associated with serum sodium imbalance were studied in bedridden elderly and healthy elderly subjects. 1. A significantly higher number of the bedridden elderly suffered from chronic wasting disease. 2. The average serum sodium concentration in bedridden elderly subjects was significantly lower than in healthy subjects, as was the sodium intake and the sodium content in urine, which indicate that the bedridden elderly subjects suffered from chronic sodium deficiency. 3. The bedridden elderly subjects had high levels of plasma PRA and antidiuretic hormone, and their aldosterone levels were low, which indicate that their condition was associated with a decrease in available circulating plasma, hypersecretion of antidiuretic hormone, and a decline in the ability to retain sodium. 4. Measurement of 24-hr creatinine clearance, albumin, and beta 2-microglobulin in urine revealed that bedridden elderly subjects had high levels of renal dysfunction, the result of which may a disturbance in water excretion. Abnormalities in serum sodium levels in the bedridden elderly subjects were related to a chronic deficiency in sodium intake, which reduced their ability to maintain sodium levels and impaired their renal function. Iatrogenic factors are likely to play an important role in the genesis of this condition, and should be taken into account in during management.

Topics: Aged; Bed Rest; Female; Fluid Therapy; Humans; Iatrogenic Disease; Kidney Diseases; Male; Sodium; Vasopressins; Water-Electrolyte Imbalance

The pathophysiology of renal colic is related to tension exerted on the excretory cavities by an obstruction, generally a stone, causing secretion of prostaglandins which, in turn, increase the renal blood flow and glomerular filtration rate. This results in a vicious circle explaining the effect of fluid restriction and NSAIDs.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Colic; Dinoprostone; Glomerular Filtration Rate; Humans; Kidney Diseases; Renal Circulation; Urinary Calculi; Vasopressins; Water-Electrolyte Balance

The binding of tritium-labelled arginine vasopressin to human platelet vasopressin receptors was investigated in patients with congenital nephrogenic diabetes insipidus. Binding characteristics, that is receptor affinity and the maximum number of binding sites, were not significantly different from those found in normal control individuals. The findings confirm the concept of intact V1 receptors in congenital nephrogenic diabetes insipidus. The defect in nephrogenic diabetes insipidus apparently only affects the cyclic adenosine monophosphate dependent V2 receptors.

Topics: Adolescent; Adult; Arginine Vasopressin; Binding Sites; Blood Platelets; Child; Diabetes Insipidus; Humans; Kidney Diseases; Receptors, Vasopressin; Vasopressins

In congenital nephrogenic diabetes insipidus (NDI) blunted responses of plasma factor VIII, von Willebrand factor, and plasminogen activator to the synthetic V2 analogue 1-desamino-8-D-arginine vasopressin (DDAVP) have been reported. In addition, vasodilatory responses to DDAVP appear to be absent in NDI. We describe a boy, who presented shortly after birth with the typical features of NDI, but who showed normal coagulation, fibrinolytic and vasodilatory responses to DDAVP. We conclude that in this patient the defect is confined to the kidney, while in other NDI patients there may be a general V2 receptor abnormality. These findings point to heterogeneity in NDI.

Topics: Diabetes Insipidus; Humans; Infant, Newborn; Kidney Diseases; Male; Receptors, Angiotensin; Receptors, Vasopressin; Vasopressins

No study has, to our knowledge, evaluated the acute effects of low immunosuppressive doses of cyclosporin (CsA) on renal function. To establish whether a relationship exists between the dosage of CsA and the onset of nephrotoxicity, 28 rats were studied by renal clearances before (control) and after i.v. administration of different doses of CsA: 3 mg/kg b.w. (group 1); 7 mg/kg b.w. (group 2); 11 mg/kg b.w. (group 3); 15 mg/kg b.w. (group 4). No change in renal function was observed between control and the post-CsA period in groups 1 and 2. GFR (inulin clearance) was decreased vs the control period in group 3 and group 4 (-22% and -37%, respectively, P less than 0.001); the difference between these two groups was statistically significant (P less than 0.01). Effective renal plasma flow (PAH clearance) was similarly decreased in groups 3 and 4 vs their control periods (-21% and -28%, respectively, P less than 0.001) due to the increase of total renal vascular resistance (+41% and +42%, respectively, P less than 0.001). Filtration fraction was significantly decreased by CsA in group 4 (P less than 0.01 vs the control period). PAH renal extraction, urinary volume, and sodium and potassium excretion were similar in all groups before and after CsA. PRA and ADH were significantly increased only in group 4 (P less than 0.01) vs the baseline values. A high and significant relationship was detected between CsA dosage and the decrease of GFR (r = 0.81, P less than 0.001) and RPF (r = 0.612, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Animals; Blood Pressure; Body Weight; Cyclosporins; Glomerular Filtration Rate; Hematocrit; Kidney Diseases; Male; Potassium; Rats; Rats, Inbred Strains; Renal Circulation; Sodium; Vasopressins

Topics: Hepatorenal Syndrome; Humans; Kidney Diseases; Kidney Failure, Chronic; Liver Cirrhosis, Alcoholic; Ornipressin; Vasopressins

In nine patients with decompensated alcoholic cirrhosis of the liver and impaired renal function the effect of 8-ornithin vasopressin (ornipressin) on renal function and haemodynamic parameters was studied. Ornipressin was infused at a dose of 6 IU/h over a period of four hours. During ornipressin infusion an improvement of renal function was achieved as indicated by an increase of creatinine clearance (76 (15)%; p less than 0.01), urine volume (108 (29)%; p less than 0.05) and sodium excretion (168 (30)%; p less than 0.05). The hyperdynamic circulation of hepatic failure, as characterised by increased cardiac index and heart rate as well as decreased systemic vascular resistance was reversed to a nearly normal circulatory state during ornipressin infusion. The raised noradrenaline plasma concentration (1.74 (0.31) ng/ml) and plasma renin activity (13.5 (3.9) ng/ml/h) were lowered during ornipressin infusion to 0.87 (0.21) ng/ml and 5.9 (2.1) ng/ml/h, respectively (p less than 0.01). The efficacy of a vasoconstrictor agent in reverting a hyperdynamic state and improving renal function provides evidence for the substantial role of accumulation of vasodilator substances and subsequent activation of sympathetic nervous system and renin-angiotensin-axis in the pathogenesis of renal dysfunction in hepatic failure. Values are expressed as mean (SE).

Topics: Female; Glomerular Filtration Rate; Humans; Kidney; Kidney Diseases; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Norepinephrine; Ornipressin; Renin; Vasopressins

A decline in renal function, similar to mild chronic renal insufficiency, normally occurs in the elderly concomitantly with various anatomic and histologic changes in the kidney. These morphologic and physiologic changes result in diminished ability to respond to body fluid or solute stresses. Superimposition of chronic renal insufficiency upon these age-related physiologic changes can accelerate renal functional decline. However, with proper management, most elderly patients with renal disease can remain highly functional.

Topics: Aged; Aged, 80 and over; Aging; Creatinine; Glomerular Filtration Rate; Humans; Kidney Diseases; Primary Health Care; Vasopressins

Topics: Brain Diseases; Calcinosis; Child, Preschool; Diabetes Insipidus; Humans; Kidney Diseases; Male; Vasopressins

Topics: Bone Marrow Transplantation; Bronchial Neoplasms; Carcinoma, Small Cell; Cyclophosphamide; Dehydration; Diabetes Insipidus; Humans; Kidney Diseases; Liver Neoplasms; Male; Middle Aged; Vasopressins

The pathogenesis of hyponatremia remains debated; therefore, we determined the roles of plasma vasopressin, fluid intake and renal free water excretion in hyponatremic medical patients. We evaluated 100 consecutive hypo-osmolar hyponatremic patients (PNa = 127 +/- 0.7 mM l-1) in a prospective manner. We observed: hyponatremia was often found in association with advanced congestive cardiac failure (twenty-five of 100 patients), liver cirrhosis (16%) and primary volume contraction (29%). There was a 17% in-hospital mortality of hyponatremic patients. This was primarily related to the severity of underlying illnesses rather than to hyponatremia per se. The most consistently observed laboratory finding of hyponatremia was non-osmotic vasopressin stimulation; mean observed PADH was 4.7 +/- 0.7 pg ml-1 and vasopressin was detectable by radioimmunoassay (RIA) in 91% of all patients. In addition to vasopressin stimulation we also found evidence of advanced 'circulatory underfilling' in most hyponatremic patients. Mean urinary osmolality was hypertonic to plasma (441 +/- 17.4 m0sm kg H2O-1). This applied to patients with hyponatremic cardiac failure, liver cirrhosis and volume contraction. Almost all of these patients received high ceiling diuretics. (v) Spontaneous mean daily fluid intake was 2.4 +/- 0.2 l. In summary, our findings suggest that disturbances of vasopressin, fluid intake and renal free water excretion co-operate in the pathogenesis of hyponatremia. In clinical states of advanced circulatory underfilling the occurrence of hyponatremia indicates a poor prognosis of the patient.

Topics: Aged; Drinking; Female; Heart Failure; Humans; Hyponatremia; Kidney Diseases; Liver Cirrhosis; Male; Middle Aged; Vasopressins

In four boys with congenital nephrogenic diabetes insipidus, plasma arginine-vasopressin (AVP) and urinary excretion of prostaglandins were studied in response to treatment with hydrochlorothiazide and indomethacin. An abnormal relationship between AVP and urine osmolality was demonstrated in all patients. In the first patient, treatment with indomethacin (3 mg/kg per day) resulted in a drop of the insulin and paraminohippurate clearances. In the other three patients urinary excretion of PGE2 was raised, and fell during treatment with hydrochlorothiazide (2 mg/kg per day) and indomethacin (2 mg/kg per day). Urine flow, free water clearance and osmolar clearance decreased during treatment. A combination of both drugs is more effective than hydrochlorothiazide alone and the effect appears to be additive.

Topics: Child; Child, Preschool; Diabetes Insipidus; Humans; Hydrochlorothiazide; Indomethacin; Infant; Kidney Diseases; Male; Prostaglandins; Vasopressins

A case of transient nephrogenic diabetes insipidus occurred in late pregnancy, the first associated with biopsy-proven hepatitis. Five previously reported cases occurred in pregnancy. All six patients demonstrated similar but transient signs, symptoms and laboratory abnormalities suggesting a syndrome peculiar to pregnancy. The characteristics of this syndrome are elevated liver function studies, decreased renal function, hyperuricemia and transient vasopressin-resistant diabetes insipidus.

Topics: Adult; Diabetes Insipidus; Female; Hepatitis; Humans; Kidney Diseases; Pregnancy; Pregnancy Complications; Pregnancy Trimester, Third; Uric Acid; Vasopressins; Water-Electrolyte Balance

When comparing iatrogenic inhibition with endogenous stimulation of renal prostaglandin production, the role of this mediator and modulator system for renal function becomes apparent. Renal perfusion and glomerular filtration as well as modulation of tubular function with respect to electrolyte and water excretion is significantly influenced by renal prostaglandin activity. Treatment with the prostaglandin cyclooxygenase inhibitor indomethacin reduces the endogenous creatinine clearance by about fifty percent in a state of a diminished circulatory blood volume, such as may exist during left-to-right shunting across a persistent ductus arteriosus in preterm infants. In addition, urinary electrolyte and water excretion is reduced by increased tubular absorption leading to marked oliguria. In contrast, electrolytes and water are lost in congenital renal tubular disorders associated with increased prostaglandin E2 (PGE2) activity (a so called hyperprostaglandin E syndrome). Patients with this renal disorder require a permanent high dosed indomethacin therapy. After this pharmacotherapy has brought electrolyte and water metabolism into balance, no deterioration of glomerular filtration and renal perfusion was observed. This is in accordance with the general principle that renal function only becomes dependent on the vasodilatory activity of renal prostaglandins in a stress situation resulting in the threat of hypoperfusion. It is essential to bear in mind the physiological and pathophysiological role of renal prostaglandins, when prescribing frequently administered prostaglandin cyclooxygenase inhibitors like aspirin, paracetamol or indomethacin in pediatrics. Otherwise, renal function may deteriorate or the kidney will be irreversibly damaged.

Topics: Angiotensin II; Aspirin; Child, Preschool; Creatinine; Ductus Arteriosus, Patent; Glomerular Filtration Rate; Humans; Indomethacin; Infant; Infant, Newborn; Infant, Premature, Diseases; Kidney Diseases; Kidney Function Tests; Oliguria; Prostaglandins; Prostaglandins E; Renal Circulation; Renin-Angiotensin System; Vasopressins; Water-Electrolyte Balance

Persistent, severe renal hemorrhage resulted from a diagnostic renal biopsy in a 19-year-old woman with chronic renal insufficiency. Infusion of vasopressin into the renal artery through an angiographic catheter produced prompt resolution of bleeding. This method has distinct advantages over surgical intervention or transcatheter embolization in the control of traumatic renal hemorrhage.

Topics: Adult; Biopsy, Needle; Female; Hemorrhage; Humans; Infusions, Intra-Arterial; Kidney; Kidney Diseases; Radiography; Renal Artery; Vasopressins

Topics: Amyloidosis; Arginine Vasopressin; Diuresis; Familial Mediterranean Fever; Humans; Kidney Concentrating Ability; Kidney Diseases; Mannitol; Vasopressins

Topics: Animals; Body Water; Diabetes Insipidus; Diagnosis, Differential; Dog Diseases; Dogs; Drinking; Kidney; Kidney Concentrating Ability; Kidney Diseases; Polyuria; Thirst; Vasopressins

Topics: Amino Acids; Ammonia; Blood Urea Nitrogen; Child; Electrolytes; Humans; Kidney Diseases; Reye Syndrome; Urea; Vasopressins

Topics: Animals; Kidney Concentrating Ability; Kidney Diseases; Kidney Function Tests; Phenolsulfonphthalein; Vasopressins; Water Deprivation

In five hyponatremic, cirrhotic patients, demeclocycline hydrochloride was used to inhibit the hydroosmotic effect of vasopressin. In four, renal impairment developed during the 7 to 20 days of demeclocycline hydrochloride (900 to 1,200 mg/day) administration. In these four patients, creatinine clearance fell (72 to 20 mL/min, P less than .01) as BUN (12 to 47 mg/dl, P less than .02) and serum creatinine (0.9 to 4.2 mg/dl, P less than .01) levels rose. The azotemic effect of the drug could not be accounted for consistently by volume depletion secondary to its natriuretic effect. However, a close correlation between plasma demeclocycline levels and its azotemic effect was observed. We conclude that a nephrotoxic effect of demeclocycline severly limits its usefulness in treating hyponatremia in the cirrhotic patient.

Topics: Adult; Creatinine; Demeclocycline; Glomerular Filtration Rate; Humans; Hyponatremia; Kidney; Kidney Diseases; Liver Cirrhosis, Alcoholic; Male; Natriuresis; Vasopressins

Topics: Adult; Diabetes Insipidus; Drug Resistance; Gout; Humans; Hydronephrosis; Kidney Diseases; Male; Vasopressins

The use of various vasoactive drugs in the angiographic investigation of renal pathology is discussed. It is concluded that vasoconstrictors (e.g., angiotensin) are to be preferred in order to demonstrate neovascularity, whereas vasodilators yield more information about "medical diseases" of the kidney. In spite of the increased use of noninvasive techniques such as ultrasound and computed tomography, it is suggested that pharmacoangiography will still remain a valuable tool in the diagnostic armamentarium of urologic radiologists.

Topics: Acetylcholine; Adolescent; Adult; Angiotensin II; Animals; Contrast Media; Dogs; Epinephrine; Humans; Kidney Diseases; Male; Radiography; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Topics: Extracellular Space; Homeostasis; Humans; Hyponatremia; Kidney Diseases; Kidney Glomerulus; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Child; Diabetes Insipidus; Female; Humans; Kidney Diseases; Male; Osmotic Pressure; Sodium Chloride; Urea; Vasopressins

Polyuria and polydipsia developed in two cases during amphotericin B therapy for deep mycoses. Neither patient could concentrate his urine in response to water deprivation or exogenous vasopressin. Other causes of vasopressin-resistant nephrogenic diabetes insipidus were not present. Three months after amphotericin B therapy had been discontinued, concentrating ability improved toward normal. A third patient was further observed and demonstrated normal diluting capacity but impaired free-water reabsorption, suggesting a distal tubular defect consistent with nephrogenic diabetes insipidus. Four months after discontinuing therapy, renal concentrating ability was normal. Amphotericin B can induce a reversible form of nephrogenic diabetes insipidus.

Topics: Amphotericin B; Diabetes Insipidus; Humans; Kidney Concentrating Ability; Kidney Diseases; Male; Middle Aged; Osmolar Concentration; Urine; Vasopressins; Water Deprivation

A 6-week-old girl with fever, hypernatraemia, dehydration, and polyuria failed to concentrate urine in response to exogenous vasopressin administration. There was no family history of nephrogenic diabetes insipidus. When she was 15 months old, the infusion of vasopressin did not produce an increase in urinary cyclic-AMP.

Topics: Cyclic AMP; Diabetes Insipidus; Female; Humans; Infant; Kidney Diseases; Vasopressins

Urinary excretion of cyclic adenosine monophosphate (cAMP) is assessed in response to pitressin stimulation in three patients with nephrogenic diabetes insipidus, four carriers and seven controls. There is no significant difference in cAMP excretion between these groups when corrected for surface area, nor is there any significant increase in excretion after pitressin stimulation. There is very close correlation between urinary cAMP and both urinary concentration and urinary creatinine excretion. Urinary cAMP after pitressin stimulation does not discriminate between carriers of nephrogenic diabetes insipidus and control subjects.

Topics: Adult; Child; Child, Preschool; Creatinine; Cyclic AMP; Diabetes Insipidus; Female; Genetic Carrier Screening; Humans; Kidney Diseases; Male; Vasopressins

The concept of the "inappropriate" has a well-defined and easily comprehended meaning when applied to tumour secretion of antidiuretic hormone (A.D.H., vasopressin). When applied to high A.D.H. in other situations such as nephrotic syndrome, congestive cardiac failure, or cirrhosis, the use of the term "inappropriate secretion" simply reflects the fact that an easily measured controlling factor (plasma tonicity) is being overridden by a less easily measured one (effective extracellular volume). Similarly, sodium excretion in hypertension is said to be inappropriately low for the raised renal perfusion pressure: in this case inappropriateness results from the antinatriuretic effect of a minor degree of sodium depletion produced by pressure natriuresis. A similar objection can be made to the application of the term to the relations between renin or angiotensin-II concentrations and blood-pressure in some forms of hypertension. Since inappropriateness merely reflects the position and predilections of the observer, the widespread use of the term should be abandoned.

Topics: Angiotensin II; Animals; Blood Pressure; Diet; Diet, Sodium-Restricted; Humans; Hypertension; Hypertension, Renal; Kidney; Kidney Diseases; Models, Biological; Natriuresis; Paraneoplastic Endocrine Syndromes; Rats; Renin; Research; Sodium; Terminology as Topic; Vasopressins

Topics: Blood Volume; Female; Humans; Hypercalcemia; Kidney Diseases; Lupus Erythematosus, Systemic; Nephrotic Syndrome; Potassium Deficiency; Retroperitoneal Fibrosis; Urogenital Neoplasms; Vasopressins

The concentration of serum sodium is determined by the external balance of water. Hyponatremia occurs when total body water is in excess of sodium, and hypernatremia develops when body water is relatively decreased in relation to sodium. Both disorders may be present in patients with various disease states in which total body sodium is either decreased, normal or increased. The symptomatology in both disorders is related to the disturbance in central nervous system due to brain edema in patients with hyponatremia and brain dehydration, and cerebrovascular hemorrhages in patients with hypernatremia. The treatment of hypo and hypernatremia is achieved by correcting the abnormalities in body water content.

Topics: Adult; Blood Volume; Edema; Endocrine System Diseases; Humans; Hypernatremia; Hyponatremia; Infant; Kidney Concentrating Ability; Kidney Diseases; Syndrome; Thirst; Vasopressins; Water; Water Loss, Insensible

Topics: Adolescent; Adult; Brain Injuries; Brain Neoplasms; Child; Child, Preschool; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuresis; Female; Humans; Kidney Diseases; Male; Vasopressins

Topics: Adolescent; Adult; Chromium; Diuresis; Female; Glomerulonephritis; Humans; Hypertension; Kidney; Kidney Diseases; Kidney Function Tests; Male; Mannitol; Middle Aged; Nephrotic Syndrome; Pyelonephritis; Vasopressins

The influence of antidiuretic hormone (ADH) and papaverine on hydroxyquinoline-induced nephropathy in rats was tested, using histotopochemistry, enzyme activity measurement and morphometric investigation. Hydroxyquinoline causes a marked increase in renal weight, the development of wedge-shaped foci with severely dilated tubule segments, and a simultaneous reduction in dehydrogenases, alkaline phosphatase, and alpha-naphthyl esterase. Both ADH and papaverine produced a significant inhibition of renal damage. The subjective findings were quantitatively confirmed by measurement of enzyme activity, using the microscope photometer, and by morphometric studies with the Leitz-Classimat (determination on the basis of the alkaline phosphatase reaction) of the surface percentage of brush border in the proximal tubules. A disturbance of the hairpin counter-current system is to be considered as the cause of the renal lesion. This disturbance is caused by hydroxyquinoline-induced impairment of Na+/K+ transport, especially in the thick ascending limb of Henle's loop. Our results show that the hydroxyquinoline nephropathy can be favourably influenced both by stimulation of water re-absorption and possibly also transepithelial Na+ transport (ADH), and by increasing the blood flow of the arteriolae rectae with a resultant lowering of the intratubular urine concentration (papaverine). The dependency of hydroxyquinoline nephropathy on the phylogenetically determined concentration capacity of the kidney, and the effective influencing of the condition by ADH and papaverine indicate the importance of the degree of efficiency of the medullary countercurrent system in the pathogenesis of this renal lesion.

Topics: Alkaline Phosphatase; Animals; Esterases; Female; Histocytochemistry; Hydroxyquinolines; Kidney; Kidney Diseases; Kidney Tubules, Proximal; Organ Size; Oxidoreductases; Papaverine; Rats; Rats, Inbred Strains; Vasopressins

Topics: Anemia, Sickle Cell; Chronic Disease; Diabetes Insipidus; Diet; Humans; Hydrogen-Ion Concentration; Hypernatremia; Hyponatremia; Kidney; Kidney Concentrating Ability; Kidney Diseases; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

We observed idiopathic light-chain proteinuria in a patient with multiple abnormalities of proximal-tubule transport mechanisms (Fanconi syndrome), nephrogenic diabetes insipidus, and distal renal tubular acidosis. Seventeen of the 19 urinary amino acid levels measured were elevated. Uric acid and phosphate clearances were greater than 60 per cent and 50 per cent, respectively, of the simultaneous inulin clearance. When water deprivation was coupled with vasopressin administration, the maximum urinary concentration observed was 384 mOsm per kilogram of water. During ammonium-chloride loading, the level of hydrogen-ion concentration in the urine remained less than 100 times that in the blood. Kappa light-chain excretion was 149 mg per 24 hours. It appears that the concurrence of proximal tubular dysfunction, distal tubular dysfunction and light-chain proteinuria represents a distinct syndrome, which we call "combined light-chain nephropathy." Available evidence indicates that excessive light-chain production with subsequent filtration, reabsorption and catabolism, causes the complex tubular dysfunctions observed.

Topics: Acidosis, Renal Tubular; Ammonium Chloride; Bence Jones Protein; Diabetes Insipidus; Fanconi Syndrome; Female; Follow-Up Studies; Humans; Immunoglobulin kappa-Chains; Immunoglobulin Light Chains; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubules; Kidney Tubules, Distal; Middle Aged; Proteinuria; Renal Aminoacidurias; Syndrome; Vasopressins

Topics: Animals; Biological Transport, Active; Capillary Permeability; Humans; Kidney; Kidney Concentrating Ability; Kidney Diseases; Kidney Medulla; Kidney Tubules; Loop of Henle; Models, Biological; Osmolar Concentration; Osmotic Pressure; Rabbits; Sodium Chloride; Vasopressins; Water

Topics: Diabetes Insipidus; Diagnosis, Differential; Humans; Kidney Diseases; Pituitary Gland, Posterior; Psychophysiologic Disorders; Vasopressins; Water-Electrolyte Balance

We have studied the effects of demeclocycline on the water metabolism of a patient with the syndrome of inappropriate antidiuretic hormone (ADH) secretion who presented with a serum sodium concentration of 110 meq/litre. Free water clearance was studied before, during, and after treatment with demeclocycline. This study shows that demeclocycline (900 mg/day) can at least partially inhibit the action of ADH in the setting of tumor-induced ADH secretion, with the production of a reversible, partial nephrogenic diabetes insipidus, and with few or no side effects. Demeclocycline may be useful in the treatment of chronic inappropriate ADH secretion.

Topics: Carcinoma, Small Cell; Demeclocycline; Diabetes Insipidus; Humans; Hyponatremia; Kidney Diseases; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Syndrome; Urine; Vasopressins

Topics: Adult; Ambulatory Care; Czechoslovakia; Female; Humans; Kidney Concentrating Ability; Kidney Diseases; Male; Middle Aged; Vasopressins

1. Healthy subjects, given a long-acting preparation of vasopressin intramuscularly, excreted a significantly less concentrated urine than when subjected to fluid deprivation for 28 h. 2. When fludrocortisone, a potent mineralocorticoid, was given in addition to vasopressin the urine was not significantly less concentrated than after fluid deprivation. 3. Oral urea-loading also enhanced the urine-concentrating power of vasopressin but its effect was less marked than that of fludrocortisone. Oral urea did not increase further the urine concentration achieved by combined fludrocortisone and vasopressin. 4. Renal concentrating power was assessed in fourteen patients with renal disease and impaired concentrating ability. Fludrocortisone significantly enhanced the urine concentration achieved by vasopressin alone and the resultant urine was not significantly less concentrated than that achieved by fluid deprivation. 5. The action of fludrocortisone in enhancing the urine-concentrating effect of vasopressin is similar to that of aldosterone and is probably due to the increased sequestration of solute in the renal medulla, caused by increased reabsorption of sodium chloride in the ascending limb of the loop of Henle. 6. In the clinical assessment of renal concentrating power, the combined use of fludrocortisone and vasopressin has potential advantages over established methods.

Topics: Adolescent; Adult; Aged; Creatinine; Female; Fludrocortisone; Humans; Kidney Concentrating Ability; Kidney Diseases; Male; Middle Aged; Osmolar Concentration; Time Factors; Urea; Urinary Bladder; Vasopressins; Water Deprivation

Nephrogenic diabetes insipidus associated with high basal levels of plasma arginine vasopressin developed in a patient during lithium therapy. Fluid deprivation was accompanied by an increase in the concentration in peripheral venous plasma of vasopressin and angiotensin II, a rise in plasma osmolality and a modest rise in urine osmolality. Infusion of arginine vasopressin produced comparable levels of plasma vasopressin to those found during fluid deprivation, with no overall change in plasma angiotensin II and little change in urine volume or osmolality. It is suggested that angiotensin II may be responsible for the difference in ability to concentrate urine under these two conditions. Following death by self-poisoning, renal histology revealed distinct structural changes in the distal tubules: such lesions have not previously been described in man and it is suggested that the occurrence of nephrogenic diabetes insipidus while on lithium therapy may be related to tubular damage.

Topics: Adult; Angiotensin II; Arginine Vasopressin; Diabetes Insipidus; Humans; Kidney Diseases; Kidney Tubules, Distal; Lithium; Male; Osmolar Concentration; Vasopressins

Topics: Diagnosis, Differential; Humans; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubules; Osmolar Concentration; Polyuria; Vasopressins

Renal function studies were done in five children with infantile polycystic disease (IPCD)of kidneys and liver and in four with congenital hepatic fibrosis (CHF). Glomerular filtration rate was reduced in all IPCD patients and in two of four CHF patients. Urinary concentrating ability following water deprivation and vasopressin administration was impaired in all IPCD patients and in three of four CHF patients. During control period, all patients had asymptomatic metabolic acidosis with total carbon dioxide content less than or equal to 20.5 millimols/liter, and net acid excretion (NAE) was reduced in all but one. Ammonium chloride was administered to seven patients; NAE increased in all, but the increments were subnormal in four. The inability to excrete maximally concentrated urine and an adequate amount of net acid may best be explained by abnormal tubular structure or alterations in medullary architecture secondary to progressive scarring, or both.

Topics: Acidosis, Renal Tubular; Adolescent; Ammonium Chloride; Child; Child, Preschool; Cystic Fibrosis; Female; Glomerular Filtration Rate; Humans; Infant; Kidney Concentrating Ability; Kidney Diseases; Kidney Function Tests; Liver Cirrhosis; Male; Vasopressins; Water Deprivation

Topics: Diabetes Insipidus; Diagnosis, Differential; Humans; Kidney Concentrating Ability; Kidney Diseases; Osmolar Concentration; Vasopressins

The age-dependent polydipsia and polyuria observed in SWR/J mice was found to be caused by relative inability of the kidneys to respond to antidiuretic hormone (ADH), resulting in a concentrating defect, which persisted even following Pitressin injection or water deprivation. Posterior pituitaries contained large amounts of ADH, which was also found in the urine and increased in output following water deprivation, indicating normal, or above normal synthesis and release of ADH. Kidneys of polydipsic SWR/J mice weighed more than those of normal strains and sometimes contained a lesion in the medullary area. No clear relationship was found between the size of the lesion and water intake.

Topics: Animals; Diabetes Insipidus; Disease Models, Animal; Drinking; Female; Kidney Concentrating Ability; Kidney Diseases; Male; Mice; Mice, Inbred Strains; Organ Size; Osmolar Concentration; Pituitary Gland; Species Specificity; Vasopressins; Water Deprivation

In uncharacteristic clinical symptomatology the excess of water or the water intoxication render themselves conspicuous less by the signs of an increased fluid content than by central-nervous disturbances. Among the results of laboratory examinations the hypoosmolarity measured cryoscopically always, the hyponatraemia in most cases prove the excess of free water. Exceptions are discussed. A decreased capacity of the elimination of water pathogenetically plays a larger role than primarily excessive water supply. Apart from acute and chronic renal insufficiency the various forms of the Schwartz-Bartter-syndrome (inadequate ADH-secretion) play an increasingly more important role. The therapy demands the reduction of every supply of free water, the treatment of the evoking cause and only in cases of exception the administration of hypertonic saline solution, at the most dialysis treatment.

Topics: Diabetic Coma; Diagnosis, Differential; Humans; Kidney Diseases; Multiple Myeloma; Osmolar Concentration; Sodium; Vasopressins; Water Intoxication; Water-Electrolyte Balance

Topics: Adenylyl Cyclases; Adult; Child; Child, Preschool; Cyclic AMP; Diabetes Insipidus; Humans; Inulin; Kidney Concentrating Ability; Kidney Diseases; Kidney Function Tests; Male; Metabolic Clearance Rate; Middle Aged; Osmolar Concentration; Vasopressins

Topics: Blood Urea Nitrogen; Diabetes Insipidus; Diet Therapy; Humans; Hydronephrosis; Infant; Kidney Diseases; Male; Osmolar Concentration; Urethra; Urethral Diseases; Urethral Stricture; Urinary Tract Infections; Urography; Vasopressins; Water-Electrolyte Balance

Topics: Amines; Animals; Biological Transport; Carbon Radioisotopes; Dehydration; Disease Models, Animal; Glomerular Filtration Rate; Inulin; Kidney; Kidney Concentrating Ability; Kidney Cortex; Kidney Diseases; Kidney Medulla; Kidney Tubules; Male; Microscopy, Electron; Osmolar Concentration; Photometry; Potassium; Punctures; Quaternary Ammonium Compounds; Rats; Sodium; Thiazoles; Urea; Vasopressins; Water

Topics: Animals; Cat Diseases; Cats; Chronic Disease; Dehydration; Diabetes Insipidus; Hydrochlorothiazide; Kidney Diseases; Male; Urine; Vasopressins

Topics: Adolescent; Age Factors; Child; Female; Humans; Kidney Concentrating Ability; Kidney Diseases; Male; Osmolar Concentration; Vasopressins

Topics: Adolescent; Aminohippuric Acids; Child; Diabetes Insipidus; Diuresis; Glomerular Filtration Rate; Humans; Infant; Inulin; Kidney Concentrating Ability; Kidney Diseases; Kidney Function Tests; Mannitol; Methods; Osmolar Concentration; Potassium; Sodium; Stimulation, Chemical; Vasopressins

Topics: Amiloride; Animals; Biological Transport; Bufo marinus; Choline; Cyclic AMP; Diabetes Insipidus; Drug Interactions; Female; Hydrogen-Ion Concentration; In Vitro Techniques; Kidney Diseases; Lithium; Magnesium; Membrane Potentials; Potassium; Propionates; Sodium; Triamterene; Urinary Bladder; Vasopressins

Topics: Aldosterone; Alkalosis; Angiotensin II; Biopsy; Blood Pressure; Child, Preschool; Diet Therapy; Female; Follow-Up Studies; Growth Disorders; Humans; Hyperaldosteronism; Hyperplasia; Hypertrophy; Hypokalemia; Juxtaglomerular Apparatus; Kidney Concentrating Ability; Kidney Diseases; Norepinephrine; Potassium; Renin; Secretory Rate; Sodium Chloride; Spironolactone; Syndrome; Vasopressins

Topics: Anesthesia, Inhalation; Blood Urea Nitrogen; Body Weight; Creatinine; Drug Synergism; Fluorides; Gentamicins; Humans; Kidney Diseases; Male; Methoxyflurane; Middle Aged; Osmolar Concentration; Postoperative Complications; Uric Acid; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Acetaminophen; Creatinine; Glomerular Filtration Rate; Humans; Kidney Diseases; Kidney Tubules; Vasopressins

Topics: Animals; Blood Proteins; Diabetes Insipidus; Diagnosis, Differential; Dog Diseases; Dogs; Hydrochlorothiazide; Kidney Diseases; Leukocyte Count; Male; Osmolar Concentration; Phenolphthaleins; Polyuria; Specific Gravity; Thirst; Urine; Vasopressins

Topics: Adolescent; Diabetes Insipidus; Diuretics; Female; Humans; Hydrochlorothiazide; Hydronephrosis; Hypertrophy; Infant; Kidney Diseases; Male; Postoperative Complications; Sodium; Ureteral Obstruction; Ureterocele; Urinary Bladder Diseases; Urography; Vasopressins; Water

Topics: Adolescent; Albumins; Body Water; Chronic Disease; Circadian Rhythm; Dehydration; Diabetes Insipidus; Glucose Tolerance Test; Humans; Hypernatremia; Hypogonadism; Hypothalamus; Intellectual Disability; Kidney Diseases; Male; Obesity; Polyuria; Renin; Sodium; Thirst; Vasopressins

Topics: Age Factors; Animals; Colorimetry; Diabetes Insipidus; Diuresis; Drug Resistance; Genotype; Kidney; Kidney Concentrating Ability; Kidney Diseases; Mathematics; Methods; Mice; Mice, Inbred Strains; Osmolar Concentration; Photometry; Potassium; Sodium; Species Specificity; Urea; Urine; Vasopressins

Topics: Acid-Base Equilibrium; Blood Cell Count; Cortisone; Depression; Diabetes Insipidus; Diuresis; Electrocardiography; Heart Failure; Hemorrhage; Humans; Hypophysectomy; Kidney Diseases; Methods; Pituitary Diseases; Pituitary Neoplasms; Postoperative Care; Postoperative Complications; Posture; Preoperative Care; Sodium; Time Factors; Vasopressins

Topics: Adult; Diabetes Insipidus; Facial Injuries; Female; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Kidney Diseases; Male; Natriuresis; Vasopressins; Water Deprivation; Water-Electrolyte Balance

Ectopic production of polypeptide hormones by tumors of nonendocrine tissues can serve as a clue to diagnosis of the tumor and as a focus for management of the patient with cancer. In the differential diagnosis of syndromes of endocrine hyperfunction, the ectopic hormone syndromes have achieved an increasingly prominent position. Available evidence on the properties of ectopic ACTH, MSH, parathyroid hormone, erythropoietin, gonadotropins, and thyrotropin is consistent with the unifying hypothesis of genetic derepression.

Topics: Abdominal Neoplasms; Adenocarcinoma; Adrenocortical Hyperfunction; Brain Neoplasms; Carcinoma, Bronchogenic; Carcinoma, Hepatocellular; Carcinoma, Small Cell; Cysts; Diagnosis, Differential; Fibroma; Hemangiosarcoma; Humans; Hyperparathyroidism; Hypoglycemia; Kidney Diseases; Kidney Neoplasms; Liver Neoplasms; Lung Neoplasms; Paraneoplastic Endocrine Syndromes; Pheochromocytoma; Polycythemia; Sarcoma; Thoracic Neoplasms; Vasopressins

Topics: Aldosterone; Anemia; Anuria; Child; Child, Preschool; Diuresis; Diuretics; Glomerulonephritis; Humans; Infant; Kidney; Kidney Concentrating Ability; Kidney Diseases; Osmolar Concentration; Osmotic Pressure; Polyuria; Pyelonephritis; Thalassemia; Vasopressins; Water; Water-Electrolyte Balance

Topics: Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; Animals; Corticotropin-Releasing Hormone; Dehydration; Diabetes Insipidus; Female; Formaldehyde; Hypertrophy; Hypothalamo-Hypophyseal System; Hypothalamus; Karyometry; Kidney Diseases; Male; Melanocyte-Stimulating Hormones; Mice; Neurosecretion; Organ Size; Pituitary Gland; Pituitary-Adrenal System; Stress, Physiological; Vasopressins

Topics: Adult; Aged; Blood Circulation Time; Blood Flow Velocity; Bradykinin; Female; Humans; Kidney; Kidney Diseases; Kidney Diseases, Cystic; Kidney Neoplasms; Male; Middle Aged; Radiography; Regional Blood Flow; Renal Artery; Technology, Radiologic; Vasopressins

Topics: Adolescent; Adult; Child; Child, Preschool; Circadian Rhythm; Female; Humans; Kidney Diseases; Male; Middle Aged; Urination; Vasopressins; Water

Topics: Acute Kidney Injury; Adult; Bacteriuria; Biopsy; Creatinine; Female; Follow-Up Studies; Glomerular Filtration Rate; Humans; Hydrogen-Ion Concentration; Kidney; Kidney Concentrating Ability; Kidney Diseases; Kidney Function Tests; Male; Middle Aged; Phenolphthaleins; Time Factors; Urine; Urography; Vasopressins

Topics: Adolescent; Adult; Ammonia; Child; Creatinine; Female; Humans; Hydrogen-Ion Concentration; Kidney Concentrating Ability; Kidney Diseases; Kidney Function Tests; Male; Methods; Middle Aged; Phenolphthaleins; Urea; Urinary Tract Infections; Urine; Vasopressins

Topics: Adenoma, Chromophobe; Adrenal Gland Neoplasms; Animals; Diabetes Insipidus; Dog Diseases; Dogs; Female; Hepatitis; Hepatitis, Animal; Hypothalamo-Hypophyseal System; Kidney; Kidney Diseases; Male; Ovarian Neoplasms; Testicular Neoplasms; Vasopressins

Topics: Adolescent; Adult; Alkaline Phosphatase; Blood Urea Nitrogen; Calcinosis; Calcium; Chronic Disease; Creatinine; Female; Humans; Hyperparathyroidism; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubules; Male; Middle Aged; Osmolar Concentration; Phosphorus; Potassium; Sodium; Urea; Vasopressins

Topics: Adult; Blood Volume; Blood Volume Determination; Cardiac Output; Cardiovascular System; Diabetes Insipidus; Female; Heart Rate; Humans; Injections, Intravenous; Kidney Diseases; Pregnancy; Pregnancy Complications, Hematologic; Puerperal Disorders; Vascular Resistance; Vasopressins

Topics: Diabetes Insipidus; Female; Humans; Kidney Diseases; Male; Vasopressins

Topics: Diagnosis, Differential; Follow-Up Studies; Glucose; Humans; Kidney Diseases; Kidney Function Tests; Methoxyflurane; Vasopressins

Topics: Diabetes Insipidus; Diabetes Mellitus; Diuresis; Female; Glomerular Filtration Rate; Humans; Hyperthyroidism; Kidney Diseases; Kidney Tubules; Male; Neurotic Disorders; Polyuria; Thirst; Vasopressins

Topics: Amides; Clopamide; Diabetes Insipidus; Diuretics; Female; Furosemide; Humans; Hypertonic Solutions; Kidney; Kidney Concentrating Ability; Kidney Diseases; Male; Middle Aged; Piperidines; Sodium Chloride; Tannins; Vasopressins

Topics: Biopsy; Humans; Kidney Diseases; Radiography; Television; Vasopressins

Topics: Adolescent; Child; Child, Preschool; Cystinosis; Diabetes Insipidus; Diuresis; Glomerulonephritis; Humans; Hydronephrosis; Infant; Infant, Newborn; Kidney Diseases; Kidney Diseases, Cystic; Polyuria; Pyelonephritis; Uremia; Vasopressins

Topics: Adolescent; Adult; Aminohippuric Acids; Animals; Creatinine; Dogs; Female; Humans; Kidney Diseases; Kidney Function Tests; Male; Middle Aged; Vasopressins

Topics: Adult; Diagnosis, Differential; Female; Heart Diseases; Humans; Hyponatremia; Kidney Diseases; Male; Middle Aged; Obesity; Potassium; Potassium Isotopes; Radioisotope Dilution Technique; Sodium; Sodium Isotopes; Vasopressins

Topics: Adult; Aged; Animals; Child; Humans; Kidney Diseases; Middle Aged; Rats; Vasopressins

Topics: Animals; Biological Assay; Humans; Hypertension, Renal; Kidney Diseases; Kidney Function Tests; Plasma; Preoperative Care; Rats; Renal Artery Obstruction; Renal Veins; Vascular Surgical Procedures; Vasopressins

Topics: Biopsy; Black People; Chlorothiazide; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diagnosis, Differential; Humans; Hypercalcemia; Hypertonic Solutions; Kidney Diseases; Pathology; Prednisone; Sarcoidosis; Skin Tests; Vasopressins

Topics: Creatine; Creatinine; Diuresis; Dogs; Fluids and Secretions; Glomerular Filtration Rate; Kidney Diseases; Kidney Function Tests; Kidney Tubules; Nephrectomy; p-Aminohippuric Acid; Physiology; Renal Insufficiency; Research; Urea; Urine; Vasopressins

Topics: Blood Pressure Determination; Diagnosis; Diuresis; Glomerular Filtration Rate; Humans; Hypertension; Hypertension, Renal; Insulin; Kidney; Kidney Diseases; Kidney Function Tests; Natriuresis; Pharmacology; Renal Artery Obstruction; Urea; Vasopressins

Topics: Demeclocycline; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diagnosis; Drug Therapy; Humans; Kidney Diseases; Photosensitivity Disorders; Toxicology; Vasopressins

Topics: Angiotensin II; Diabetes Insipidus; Diet, Sodium-Restricted; Glomerular Filtration Rate; Humans; Hypertension, Malignant; In Vitro Techniques; Kidney Diseases; Male; Middle Aged; Natriuresis; Periodicity; Polyuria; Renin; Vasopressins

Topics: Humans; Hypertension, Renal; Kidney Diseases; Kidney Function Tests; Osmosis; Urine; Vasopressins

Topics: Animals; Dietary Proteins; Kidney Diseases; Phenacetin; Rats; Urea; Vasopressins

Topics: Adult; Animals; Chlorides; Chlorthalidone; Diabetes Insipidus; Diuresis; Female; Humans; Hydrochlorothiazide; Kidney; Kidney Diseases; Male; Mannitol; Middle Aged; Rabbits; Sodium; Urea; Urine; Vasopressins

Topics: Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diarrhea; Diarrhea, Infantile; Humans; Infant; Kidney Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Alcoholic Intoxication; Calcium Metabolism Disorders; Child; Diabetes Insipidus; Diagnosis; Diuresis; Genetics, Medical; Histiocytosis, Langerhans-Cell; Humans; Kidney Diseases; Measles; Polyuria; Prednisone; Psychosomatic Medicine; Sarcoidosis; Syndrome; Thirst; Toxicology; Urine; Vasopressins; Whooping Cough

Topics: Blood Chemical Analysis; Creatine; Creatinine; Early Diagnosis; Inulin; Kidney Diseases; Kidney Function Tests; Nitrogen; Pyelonephritis; Vasopressins

Topics: Diuretics; Edema; Heart Failure; Kidney Diseases; Liver Diseases; Organomercury Compounds; Physiology; Vasopressins

Topics: Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Humans; Kidney Diseases; Kidney Tubules; Vasopressins

The reciprocals of the blood urea nitrogen and plasma creatinine levels, the maximum specific gravity of the urine after vasopressin, and three modified forms of the phenolsulphonphthalein (P.S.P.) excretion test were found to be directly related to the glomerular filtration rate (G.F.R.) in hospital patients. From 34 to 75 patients were studied for each test, and in 21 patients all tests were performed concurrently. The plasma creatinine level and the 15-minute urinary excretion of P.S.P. were found to be the most useful simple tests of renal function and gave sufficiently accurate estimates of total function (G.F.R.) to justify their more extensive use. The G.F.R. (ml./min./1.73 sq. m. of body surface area) could be calculated from each test, using the following equations:- [Formula: see text] G.F.R. = 3.15 x P.S.P.% + 19, where P.S.P.% is the 15-minute urinary excretion of P.S.P., expressed as a percentage of the administered dose. Satisfactory estimates of G.F.R. were also given by the simplified relationships [Formula: see text]. In the presence of impaired renal function more accurate estimates of G.F.R. were obtained from the plasma creatinine and P.S.P. excretion tests (S.D. of estimate 8 and 13 ml./min. respectively). It was thought that these tests could well replace the commonly used blood urea nitrogen estimation as simple tests of renal function.

Topics: Blood Chemical Analysis; Blood Urea Nitrogen; Creatine; Creatinine; Glomerular Filtration Rate; Humans; Kidney Diseases; Kidney Function Tests; Pathology; Phenolphthaleins; Phenolsulfonphthalein; Urea; Vasopressins

Observations are presented on two patients with chronic compulsive polydipsia who showed a relative defect in renal concentrating capacity. After excluding all possible metabolic and renal causes of hyposthenuria and after obtaining normal kidney biopsies, both patients were studied in metabolic balance on a constant diet under the following conditions: (a) dehydration (loss of 3-5% body weight), (b) water loading and response to hypertonic saline, and (c) water loading and response to intravenous vasopressin (Pitressin). Throughout these studies the following parameters were observed: plasma and urine osmolality, glomerular filtration rate (inulin), renal plasma flow (P.A.H.), osmolar clearance and clearance of free water. In both patients the concentration defect was not related to variations in glomerular filtration rate or osmotic load. There was no correlation between the degree of hypoosmolality and the renal concentrating defect. Contrary to reports from other laboratories, restriction of water intake and chronic administration of intramuscular vasopressin did not correct the concentration defect.

Topics: Arginine Vasopressin; Body Weight; Compulsive Behavior; Drinking; Glomerular Filtration Rate; Humans; Inulin; Kidney; Kidney Diseases; Osmolar Concentration; Osmosis; Polydipsia; Polyuria; Saline Solution, Hypertonic; Thirst; Vasopressins

Topics: Acidosis; Acidosis, Renal Tubular; Amino Acids; Humans; Kidney Diseases; Polyuria; Vasopressins

Topics: Autonomic Nerve Block; Carcinoma; Chlorpromazine; Geriatrics; Histocytochemistry; Humans; Kidney Diseases; Lung Neoplasms; Neoplasm Metastasis; Neoplasms; Nitrogen Mustard Compounds; Vasopressins

Topics: Adolescent; Cortisone; Diabetes Mellitus; Diabetes Mellitus, Type 1; Diabetic Angiopathies; Diabetic Retinopathy; Geriatrics; Gonadal Steroid Hormones; Humans; Hypophysectomy; Insulin; Kidney Diseases; Thyroxine; Vasopressins

Topics: Aristolochic Acids; Blood Chemical Analysis; Creatine; Creatinine; Electrolytes; Kidney Diseases; Kidney Tubules; Pathology; Phenanthrenes; Plant Poisoning; Rats; Research; Urea; Urine; Vasopressins

Topics: Arginine Vasopressin; Humans; Kidney Diseases; Nephrotic Syndrome; Vasopressins

Negligible antidiuretic activity (less than 0.17 mU./g.) was found in extracts of the kidneys either of unanaesthetized adult rats in normal water balance or of rats in whose blood a rise of the level of endogenous antidiuretic hormone had been induced by ether anaesthesia. Extracts of the livers of unanaesthetized rats had negligible antidiuretic activity (less than 0.06 mU./g.), but liver extracts from rats anaesthetized with ether showed antidiuretic effects equivalent to 0.74+/-0.24 mU. Pitressin/g. liver. When Pitressin was injected intravenously into unanaesthetized rats, small amounts of antidiuretic activity were occasionally found in the livers and the kidneys of animals killed up to 3 min. after the injection but none in animals killed later. Some 3% of the antidiuretic activity of an injected dose of Pitressin was found in the urine and the "dead space" of the kidneys in rats decapitated 3 min. after the intravenous injection. When Pitressin was added to rat kidney homogenate and the mixture was incubated at 38 degrees , only 0.75% of the initial antidiuretic activity was recovered after 30 min. and less than 0.40% after 60 min. Experiments with "glomerular" and "tubular" fractions of rat kidney indicated that the inactivation was essentially due to tubular tissue. It is suggested that, in the rat, the kidneys and perhaps the liver are not only sites of clearance of the antidiuretic hormone but also sites of irreversible inactivation.

Topics: Animals; Antidiuretic Agents; Arginine Vasopressin; Kidney; Kidney Diseases; Liver; Rats; Vasopressins

Topics: Child; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Humans; Infant; Kidney Diseases; Vasopressins

Topics: Arginine Vasopressin; Blood; Deamino Arginine Vasopressin; Kidney Diseases; Renal Insufficiency, Chronic; Vasopressins

Topics: Diabetes Insipidus; Hormones; Humans; Kidney Diseases; Pituitary Gland; Pituitary Gland, Posterior; Renal Insufficiency, Chronic; Vasopressins; Water

Topics: Arginine Vasopressin; Humans; Kidney Cortex Necrosis; Kidney Diseases; Vasopressins