pituitrin and Kidney-Failure--Chronic

Homeostatic regulation of plasma osmolality (POsm) is critical for normal cellular function in humans. Arginine vasopressin (AVP) is the major hormone responsible for the maintenance of POsm and acts to promote renal water retention in conditions of increased POsm. However, AVP also exerts pressor effects, and its release can be stimulated by the development of effective arterial blood volume depletion. Patients with end-stage renal disease on hemodialysis, particularly those with minimal or no residual renal function, have impaired ability to regulate water retention in response to AVP. While hemodialysis can assist with this task, patients are subject to relatively rapid shifts in volume and electrolytes during the procedure. This can result in the development of transient osmotic gradients that lead to the movement of water from the extracellular to the intracellular space. Hypotension may result-both as a consequence of water movement out of the intravascular compartment, but also from impaired AVP release and inadequate vascular tone. In this review, we explore the evidence for POsm changes during hemodialysis, associations with adverse outcomes, and methods to minimize the rapidity of changes in POsm in an effort to reduce patient symptoms and minimize intra-dialytic hypotension.

Topics: Blood Pressure; Hemodialysis Solutions; Humans; Hypotension; Kidney Failure, Chronic; Neurophysins; Osmolar Concentration; Protein Precursors; Renal Dialysis; Vasopressins; Water-Electrolyte Balance

Arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), is released in response to osmotic and non-osmotic stimuli and plays a key role in many physiologic and pathologic processes. The main function of AVP is the control of fluid homeostasis by inducing water conservation by the kidney, but it also stimulates arteriolar vasoconstriction and the release of adrenocorticotropic hormone (ACTH). These actions are mediated by different AVP receptors located on various target cells. Produced in hypothalamus from a larger precursor, pre-proAVP, AVP is produced in equimolar amounts to copeptin, a glycopeptide with yet unknown biologic function. Copeptin remains stable in plasma and its circulating concentrations correlate directly with those of AVP. Because AVP is unstable in isolated plasma or serum and its half-life is short, copeptin has become an easily measured surrogate marker reflecting vasopressin concentration. Recently, associations between high circulating copeptin and decline in glomerular filtration rate as well as greater risk of new-onset chronic kidney disease (CKD) have been reported. In addition, copeptin has been shown to be associated with increased risk of complications such as myocardial infarction, heart failure, diabetes mellitus and metabolic syndrome. In this brief review, studies on the prognostic value of copeptin measurement in the general population and in CKD are presented and discussed.

Topics: Adrenocorticotropic Hormone; Arginine Vasopressin; Biomarkers; Disease Progression; Female; Gene Expression Regulation; Glomerular Filtration Rate; Glycopeptides; Humans; Hypothalamus; Kidney Failure, Chronic; Male; Prognosis; Receptors, Vasopressin; Sex Factors; Signal Transduction; Vasopressins

Anorexia nervosa (AN) is a serious eating disorder associated with numerous medical complications, including alterations in water balance and impaired osmoregulation.. The aim of this paper is to review the evidence-based literature and discuss the potential pathophysiological mechanisms of impaired osmoregulation observed in patients with AN.. Although limited, the evidence suggests that the pathophysiological mechanisms causing impaired osmoregulation in AN is multifactorial and includes abnormalities in osmoregulation of vasopressin, intrinsic renal defects and the influence of antidepressants often used in the treatment of patients with AN. Physicians treating patients with AN should be aware of this complication and the possible multifactorial etiology contributing to this medical complication.

Topics: Adolescent; Anorexia Nervosa; Antidepressive Agents; Evidence-Based Medicine; Humans; Kidney; Kidney Failure, Chronic; Vasopressins; Water-Electrolyte Imbalance

Concomitant anemia, heart failure, and renal disease can be seen in a large proportion of patients with heart failure. The purpose of this review is to discuss the current definitions and mechanisms involved in this pathophysiological relationship, as well as the potential management and treatment options available for these patients.. Dysfunctional heart can promote the dysfunction of the kidneys through a variety of pathophysiological mechanism, the reciprocal holds true as well. Heart failure has been considered as the most common type of cardiovascular complication seen in patients with renal failure. Central to this relationship lies anemia, which can be the result or the cause of either heart or kidney disease.. Cardiorenal syndrome is a complex condition, which requires the collaboration and resources from cardiology, cardiac surgery, nephrology, and critical care. Of great importance is recognizing the presence of cardiorenal syndrome and appreciating the impact it can play on treatment options and survival.

Topics: Adenosine; Anemia; Chronic Disease; Diuretics; Heart Failure; Hemofiltration; Humans; Kidney Failure, Chronic; Prognosis; Renin-Angiotensin System; Risk Factors; Vasodilator Agents; Vasopressins

Hyponatremia in virtually all patients results from water retention due to an inability to excrete ingested water. In most cases, this defect represents the persistent secretion of ADH (such as in effective circulating volume depletion, and in the syndrome of inappropriate ADH secretion), although free water excretion can also be limited in disorders in which ADH levels may be appropriately suppressed (such as in advanced renal failure, and in primary polydipsia). The symptoms of hyponatremia primarily reflect neurologic dysfunction induced by cerebral edema and are related both to the severity and to the rapidity of reductions in the plasma sodium concentration. The degree of cerebral edema which occurs in acute hyponatremia is much less with chronic hyponatremia, because the brain cells lose solutes, leading to the osmotic movement of water out the cells and less brain swelling. In general, hyponatremia is corrected acutely by giving Na+ to patients who are volume-depleted and by restricting water intake in patients who are normovolemic or edematous. The optimal rate of correction should be defined to prevent the risk of central demyelinating lesions.

Topics: Adrenal Insufficiency; Adult; Brain Edema; Edema; Female; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Models, Biological; Osmolar Concentration; Potassium; Pregnancy; Syndrome; Vasopressins

Ageing of the kidneys has long been associated with a fall in the number of functioning nephrons resulting in a reduction of renal blood flow and glomerular filtration. This narrow concept of age-related changes in renal function has been developed chiefly during the last few years by Brenner et al. on the basis of experimental studies conducted on rodents. According to these authors, the size and frequency of segmental and focal lesions of glomerulosclerosis increase regularly with age, and in its final phase this pathology results in occlusion of glomerular capillaries. Renal ageing, therefore, can be assimilated to the nephron reduction models obtained by surgical ablation. The hypothesis that hypofiltration in certain nephrons is compensated by hyperfiltration in healthy glomerulis, leading to a vicious circle of self-destruction, was then applied to both ageing and experimental renal impairment: the smaller the number of nephrons, the greater the filtration achieved by the remaining nephrons, a process that accelerates the probability of their destruction. Conversely, any attempt to reduce intracapillary pressure or glomerular filtration slows down the progression of renal failure. This hypothesis is supported by experiments showing that reduction of protein intake or chronic inhibition of angiotensin I-converting enzyme activity are truly capable of limiting the progression of glomerulosclerosis induced in rats by partial renal mass ablation. Similarly, prolonged food restriction increases the life expectancy of rodents and almost totally prevents the occurrence of glomerulosclerosis. The experimental finding that degenerative renal lesions do not necessarily develop with age raises the problem of normal and pathological ageing. With an adequate choice of rats' food, strain and sanitary surroundings it is possible to obtain very old animals devoid of occluded glomerular capillaries and loss of nephron. What about the functional and structural changes due to ageing and not to pathology? This question has given rise to numerous studies which concluded, on the whole, that there exists a normal ageing of the kidneys without loss of nephron and that ageing is expressed by the fact that the kidneys have difficulties in adjusting themselves to disturbances in the inner environment. As regards renal functional reserve, response to the antidiuretic hormone in case of water restriction, or stimulation of the renin-angiotensin system in response to decrease of

Topics: Aging; Angiotensin-Converting Enzyme Inhibitors; Animals; Glomerular Filtration Rate; Glomerulosclerosis, Focal Segmental; Hydronephrosis; Hyperparathyroidism; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Nephrons; Rats; Vasopressins

Topics: Animals; Dietary Proteins; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Nephrons; Rats; Risk Factors; Urea; Vasopressins

This paper reviews experimental findings which support the concept that vasopressin (VP) and the process of urine concentration may be involved in the progression of chronic renal failure (CRF). The influence of dietary protein intake on the progression of CRF may also involve VP and the operation of the concentrating process. VP receptors have been identified in glomeruli and VP is able to constrict mesangial cells as does angiotensin II. Acute VP infusion increases the glomerular transcapillary hydraulic pressure difference, and chronic VP infusion increases GFR. In rats with CRF (induced by 5/6 nephrectomy), VP levels were found elevated. In rats with 5/6 nephrectomy, we increased experimentally water intake in order to decrease circulating VP levels, urine concentration, and free water reabsorption. Several indices of progression of CRF, including proteinuria, hypertension and glomerulosclerosis, were significantly reduced, thus suggesting a contribution of VP in progression. Lowering protein intake in CRF could be beneficial because proteins, but not carbohydrates or lipids, produce metabolic end products (mainly urea, ammonia, protons, etc.) that are excreted by the kidney, and concentrated in the urine. In healthy subjects (man or rat), high protein (HP) intake favors urine concentration and causes changes in kidney function and morphology very similar to those induced by chronic VP infusion or water restriction. These changes involve an increase in transport activity of the thick ascending limb (where the initial active step of the concentrating process takes place) and may affect filtration rate and/or glomerular hemodynamics secondarily, by decreasing salt concentration at the macula densa and depressing tubuloglomerular feedback.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Dietary Proteins; Humans; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Vasopressins

The vasoconstrictor and vasopressor actions of vasopressin have been revealed in recent research through the use of highly specific and sensitive radioimmunoassays, employment of peptide antagonists, and comparison with an animal model which has hereditary absence of this hormone, the Brattleboro rat. Factors now known to modify the pressor effect of vasopressin are the baroreflexes, local vascular prostaglandin production, and a specific interaction with angiotensin II. In experimental models the volume retaining, but not the vasoconstrictor effect of vasopressin is necessary for mineralocorticoid-salt hypertension. Vasopressin contributes directly to the increase in arterial pressure of glycerol induced acute renal failure. In nephrectomized rats, plasma vasopressin is elevated and contributes directly to maintenance of pressure. Vasopressin antagonism may reduce arterial pressure in Goldblatt 1 and 2 kidney hypertension and in one genetic model, spontaneously hypertensive rat (SHR), but the peptide is not necessary for hypertension in these models. Plasma vasopressin is reduced in primary aldosteronism, but may be elevated in malignant hypertension. In essential hypertension, there is considerable disagreement among various studies in which plasma vasopressin, urine vasopressin excretion, platelet associated vasopressin, or vasopressin-neurophysin were measured as to whether there is evidence for increased secretion of vasopressin. Only preliminary studies of vasopressin antagonism in clinical hypertension have been reported. At present, there is no conclusive evidence that elevated vasopressin secretion occurs or is necessary for any form of clinical hypertension.

Topics: Acute Disease; Acute Kidney Injury; Animals; Central Nervous System Diseases; Desoxycorticosterone; Humans; Hypertension; Hypertension, Malignant; Hypertension, Renal; Hypertension, Renovascular; Kidney Failure, Chronic; Rats; Rats, Brattleboro; Rats, Inbred SHR; Vasopressins

Topics: Body Water; Diuretics; Extracellular Space; Glucocorticoids; Humans; Hyperlipidemias; Hyponatremia; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Lithium; Lithium Carbonate; Osmolar Concentration; Sodium; Vasodilator Agents; Vasopressins

Topics: Age Factors; Animals; Ascites; Blood; Body Water; Heart Diseases; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Osmolar Concentration; Rats; Renal Dialysis; Ultrafiltration; Vasopressins

Topics: Acid-Base Equilibrium; Animals; Buffers; Calcitonin; Colchicine; Diphosphonates; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Parathyroid Hormone; Phosphates; Rats; Vasopressins; Vitamin D

Nonsteroidal antiinflammatory drugs can adversely affect the kidney. They may induce sodium retention and antagonize the action of diuretics, impair free-water clearance and cause hyponatremia, and prevent aldosterone production and cause hyperkalemic hyperchloremic acidosis. If patients taking these drugs are exposed to a renal insult, acute renal failure becomes more likely. Similarly, patients with chronic renal disease who are taking them appear to be at greater risk of chronic renal failure. However, not all renal effects of nonsteroidal antiinflammatory drugs are adverse. Beneficial effects have been reported in patients with Bartter's syndrome and in those with severe orthostatic hypotension.

Topics: Acidosis; Acute Kidney Injury; Aged; Anti-Inflammatory Agents; Bartter Syndrome; Female; Humans; Hyponatremia; Hypotension, Orthostatic; Ibuprofen; Indomethacin; Kidney; Kidney Failure, Chronic; Lupus Erythematosus, Systemic; Nephrotic Syndrome; Prostaglandin Antagonists; Sodium; Vasopressins

Many hormones initiate their biologic actions by augmenting the intracellular concentrations of 3',5'-adenosine monophosphate (cyclic AMP). The nucleotide has been found in body fluids; its determination in plasma and urine can be performed by a rapid, simple and specific method: the cyclic AMP assay kit of the Radiochemical Centre (Amersham, England). The assay is based on the competition between unlabelled cAMP and a fixed quantity of the tritium labelled compound for binding to a bovine muscle protein which has a high specificity and affinity for cAMP. Different factors must be considered in evaluating the 24 h urinary content of the nucleotide: the renal or extrarenal origin of cAMP and the functional status of the kidneys. In basal conditions the urinary cAMP excretion is significantly correlated with creatinine excretion (n = 67; r = 0.47; p less than 0.001) thus confirming that the most part of cAMP excreted is derived from the plasma by glomerular filtration. Parathyroid hormone (PTH) stimulates adenylate cyclase predominantly in the renal cortex, whereas vasopressin (ADH) stimulated the enzyme in the medulla; thus PTH and ADH could increase the amount of cAMP in the urine from the renal source. In a case of diabetes insipidus and infusion of ADH caused a prompt rise in cAMP urinary excretion. In 5 normals an infusion of bovine synthetic parathyroid hormone caused an increased excretion of cAMP that preceded the phosphaturic response. An infusion of salmon synthetic calcitonin caused a rise in phosphate excretion and no increase in cAMP urinary content. As it concerns the two calciotopic hormones, PTH and CT, it is reasonable to assume that renal receptors are distinct. The 24 h urinary excretion of cAMP in 55 control subjects (3613 +/- 1460 D.S. n moles) was contrasted with the lower excretion in 25 elderly subjects (70-93 years: 1804 +/- 699 n moles), with the high cAMP excretion in a patient with hyperparathyroidism (that fell to normal values following removal of the parathyroid adenoma) and with the low cAMP excretion in patients with primary or surgical hypoparathyroidism. The mean 24 h cAMP excretion in patients with renal insufficiency was significantly decreased when compared to control subjects. These findings and recent reports confirm that the 24 h urinary output of cAMP may be considered an useful index of pharathyroid function in man.

Topics: Adult; Aged; Calcitonin; Circadian Rhythm; Cyclic AMP; Humans; Kidney Failure, Chronic; Parathyroid Diseases; Parathyroid Hormone; Parathyroid Neoplasms; Pseudohypoparathyroidism; Vasopressins

Topics: Acidosis, Renal Tubular; Aldosterone; Ascites; Diuretics; Hepatic Encephalopathy; Humans; Hypokalemia; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules, Distal; Liver Cirrhosis; Liver Transplantation; Sodium; Transplantation, Homologous; Uremia; Vasopressins; Water-Electrolyte Imbalance

Topics: Aging; Angiotensin II; Animals; Atropine; Bartter Syndrome; Bone and Bones; Carbohydrate Metabolism; Cardiovascular Diseases; Drug Hypersensitivity; Gastric Mucosa; Gastrointestinal Diseases; Heart; Hematologic Diseases; Humans; Kidney Failure, Chronic; Parathyroid Diseases; Parathyroid Hormone; Pharmaceutical Preparations; Rabbits; Rats; Thyroid Diseases; Uremia; Vasopressins; Vitamin D

Topics: Addison Disease; Ascites; Edema; Extracellular Space; Heart Failure; Humans; Hyponatremia; Intestinal Secretions; Kidney Failure, Chronic; Liver Cirrhosis; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

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: Acute Kidney Injury; Animals; Blood; Cardiac Glycosides; Dehydration; Diuretics; Glomerular Filtration Rate; Heart Failure; Hyponatremia; Kidney Failure, Chronic; Liver Cirrhosis; Mineralocorticoid Receptor Antagonists; Nephrotic Syndrome; Sodium; Syndrome; Vasopressins; Water

Topics: Angiography; Biological Transport, Active; Contrast Media; Dehydration; Diuresis; Furosemide; Glomerular Filtration Rate; Humans; Hypertension; Kidney; Kidney Calculi; Kidney Concentrating Ability; Kidney Failure, Chronic; Kidney Tubules; Male; Metaraminol; Prostatic Diseases; Renal Artery Obstruction; Sodium; Urinary Calculi; Urography; Vasopressins

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

Topics: Adrenal Insufficiency; Diuresis; Glucocorticoids; Humans; Hypothyroidism; Kidney; Kidney Failure, Chronic; Osmolar Concentration; Urination Disorders; Vasopressins; Water; Water Intoxication

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

Topics: Adolescent; Adult; Aged; Animals; Arginine; Child; Dehydration; Diabetes Insipidus; Female; Humans; Hyperaldosteronism; Hypertonic Solutions; Hypocalcemia; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules; Male; Middle Aged; Nicotine; Osmolar Concentration; Polyuria; Sex Factors; Sodium Chloride; Thirst; Time Factors; Urine; Urologic Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Alcoholism; Aldosterone; Animals; Diuretics; Dogs; Humans; Kidney; Kidney Failure, Chronic; Magnesium; Magnesium Deficiency; Parathyroid Hormone; Rats; Uremia; Vasopressins

Arginine vasopressin (AVP), an endogenous hormone with vasopressor properties, may be inadequately secreted during episodes of intradialytic hypotension (IDH).. To evaluate this, we performed a prospective, observational pilot study of 20 chronic hemodialysis patients assessing the baseline AVP level and trend of AVP with ultrafiltration in patients with a diagnosis of IDH compared with patients without IDH. Ten symptomatic IDH patients and 10 controls were enrolled and matched for age, gender, and dialysis vintage. AVP levels were obtained hourly throughout the dialysis session and during hypotensive episodes.. We observed that IDH patients experienced greater decreases in both systolic and diastolic blood pressure during the dialysis session despite equivalent ultrafiltration in both groups. AVP concentration did not increase in the IDH patients (5.0 +/- 1.8) compared with controls (6.4 +/- 6.0) (P = 0.5) despite hypotensive events.. This study suggests that symptomatic IDH patients are unable to mount an appropriate increase in AVP secretion in the setting of hypotension. These findings support the possibility of AVP as a mechanism driven therapy for patients with symptomatic IDH.

Topics: Adult; Aged; Aged, 80 and over; Blood Pressure; Case-Control Studies; Diastole; Female; Hemodiafiltration; Humans; Hypotension; Kidney Failure, Chronic; Male; Middle Aged; Neurophysins; Pilot Projects; Prospective Studies; Protein Precursors; Renal Dialysis; Research Design; Severity of Illness Index; Sodium; Systole; Time Factors; Vasopressins

Inadequate secretion of vasopressin during fluid removal by hemodialysis may contribute to the cardiovascular instability that complicates this therapy and administration of exogenous hormone, by supporting arterial pressure, may facilitate volume removal. To test this, we measured plasma vasopressin in patients with end-stage renal disease (ESRD) during hemodialysis and found that despite significant fluid removal, plasma vasopressin concentration did not increase. We further found that ESRD did not alter the endogenous removal rate of plasma vasopressin and that plasma hormone is not dialyzed. Finally, in a randomized, double-blinded, placebo-controlled trial in 22 hypertensive patients, we examined the effect of a constant infusion of a non-pressor dose of vasopressin on the arterial pressure response during a hemodialysis in which the target fluid loss was increased by 0.5 kg over the baseline prescription. We found that arterial pressure was more stable in the patients receiving vasopressin and that while only one patient (9%) in the vasopressin group had a symptomatic hypotensive episode, 64% of the patients receiving placebo had such an episode (P=0.024). Moreover, increased fluid removal was achieved only in the vasopressin group (520+/-90 ml vs 64+/-130 ml, P=0.01). Thus, administration of non-pressor doses of vasopressin to hypertensive subjects improves cardiovascular stability during hemodialysis and allows increased removal of excess extracellular fluid. Inadequate vasopressin secretion during hemodialysis-induced fluid removal is a likely contributor to the intradialytic hypotension that limits fluid removal.

Topics: Antidiuretic Agents; Blood Pressure; Double-Blind Method; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Vasopressins

Two groups of subjects (uraemic and control) were studied. The uraemic group consisted of 30 patients treated by HD (haemodialysis). The mean age was x +/- SD-35.4 +/- 8.4 years, duration of haemodialysis treatment 42.8 +/- 12.1 months, cuprophan dialyzers and acetate containing solution--35 mEq/l--were used, duration of HD-4 hours 3 times weekly, predialysis serum creatinine was 1060 +/- 218 mumol/l (12.8 +/- 2.5 mg%). The control group comprised 23 healthy subjects (mean age 33.0 +/- 8.0 years, serum creatinine level 88.4 +/- 14 mumol/l (1.0 +/- 0.16 mg%). In all examined subjects the following experimental protocol was used. Blood pressure (BP) was determined at about 8 a.m. after an overnight rest. Then blood samples were withdrawn for estimation of ANP, AVP, sodium and potassium, protein, osmolality and creatinine concentrations. Between 8 and 12 a.m. all examined uraemic subjects were dialysed. After each hour of dialysis BP was measured and blood samples were taken. ANP (Peninsula Lab. Kids.) and AVP (DRG) were measured using RIA method, and other biochemical parameters using routine methods. Plasma creatinine and plasma ANP levels significantly decreased, but AVP significantly increased after HD.. 1. In all uraemic subjects, plasma ANP and AVP levels were significantly higher than in control subjects; 2. During haemodialysis with ultrafiltration a significant increase AVP level and decrease ANP level was observed; 3. A significant correlation between ANP concentration and blood pressure may suggest participation of above mentioned hormone in pathogenesis of hypertension in patients with uraemia; 4. It's possible, in pathogenesis plasma AVP increase takes part plasma ANP decrease, too.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Creatinine; Humans; Hypertension; Kidney Failure, Chronic; Middle Aged; Renal Dialysis; Vasopressins

An enzyme-linked immunosorbent assay is described for the measurement of ouabain in human plasma. This assay is specific for ouabain, strophanthidin, and ouabagenin, with other steroids, including digoxin and vasopressor hormones, exhibiting negligible cross-reactivity. Assay sensitivity was 0.06 nmol/L if 1 mL plasma was extracted and less than 0.005 nmol/L when 20 mL plasma was analyzed. Extracted plasma samples showed ouabainlike immunoreactivity that diluted in parallel with the ouabain standard curve. Repeated extraction and assay of single plasma samples, however, did not produce consistent results in the assay. Increased specificity was obtained by high-performance liquid chromatography of sample extracts before assay. When high-performance liquid chromatographic profiles of plasma spiked with ouabain standard or following bolus intravenous injections of ouabain into normal human volunteers were compared with profiles of unspiked plasma, there was no support for the immunoreactive material in the latter samples being ouabain. We propose that if ouabain is present in the human circulation, its concentration is less than 0.005 nmol/L.

Topics: Animals; Antibodies; Antibody Specificity; Chromatography, High Pressure Liquid; Cross Reactions; Digoxin; Enzyme-Linked Immunosorbent Assay; Female; Fetal Blood; Heart Failure; Humans; Kidney Failure, Chronic; Ouabain; Pre-Eclampsia; Pregnancy; Rabbits; Sensitivity and Specificity; Steroids; Strophanthidin; Vasopressins

A 72-year-old man with end-stage renal disease (ESRD) undergoing transurethral resection of a bladder tumor experienced severe and prolonged hypotension after receiving oral 5-aminolevulinic acid (5-ALA). Continuous infusions of norepinephrine and vasopressin ultimately resolved the hypotension over the course of 26 hours. It is uncertain whether 5-ALA is causative or is a contributing factor that influences other factors, such as hypovolemia after hemodialysis and autonomic nerve dysfunction associated with ESRD. Our findings suggest that anesthesiologists should be aware of the possible occurrence of hypotension after administration of 5-ALA, and urologists should consider intravesical 5-ALA administration in patients with ESRD.

Topics: Administration, Oral; Aged; Aminolevulinic Acid; Humans; Hypotension; Kidney Failure, Chronic; Norepinephrine; Treatment Outcome; Urinary Bladder Neoplasms; Urologic Surgical Procedures; Vasopressins

Chronically elevated vasopressin (VP) plasma levels have been shown to induce accelerated renal function decline in rats with chronic renal failure. Whether endogenous VP is a renal risk factor in humans has not been investigated yet. We aimed to investigate whether, in renal transplant recipients, VP concentration is associated with change in renal function during follow-up.. In this prospective study, all consecutive patients visiting our kidney transplant outpatient clinic between August 2001 and July 2003 were asked to participate. Serum creatinine was assessed at baseline and at follow-up. Copeptin, the C-terminal portion of the precursor of VP, was determined at baseline (immunoassay). Univariate and multivariate regression analyses were performed to investigate the association between copeptin and renal function decline.. Overall, 548 patients were included 6.0 (2.8-11.6) years after transplantation (men 54%, age 52 [43-60] years). Median follow-up was 3.2 (2.7-3.7) years. Median copeptin level was 9.1 (5.0-18.6) pmol/L at baseline. Copeptin was significantly associated with change in estimated Glomerular Filtration Rate (eGFR; MDRD) during follow-up. When our study population was subdivided according to gender-stratified tertiles of increasing copeptin concentration, mean changes in eGFR during follow-up were -0.03, -0.44, and -1.06 mL/min/1.73 m2 per year. In multivariate regression analysis, the association of copeptin at baseline with change in eGFR during follow-up remained significant after adjustment for age, gender, baseline eGFR, and known risk factors for renal function decline.. These findings suggest that in renal transplant patients, VP may play a role in renal function decline.

Topics: Adult; Animals; Biomarkers; Female; Glomerular Filtration Rate; Glycopeptides; Humans; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Models, Biological; Prospective Studies; Rats; Vasopressins

Previous reports have shown a stimulatory effect of vasopressin (VP) on Na-K-ATPase and rBSC-1 expression and activity. Whether these VP-dependent mechanisms are operating in vivo in physiological conditions as well as in chronic renal failure (CRF) has been less well studied. We measured ATPase expression and activity and rBSC-1 expression in the outer medulla of controls and moderate CRF rats both before and under in vivo inhibition of VP by OPC-31260, a selective V(2)-receptor antagonist. OPC-31260 decreased Na-K-ATPase activity from 11.2 +/- 1.5 to 3.7 +/- 0.8 in controls (P < 0.05) and from 19.0 +/- 0.8 to 2.9 +/- 0.5 micromol P(i). mg protein(-1) x h(-1) in moderate CRF rats (P < 0.05). CRF was associated with a significant increase in Na-K-ATPase activity (P < 0.05). Similarly, CRF was also associated with a significant increase in Na-K-ATPase expression to 164.4 +/- 21.5% compared with controls (P < 0.05), and OPC-31260 decreased Na-K-ATPase expression in both controls and CRF rats to 57.6 +/- 9.5 and 105.3 +/- 10.9%, respectively (P < 0.05). On the other hand, OPC-31260 decreased rBSC-I expression in both controls and CRF rats to 60.8 +/- 6.5 and 30.0 +/- 6.9%, respectively (P < 0.05), and was not influenced by CRF (95.7 +/- 5.2%). We conclude that 1) endogenous VP modulated Na-K-ATPase and rBSC-1 in both controls and CRF; and 2) CRF was associated with increased activity and expression of the Na-K-ATPase in the outer medulla, in contrast to the unaltered expression of the rBSC-1. The data suggest that endogenous VP could participate in the regulation of electrolyte transport at the level of the outer medulla.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Disease Models, Animal; Kidney Failure, Chronic; Kidney Medulla; Male; Mucoproteins; Rats; Rats, Wistar; Receptors, Vasopressin; Sodium-Potassium-Chloride Symporters; Sodium-Potassium-Exchanging ATPase; Solute Carrier Family 12, Member 1; Uromodulin; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Blood Pressure; Disease Progression; Diuresis; Endothelins; Female; Glomerulonephritis, IGA; Humans; Kidney Failure, Chronic; Kidney Tubules; Male; Nitric Oxide; Oxidative Stress; Polycystic Kidney, Autosomal Dominant; Retrospective Studies; Risk Factors; Sex Factors; Smoking; Vasopressins

The effect of volume reduction on vasoactive substances and their role in estimating dry weight in haemodialysis patients was studied. Plasma atrial natriuretic peptide (ANP), catecholamines, antidiuretic hormone, renin activity and serum aldosterone were measured in 12 patients before and after bicarbonate haemodialysis. Haemodynamical changes were registered and cardiac function and diameter of the inferior vena cava were measured by echocardiography before and after dialysis. Plasma concentration of ANP was significantly reduced by haemodialysis from 209 +/- 51 to 69 +/- 13 pg mL(-1) (n = 12, P < 0.05), whereas concentrations of the other hormones were unchanged. The change in the concentration of ANP did not have significant correlation with weight reduction. The concentration of ANP correlated positively with the diameter of the inferior vena cava (r = 0.70, P < 0.05) after dialysis, but not before dialysis. The concentration of ANP before or after haemodialysis or its change during dialysis did not correlate with any other biochemical parameter. The results show that plasma ANP level is decreased after volume reduction in patients with chronic renal failure, whereas other hormonal systems are unresponsive. However, plasma concentration of ANP seems to have no role in estimating dry weight in chronic haemodialysis patients.

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Body Weight; Catecholamines; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Neurotransmitter Agents; Renal Dialysis; Renin; Ultrasonography; Vasopressins

Diabetic nephropathy represents a major complication of diabetes mellitus (DM), and the origin of this complication is poorly understood. Vasopressin (VP), which is elevated in type I and type II DM, has been shown to increase glomerular filtration rate in normal rats and to contribute to progression of chronic renal failure in 5/6 nephrectomized rats. The present study was thus designed to evaluate whether VP contributes to the renal disorders of DM. Renal function was compared in Brattleboro rats with diabetes insipidus (DI) lacking VP and in normal Long-Evans (LE) rats, with or without streptozotocin-induced DM. Blood and urine were collected after 2 and 4 weeks of DM, and creatinine clearance, urinary glucose and albumin excretion, and kidney weight were measured. Plasma glucose increased 3-fold in DM rats of both strains, but glucose excretion was approximately 40% lower in DI-DM than in LE-DM, suggesting less intense metabolic disorders. Creatinine clearance increased significantly in LE-DM (P < 0.01) but failed to increase in DI-DM. Urinary albumin excretion more than doubled in LE-DM but rose by only 34% in DI-DM rats (P < 0.05). Kidney hypertrophy was also less intense in DI-DM than in LE-DM (P < 0.001). These results suggest that VP plays a critical role in diabetic hyperfiltration and albuminuria induced by DM. This hormone thus seems to be an additional risk factor for diabetic nephropathy and, thus, a potential target for prevention and/or therapeutic intervention.

Topics: Albuminuria; Animals; Creatinine; Diabetes Insipidus; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Glomerular Filtration Rate; Glycosuria; Hypertrophy; Kidney; Kidney Failure, Chronic; Male; Nephrectomy; Organ Size; Rats; Rats, Brattleboro; Rats, Long-Evans; Vasopressins

We have previously shown that a chronic reduction in plasma vasopressin level slowed the progression of chronic renal failure (CRF) in Sprague Dawley rats. The aim of the present study was to determine the respective contribution of pressor (V1) and antidiuretic (V2) effects of vasopressin on progression. Male homozygous Brattleboro rats with hereditary central diabetes insipidus were submitted to 5/6 nephrectomy. They were divided into three groups, two of which received chronic i.p. infusion of AVP (V1 + V2 effects) or dDAVP (V2 effects). The third group served as control (CONT). The doses of AVP and dDAVP were chosen so as to produce urine osmolality similar to that observed in 5/6 Nx Sprague Dawley rats. All rats ate the same amount of food and drank water ad libitum. Renal function was studied for 13 weeks. All three groups showed a marked hypertension. Rats infused with dDAVP, but not those infused with AVP, had a higher creatininemia, anemia and urinary protein excretion than CONT rats. In the dDAVP but not the AVP group, fractional excretion of urea was markedly decreased and plasma urea concentration rose much more than that of creatinine. These results show that V2 but not V1 effects play a major role in the deleterious influence of vasopressin on progression, at least in Brattleboro rats. The more severe progression seen in dDAVP rats could indirectly result from the V2-mediated effects on the collecting duct resulting in a decreased efficiency of urea excretion, an increased intrarenal urea recycling, and a rise in plasma urea concentration. Both the toxic effects of urea and the recently demonstrated V2-mediated increase in glomerular hemodynamics might be involved in the deleterious influence of V2 agonism.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Body Weight; Creatinine; Diabetes Insipidus; Disease Models, Animal; Disease Progression; Kidney; Kidney Failure, Chronic; Male; Proteinuria; Rats; Rats, Brattleboro; Rats, Sprague-Dawley; Uremia; Vasopressins

Chronic renal failure (CRF) is accompanied by adaptive changes in electrolyte reabsorption in the thick ascending limb of Henle of surviving nephrons. To study the cellular mechanism of this adaptation, we measured intracellular cAMP in micro-dissected medullary thick ascending limb (mTAL) segments in rats with CRF. mTAL exhibited in CRF an increase of basal cAMP from 25.6 +/- 10.0 in controls to 65.8 +/- 11.3 fmol mm-1 tubule in CRF (P < 0.05). Vasopressin and calcitonin stimulated mTAL adenylate-cyclase in a dose-dependent manner in controls but failed to stimulate in CRF. Likewise, maximal stimulation with 10(-3) M 3-isobutyl-1-methylxanthine (IBMX) plus 10(-5) M forskolin increased cAMP in controls to 63.0 +/- 16.0 but not in CRF, where maximal stimulated values remained at 63.1 +/- 18.8 fmol mm-1 tubule (P NS). Alpha2-adrenoreceptor activation with clonidine at concentrations ranging from 10(-8) to 10(-6) M diminished cAMP production by 37% in CRF (P < 0.05), whereas no differences were found in controls. Thus, the basal intracellular cAMP is increased in rat mTAL in CRF. The finding that neither forskolin nor vasopressin were able to further augment intracellular cAMP would suggest that stimulatory pathways of the adenylate-cyclase system are activated in the basal state. However, mTAL cells in CRF seem to retain the response of normal epithelium to inhibitory pathways such as the one mediated by alpha2-adrenoreceptors.

Topics: 1-Methyl-3-isobutylxanthine; Adrenergic alpha-Agonists; Animals; Calcitonin; Cell Separation; Clonidine; Colforsin; Creatinine; Cyclic AMP; Disease Models, Animal; Dose-Response Relationship, Drug; Glomerular Filtration Rate; In Vitro Techniques; Kidney Failure, Chronic; Loop of Henle; Male; Osmolar Concentration; Rats; Rats, Wistar; Vasopressins

We report the first case of the syndrome of periodic adrenocorticotropin (ACTH) and vasopressin (ADH) discharge associated with focal glomerulosclerosis. Approximately 30 cases of this syndrome have so far been reported in Japan, but no cases associated with renal dysfunction have yet been reported. The patient, a 10-year-old Japanese boy, was referred to our hospital because of recurrent attacks of vomiting. He was diagnosed as having this syndrome from clinical and laboratory findings. While various drugs were tried to manage his vomiting attacks, only valproic acid appeared to be effective in reducing the frequency of the attacks. Chronic nephritis was manifested when the patient was 12 years old, which required treatment with continuous ambulatory peritoneal dialysis. Valproic acid was proved to be effective in reducing the number of attacks over 4 months.

Topics: Adrenocorticotropic Hormone; Child; Glomerulosclerosis, Focal Segmental; Humans; Kidney Failure, Chronic; Male; Periodicity; Recurrence; Syndrome; Valproic Acid; Vasopressins; Vomiting

Topics: Animals; Body Water; Dietary Proteins; Glomerular Filtration Rate; Humans; Kidney Concentrating Ability; Kidney Failure, Chronic; Rats; Vasopressins

Elderly patients may exhibit changes in plasma hormone levels, as well as thirst disorders. Two groups of elderly hemodialysis patients were evaluated to determine if excessive interdialytic weight gain was related to differences in postdialysis plasma osmolality or postdialysis measurement of plasma renin activity, or plasma levels of angiotensin II (a dipsogenic hormone), aldosterone, and vasopressin. Patients mean age was 77.0 +/- 8.8 years and patients were divided into groups, I and II, with less than or greater than 2 kg interdialytic weight gain. Postdialysis plasma osmolality was similar in both groups of patients (309.3 +/- 2.3 vs. 309.6 +/- 2.4 mOsm/Kg, p = 0.8) and postdialysis AVP levels also were no different (2.7 +/- 0.6 vs. 2.1 +/- 0.2 pg/mL, p = 0.3). There was also no statistical difference between postdialysis angiotensin II and aldosterone levels in either group of patients. Plasma renin activity (PRA) was also not different in either group (2.3 +/- 1.1 vs. 0.43 +/- 0.1 ng/mL/hr, p = 0.1), but group I patients, with less than 2 kg weight gain, tended to exhibit higher PRA values perhaps reflecting proximity to their dry weight postdialysis. Since excessive fluid intake did not appear to relate to plasma osmolality and hormone levels studied, it might be suggested that excessive drinking could be due to excessive sodium intake associated with personal dietary habits or perhaps other as yet unmeasured factors.

Topics: Aged; Aged, 80 and over; Aldosterone; Angiotensin II; Humans; Kidney Failure, Chronic; Osmolar Concentration; Renal Dialysis; Renin; Vasopressins; Weight Gain

Factors related to atrial natriuretic peptide (alpha-ANP) regulation and its potential impact on excretory transplant function were examined in a prospective cohort study of 20 patients with end-stage renal disease over 21 days after allogenic kidney transplantation. Depending on posttransplant graft function, patients were separated into those with primary renal function (PF group, n = 10) and posttransplant acute renal failure (ARF group, n = 10). ANP concentrations were markedly elevated in both PF and ARF immediately after renal transplantation, even when compared with the pretransplant dialysis phase (PF group: 939 +/- 467 pg/ml; ARF group: 648 +/- 306 pg/ml, on 3rd postoperative day; "normals': 72 +/- 35 pg/ml). Whilst ANP levels were persistently elevated in patients with acute renal failure, there was a steady decrease in plasma concentrations in patients with primary renal function (PF: 270 +/- 122 pg/ml on 21st day). ANP concentration correlated with endogenous creatinine clearance (rz = 0.56, p < 0.01, PF group). Moreover, there was a greater correlation between ANP levels and postoperative hydration status, measured as central venous pressure or the difference from predialysis dry weight (rz = 0.79 and rz = 0.74, p < 0.01, PF group). Systolic blood pressure was also positively correlated with ANP concentrations. Together, these factors accounted for a total correlation coefficient of r = 0.87 (p < 0.001) in multiple regression analysis. No significant relation was found between plasma ANP levels and total or fractional sodium excretion or free water clearance. With the restoration of renal function most vasoactive hormones (renin-aldosterone system, catecholamines, vasopressin) decreased towards normal values, whilst ANP plasma concentrations remained elevated.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Body Weight; Catecholamines; Central Venous Pressure; Cohort Studies; Creatinine; Cyclic GMP; Female; Humans; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Postoperative Period; Prospective Studies; Renin; Transplantation, Homologous; Vasopressins

The effects of hormone stimulation on atrial natriuretic factor (ANF) release in atria were studied in experimental renal failure rats. In vitro experiments were done in two groups of male Wistar rats. Group 1 rats were sham operated, and group 2 rats were subjected to 5/6 nephrectomy. Overall glomerular filtration rate was significantly reduced (1.98 +/- 0.10 vs. 0.75 +/- 0.05 ml/min, p < 0.001) in nephrectomized rats. These rats were also mildly uremic [blood urea nitrogen (BUN): 18 +/- 0.6 vs. 60 +/- 3.9 mg/dl p < 0.001]. The right atria of partially nephrectomized and sham-operated rats were isolated and perfused in a modified Langendorff apparatus to measure ANF release rate. Experiments were done in two phases. In the initial phase, spontaneous release of ANF was measured. In the second phase, angiotensin II (10(-6) M), vasopressin (10(-6) M) or endothelin (ET 1; 10(-6) M) were added into the perfusate. Spontaneous ANF release by the atria of renal failure rats was significantly elevated compared to intact rats. A significant positive correlation was found between ANF release rate and BUN (r = 0.65, p < 0.01). This suggests that the increase in ANF release by the atria of chronic renal failure (CRF) rats is related to the severity of renal impairment. Angiotensin II, vasopressin and endothelin induced exaggerated increases in ANF release by the atria of CRF rats. These results show that a shift in stimulus response curve is present and can contribute to the observed increase in plasma ANF levels in CRF rats.

Topics: Angiotensin II; Animals; Atrial Natriuretic Factor; Blood Urea Nitrogen; Endothelins; Glomerular Filtration Rate; Heart; Heart Atria; Hormones; Kidney Failure, Chronic; Male; Nephrectomy; Rats; Rats, Wistar; Stimulation, Chemical; Vasopressins

Topics: Animals; Atrial Natriuretic Factor; Brain; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Vasopressins; Water-Electrolyte Balance

We explored the role of angiotensin II and vasopressin in the maintenance of blood pressure during the nephrotic syndrome of adriamycin-induced nephropathy in rats. All 91 rats treated with adriamycin developed chronic renal failure with nephrotic syndrome, which was more pronounced in the normotensive rats than the 35% who became hypertensive. Angiotensin II blockade with DuP 753 produced a significantly greater hypotensive response in both the adriamycin-hypertensive (-16 +/- 3 mm Hg) and adriamycin-normotensive (-14 +/- 5 mm Hg) groups than the saline-treated controls (-5 +/- 1 mm Hg, P < .05). Vasopressin blockade with either a V1V2 inhibitor or a selective V1 inhibitor produced a hypotensive response in adriamycin-hypertensive rats only (by -16 +/- 4 and -17 +/- 2 mm Hg, respectively, P < .01), although the nonselective vasopressin inhibitor produced similar fluid loss and body weight reduction in all three groups. The data suggest that in adriamycin-induced nephropathy with nephrotic syndrome, angiotensin II contributes to blood pressure maintenance in both hypertensive and normotensive animals, whereas the pressor action of vasopressin contributes to elevated blood pressure in hypertensive animals only.

Topics: Angiotensin II; Animals; Biphenyl Compounds; Blood Pressure; Cholesterol; Creatinine; Doxorubicin; Hypertension; Imidazoles; Kidney; Kidney Failure, Chronic; Losartan; Male; Nephrotic Syndrome; Potassium; Rats; Rats, Wistar; Serum Albumin; Sodium; Tetrazoles; Time Factors; Urea; Vasopressins

To investigate the cause and the mechanisms responsible of the compulsive thirst and excessive fluid intake observed in many patients on chronic dialysis treatment, we measured plasma antidiuretic hormone (ADH), angiotensin II (Ang II) and some hemodynamic parameters in seven polydipsic and in six normodipsic patients before hemodialysis, at the end of it and several times during the interdialytic interval. Before dialysis we found that ADH was elevated in both groups (6.9 +/- 1.9 vs. 6.9 +/- 1.3 pg/ml, respectively in polydipsics and controls), whereas Ang II was abnormally high only in polydipsics (51 +/- 12 vs. 11 +/- 3 pg/ml, P < 0.01); these patients also had significantly higher heart rate and cardiac indices and lower total peripheral resistances than control patients. Overall these hemodynamic indices were related with Ang II but not with ADH. Ang II rose markedly in polydipsics after dialysis, reaching a peak at the fourth hour after its termination (136 +/- 12 pg/ml) and remained consistently elevated throughout the interdialytic period, whereas in controls Ang II was practically unchanged with respect to baseline. In contrast, ADH had minor and similar modifications in both groups, in whom also the hemodynamic changes were superimposable. Significant correlations were found between the absolute and percent changes of Ang II and those of plasma volume during the interdialytic interval (P < 0.001 for both), and between the individual values of Ang II measured during the whole study and the interdialytic weight gain (P < 0.05). These results demonstrate that polydipsic patients have abnormally high levels of Ang II before and after the hemodialysis-induced volume depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Angiotensin II; Drinking; Female; Hemodynamics; Humans; Kidney Failure, Chronic; Male; Middle Aged; Osmolar Concentration; Renal Dialysis; Thirst; Vasopressins

To determine whether thirst mechanisms are altered in nondiabetic patients with chronic renal failure on hemodialysis, 4 patients with an average weight gain between dialysis sessions of more than 5% of dry body weight (group I), 5 patients with less than 3% weight gain (group II), and a group of 6 healthy subjects (group III) were submitted to infusion of hypertonic saline. After infusion the subjects had free access to water. Thirst was evaluated by visual analogue rating scales. Despite similar increments of effective plasma osmolality during saline infusion, patients of group I were thirstier than groups II and III (p less than 0.005 and p less than 0.01, respectively). Changes in thirst ratings were similar in groups II and III. Osmotic thresholds for thirst onset were similar in groups II and III (288.9 +/- 8.5 and 289.8 +/- 3.4 mosm/kg, respectively), but lower in group I (277.6 +/- 7.6 mosm/kg). Nevertheless, great variations were observed in the latter group. Thus, 2 patients showed thresholds for thirst within the normal range, whereas the others had low osmolar thresholds for thirst and baseline plasma osmolalities and high basal thirst scores. During the drinking period, the patients of group I drank more (14.2 +/- 2.8 ml/kg) than those of groups II (5.3 +/- 1.6 ml/kg; p less than 0.02) and III (10.2 +/- 1.6 ml/kg; n.s.) The plasma levels of angiotensin II in uremic patients were higher than in healthy subjects, although there were no differences between groups I and II and no correlation between basal angiotensin II levels and the interdialytic weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Angiotensin II; Body Weight; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Osmolar Concentration; Renal Dialysis; Saline Solution, Hypertonic; Thirst; Vasopressins; Water-Electrolyte Balance

Influence of blockade converting enzyme on plasma renin activity (PRA), aldosterone and vasopressin secretion in 12 hemodialyzed patients with chronic renal failure and in 21 healthy subjects was observed. Our observation were provided during bed rest and water immersion tests. We didn't observe statistically significant influence PRA (increase after converting enzyme blockade) on vasopressin secretion in patients with chronic renal failure and in healthy subjects. Correlation between PRA and vasopressin secretion was absent.

Topics: Adult; Angiotensin-Converting Enzyme Inhibitors; Humans; Kidney Failure, Chronic; Reference Values; Renin-Angiotensin System; Vasopressins

Recent experiments have shown that the kidney adapts to chronic variations in urine concentration. Glomerular filtration rate (GFR), kidney weight relative to body weight, thickness of inner stripe of the outer medulla, volume of epithelium in early thick ascending limb, and internephron heterogeneity are all decreased by chronic water diuresis and increased by chronic stimulation of urine concentration. It was further shown that the intrarenal pattern of hypertrophy observed after high protein (HP) intake, but not that observed after compensatory hypertrophy or normal growth with age, is exactly similar to that observed after chronic stimulation of urine concentration. Since solute-free water reabsorption (TcH2O) is markedly enhanced by HP diet, this suggests that the increases in GFR and renal mass observed after HP intake are, at least in part, an adaptive response of the kidney to increased urinary concentrating activity. The beneficial effects are induced by protein restriction in chronic renal failure (CRF) could thus be due, in part, to the reduction of this concentrating activity. This hypothesis was confirmed by an experiment performed in rats with experimental chronic renal failure (CRF) in which a chronic increase in water intake, reducing urine osmolality and TcH2O, without any change in food composition or consumption, reduced proteinuria, systemic hypertension, kidney hypertrophy, incidence of glomerulosclerosis, and mortality.

Topics: Adaptation, Physiological; Animals; Dietary Proteins; Glomerular Filtration Rate; Hypertrophy; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Organ Size; Rats; Rats, Brattleboro; Vasopressins

Plasma immunoreactive human atrial natriuretic peptide (hANP) levels were measured in 9 patients with chronic renal failure treated with maintenance hemodialysis in order to evaluate the effects of fluid removal and osmotic pressure. Under hemodialysis without fluid removal plasma hANP levels remained unchanged, but the levels were significantly decreased during extra-corporeal ultrafiltration (p less than 0.01). The present study provided strong evidence that the fall in plasma hANP levels in hemodialysis patients is mainly due to the reduction in circulating plasma volume.

Topics: Adult; Aged; Atrial Natriuretic Factor; Body Weight; Extracorporeal Circulation; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Ultrafiltration; Vasopressins

Renal function was evaluated in normal and after 30 days of 5/6 renal mass reduction (CRF) in Munich-Wistar (MW) rats, spontaneously hypertensive rats with superficial glomeruli (EPM), and in Brattleboro rats with congenital diabetes insipidus (DI). Mean arterial pressure was higher in EPM-Control and EPM-CRF rats as compared with MW and DI rats. MW and EPM rats with CRF showed increases of 120% and 196%, respectively, in single nephron glomerular filtration rate as compared with their controls. However, DI rats with CRF did not show any increase in single nephron glomerular filtration rate as compared with the control group. Therefore, the data suggest that the presence of hypertension enhances the adaptive mechanisms on remnant kidney's function. Conversely, in the absence of antidiuretic hormone, adaptive mechanisms of remnant nephrons did not occur. In addition, it was observed that rats with CRF submitted to prostaglandin blockade with indomethacin showed for MW rats a 55% and 20% reduction in ultrafiltration coefficient and in single nephron glomerular filtration rate, respectively. Decreases of 60% and 30% in ultrafiltration coefficient and single nephron glomerular filtration rate, respectively, were observed for EPM rats. In contrast, DI rats did not show any alteration on renal function after indomethacin. It seems, therefore, that prostaglandins play a role in remnant nephron function of MW and EPM rats, but in the absence of antidiuretic hormone, prostaglandins do not affect remnant glomerular hemodynamics.

Topics: Animals; Blood Pressure; Diabetes Insipidus; Glomerular Filtration Rate; Hypertension; Kidney Failure, Chronic; Kidney Glomerulus; Male; Nephrectomy; Nephrons; Prostaglandins; Rats; Rats, Inbred Strains; Vasopressins

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

1. Partial (5/6) renal ablation was performed in Long Evans rats treated with vehicle or a vasopressin V1-receptor antagonist, in control Long Evans rats, and in homozygous Brattleboro rats which lack endogenous vasopressin. 2. In control and vasopressin-blocked Long Evans rats, 3 weeks following partial renal ablation, systolic blood pressure was 215 +/- 5 and 199 +/- 9 mmHg and, urinary protein excretion was 54 +/- 4 and 50 +/- 3 mg day-1, respectively. 3. The pressor response to exogenous vasopressin was significantly (P less than 0.05) reduced in rats treated with the V1-receptor antagonist (ED50 mmHg 5.0 +/- 1.6 vs. 0.09 +/- 0.01 micrograms kg-1). 4. In control Long Evans and in Brattleboro rats, 3 weeks following renal ablation, systolic blood pressure was 204 +/- 10 and 191 +/- 7 mmHg, and urinary protein excretion was 97 +/- 27 and 71 +/- 5 mg day-1, respectively. 5. Histological examination of the remaining kidney tissue demonstrated significant glomerular hyalinization following renal ablation but no differences between any of the groups. 6. The data indicate that neither vasopressin nor the urinary concentrating mechanism is likely to be involved in the hypertension and proteinuria associated with partial renal ablation.

Topics: Animals; Blood Pressure; Body Weight; Hypertension, Renal; Kidney; Kidney Failure, Chronic; Kidney Glomerulus; Male; Osmolar Concentration; Proteinuria; Rats; Rats, Brattleboro; Urodynamics; Vasopressins

Water immersion (WI)-induced alterations of circulating plasma volume (PV), plasma renin activity (PRA), plasma levels of aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) were examined in 12 patients with noninflammatory acute renal failure (ARF) at the anuric/oliguric phase, in 20 hemodialyzed patients with chronic renal failure and in 15 healthy subjects. Patients with acute and chronic renal failure showed significantly elevated basal ANP concentrations (138.67 +/- 12.88 and 295.8 +/- 21.87 pg/ml, respectively) as compared with normals (74.54 +/- 4.1 pg/ml) and significantly elevated PRA (20.85 +/- 3.24 and 6.60 +/- 0.94 ng/ml/h, respectively versus 2.33 +/- 0.31 ng/ml/h), plasma levels of Ald (16.11 +/- 1.26 and 18.11 +/- 1.58 ng/dl, respectively versus 12.71 +/- 1.03 ng/dl) and AVP (6.95 +/- 0.62 and 6.08 +/- 0.54 pg/ml, respectively versus 2.68 +/- 0.48 pg/ml). After 2 hrs of WI a significant decline of PRA, Ald and AVP but an increase of ANP was noted in all examined groups. The absolute WI-induced increase in plasma ANP was significantly less marked in uremic patients than in normals. The endocrine profile of patients with ARF differed only quantitatively from that of patients with CRF both under basal and WI conditions. WI was followed by a significant increase of PV which was significantly more marked in patients with ARF (+ 16.42 +/- 1.73%) than in CRF (10.57 +/- 0.37%) and in normals (+11.3 +/- 1.6%). Only in healthy subjects a significant correlation was found between WI-induced changes of PV and ANP, PRA and Ald, and between PRA and AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Kidney Injury; Adult; Atrial Natriuretic Factor; Humans; Immersion; Kidney Failure, Chronic; Renal Dialysis; Renin-Angiotensin System; Rest; Time Factors; Vasopressins

Echocardiographically determined left ventricular function and cardiovascular hormone balance were assessed before and after hemodialysis in 10 patients who had been on hemodialysis for 4 months to 15 years. Plasma levels of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), renin activity and aldosterone were determined. All patients had vector- and echocardiographic evidences of slight to moderate left ventricular hypertrophy. The body weight decreased 2.0 kg (3.3 +/- 0.5%) with dialysis. Nine out of ten patients showed a slightly reduced ejection fraction that normalized after dialysis (p less than 0.05). Left atrial and ventricular systolic dimensions were around the upper reference limit before dialysis with a decrease after dialysis (p less than 0.05 and p less than 0.02, respectively). The levels of ANP decreased with dialysis from 2-17 times to 1 to 15 times the upper reference value in nine out of the ten patients. In the whole group the decrease was 117 +/- 35% (p less than 0.005). A significant regression was obtained between percentage decrease of body weight and percentage change of ANP (r = 0.67; p less than 0.05). The plasma concentration of ADH did not change following dialysis but the mean value was significantly higher than the mean value of the reference group of the laboratory (p less than 0.05 before and p less than 0.005 after dialysis). Renin activity and aldosterone levels were low and did not change during dialysis. In conclusion, the slight left ventricular hypertrophy may partly be a response to volume overload with hyperdynamic circulation and partly to metabolically depressed myocardial function.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Cardiomegaly; Echocardiography; Female; Heart; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Renin; Vasopressins

Topics: Acute Kidney Injury; Adult; Blood Pressure; Humans; Immersion; Kidney Failure, Chronic; Middle Aged; Osmolar Concentration; Plasma Volume; Potassium; Sodium; Vasopressins

Atrial natriuretic factor, plasma renin activity, and plasma vasopressin were measured in 38 patients with chronic renal failure prior to and after hemodialysis. The objective of the study was to evaluate the effect of acute volume changes on the level of atrial natriuretic factor. Blood pressure prior to dialysis was 154 +/-/83 +/- mmHg, and 132 +/-/78 +/- mmHg post dialysis (p less than 0.005) while heart rate increased from 82.5 +/- 1.8 beats per minute to 91.2 +/- 2.4 after dialysis (p less than 0.005). The average weight of patients was reduced from 60.2 +/- 2.4 kg to 57.8 +/- 2.4 kg (p less than 0.005). While the plasma levels of atrial natriuretic factor in normal individuals were 65.3 +/- 2.9 pg/ml (n = 59), these levels were 251.4 +/- 28 pg/ml prior to dialysis in the patients with renal failure, and 173.3 +/- 18.0 pg/ml after dialysis (p less than 0.005). Twenty-nine patients had a reduction in the levels of this atrial natriuretic factor, 5 had no change, and 4 had an increase. The atrial factor was not detected in the dialysate fluid of 6 patients in whom it was measured. Peripheral renin values were unchanged from 2.12 +/- 0.68 to 2.07 +/- 0.8 ng/ml/hr. Plasma vasopressin before dialysis was significantly higher than normal, and increased from 7.04 +/- 0.56 to 9.95 +/- 1.55 pg/ml following dialysis (p less than 0.05). The changes in atrial natriuretic factor values correlated most significantly (r = 0.47, p less than 0.005) with the changes in weight, but no single variable could explain the changes in atrial natriuretic factor.

Topics: Adult; Aged; Atrial Natriuretic Factor; Blood Pressure; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Pulse; Renal Dialysis; Renin; Vasopressins

The blood pressure changes and behavior of vasoactive hormones after various stimuli were studied in eighteen patients with end-stage renal disease maintained on chronic hemodialysis. Group A patients (n = 9) were not subject to intra- or post-dialysis hypotensive episodes, and Group B (n = 9) frequently had such episodes. A 500 ml hypertonic saline infusion produced no change in blood pressure in either group, despite significant rise of vasopressin levels in both. Plasma renin activity levels were similar and became appropriately suppressed by the infusion in both groups, whereas norepinephrine rose significantly only in Group A, but not Group B where it was already higher at baseline. The regular dialysis session produced, as expected, a significantly more profound hypotensive effect in Group B, but was accompanied in both groups by decrease in vasopressin and increase in plasma renin activity. Norepinephrine change differed in the two groups: it decreased in Group A as expected from its capacity to be dialyzed, but rose in several hypotensive patients in Group B, indicating appropriate response to baroreceptor stimulation and leading to an unchanged average. These findings suggest that dialysis-induced hypotensive episodes are not necessarily associated with autonomic neuropathy or with abnormal patterns of vasopressor hormone response to stimuli. They also shed new light on the factors regulating vasopressin secretion under these circumstances, since they indicate that the osmoreceptor and/or sodium-sensitive receptor may be a more dominant mechanism in the regulation of vasopressin release than the volumetric mechanism responding to fluid volume changes.

Topics: Adult; Aged; Blood Pressure; Catecholamines; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Renin; Saline Solution, Hypertonic; Sodium Chloride; Vasopressins

Fluid excess can cause hyporeninemia and hypoaldosteronemia in hemodialysis patients. In six patients on CAPD, plasma renin activity (PRA) and plasma aldosterone (PA) were elevated to levels of : PRA 10.2 +/- 2.9 nl (1-5 ng/ml/h), and PA: 47.4 +/- 16.2 (normal 5-20 ng/dl). In 4 patients, data posthemodialysis and later during CAPD revealed that PRA increased from 0.9 +/- 0.3 to 14.1 +/- 4.6 and PA increased from 3.4 +/- 0.3 to 67.4 +/- 24.9 on CAPD (p less than 0.05). Mean arterial pressure was lower on CAPD and serum glucose was higher. No significant difference was seen in weight, hematocrit, BUN, or potassium, however. Plasma volume was not decreased in five CAPD patients: 3619 +/- 358 ml (predicted 3083 +/- 201 ml). Elevated catecholamine levels were seen in CAPD patients: norepinephrine 868.0 +/- 104.1 (normal 358.4 +/- 41.5 pg/ml), epinephrine 386.3 +/- 49.2 (normal 58.3 +/- 10.6 pg/ml). Plasma vasopressin levels were elevated to the range usually seen with hyperosmolality. In eight patients who lost or gained weight on CAPD, levels of PRA and PA changed as expected, but catecholamine levels did not correlate with weight changes. The data suggest that in CAPD patients, PRA and PA may be elevated in association with augmented sympathetic stimulation and elevated vasopressin levels. Serial observations demonstrated that PRA and PA can respond appropriately to changes in body weight, while catecholamine and vasopressin levels seem to be influenced by other factors.

Topics: Aldosterone; Blood Urea Nitrogen; Creatinine; Electrolytes; Epinephrine; Hematocrit; Humans; Kidney Failure, Chronic; Norepinephrine; Peritoneal Dialysis, Continuous Ambulatory; Renin; Vasopressins; Water-Electrolyte Balance

Levels of immunoreactive (IR) oxytocin (OT)-associated or estrogen-stimulated neurophysin (ESN) and vasopressin-associated or nicotine-stimulated neurophysin (NSN) were measured in plasma of patients with chronic renal failure before and after hemodialysis (HD) and intermittent peritoneal dialysis (IPD), and during continuous ambulatory peritoneal dialysis (CAPD). ESN-IR in 17 patients before HD was 24.4 +/- 2.7 ng/ml (mean +/- SEM) and increased after HD to 33.2 +/- 4.1 ng/ml (P less than 0.001). ESN-IR in 17 patients with CAPD was 15.2 +/- 3.4 ng/ml, significantly lower than in patients undergoing HD, P less than 0.001. In patients receiving IPD (n = 6), ESN was 11.6 +/- 3.7 ng/ml and did not change significantly after IPD. Levels of ESN in patients with renal failure were increased compared with levels in normal individuals, 1.0 +/- 0.1 ng/ml. Levels of ESN were not correlated with laboratory parameters that may be abnormal in renal failure. NSN levels in 16 of 17 patients undergoing HD were 3.2 +/- 0.34 ng/ml and in 14 of 17 patients with CAPD were 2.9 +/- 0.4 ng/ml, respectively. ESN before HD (r = 0.63, P less than 0.01), after HD (r = 0.85, P less than 0.001), and in patients with CAPD (r = 0.83, P less than 0.001) and IPD (r = 0.81, P less than 0.05) correlated significantly with an OT-like peptide previously found to be increased in renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Chromatography, High Pressure Liquid; Estrogens; Humans; Kidney Failure, Chronic; Middle Aged; Neurophysins; Nicotine; Oxytocin; Peritoneal Dialysis; Peritoneal Dialysis, Continuous Ambulatory; Pituitary Gland, Posterior; Renal Dialysis; Vasopressins

The systemic effects of local anesthetic drugs, especially bupivacaine, on myocardial conduction and the increase of cardiotoxicity by hypoxemia, acidosis, and hyperkalemia has been proven in numerous animal experiments. In our department, supraclavicular brachial block with bupivacaine is the method of choice for patients with chronic renal failure requiring operations of the upper limb. The question may be raised whether or not these patients with their concomitant disease--electrolyte and acid-base imbalances, uremic cardiomyopathy--are especially endangered by the use of this drug. Supraclavicular brachial blockade (3 mg/kg bupivacaine 0.5% + 0.1 IU vasopressin/ml) was performed in 10 patients with chronic renal failure requiring hemodialysis. The control group consisted of 10 healthy patients who were admitted for minor hand surgery. Preoperative blood samples were taken for measurements of blood urea nitrogen, serum creatinine, serum electrolytes, and arterial blood gas analysis. Long-term ECG monitoring begun 20 min before injection of the block and continued over a total of 200 min. Serum concentrations of bupivacaine were determined at 10, 20, 30, 60, 120, and 180 min after injection. Comparing the two groups, no severe changes in electrolytes or acid-base status could be found despite some statistical significances. Even though bupivacaine serum concentrations proved to be 3 times higher in the study group than in the control group, no changes in cardiac conduction could be registered. We conclude that bupivacaine is as safe in dialyzed patients with chronic renal failure with regard to possible changes in circulatory parameters and myocardial conduction as in healthy patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Blood Chemical Analysis; Blood Pressure; Brachial Plexus; Bupivacaine; Electrocardiography; Electrolytes; Heart Rate; Humans; Kidney Failure, Chronic; Nerve Block; Renal Dialysis; Vasopressins

Topics: Acute Kidney Injury; Blood; Humans; Kidney Failure, Chronic; Metabolic Clearance Rate; Polyuria; Renin-Angiotensin System; Ultrafiltration; Uremia; Vasopressins

Topics: Humans; Hyponatremia; Kidney Concentrating Ability; Kidney Failure, Chronic; Osmolar Concentration; Renal Dialysis; Vasopressins; Water-Electrolyte Balance

Topics: Acute Kidney Injury; Adult; Depression, Chemical; Endorphins; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Naloxone; Receptors, Opioid; Vasopressins

Changes in plasma ADH levels and plasma aldosterone levels (PA) were studied in patients with end-stage renal disease (N = 40). The patients were divided into two groups according to their plasma renin activity (PRA) into a low renin (LR, n = 9) and a high renin group (HR, n = 31). The metabolic clearance rate (MCR) of plasma ADH was also investigated in 4 patients and 5 normal volunteers. Additionally, it was examined whether plasma ADH, aldosterone and renin were permeable through the dialysis membrane. Pre- and post-dialysis plasma ADH levels in LR were similar to those in the HR group. However, pre- and post-dialysis PA in the HR group were significantly greater than those in the LR group. Post-dialysis PRA was significantly increased in HR compared to pre-dialysis, but not in LR. Pre- and post-dialysis plasma osmolality was increased in both groups, but effective plasma osmolality (EPosm) was within the normal range. There was a significant correlation between EPosm and plasma ADH level both before and after haemodialysis, but the majority of the abnormally high values of ADH compared to the normal values was found within the normal range of EPosm. The patients exhibited high blood pressure and a rise in body weight, and haemodialysis caused a significant fall in body weight and blood pressure in both groups. MCR of ADH was significantly lower in the patients than that in normal subjects. Plasma ADH proved to be permeable through the dialysis membrane in all cases, but aldosterone in only a few cases. Renin was not permeable.

Topics: Adolescent; Adult; Aged; Aldosterone; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Osmolar Concentration; Renal Dialysis; Renin; Vasopressins

We examined renal function and Na+ balance in a patient with congestive heart failure who was treated with demeclocycline (DMC) on three separate occasions under strict metabolic balance conditions. Natriuresis and reversible renal insufficiency, which could not be explained solely on the basis of negative Na+ balance, developed on each occasion. In contrast to reports of an association between elevated serum DMC levels and renal insufficiency in patients with cirrhotic edema, the renal insufficiency in this patient with cardiac edema occurred in the absence of high DMC levels. Consequently, markedly elevated serum DMC levels do not appear to be a prerequisite for the development of natriuresis or renal insufficiency in edematous patients receiving this drug. In an attempt to clarify the mechanism of the natriuresis, we also examined the effects of DMC on Na+ transport in an in-vitro model system, the toad urinary bladder. DMC inhibited aldosterone-stimulated Na+ transport, but had no effect on Na+ transport when the latter was jointly stimulated by ADH and theophylline. Despite this selective inhibition of the natriferic effect of aldosterone in vitro, it is unlikely that such a mechanism completely accounts for the natriuresis observed in-vivo since the natriuresis is generally of large magnitude and is usually accompanied by some degree of kaliuresis, and DMC had no consistent effect on urinary aldosterone excretion. Consequently, other mechanisms must be sought to explain the natriuretic effect of DMC in edematous patients. Likewise, mechanisms other than negative Na+ balance (perhaps primary alterations in renal hemodynamics) must underly the development of renal insufficiency in such individuals.

Topics: Administration, Oral; Aldosterone; Animals; Anura; Biological Transport; Blood Urea Nitrogen; Body Weight; Demeclocycline; Glomerular Filtration Rate; Heart Failure; Humans; In Vitro Techniques; Kidney Failure, Chronic; Male; Middle Aged; Natriuresis; Nephrons; Potassium; Sodium; Theophylline; Vasopressins

The effect of changes in extracellular volume versus changes in plasma osmolality on arginine vasopressin (AVP) release was studied in 6 patients with terminal renal failure maintained on chronic hemodialysis. The day of the study, the patients were treated by sequential ultrafiltration lasting 1 hour followed by a 3-hour conventional hemodialysis session. The ultrafiltration resulted in the removal of 460 to 1,170 ml (mean = 860 ml) of volume. Body weight during the combined procedures fell by 1.6 +/- 0.4 kg (mean +/- s.e.m.) while mean arterial pressure decreased only slightly. Plasma osmolality was unaffected by sequential ultrafiltration, but decreased from 313 +/- 4 mosm/kg H2O to 291 +/- 4 mosm/kg H2O during hemodialysis. Initial plasma AVP concentration was high at 4.45 +/- 0.25 pg/ml and remained unchanged during the sequential ultrafiltration at 4.55 +/- 0.37 pg/ml, but it fell during the hemodialysis to 2.47 +/- 0.45 pg/ml. A hypotensive episode observed in one patient towards the end of hemodialysis resulted in a sharp increase in plasma AVP concentration from 5.5 to 18 pg/ml. During the combined procedures, plasma AVP and plasma osmolality showed a close and linear correlation (r = 0.63, n = 23, p less than 0.001). These findings suggest that in patients on maintenance hemodialysis, changes in plasma osmolality play a predominant role in determining AVP secretion whereas a marked decrease in volume without ensuing hypotension has no effect on AVP release.

Topics: Blood Pressure; Blood Volume; Extracellular Space; Humans; Kidney Failure, Chronic; Osmolar Concentration; Renal Dialysis; Ultrafiltration; Vasopressins

Urinary clearance of antidiuretic hormone (ADH) has been measured under basal conditions and during intravenous administration of arginine vasopressin in ten healthy subjects, and only under basal conditions in 18 patients with chronic renal failure and seven patients with acute renal failure at the polyuric phase of the disease. In healthy subjects studied under conditions of mild water diuresis plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 3.3 +/- 0.36 pg/ml, 25.2 +/- 5.5 pg/min, 7.5 +/- 1.2 ml/min and 6.4 +/- 1.0% (means +/- SEM) respectively. When plasma ADH was raised to levels between 7 and 26 pg/ml during intravenous administration of the hormone, urinary excretion rate and urinary clearance of ADH increased. Tubular reabsorption of ADH did not reach a plateau but progressively increased in the range of plasma ADH studied. In patients with chronic renal failure, plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 2.8 +/- 0.19 pg/ml, 9.4 +/- 2.0 pg/min, 3.4 +/- 0.6 ml/min and 10.0 +/- 2.9% (means +/- SEM) respectively. Urinary excretion rate and urinary clearance were significantly lower than in healthy subjects. In patients with acute renal failure, plasma concentration, urinary excretion rate, urinary clearance and fractional clearance of ADH were 4.6 +/- 0.47 pg/ml, 52.8 +/- 15.8 pg/min, 9.5 +/- 2.7 ml/min and 24.9 +/- 4.4% (means +/- SEM) respectively. Urinary excretion rate and fractional clearance were higher than in healthy subjects and patients with chronic renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Kidney Injury; Arginine Vasopressin; Creatinine; Female; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Male; Vasopressins

A case of solitary cecal ulcer with major hemorrhage followed by perforation after treatment with intra-arterial vasopressin in a patient with end-stage renal failure is presented. Though vasopressin has been used with success in the treatment of colonic hemorrhage, caution should be applied in patients with a bleeding cecal ulcer as the vasoconstriction produced by vasopressin may cause perforation in an area whose blood supply is already compromised.

Topics: Cecal Diseases; Female; Gastrointestinal Hemorrhage; Humans; Intestinal Perforation; Kidney Failure, Chronic; Middle Aged; Radiography; Ulcer; Vasopressins

Topics: Acute Kidney Injury; Adult; Blood Pressure; Blood Volume; Brain Edema; Chemoreceptor Cells; Edema; Female; Humans; Kidney; Kidney Concentrating Ability; Kidney Failure, Chronic; Male; Pressoreceptors; Renin-Angiotensin System; Vasopressins; Water-Electrolyte Balance

Topics: Adrenocorticotropic Hormone; Aldosterone; Angiotensins; Carbohydrate Metabolism; Catecholamines; Endocrine System Diseases; Erythropoietin; Female; Gastrins; Gonadal Steroid Hormones; Humans; Hydrocortisone; Kidney Failure, Chronic; Male; Renal Dialysis; Renin; Thyroid Gland; Uremia; Vasopressins

In 13 patients suffering from renal dysfunction and treated by chronic haemodialysis, the mnemic functions appeared within the limits of normality and there was no positive correlation between blood levels of neurophysines and free cortisol. On the other hand, a negative correlation was found between levels of neurophysine I and items 3 and 5 of the memory test PRM. This negative result indicates that in haemodialyzed patients a discrepancy may exist between blood levels of neurophysines and vasopressin release, or that there is no direct relationship between plasma and CSF concentrations of such hormones.

Topics: Adrenocorticotropic Hormone; Adult; Aged; Humans; Hydrocortisone; Kidney Failure, Chronic; Male; Memory; Middle Aged; Oxytocin; Pituitary Gland, Posterior; Psychological Tests; Renal Dialysis; Vasopressins

Quantative data on plasma levels of antidiuretic hormone (ADH) in renal failure are limited. We measured predialysis plasma ADH levels using a double antibody radioimmunoassay in 14 patients with end-stage renal failure. Plasma ADH was inappropriately elevated in the majority of tested patients despite normal plasma osmolality, moderately elevated blood pressure, and hypervolemia. The etiology of increased plasma ADH in our population is unclear.

Topics: Adult; Aged; Blood Pressure; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Osmolar Concentration; Renal Dialysis; Vasopressins

The effect of isoosmolar volume reduction on plasma ADH level was studied in 8 patients with chronic renal failure utilizing hemofiltration technique. Plasma ADH fell significantly (P less than 0.001) after one hour of hemofiltration despite volume reduction which was expected to elevate the ADH level. After two hours of hemofiltration, ADH remained low in 5 patients and increased in 3. Post-hemofiltration mean blood pressure was generally lower in patients whose ADH rose than those whose ADH remained low. The two groups were otherwise comparable with respect to total fluid loss, hemofiltration rate, and fluid removed expressed as percent body weight. It can thus be suggested that in these patients a rise in plasma ADH in response to fluid reduction may require a fall in the arterial blood pressure below a critical level. While the rise in plasma ADH observed with continued fluid removal in some patients can be readily explained, we have no clear explanation for the paradoxical initial fall of ADH in all patients and subsequent maintenance of low levels observed in the majority of patients. This unusual ADH response to isoosmolar volume reduction may represent some unidentified mechanism of ADH regulation in patients with end-stage renal disease.

Topics: Adult; Aged; Blood; Blood Pressure; Extracellular Space; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Osmolar Concentration; Ultrafiltration; Vasopressins; Water-Electrolyte Balance

Topics: Demeclocycline; Humans; Kidney Failure, Chronic; Liver Cirrhosis, Alcoholic; Radioimmunoassay; Vasopressins

Topics: Blood Volume; Diuretics; Heart Failure; Hospitalization; Humans; Hyperglycemia; Hyponatremia; Kidney Failure, Chronic; Liver Cirrhosis; Stress, Physiological; Surgical Procedures, Operative; Vasopressins

Topics: Adult; Body Water; Diabetes Insipidus; Diuresis; Extracellular Space; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Intracellular Fluid; Kidney Concentrating Ability; Kidney Failure, Chronic; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Adult; Arginine Vasopressin; Female; Homeostasis; Humans; Kidney Failure, Chronic; Male; Middle Aged; Osmolar Concentration; Renal Dialysis; Vasopressins

Plasma vasopressin (VP) was determined in 28 patients with chronic renal failure undergoing hemodialysis. Plasma VP levels were significantly higher in the patients than in the normal subjects. It was also observed that plasma VP levels did not fall significantly despite a marked decrease of effective plasma osmolality following hemodialysis, and that no correlation was obtained between the plasma VP levels and effective plasma osmolality, both before and after hemodialysis. By analyzing the changes in blood volume and blood pressure in addition to plasma osmolality in each case, a dysfunction of VP release in response to osmotic stimulus was found in 5 out of 28 patients.

Topics: Adolescent; Adult; Blood Pressure; Blood Volume; Body Weight; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Osmolar Concentration; Renal Dialysis; Vasopressins

The excretion of cyclic AMP in urine has been examined in normal children and in children with nephrogenic diabetes insipidus or moderate renal failure (predominantly defective concentrating ability) under basal conditions and in response to antidiuretic hormone (ADH) and parathyroid hormone (PTH). In contrast to other reported data, we could not confirm an ADH- and (PTH-unresponsiveness in hereditary, congenital nephrogenic diabetes insipidus, but our patients with structural renal disorders characterized by a defective urine concentrating ability did have reduced hormonal responses. It seems necessary to define nephrogenic diabetes insipidus very carefully, and until more data are collected, there appears to be no value in the measurement of urinary cyclic AMP level in the individual patient in the differential diagnosis of disorders due to renal concentrating defects.

Topics: Adolescent; Child; Child, Preschool; Cyclic AMP; Diabetes Insipidus; Diabetic Nephropathies; Humans; Infant; Kidney Failure, Chronic; Male; Parathyroid Hormone; Vasopressins

U-Deamino-8-D-arginine-vasopressin (DDAVP) is a new synthetic antidiuretic hormone with prolonged action. 0.02 mg given intranasally to 38 patients with far advanced chronic renal failure effected an instantaneous decrease in urine volume as well as an augmentation of U/P-inulin ratio, fraction of filtered sodium and chloride excreted and of the absolute elimination of these ions. These findings suggest an improvement of permeability at the descending limb of Henle, too, the latter and a diminution of circulation in the renal medulla being responsible for the increase in renal salt loss after DDAVP. A rise of blood pressure or other side effects could not be observed.

Topics: Administration, Intranasal; Arginine; Chlorides; Diuresis; Glomerular Filtration Rate; Glomerulonephritis; Humans; Kidney Failure, Chronic; Kidney Function Tests; Male; Pyelonephritis; Sodium; Vasopressins

Topics: Aldosterone; Angiotensin II; Heart Failure; Hematuria; Humans; Kidney; Kidney Failure, Chronic; Natriuresis; Renin; Vasopressins

Topics: Creatinine; Electrophoresis; Humans; Kidney Failure, Chronic; Kidney Tubules; Neurophysins; Pituitary Gland, Posterior; Pyelonephritis; Vasopressins

Topics: Adult; Carbamazepine; Clofibrate; Diabetes Insipidus; Diuresis; Female; Glomerular Filtration Rate; Humans; Kidney Failure, Chronic; Lysine; Nephritis; Osmolar Concentration; Pituitary Gland; Vasopressins; Water

Topics: Adrenal Glands; Aldosterone; Ascites; Blood Pressure; Calcium; Creatinine; Cyclic AMP; Edema; Glomerular Filtration Rate; Humans; Hydrocortisone; Hypertension; Kidney; Kidney Failure, Chronic; Kidney Tubules; Liver Cirrhosis; Magnesium; Osmolar Concentration; Phosphates; Potassium; Prostaglandins; Renin; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Blood; Blood Urea Nitrogen; Body Water; Creatinine; Desoxycorticosterone; Diet, Sodium-Restricted; Extracellular Space; Feces; Glomerular Filtration Rate; Humans; Hydrocortisone; Kidney Concentrating Ability; Kidney Failure, Chronic; Mannitol; Osmolar Concentration; Plasma Volume; Potassium; Sodium; Spironolactone; Urea; Urine; Vasopressins

Topics: Adolescent; Adult; Aged; Blood; Child; Dehydration; Female; Glomerular Filtration Rate; Humans; Iodine Radioisotopes; Iothalamic Acid; Kidney Concentrating Ability; Kidney Failure, Chronic; Kidney Medulla; Loop of Henle; Male; Middle Aged; Osmolar Concentration; Polycystic Kidney Diseases; Sodium; Sodium Chloride; Urine; Vasopressins; Water

The effect of octapressin (2-phenylalanine-8-lysine vasopressin) on renal and intrarenal blood flow was studied in 11 normotensive cirrhotic patients with abnormal renal perfusion. Renal haemodynamic changes were assessed with the (133)Xenon washout technique. Of the six patients given suppressor doses of octapressin intravenously renal blood flow improved in one only. A further three patients responded to the drug in a dose which increased the mean arterial pressure by 5 or more mm Hg. The increase in mean renal blood flow was accompanied by an improvement in renal cortical perfusion. In two patients renal blood flow decreased after the administration of octapressin. These findings, in conjunction with previous reports, suggest that octapressin will only consistently improve renal perfusion in cirrhotic subjects who are hypotensive and in whom the mean arterial blood pressure is raised by the drug, but do not exclude the possibility that octapressin may have a direct renal circulatory effect in some patients.

Topics: Adult; Alkaline Phosphatase; Bilirubin; Blood Flow Velocity; Blood Pressure; Creatinine; Felypressin; Female; Humans; Hypertension, Portal; Hypotension; Kidney; Kidney Failure, Chronic; Liver Cirrhosis; Male; Middle Aged; Serum Albumin; Vasopressins; Xenon

Topics: Adrenal Cortex Hormones; Alkalosis; Blood Urea Nitrogen; Blood Volume; Diuretics; Edema; Ethacrynic Acid; Furosemide; Glomerular Filtration Rate; Humans; Hyperaldosteronism; Hyperkalemia; Hypokalemia; Hyponatremia; Kidney Failure, Chronic; Kidney Tubules; Liver Cirrhosis; Spironolactone; Triamterene; Vasopressins

Topics: Adult; Aged; Anemia, Hemolytic; Anemia, Hypochromic; Anemia, Sideroblastic; Aspirin; Blood Urea Nitrogen; Creatinine; Diagnosis, Differential; Female; Hematuria; Humans; Kidney Failure, Chronic; Male; Middle Aged; Phenacetin; Pyelonephritis; Radioisotope Renography; Scotland; Substance-Related Disorders; Uremia; Urinary Tract Infections; Urine; Urography; Vasopressins

Topics: Adult; Angiotensin II; Blood Pressure; Creatinine; Diabetes Insipidus; Female; Humans; Kidney Failure, Chronic; Kidney Function Tests; Male; Potassium; Sodium; Vasopressins