pituitrin and Renal-Insufficiency

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of numerous kidney cysts which leads to kidney failure. ADPKD is responsible for approximately 10% of patients with kidney failure. Overwhelming evidence supports that vasopressin and its downstream cyclic adenosine monophosphate signaling promote cystogenesis, and targeting vasopressin 2 receptor with tolvaptan and other antagonists ameliorates cyst growth in preclinical studies. Tolvaptan is the only drug approved by Food and Drug Administration to treat ADPKD patients at the risk of rapid disease progression. A major limitation of the widespread use of tolvaptan is aquaretic events. This review discusses the potential strategies to improve the tolerability of tolvaptan, the progress on the use of an alternative vasopressin 2 receptor antagonist lixivaptan, and somatostatin analogs. Recent advances in understanding the pathophysiology of PKD have led to new approaches of treatment via targeting different signaling pathways. We review the new pharmacotherapies and dietary interventions of ADPKD that are promising in the preclinical studies and investigated in clinical trials.

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Polycystic Kidney, Autosomal Dominant; Receptors, Vasopressin; Renal Insufficiency; Tolvaptan; United States; Vasopressins

Autosomal-dominant polycystic kidney disease (ADPKD) is the most common genetic renal disease in adults, affecting one in every 1000 Australians. It is caused by loss-of-function heterozygous mutations in either PKD1 or PKD2 , which encode the proteins, polycystin-1 and polycystin-2 respectively. The disease hallmark is the development of hundreds of microscopic fluid-filled cysts in the kidney during early childhood, which grow exponentially and continuously through life at varying rates (between 2% and 10% per year), causing loss of normal renal tissue and up to a 50% lifetime risk of dialysis-dependent kidney failure. Other systemic complications include hypertensive cardiac disease, hepatic cysts, intracranial aneurysms, diverticular disease and hernias. Over the last two decades, advances in the genetics and pathogenesis of this disease have led to novel treatments that reduce the rate of renal cyst growth and may potentially delay the onset of kidney failure. New evidence indicates that conventional therapies (such as angiotensin inhibitors and statins) have mild attenuating effects on renal cyst growth and that systemic levels of vasopressin are critical for promoting renal cyst growth in the postnatal period. Identifying and integrating patient-centred perspectives in clinical trials is also being advocated. This review will provide an update on recent advances in the clinical management of ADPKD.

Topics: Angiotensin Receptor Antagonists; Disease Management; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypertension; Mutation; Polycystic Kidney, Autosomal Dominant; Randomized Controlled Trials as Topic; Renal Dialysis; Renal Insufficiency; TRPP Cation Channels; Vasopressins

Autosomal dominant polycystic kidney disease (ADPKD) is the commonest inherited cause of renal failure in adults, and is due to loss-of-function mutations in either the PKD1 or PKD2 genes, which encode polycystin-1 and polycystin-2, respectively. These proteins have an essential role in maintaining the geometric structure of the distal collecting duct in the kidney in adult life, and their dysfunction predisposes to renal cyst formation. The typical renal phenotype of ADPKD is the insidious development of hundreds of renal cysts, which form in childhood and grow progressively through life, causing end-stage kidney failure in the fifth decade in about half affected by the mutation. Over the past 2 decades, major advances in genetics and disease pathogenesis have led to well-conducted randomized controlled trials, and observational studies that have resulted in an accumulation of evidence-based data, and raise hope that the lifetime risk of kidney failure due to ADPKD will be progressively curtailed during this century. This review will provide a contemporary summary of the current state of the field in disease pathogenesis and therapeutics, and also briefly highlights the importance of clinical practice guidelines, patient perspectives, patient-reported outcomes, uniform trial reporting, and health-economics in ADPKD.

Topics: Age of Onset; Humans; Polycystic Kidney, Autosomal Dominant; Practice Guidelines as Topic; Renal Insufficiency; Signal Transduction; TRPP Cation Channels; Vasopressins

This is a review of the management of septic shock that suggests an approach to treatment (ABCDEF: Airway, Breathing, Circulation, Drugs, Evaluate the source of sepsis, Fix the source of sepsis) for clinicians. The incidence of septic shock is increasing and mortality ranges from 30% to 70%. The commonest sources of infection are lung (25%), abdomen (25%), and other sources. Septic shock occurs because of highly complex interactions between the infecting microorganism(s) and the responses of the human host. The innate immune response is rapidly followed by the more specific adaptive immune response. Septic shock is characterized by alterations in the coagulant/anticoagulant balance such that there is a more pro-coagulant phenotype. Lung protective ventilation (which means the use of relatively low tidal volumes of 4 -6 mL/kg ideal body weight) is recommended for treatment of patients who have septic shock. Rivers early goal-directed therapy is recommended because it showed a significant increase in survival. Surviving Sepsis guidelines recommend resuscitation of septic shock with either crystalloid or colloid. Patients who have septic shock should be treated with intravenous broad-spectrum antibiotics as rapidly as possible and certainly within one hour. Activated protein C (APC) is a vitamin K dependent serine protease that is an anticoagulant and is also cytoprotective and anti-inflammatory. APC (24 mg/kg/hour infusion for 96 hours) decreased mortality (APC 25% vs placebo 31%, relative risk 0.81P=0.005) and improved organ dysfunction in patients at high risk of death (e.g. APACHE II >25 [APC 31% vs placebo 44%]). APC is not recommended to treat surgical patients who have one organ system dysfunction. In 2006, the European regulatory authority indicated that there must be another randomized placebo-controlled trial of APC to further establish efficacy as assessed by mortality reduction. Vasopressin is a key stress hormone in response to hypotension. The VASST study was a randomized trial of vasopressin versus norepinephrine in septic shock. There was no difference in mortality between vasopressin versus norepinephrine-treated patients (35% versus 39% respectively). In patients who had less severe septic shock, patients treated with vasopressin may have lowered mortality compared with norepinephrine (26% vs 36%). Annane et al. found that hydrocortisone plus fludrocortisone (compared to placebo) was associated with lower mortality in patients who had an in

Topics: Adrenal Cortex Hormones; Anemia; Anti-Bacterial Agents; Anticoagulants; Blood Coagulation; Fluid Therapy; Humans; Hyperglycemia; Hypoglycemic Agents; Insulin; Protein C; Renal Insufficiency; Shock, Septic; Vasopressins

Heart failure is one of the leading causes of hospitalizations in the United States. Concomitant and significant renal dysfunction is common in patients with heart failure. Increasingly, the syndrome of heart failure is one of cardiorenal failure, in which concomitant cardiac and renal dysfunctions exist, with each accelerating the progression of the other. One fourth of patients hospitalized for the treatment of acute decompensated heart failure will experience significant worsening of renal function, which is associated with worse outcomes. It remains unclear whether worsening renal function specifically contributes to poor outcomes or whether it is merely a marker of advanced cardiac and renal dysfunction. Diuretic resistance, with or without worsening renal function, is also common in acute decompensated heart failure, although the definition of diuretic resistance, its prevalence, and prognostic implications are less well defined. The term cardiorenal syndrome has been variably associated with cardiorenal failure, worsening renal function, and diuretic resistance but is more comprehensively defined as a state of advanced cardiorenal dysregulation manifest by one or all of these specific features. The pathophysiology of the cardiorenal syndrome is poorly understood and likely involves interrelated hemodynamic and neurohormonal mechanisms. When conventional therapy for acute decompensated heart failure fails, mechanical fluid removal via ultrafiltration, hemofiltration, or hemodialysis may be needed for refractory volume overload. While ultrafiltration can address diuretic resistance, whether ultrafiltration prevents worsening renal function or improves outcomes in patients with cardiorenal syndrome remains unclear. Evidence regarding the potential renal-preserving effects of nesiritide is mixed, and further studies on the efficacy and safety of different doses of nesiritide in heart failure therapy are warranted. Newer therapeutic agents, including vasopressin antagonists and adenosine antagonists, hold promise for the future, and clinical trials of these agents are underway.

Topics: Acute Disease; Adenosine; Cardiotonic Agents; Dopamine; Heart Failure; Humans; Natriuretic Agents; Natriuretic Peptide, Brain; Renal Insufficiency; Risk Factors; Sodium Potassium Chloride Symporter Inhibitors; Ultrafiltration; Vasopressins

Renal insufficiency is becoming an increasingly common and devastating comorbidity in both acute and chronic heart failure settings. Part of the problem is due to the lack of insight into the underlying pathophysiology of salt and water balance leading to the congestive states. This review summarizes our current understanding regarding the cause and consequences of renal insufficiency in patients with heart failure, and addresses some of the limitations of current therapeutic strategies. Based on these limitations, this paper will explore the ongoing efforts to develop novel drug therapeutics to prevent or ameliorate renal impairment in patients with heart failure. These include natriuretic peptides and other vasodilators, adenosine receptor antagonists, and vasopressin receptor antagonists all currently undergoing late-stage clinical trials.

Topics: Adenosine; Angiotensin-Converting Enzyme Inhibitors; Antidiuretic Agents; Diuretics; Drug Therapy, Combination; Heart Failure; Humans; Mineralocorticoid Receptor Antagonists; Natriuretic Agents; Natriuretic Peptide, Brain; Natriuretic Peptides; Neurotransmitter Agents; Prognosis; Renal Insufficiency; Treatment Outcome; Vasodilator Agents; Vasopressins

Endocrinopathy during sepsis can manifest as hyperglycemia and insulin resistance or as insufficient production of either adrenal corticosteroids or vasopressin. The results of a recent large clinical trial have demonstrated that tight glycemic control with insulin can confer survival benefit to selected intensive care unit patients. Relative impairment of adrenocortical reserve has been suggested to be an important contributor to the pathogenesis of shock in sepsis. Replacement doses of glucocorticoids and mineralocorticoids have been associated with improved survival in the subset of patients with blunted results on adrenocorticotropin hormone stimulation tests. Posterior pituitary production of vasopressin is diminished in septic shock while sensitivity to its vasopressor effects is enhanced. Clinical trials are underway to determine whether administration of vasopressin can improve outcomes in patients with septic shock. Whether the euthyroid sick syndrome represents an adaptive or a maladaptive response to severe illness remains unclear.

Topics: Animals; Clinical Trials as Topic; Endocrine System; Humans; Renal Insufficiency; Sepsis; Vasopressins

Physiologic data provided evidence for specific urea transporter proteins in red blood cells and kidney inner medulla. During the past decade, molecular approaches resulted in the cloning of several urea transporter cDNA isoforms derived from two gene families: UT-A and UT-B. Polyclonal antibodies were generated to the cloned urea transporter proteins, and their use in integrative animal studies resulted in several novel findings, including: (1) UT-B is the Kidd blood group antigen; (2) UT-B is also expressed in many non-renal tissues and endothelial cells; (3) vasopressin increases UT-A1 phosphorylation in rat inner medullary collecting duct; (4) the surprising finding that UT-A1 protein abundance and urea transport are increased in the inner medulla during conditions in which urine concentrating ability is reduced; and (5) UT-A protein abundance is increased in uremia in both liver and heart. This review will summarize the knowledge gained from studying molecular mechanisms of urea transport and from integrative studies into urea transporter protein regulation.

Topics: Angiotensins; Animals; Biological Transport, Active; Cell Membrane Permeability; Diabetes Mellitus; Homeostasis; Humans; Kidney; Kidney Concentrating Ability; Kidney Medulla; Membrane Transport Proteins; Mice; Rats; Renal Insufficiency; Urea; Urea Transporters; Uremia; Urine; Vasopressins

The changes in sodium homeostasis most frequently are expression of water-electrolyte balance disturbances in patients with liver cirrhosis. Hyponatremia of water excess is found in 35% of the patients with cirrhosis and ascites. This disturbance is most frequently connected with raised antidiuretic hormone (vasopressin) secretion and is realized by including of nonosmotic stimulating mechanisms. The vasopressin plays a leading role in pathogenesis of disturbed water metabolism in the liver cirrhosis. Some patients with hepatorenal syndrome are established with highest plasma vasopressin concentrations. Gene expression of the regulation of kidney vasopressin-sensitive water channels (aquaporin-2 proteins) is also raised in the liver cirrhosis. Using in practice vasopressin-type 2 (V-2) receptor antagonists gives hopeful results in medical treatment of water-electrolyte disturbances in patients with advanced liver cirrhosis.

Topics: Gene Expression; Humans; Hyponatremia; Liver Cirrhosis; Renal Insufficiency; Sodium; Vasopressins; Water-Electrolyte Imbalance

Norepinephrine is currently recommended as the first-line vasopressor in septic shock; however, early vasopressin use has been proposed as an alternative.. To compare the effect of early vasopressin vs norepinephrine on kidney failure in patients with septic shock.. A factorial (2×2), double-blind, randomized clinical trial conducted in 18 general adult intensive care units in the United Kingdom between February 2013 and May 2015, enrolling adult patients who had septic shock requiring vasopressors despite fluid resuscitation within a maximum of 6 hours after the onset of shock.. Patients were randomly allocated to vasopressin (titrated up to 0.06 U/min) and hydrocortisone (n = 101), vasopressin and placebo (n = 104), norepinephrine and hydrocortisone (n = 101), or norepinephrine and placebo (n = 103).. The primary outcome was kidney failure-free days during the 28-day period after randomization, measured as (1) the proportion of patients who never developed kidney failure and (2) median number of days alive and free of kidney failure for patients who did not survive, who experienced kidney failure, or both. Rates of renal replacement therapy, mortality, and serious adverse events were secondary outcomes.. A total of 409 patients (median age, 66 years; men, 58.2%) were included in the study, with a median time to study drug administration of 3.5 hours after diagnosis of shock. The number of survivors who never developed kidney failure was 94 of 165 patients (57.0%) in the vasopressin group and 93 of 157 patients (59.2%) in the norepinephrine group (difference, -2.3% [95% CI, -13.0% to 8.5%]). The median number of kidney failure-free days for patients who did not survive, who experienced kidney failure, or both was 9 days (interquartile range [IQR], 1 to -24) in the vasopressin group and 13 days (IQR, 1 to -25) in the norepinephrine group (difference, -4 days [95% CI, -11 to 5]). There was less use of renal replacement therapy in the vasopressin group than in the norepinephrine group (25.4% for vasopressin vs 35.3% for norepinephrine; difference, -9.9% [95% CI, -19.3% to -0.6%]). There was no significant difference in mortality rates between groups. In total, 22 of 205 patients (10.7%) had a serious adverse event in the vasopressin group vs 17 of 204 patients (8.3%) in the norepinephrine group (difference, 2.5% [95% CI, -3.3% to 8.2%]).. Among adults with septic shock, the early use of vasopressin compared with norepinephrine did not improve the number of kidney failure-free days. Although these findings do not support the use of vasopressin to replace norepinephrine as initial treatment in this situation, the confidence interval included a potential clinically important benefit for vasopressin, and larger trials may be warranted to assess this further.. clinicaltrials.gov Identifier: ISRCTN 20769191.

Topics: Adult; Aged; Aged, 80 and over; Critical Care; Double-Blind Method; Drug Administration Schedule; Female; Fluid Therapy; Humans; Hydrocortisone; Intensive Care Units; Male; Middle Aged; Norepinephrine; Renal Insufficiency; Renal Replacement Therapy; Shock, Septic; Treatment Outcome; United Kingdom; Vasoconstrictor Agents; Vasopressins

Time-velocity wave-form analysis of Doppler signals from small intrarenal arteries allows estimation of intrarenal arteriolar vascular resistance. Among the various indexes proposed, the resistive index is the most widely used for this estimation. To investigate whether the resistive index is useful in the diagnosis of functional kidney failure and prediction of survival in cirrhotic patients with ascites, we measured resistive index, kidney and liver function and plasma levels of renin, aldosterone and antidiuretic hormone in 10 healthy subjects, 12 patients with compensated cirrhosis and 32 patients with cirrhosis and ascites (17 with kidney failure). A total of 28 clinical and laboratory variables were analyzed for prognostic value. Resistive index was significantly increased in patients with kidney failure (0.74 +/- 0.01) compared with those in the other three groups (0.64 +/- 0.01, 0.64 +/- 0.02 and 0.67 +/- 0.01) and correlated significantly with glomerular filtration rate, arterial pressure, plasma renin activity and free water clearance in the cirrhotic patients. The sensitivity and specificity of the resistive index in detecting kidney failure in patients with ascites were 71% and 80%, respectively. Nine variables were correlated with survival in the univariate analysis, including resistive index, age, hepatomegaly, blood urea nitrogen, serum creatinine, plasma sodium concentration, glomerular filtration rate, plasma renin activity and plasma concentration of antidiuretic hormone. Multivariate analysis disclosed only three independent predictors of survival: plasma renin activity, plasma concentration of antidiuretic hormone and serum sodium concentration. In conclusion, resistive index is a sensitive method to assess intrarenal hemodynamics in patients with cirrhosis and ascites. It also has predictive value for survival in these patients.

Topics: Analysis of Variance; Blood Pressure; Female; Glomerular Filtration Rate; Humans; Liver Cirrhosis; Male; Middle Aged; Multivariate Analysis; Predictive Value of Tests; Prognosis; Regression Analysis; Renal Artery; Renal Insufficiency; Renin; Sensitivity and Specificity; Sodium; Survival Rate; Ultrasonography, Doppler; Vascular Resistance; Vasopressins

Topics: Humans; Norepinephrine; Renal Insufficiency; Sepsis; Shock, Septic; Vasopressins

Intrauterine environments are related to fetal renal development and postnatal health. Influence of salty diets during pregnancy on renal functions and renin-angiotensin system (RAS) was determined in the ovine fetuses and offspring. Pregnant ewes were fed high-salt diet (HSD) or normal-salt diet (NSD) for 2 months during middle-to-late gestation. Fetal renal functions, plasma hormones, and mRNA and protein expressions of the key elements of renal RAS were measured in the fetuses and offspring. Fetal renal excretion of sodium was increased while urine volume decreased in the HSD group. Fetal blood urea nitrogen was increased, while kidney weight:body weight ratio decreased in the HSD group. The altered ratio was also observed in the offspring aged 15 and 90 days. Maternal and fetal plasma antidiuretic hormone was elevated without changes in plasma renin activity and Ang I levels, while plasma Ang II was decreased. The key elements of local renal RAS, including angiotensinogen, angiotensin converting enzyme (ACE), ACE2, AT1, and AT2 receptor expression in both mRNA and protein, except renin, were altered following maternal high salt intake. The results suggest that high intake of salt during pregnancy affected fetal renal development associated with an altered expression of the renal key elements of RAS, some alterations of fetal origins remained after birth as possible risks in developing renal or cardiovascular diseases.

Topics: Angiotensin II; Angiotensinogen; Animals; Electrolytes; Female; Fetal Blood; Gene Expression Regulation, Developmental; Kidney; Male; Maternal Nutritional Physiological Phenomena; Peptidyl-Dipeptidase A; Pregnancy; Receptors, Angiotensin; Renal Insufficiency; Renin-Angiotensin System; RNA, Messenger; Sheep, Domestic; Sodium Chloride, Dietary; Urine; Vasopressins

The Na-Cl cotransporter (NCC), which is the target of inhibition by thiazides, is located in close proximity to the chloride-absorbing transporter pendrin in the kidney distal nephron. Single deletion of pendrin or NCC does not cause salt wasting or excessive diuresis under basal conditions, raising the possibility that these transporters are predominantly active during salt depletion or in response to excess aldosterone. We hypothesized that pendrin and NCC compensate for loss of function of the other under basal conditions, thereby masking the role that each plays in salt absorption. To test our hypothesis, we generated pendrin/NCC double knockout (KO) mice by crossing pendrin KO mice with NCC KO mice. Pendrin/NCC double KO mice displayed severe salt wasting and sharp increase in urine output under basal conditions. As a result, animals developed profound volume depletion, renal failure, and metabolic alkalosis without hypokalemia, which were all corrected with salt replacement. We propose that the combined inhibition of pendrin and NCC can provide a strong diuretic regimen without causing hypokalemia for patients with fluid overload, including patients with congestive heart failure, nephrotic syndrome, diuretic resistance, or generalized edema.

Topics: Alkalosis; Animals; Anion Transport Proteins; Body Weight; Diuresis; Kidney; Kidney Function Tests; Mice; Mice, Knockout; Models, Biological; Potassium; Receptors, Drug; Renal Insufficiency; Sodium; Sodium Chloride; Sodium Chloride, Dietary; Solute Carrier Family 12, Member 3; Sulfate Transporters; Symporters; Vasopressins; Water-Electrolyte Balance

Copeptin is a marker of endogenous vasopressin secretion. Population-based data of the PREVEND Study show that men and women with high plasma copeptin have a highly prevalent microalbuminuria in addition to the low level of hydration typical of persons with high vasopressin secretion. The association of plasma copeptin with microalbuminuria suggests that vasopressin might have a role in kidney dysfunction via effects on the permselectivity of the glomerulus and/or on tubular albumin reabsorption.

Topics: Albuminuria; Biomarkers; Female; Glycopeptides; Humans; Male; Renal Insufficiency; Vasopressins

Chloroquine is one of the antimalaria drugs, also used to treat rheumatoid arthritis and systemic lupus erythematosus (SLE). Although well tolerated in most individuals, it was suggested that chloroquine can exert a profound influence on renal function, especially in individuals with compromised body fluid status. However, epidemiological studies are still lacking. The renal actions of chloroquine are further exacerbated by co-administration of other commonly used drugs such as paracetamol. The following discussion will focus on the evidence that chloroquine is a stimulator of nitric oxide (NO), which mediates many of its renal actions (diuresis, natriuresis and an increase in both glomerular filtration rate (GFR) and plasma vasopressin). Chloroquine appears to modulate the renal tubular response to vasopressin either by directly inhibiting cAMP generation or indirectly via NO.

Topics: Animals; Antimalarials; Chloroquine; Cyclic AMP; Humans; Kidney Tubules; Models, Biological; Nitric Oxide; Renal Insufficiency; Vasopressins

Up to 21% of severe cases of malaria tropica are associated with polyuria and are life-threatening. We describe a 39-yr-old man with malaria tropica who developed disseminated intravascular coagulation, polyuria, and a pituitary lesion. Empiric treatment with vasopressin improved the polyuria. This is the first case of malaria tropica in which central diabetes insipidus has been documented.

Topics: Adrenal Insufficiency; Adult; Diabetes Insipidus, Neurogenic; Disseminated Intravascular Coagulation; Humans; Hydrocortisone; Magnetic Resonance Imaging; Malaria, Falciparum; Male; Natriuresis; Pituitary Gland, Posterior; Polyuria; Pulmonary Embolism; Renal Insufficiency; 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: 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: Acute Kidney Injury; Atropine; Biomedical Research; Blood Volume; Convalescence; Dehydration; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Edema; Epinephrine; Female; Heart Failure; Hemorrhage; Humans; Hypertonic Solutions; Menstruation; Pharmacology; Placebos; Pregnancy; Renal Insufficiency; Salivation; Sweating; Uremia; Vasopressins; Water-Electrolyte Balance

Topics: Diuresis; Hemorrhagic Fever with Renal Syndrome; Humans; Kidney; Renal Insufficiency; Vasopressins