pituitrin and Acute-Kidney-Injury

The effect of early vasopressin initiation on clinical outcomes in patients with septic shock is uncertain. A systematic review and meta-analysis was performed to evaluate the impact of early start of vasopressin support within 6 h after the diagnosis on clinical outcomes in septic shock patients.. We searched the PubMed, Cochrane, and Embase databases for randomized controlled trials (RCTs) and cohort studies from inception to the 1st of February 2021. We included studies involving adult patients (> 16 years)with septic shock. All authors reported our primary outcome of short-term mortality and in the experimental group patients in the studies receiving vasopressin infusion within 6 h after diagnosis of septic shock and in the control group patients in the studies receiving no vasopressin infusion or vasopressin infusion 6 h after diagnosis of septic shock, clearly comparing with clinically relevant secondary outcomes(use of renal replacement therapy(RRT),new onset arrhythmias, ICU length of stay and length of hospitalization). Results were expressed as odds ratio (OR) and mean difference (MD) with accompanying 95% confidence interval (CI).. Five studies including 788 patients were included. The primary outcome of this meta-analysis showed that short-term mortality between the two groups was no difference (odds ratio [OR] = 1.09; 95% CI, 0.8 to 1.48; P = 0.6; χ2 = 0.83; I2 = 0%). Secondary outcomes demonstrated that the use of RRT was less in the experimental group than that of the control group (OR = 0.63; 95% CI, 0.44 to 0.88; P = 0.007; χ2 = 3.15; I2 = 36%).The new onset arrhythmias between the two groups was no statistically significant difference (OR = 0.59; 95% CI, 0.31 to 1.1; P = 0.10; χ2 = 4.7; I2 = 36%). There was no statistically significant difference in the ICU length of stay(mean difference = 0.16; 95% CI, - 0.91 to 1.22; P = 0.77; χ2 = 6.08; I2 = 34%) and length of hospitalization (mean difference = -2.41; 95% CI, -6.61 to 1.78; P = 0.26; χ2 = 8.57; I2 = 53%) between the two groups.. Early initiation of vasopressin in patients within 6 h of septic shock onset was not associated with decreased short-term mortality, new onset arrhythmias, shorter ICU length of stay and length of hospitalization, but can reduce the use of RRT. Further large-scale RCTs are still needed to evaluate the benefit of starting vasopressin in the early phase of septic shock.

Topics: Acute Kidney Injury; Arrhythmias, Cardiac; Early Medical Intervention; Humans; Intensive Care Units; Length of Stay; Mortality; Renal Replacement Therapy; Shock, Septic; Vasoconstrictor Agents; Vasopressins

Hyponatremia is frequently seen in patients with ascites secondary to advanced cirrhosis and portal hypertension. Although not apparent in the early stages of cirrhosis, the progression of cirrhosis and portal hypertension leads to splanchnic vasodilation, and this leads to the activation of compensatory mechanisms such as renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system, and antidiuretic hormone (ADH) to ameliorate low circulatory volume. The net effect is the avid retention of sodium and water to compensate for the low effective circulatory volume, resulting in the development of ascites. These compensatory mechanisms lead to impairment of the kidneys to eliminate solute-free water in decompensated cirrhosis. Nonosmotic secretion of antidiuretic hormone (ADH), also known as arginine vasopressin, further worsens excess water retention and thereby hyponatremia. The management of hyponatremia in this setting is a challenge as conventional therapies for hyponatremia including fluid restriction and correction of hypokalemia are frequently inefficacious. In this review, we discuss the pathophysiology, complications, and various treatment modalities, including albumin infusion, selective vasopressin receptor antagonists, or hypertonic saline for patients with severe hyponatremia and those awaiting liver transplantation.

Topics: Acute Kidney Injury; Acute-On-Chronic Liver Failure; Albumins; Antidiuretic Hormone Receptor Antagonists; Ascites; Fluid Therapy; Hepatic Encephalopathy; Hepatorenal Syndrome; Humans; Hypertension, Portal; Hyponatremia; Liver Cirrhosis; Liver Transplantation; Renin-Angiotensin System; Saline Solution, Hypertonic; Splanchnic Circulation; Tolvaptan; Vasodilation; Vasopressins

Acute kidney injury (AKI) is common in the setting of shock. Hemodynamic instability is a risk factor for the development of AKI, and pathophysiological mechanisms include loss of renal perfusion pressure and impaired microcirculation. Although restoration of mean arterial pressure (MAP) may mitigate the risk of AKI to some extent, evidence on this is conflicting. Also debatable is the optimal blood pressure needed to minimize the risk of kidney injury. A MAP of 65 mm Hg traditionally has been considered adequate to maintain renal perfusion pressure, and studies have failed to consistently show improved outcomes at higher levels of MAP. Therapeutic options to support renal perfusion consist of catecholamines, vasopressin, and angiotensin II. Although catecholamines are the most studied, they are associated with adverse events at higher doses, including AKI. Vasopressin and angiotensin II are noncatecholamine options to support blood pressure and may improve microcirculatory hemodynamics through unique mechanisms, including differential vasoconstriction of efferent and afferent arterioles within the nephron. Future areas of study include methods by which clinicians can measure renal blood flow in a macrocirculatory and microcirculatory way, a personalized approach to blood pressure management in septic shock using patient-specific measures of perfusion adequacy, and novel agents that may improve the microcirculation within the kidneys without causing adverse microcirculatory effects in other organs.

Topics: Acute Kidney Injury; Angiotensin II; Biomedical Research; Blood Pressure; Catecholamines; Humans; Microcirculation; Vasoconstrictor Agents; Vasopressins

To systematically review the literature and synthesize evidence concerning the effects of vasopressin and its analogs compared with other vasopressors in distributive shock, focusing on renal outcomes.. We performed a systematic review in MEDLINE, Embase, Cochrane Central, and Clinicaltrials.gov databases.. Randomized clinical trials that compared vasopressin and its analogs with other vasopressors and reported renal outcomes in adult patients with distributive shock.. Paired reviewers independently screened citations, conducted data extraction and assessed risk of bias. Three prespecified subgroup analyses were conducted. Three main outcomes related to acute renal failure were analyzed: the need for renal replacement therapy, acute kidney injury incidence, and acute kidney injury-free days. I test was used to evaluate heterogeneity between studies. Substantial heterogeneity was defined as I greater than 50%. A random-effects model with Mantel-Haenszel weighting was used for all analyses. Heterogeneity was explored using subgroup analysis. The quality of evidence for intervention effects was summarized using Grading of Recommendations Assessment, Development, and Evaluation methodology. This study was registered in the PROSPERO database (CRD42017054324).. Three-thousand twenty-six potentially relevant studies were identified, and 30 articles were reviewed in full. Seventeen studies met the inclusion criteria, including a total of 2,833 individuals. Of these, 11 studies (2,691 individuals) were suitable for quantitative meta-analysis. Overall, the evidence was of low to moderate quality. Patients who received vasopressin and its analogs had a reduced need for renal replacement therapy (odds ratio, 0.59 [0.37-0.92]; p = 0.02; I = 49%) and a lower acute kidney injury incidence (odds ratio, 0.58 [0.37-0.92]; p = 0.02; I = 63%). These results should be interpreted with caution, due to excessive heterogeneity. Acute kidney injury-free data was not pooled, since the small number of studies and extreme heterogeneity.. In patients with distributive shock, vasopressin and its analogs use is associated with a reduced need for renal replacement therapy and lower acute kidney injury incidence. These results are supported by high risk of bias evidence.

Topics: Acute Kidney Injury; Humans; Incidence; Randomized Controlled Trials as Topic; Renal Replacement Therapy; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

Liver cirrhosis is a major cause of morbidity and mortality worldwide, mainly due to complications of portal hypertension. In this article, we review the current understanding on the pathophysiology, the diagnostic criteria and the available therapeutic options for patients with emerging hepatic syndromes in cirrhosis, namely the hepatorenal, hepato-adrenal and hepatopulmonary syndrome. The hepatorenal syndrome is a well-recognized complication of advanced cirrhosis and is usually associated with an accelerated course to death unless liver transplantation is performed. The hepatopulmonary syndrome is often missed in the evaluation of patients with cirrhosis; however, early recognition is essential for the efficient management of individual patients. The hepato-adrenal syndrome, although not fully characterized, offers an exciting field for research and potential therapeutic interventions.

Topics: Acute Kidney Injury; Adrenal Insufficiency; Ascites; Creatinine; Evidence-Based Medicine; Hepatorenal Syndrome; Humans; Hypertension, Portal; Liver Cirrhosis; Liver Transplantation; Lypressin; Midodrine; Norepinephrine; Octreotide; Plasma Substitutes; Portasystemic Shunt, Transjugular Intrahepatic; Serum Albumin; Terlipressin; Vasodilator Agents; Vasopressins

Acute variceal bleeding is a potentially life-threatening complication of portal hypertension. Management consists of emergent hemostasis, therapy directed at hemodynamic resuscitation, protection of the airway, and prevention and treatment of complications including prophylactic use of antibiotics. Endoscopic treatment remains the mainstay in the management of acute variceal bleeding in combination with pharmacotherapy aimed at reducing portal pressure. This article intends to highlight only the current nonendoscopic treatment approaches for control of acute variceal bleeding.

Topics: Acute Disease; Acute Kidney Injury; Anti-Bacterial Agents; Balloon Occlusion; Blood Transfusion; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hepatic Encephalopathy; Hormones; Humans; Hypertension, Portal; Intubation, Intratracheal; Liver Cirrhosis; Portasystemic Shunt, Transjugular Intrahepatic; Somatostatin; Vasoconstrictor Agents; Vasopressins

This review will summarize the recent advances in our understanding of the relationship between liver and kidney function. It will outline the new concepts of the pathophysiology of renal dysfunction in chronic liver disease and examine novel renal biomarkers to detect acute kidney injury (AKI) in cirrhosis and following liver transplantation. We will further review new treatments for hepatorenal syndrome (HRS) and approaches to kidney dysfunction in liver transplantation recipients.. Recent studies evaluated the effect of the renin-angiotensin system on hepatic fibrosis and the role of the gut in mediating AKI after hepatic ischemia reperfusion injury. Multiple studies have investigated novel biomarkers such as neutrophil gelatinase-associated lipocalin to predict AKI (and HRS) in cirrhosis and after liver transplantation. Furthermore, there were recent advances in the management of kidney dysfunction including management of HRS with vasopressin analogs and kidney-sparing immunosuppression after liver transplantation.. Greater knowledge of the physiologic relationship between kidney and liver may open avenues for specific therapies of liver and kidney injury. Renal biomarkers may allow early diagnosis and targeted treatment of AKI, and improved management of kidney disease in the preliver and postliver transplantation setting will be crucial to improving long-term outcomes in these patients.

Topics: Acute Kidney Injury; Early Diagnosis; Female; Hepatorenal Syndrome; Humans; Immunosuppressive Agents; Liver Diseases; Liver Transplantation; Male; Renin-Angiotensin System; Vasopressins

Severe sepsis is a common occurrence in critically ill patients and a major cause of morbidity and mortality in this population. Management relies on the early identification and treatment of the underlying causative infection, adequate and rapid hemodynamic resuscitation, support of associated organ failure and modulation of the immune response with drotrecogin alfa (activated) when it is not contraindicated, and corticosteroids in severe septic shock. We will review current approaches to each of these categories.

Topics: Acute Kidney Injury; Adrenal Cortex Hormones; Adult; Anti-Bacterial Agents; Critical Illness; Fluid Therapy; Gram-Negative Bacteria; Gram-Positive Bacteria; Humans; Immunologic Factors; Protein C; Recombinant Proteins; Resuscitation; Sepsis; Vasopressins

Type 1 hepatorenal syndrome (HRS) is prerenal failure specific to decompensated cirrhosis. In patients with HRS, there is marked splanchnic/systemic vasodilation resulting in arterial hypotension, arterial baroreceptor unloading, overstimulation of the sympathetic nervous and renin-angiotensin systems. This reflex neurohumoral hyperactivity via endogenous vasoconstrictors/vasopressors such as angiotensin II and noradrenaline induces arterial vasoconstriction in different extrasplanchnic vascular beds (including preglomerular arteries in the kidneys). Decreased arterial pressure (i.e. low renal perfusion pressure) and preglomerular vasoconstriction are thought to play a major role in the decline of the glomerular filtration rate (GFR). Nonrandomized studies in patients with HRS have shown that the administration of a splanchnic vasoconstrictor (vasopressin analogue or alpha(1)-adrenoceptor agonist), usually combined with intravenous albumin, causes increases in arterial pressure, arterial baroreceptor uploading, decreased neurohumoral activity, decreased renal vascular resistance, and increased GFR. Randomized clinical trials have shown that treatment with a combination of the vasopressin analogue terlipressin and intravenous albumin improves renal function in patients with type 1 HRS. Vasopressor therapy with terlipressin plus intravenous albumin is the medical treatment of choice for type 1 HRS.

Topics: Acute Kidney Injury; Antihypertensive Agents; Humans; Hypertension, Portal; Lypressin; Terlipressin; Treatment Outcome; Vasopressins

The use of norepinephrine, and probably vasopressor therapy in general, in intensive care patients with hypotensive vasodilatation despite fluid resuscitation and evidence of acute kidney injury remains the subject of much debate and controversy. Although there is concern about the use of these drugs, these concerns are unfounded. At this time, the experimental and human data strongly suggest that, in these patients, vasopressor therapy is safe and probably beneficial from a renal, and probably general, point of view. On the basis of currently available evidence, in hypotensive vasodilated patients with acute kidney injury, restoration of blood pressure within autoregulatory values should occur promptly with noradrenaline and be sustained until such vasodilatation dissipates. The additional role of other vasopressors in these situations remains unclear. The addition of vasopressin may be helpful in individual patients, but widespread use is not supported by evidence. Alpha-dose dopamine has no advantages over noradrenaline and is not as reliably effective in restoring blood pressure and urine output. Its widespread use cannot be supported in patients with vasodilatation and acute kidney injury. Other vasopressor drugs such as epinephrine and phenylephrine may be similar in efficacy to noradrenaline. However, experience and available data with their use is vastly less than with noradrenaline. Adrenaline, in addition, is associated with hyperglycemia, hyperlactatemia, acidosis, and hypokalemia. Terlipressin appears useful in patients with acute kidney injury secondary to hepatorenal syndrome. Whether it is superior to noradrenaline in this setting remains uncertain, and more studies are needed before recommendations can be made.

Topics: Acute Kidney Injury; Animals; Blood Pressure; Critical Care; Glomerular Filtration Rate; Humans; Hypotension; Norepinephrine; Renal Circulation; Vasoconstrictor Agents; Vasopressins

Topics: Acute Kidney Injury; Apoptosis; Calcium; Capillary Permeability; Humans; Inflammation; Kidney Glomerulus; Kidney Tubules; Prognosis; Reactive Oxygen Species; Renal Circulation; Renin; Vasopressins

The hepatorenal syndrome is a form of renal failure occurring in patients with advanced liver disease. The diagnosis is based both on the demonstration of low GFR and exclusion of other common causes of renal failure that may occur in patients with cirrhosis. Orthotopic liver transplantation remains the only curative treatment for this poor outcome disease; other modalities such as vasopressin analogues, transjugular intrahepatic portosystemic shunt or renal replacement therapies may serve as a bridge to transplantation. This article reviews the pathophysiology, diagnosis and current treatment of hepatorenal syndrome.

Topics: Acute Kidney Injury; Creatinine; Diagnosis, Differential; Edema; Glomerular Filtration Rate; Hepatorenal Syndrome; Humans; Liver Cirrhosis; Liver Transplantation; Peritoneovenous Shunt; Portasystemic Shunt, Surgical; Renal Circulation; Renal Replacement Therapy; Renin-Angiotensin System; Serum Albumin; Splanchnic Circulation; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins; Water-Electrolyte Imbalance

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

The antidiuretic hormone, arginine-vasopressin (AVP), may participate in the regulation of blood pressure (BP) through its vasoconstrictor effects. In anesthetized rats, exogenous AVP induced stronger vasoconstriction in the mesenteric than in the renal vascular bed. Conversely, mesenteric but not renal vascular resistance was reduced by a vascular antagonist of AVP, d(CH2)5 VDAVP, in rats with increased endogenous AVP after anesthesia, dehydration, or injection of glycerol. Another vascular AVP-antagonist, d(CH2)5 Tyr (Me) AVP, induced a transient fall in BP in conscious primates (marmosets) after diuretic-induced volume depletion. In conscious rats with established deoxycorticosterone acetate (DOCA)/salt hypertension, d(CH2)5 Tyr (Me) AVP decreased systolic BP after acute administration. After chronic administration of this antagonist during 6 weeks after the beginning of DOCA/salt treatment, the severity of hypertension was reduced. When another, AVP-antagonist, d(CH2)5-D-Tyr (Et) VAVP, which blocks vascular and renal tubular AVP-receptors, was administered chronically, the development of DOCA/salt hypertension was prevented at the expense of severe and persistent hypernatremia. These results demonstrate that under certain conditions the vascular effects of AVP may contribute to the maintenance of BP, AVP appears to participate in the pathogenesis of DOCA/salt hypertension through both its vasoconstrictor and its antidiuretic effects.

Topics: Acute Kidney Injury; Animals; Arginine Vasopressin; Blood Pressure; Desoxycorticosterone; Glycerol; Hemodynamics; Humans; Hypertension; Kidney Tubules; Vasopressins

Topics: Acute Kidney Injury; Animals; Disease Models, Animal; Female; Furosemide; In Vitro Techniques; Ischemia; Kidney; Kidney Tubules; Mannitol; Perfusion; Rabbits; Ureteral Obstruction; Vasopressins

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

Topics: Acids; Acute Kidney Injury; Angiotensin II; Bicarbonates; Diuretics; Glomerular Filtration Rate; Hematuria; Homeostasis; Humans; Infant, Newborn; Infant, Newborn, Diseases; Infant, Premature; Infant, Premature, Diseases; Kidney; Kidney Function Tests; Kidney Tubules; Phosphates; Potassium; Renal Veins; Renin; Sodium; Uric Acid; Vasopressins

Topics: Acetylcholine; Acute Kidney Injury; Angiotensin II; Animals; Bradykinin; Diuretics; Dogs; Dopamine; Electric Stimulation; Epinephrine; Heart Failure; Hemorrhage; Humans; Hypotension; Isoproterenol; Kidney Cortex; Kidney Transplantation; Liver Cirrhosis; Norepinephrine; Oxytocin; Prostaglandins; Regional Blood Flow; Transplantation, Homologous; Ureter; Vasomotor System; Vasopressins; Vena Cava, Inferior; Water-Electrolyte Balance

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

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

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

Topics: Acute Kidney Injury; Anesthesia, General; Angiotensin II; Blood Pressure; Burns; Cell Membrane Permeability; Glomerular Filtration Rate; Glucocorticoids; Humans; Kidney; Methoxyflurane; Mineralocorticoids; Pressoreceptors; Renin; Sodium; Surgical Procedures, Operative; Vasopressins; Water-Electrolyte Balance

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: Accidents, Traffic; Acidosis; Acute Kidney Injury; Adult; Aged; Alkalosis; Aortic Diseases; Aortic Rupture; Body Composition; Calorimetry; Cholecystectomy; Convalescence; Craniocerebral Trauma; Dehydration; Duodenal Ulcer; Endocrine Glands; Female; Homeostasis; Humans; Iliac Artery; Infusions, Parenteral; Kidney; Lung Neoplasms; Male; Metabolism; Middle Aged; Natriuresis; Pancreatitis; Peptic Ulcer Perforation; Postoperative Care; Postoperative Complications; Thoracic Injuries; Thrombosis; Vasopressins; Water-Electrolyte Balance

Topics: Acute Kidney Injury; Aminohippuric Acids; Animals; Blood Flow Velocity; Calorimetry; Dogs; Glomerular Filtration Rate; Hemodynamics; Humans; Hydrogen; Hypertension; Indicator Dilution Techniques; Indicators and Reagents; Kidney; Krypton; Regional Blood Flow; Renin; Sodium; Vasopressins

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

Sepsis-induced acute kidney injury (AKI) is a common condition with high morbidity and mortality. Neutrophil-derived heparin-binding protein (HBP) induces vascular leakage and is a promising biomarker of sepsis-induced organ dysfunction. It remains unknown if HBP is prognostic of AKI in septic shock and if HBP could play a role in the pathophysiology of sepsis-induced AKI.. To determine the association of plasma HBP levels with development of AKI, investigate the role of HBP in the pathophysiology of sepsis-induced AKI, and test the effect of blocking HBP using heparin derivatives.. In 296 septic shock patients from the randomized multicenter Vasopressin and Septic Shock Trial (VASST) plasma HBP levels were associated with development of AKI and need for renal replacement therapy (RRT). Human renal tubular cells were exposed to recombinant HBP to evaluate inflammation and heparin derivatives were used to abrogate these effects. Finally, mice were exposed to HBP with and without heparin derivatives and the kidneys examined for signs of inflammation.. Plasma HBP levels were significantly higher in patients with AKI and those requiring RRT. HBP levels identified patients with moderate AKI with an area under curve (AUC) of 0.85. HBP increased IL-6 production in renal tubular epithelial cells. Different heparin derivatives abrogated the HBP-induced increased inflammatory response in vitro and in vivo.. Elevated plasma HBP is associated with development of sepsis-induced AKI and HBP is involved in its pathophysiology. Our studies suggest that heparin(s) could be tested for efficacy and safety of prevention of sepsis-induced AKI.

Topics: Acute Kidney Injury; Adult; Aged; Antimicrobial Cationic Peptides; Biomarkers; Blood Proteins; Carrier Proteins; Cell Line; Female; Heparin; Humans; Male; Middle Aged; Sepsis; Vasopressins

To compare the effects of vasopressin versus norepinephrine infusion on the outcome of kidney injury in septic shock.. Post-hoc analysis of the multi-center double-blind randomized controlled trial of vasopressin versus norepinephrine in adult patients who had septic shock (VASST).. Seven hundred seventy-eight patients were randomized to receive a blinded infusion of either low-dose vasopressin (0.01-0.03 U/min) or norepinephrine infusion (5-15 microg/min) in addition to open-label vasopressors and were included in the outcome analysis. All vasopressors were titrated and weaned to maintain a target blood pressure.. RIFLE criteria for acute kidney injury were used to compare the effects of vasopressin versus norepinephrine. In view of multiple simultaneous comparisons, a p value of 0.01 was considered statistically significant. Kidney injury was present in 464 patients (59.6%) at study entry. In patients in the RIFLE "Risk" category (n = 106), vasopressin as compared with norepinephrine was associated with a trend to a lower rate of progression to renal "Failure" or "Loss" categories (20.8 vs. 39.6%, respectively, p = 0.03), and a lower rate of use of renal replacement therapy (17.0 vs. 37.7%, p = 0.02). Mortality rates in the "Risk" category patients treated with vasopressin compared to norepinephrine were 30.8 versus 54.7%, p = 0.01, but this did not reach significance in a multiple logistic regression analysis (OR = 0.33, 99% CI 0.10-1.09, p = 0.02). The interaction of treatment group and RIFLE category was significant in predicting mortality.. Vasopressin may reduce progression to renal failure and mortality in patients at risk of kidney injury who have septic shock.

Topics: Acute Kidney Injury; Double-Blind Method; Female; Humans; Infusions, Intravenous; Male; Middle Aged; Norepinephrine; Shock, Septic; Vasoconstrictor Agents; Vasopressins

Topics: Acute Kidney Injury; Humans; Norepinephrine; Shock, Septic; Vasoconstrictor Agents; Vasopressins

To compare the effects of restoring mean arterial pressure with vasopressin or norepinephrine on systemic hemodynamics, renal blood flow, intrarenal perfusion and oxygenation, and renal function in ovine septic acute kidney injury.. Interventional Study.. Research Institute.. Adult Merino ewes.. Flow probes were implanted on the pulmonary and renal arteries (and the mesenteric artery in sheep that received vasopressin). Fiber-optic probes were implanted in the renal cortex and medulla to measure tissue perfusion and oxygen tension (PO2). Conscious sheep were administered Escherichia coli to induce septic acute kidney injury. Vasopressin (0.03 IU/min [0.03-0.05 IU/min]; n = 7) or norepinephrine (0.60 μg/kg/min [0.30-0.70 μg/kg/min]; n = 7) was infused IV and titrated to restore baseline mean arterial pressure during 24-30 hours of sepsis.. Ovine septic acute kidney injury was characterized by reduced mean arterial pressure (-16% ± 2%) and creatinine clearance (-65% ± 9%) and increased renal blood flow (+34% ± 7%) but reduced renal medullary perfusion (-44% ± 7%) and PO2 (-47% ± 10%). Vasopressin infusion did not significantly affect renal medullary perfusion or PO2 and induced a sustained (6 hr) ~2.5-fold increase in creatinine clearance. Vasopressin reduced sepsis-induced mesenteric hyperemia (+61 ± 13 to +9% ± 6%). Norepinephrine transiently (2 hr) improved creatinine clearance (by ~3.5-fold) but worsened renal medullary ischemia (to -64% ± 7%) and hypoxia (to -71% ± 6%).. In ovine septic acute kidney injury, restoration of mean arterial pressure with vasopressin induced a more sustained improvement in renal function than norepinephrine, without exacerbating renal medullary ischemia and hypoxia or reducing mesenteric blood flow below baseline values.

Topics: Acute Kidney Injury; Animals; Arterial Pressure; Disease Models, Animal; Female; Hemodynamics; Kidney; Kidney Function Tests; Norepinephrine; Sepsis; Sheep; Vasoconstrictor Agents; Vasopressins

Currently, no safe and effective pharmacologic interventions exist for acute kidney injury (AKI). One reason may be that heterogeneity exists within the AKI population, thereby hampering the identification of specific pathophysiologic pathways and therapeutic targets.. The aim of this study was to identify and test whether AKI subphenotypes have prognostic and therapeutic implications.. First, latent class analysis methodology was applied independently in two critically ill populations (discovery [n = 794] and replication [n = 425]) with AKI. Second, a parsimonious classification model was developed to identify AKI subphenotypes. Third, the classification model was applied to patients with AKI in VASST (Vasopressin and Septic Shock Trial; n = 271), and differences in treatment response were determined. In all three populations, AKI was defined using serum creatinine and urine output.. A two-subphenotype latent class analysis model had the best fit in both the discovery (P = 0.004) and replication (P = 0.004) AKI groups. The risk of 7-day renal nonrecovery and 28-day mortality was greater with AKI subphenotype 2 (AKI-SP2) relative to AKI subphenotype 1 (AKI-SP1). The AKI subphenotypes discriminated risk for poor clinical outcomes better than the Kidney Disease: Improving Global Outcomes stages of AKI. A three-variable model that included markers of endothelial dysfunction and inflammation accurately determined subphenotype membership (C-statistic 0.92). In VASST, vasopressin compared with norepinephrine was associated with improved 90-day mortality in AKI-SP1 (27% vs. 46%, respectively; P = 0.02), but no significant difference was observed in AKI-SP2 (45% vs. 49%, respectively; P = 0.99) and the P value for interaction was 0.05.. This analysis identified two molecularly distinct AKI subphenotypes with different clinical outcomes and responses to vasopressin therapy. Identification of AKI subphenotypes could improve risk prognostication and may be useful for predictive enrichment in clinical trials.

Topics: Acute Kidney Injury; Aged; Biomarkers; Female; Humans; Male; Middle Aged; Phenotype; Vasopressins; Washington

Topics: Acute Kidney Injury; Humans; Precision Medicine; Vasopressins

The purpose of this study was to test the hypothesis that consuming a soft drink (i.e., a high-fructose, caffeinated beverage) during and following exercise in the heat elevates biomarkers of acute kidney injury (AKI) in humans. Twelve healthy adults drank 2 liters of an assigned beverage during 4 h of exercise in the heat [35.1 (0.1)°C, 61 (5)% relative humidity] in counterbalanced soft drink and water trials, and ≥1 liter of the same beverage after leaving the laboratory. Stage 1 AKI (i.e., increased serum creatinine ≥0.30 mg/dl) was detected at postexercise in 75% of participants in the Soft Drink trial compared with 8% in Water trial ( P = 0.02). Furthermore, urinary neutrophil gelatinase-associated lipocalin (NGAL), a biomarker of AKI, was higher during an overnight collection period after the Soft Drink trial compared with Water in both absolute concentration [6 (4) ng/dl vs. 5 (4) ng/dl, P < 0.04] and after correcting for urine flow rate [6 (7) (ng/dl)/(ml/min) vs. 4 (4) (ng/dl)/(ml/min), P = 0.03]. Changes in serum uric acid from preexercise were greater in the Soft Drink trial than the Water trial at postexercise ( P < 0.01) and 24 h ( P = 0.05). There were greater increases from preexercise in serum copeptin, a stable marker of vasopressin, at postexercise in the Soft Drink trial ( P < 0.02) than the Water trial. These findings indicate that consuming a soft drink during and following exercise in the heat induces AKI, likely via vasopressin-mediated mechanisms.

Topics: Acute Kidney Injury; Adult; Biomarkers; Carbonated Beverages; Creatinine; Drinking; Exercise; Female; Glycopeptides; Hemodynamics; Hot Temperature; Humans; Lipocalin-2; Male; Vasopressins; Water-Electrolyte Balance; Young Adult

Topics: Acute Kidney Injury; Animals; Diuretics; Heart Failure; Humans; Rats, Wistar; Tolvaptan; Vasopressins

We conducted this study to assess the clinical application of obestatin and arginine vasopressin (AVP) levels in cases of acute renal failure (ARF) and acute heart failure (AHF).. 30 cases of ARF, 30 cases of AHF, 30 cases of ARF complicated with AHF, and 30 cases of healthy subjects (control group) were successively selected. An ELISA test was conducted to detect levels of obestatin and AVP. Routine biochemistry testing was applied to detect the levels of serum creatinine and calculate the glomerular filtration rate (GFR). Electrochemiluminescence double antibody sandwich fluorescence immune testing was applied to detect NT-proBNP and color Doppler ultrasound diagnostic apparatus was applied to detect renal arterial resistive index (RI) and left ventricular ejection fraction (LVEF). The 30-day mortality was documented.. Compared to other groups, the group of patients suffering from ARF complicated with AHF had significantly higher levels of obestatin and AVP, and significantly higher levels of serum creatinine, NT-proBNP and RI; however, their GFR and LVEF levels were the lowest. Differences were statistically significant (p < 0.05). Levels of obestatin and AVP are positively correlated with serum creatinine, NT-proBNP and RI levels, but negatively correlated with GFR and LVEF levels. The mortality rate of the group suffering from ARF complicated with AHF was markedly increased (p = 0.035). The obestatin and AVP levels of the death group were significantly higher than that of the survival group. However, the comparison among levels of serum creatinine, GFR, NT-proBNP, RI and LVEF revealed no statistical significance (p > 0.05).. Obestatin and AVP levels were closely related to the severity of ARF and AHF and survival prognosis, which could be a sensitive indicator for diagnoses and prognoses.

Topics: Acute Disease; Acute Kidney Injury; Adult; Aged; Female; Ghrelin; Glomerular Filtration Rate; Heart Failure; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Neurophysins; Peptide Fragments; Protein Precursors; Vasopressins; Ventricular Function, Left

Topics: Acute Kidney Injury; Cardiopulmonary Bypass; Coronary Artery Bypass; Humans; Postoperative Complications; Postoperative Period; Risk Factors; Vasopressins

Topics: Acute Kidney Injury; Cardiopulmonary Bypass; Coronary Artery Bypass; Humans; Postoperative Complications; Postoperative Period; Risk Factors; Vasopressins

Topics: Acute Kidney Injury; Albumins; Aldosterone; Arterial Pressure; Female; Fluid Therapy; Humans; Hydroxyethyl Starch Derivatives; Kidney; Liver Transplantation; Male; Plasma Substitutes; Prostatectomy; Vasopressins

Pneumoperitoneum during laparoscopy results in transient oliguria and decreased glomerular filtration and renal blood flow. The presence of oliguria and elevated serum creatinine is suggestive of acute renal injury. Serum cystatin C has been described as a new marker for the detection of this type of injury. In this study, our aim was to compare the glomerular filtration rate estimated using cystatin C levels with the rate estimated using serum creatinine in patients with normal renal function who were undergoing laparoscopic surgery.. In total, 41 patients undergoing laparoscopic cholecystectomy or hiatoplasty were recruited for the study. Blood samples were collected at three time intervals: first, before intubation (T1); second, 30 minutes after the establishment of pneumoperitoneum (T2); and third, 30 minutes after deflation of the pneumoperitoneum (T3). These blood samples were then analyzed for serum cystatin C, creatinine, and vasopressin. The Larsson formula was used to calculate the glomerular filtration rate based on the serum cystatin C levels, and the Cockcroft-Gault formula was used to calculate the glomerular filtration rate according to the serum creatinine levels.. Serum cystatin C levels increased during the study (T1 = T2T3; p<0.05). The calculated eGlomerular filtration rate-Larsson decreased, whereas the eGlomerular filtration rate-Cockcroft-Gault increased. There was no correlation between cystatin C and serum creatinine. Additionally, Pearson's analysis showed a better correlation between serum cystatin C and the eGlomerular filtration rate than between serum creatinine and the eGlomerular filtration rate.. This study demonstrates that serum cystatin C is a more sensitive indicator of changes in the glomerular filtration rate than serum creatinine is in patients with normal renal function who are undergoing laparoscopic procedures.

Topics: Acute Kidney Injury; Adult; Biomarkers; Creatinine; Cystatin C; Female; Glomerular Filtration Rate; Humans; Laparoscopy; Male; Middle Aged; Sensitivity and Specificity; Vasopressins; Young Adult

Contrast-induced nephropathy (CIN) remains a leading cause of iatrogenic acute renal failure. Terlipressin, a long-acting analog of vasopressin, may improve renal function. This study aimed to investigate the possible protective effect of terlipressin against the development of experimental CIN in rats.. Wistar albino rats (n = 32) were allocated randomly into four equal groups of 8 each, i.e. control, terlipressin, contrast media (CM), and terlipressin plus contrast media (TCM). CIN was induced by intravenous administration of indomethacin (10 mg/kg), N-nitro L-arginine methyl ester (L-NAME, 10 mg/kg, twice at 15 and 30 min), and high-osmolar contrast media meglumine amidotrizoate 60%. Renal function parameters, kidney histology, and tubular expression of vascular endothelial growth factor (VEGF) were determined.. Mean serum creatinine levels were decreased (p < 0.05) and creatinine clearance (p < 0.05) increased in the TCM group compared with the CM group. Notably, rats in the TCM group displayed less tubular necrosis (p < 0.05), medullary congestion (p < 0.05), and a reduced tubular expression of VEGF (p < 0.05) compared with the CM group.. These results demonstrate that terlipressin can inhibit the development of CIN.

Topics: Acute Kidney Injury; Animals; Contrast Media; Disease Models, Animal; Kidney Function Tests; Lypressin; Rats; Rats, Inbred BB; Terlipressin; Vasoconstrictor Agents; Vasopressins

Acute renal failure (ARF) is frequently associated with polyuria and urine concentration defects and it is a severe complication of sepsis because it increases the mortality rate. Inhibition of NF-kappaB activation has been suggested to provide a useful strategy for the treatment of septic shock. However, the impact on sepsis-induced ARF is still unclear. Therefore, we examined the effect of pyrrolidine dithiocarbamate (PDTC) and of small interfering RNA (siRNA) silencing NF-kappaB p50/p105 on sepsis-induced downregulation of vasopressin V(2) receptors and aquaporin (AQP)-2 channels using a cecal ligation and puncture (CLP) mouse model. CLP caused a time-dependent downregulation of renal vasopressin V(2) receptor and of AQP2 expression without alterations in plasma vasopressin levels. Renal activation of NF-kappaB in response to CLP was attenuated by PDTC pretreatment, which also attenuated the downregulation of V(2) receptor and AQP2 expression. Furthermore, a strong nuclear staining for the NF-kappaB p50 subunit throughout the whole kidney in response to CLP was observed. siRNA against NF-kappaB p50 attenuated the CLP-induced nuclear translocation of the p50 subunit and the CLP-induced downregulation of V(2) receptor and AQP2 expression. Additionally, PDTC and siRNA pretreatment inhibited the CLP-induced increase in renal TNF-alpha and IL-1beta concentration and NOS-2 mRNA abundance. Moreover, PDTC and siRNA pretreatment ameliorated CLP-induced hypotension and ARF. Our findings suggest that NF-kappaB activation is of importance for the downregulation of AQP2 channel and vasopressin V(2) receptor expression during sepsis. In addition, our data indicate that NF-kappaB inhibition ameliorates sepsis-induced ARF.

Topics: Acute Kidney Injury; Animals; Antioxidants; Aquaporin 2; Cecum; Disease Models, Animal; Down-Regulation; Interleukin-1beta; Ligation; Male; Mice; Mice, Inbred C57BL; NF-kappa B; Pyrrolidines; Receptors, Vasopressin; Sepsis; Thiocarbamates; Tumor Necrosis Factor-alpha; Vasopressins

Topics: Acute Kidney Injury; Adolescent; Age Factors; Child, Preschool; Critical Care; Dose-Response Relationship, Drug; Female; Glomerular Filtration Rate; Humans; Infant, Newborn; Intensive Care Units, Pediatric; Kidney Function Tests; Male; Severity of Illness Index; Shock; Survival Rate; Treatment Outcome; Vasopressins

Topics: Acute Kidney Injury; Fluid Therapy; Humans; Respiratory Distress Syndrome; Sepsis; Vasoconstrictor Agents; Vasopressins

Milrinone is a phosphodiesterase type III inhibitor with positive inotropic and vasodilatory effects. A common side effect of milrinone is hypotension from the peripheral vasodilation. Although mild elevations in serum creatinine have been described previously in the setting of milrinone-induced hypotension, acute oligoanuric renal failure requiring renal replacement therapy has not yet been described. This case report is the first to document such a result and to report the successful use of peritoneal dialysis in this setting. Previous case reports documented vasopressin as an effective alternative to catecholamines in the treatment of milrinone-induced hypotension. This report documents the use of four vasopressor agents (including vasopressin) in this patient, with only vasopressin resulting in improvement in systemic vascular resistance and blood pressure. Vasopressin may be the most effective vasopressor agent in the treatment of milrinone-induced hypotension.

Topics: Acute Kidney Injury; Adrenergic beta-Agonists; Amyloidosis; Cardiotonic Agents; Dobutamine; Drug Administration Schedule; Drug Therapy, Combination; Heart Diseases; Humans; Hypotension; Male; Middle Aged; Milrinone; Norepinephrine; Peritoneal Dialysis; Phenylephrine; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Xanthopterin (XPT), an unconjugated pteridine compound, affects cell growth and differentiation. When injected into rats, XPT has caused changes that have been interpreted as renal growth and hypertrophy. In the present study, we investigated the effect of intraperitoneal administration of XPT on the renal function in the rat. XPT administration was associated with polyuria and a reversible form of nonoliguric acute renal failure (ARF), with renal function declining maximally after 2 days and returning to normal after 7 days. The polyuria was due, at least in part, to a concentrating defect that was vasopressin resistant. The ability of XPT to induce ARF was modulated by dietary salt intake, being enhanced by a low-sodium diet and prevented by a high sodium intake. Histological examination of the kidneys showed intratubular crystal deposition and acute tubule necrosis, suggesting that XPT induces crystal nephropathy. There was an increase in wet and dry weights of the kidney and an increased DNA/protein ratio, compatible with a hyperplastic response. Because the severity of other crystal nephropathies may be modulated by urine flow rate and pH, we studied the ability of water diuresis or alkaline diuresis to protect against XPT-induced ARF. Both water diuresis and HCO3 loading blunted the ability of XPT to decrease renal function. The change in renal function induced by XPT in the various groups was paralleled by corresponding changes in the levels of XPT-like substances in the kidney and by the amount of crystal deposition. Thus, XPT injection induces crystal nephropathy, the severity of which can be modulated by dietary salt intake, urine pH, and urine flow rate.

Topics: Acute Kidney Injury; Animals; Ascitic Fluid; Diabetes Insipidus, Nephrogenic; Disease Models, Animal; Kidney; Male; Organ Size; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Sodium, Dietary; Urine; Urodynamics; Vasopressins; Xanthopterin

Continuous pump-driven veno-venous hemofiltration (CVVH) has become an established method for treatment of acute renal failure (ARF). Since severe disturbances of (micro-) circulation are intimately involved in the bad outcome of these patients, the profile of endocrinological regulators of circulation was prospectively and serially measured in patients undergoing pump-driven CVVH (n = 15). 15 patients with similar APACHE II score, but without ARF and without CVVH were also studied. Endothelin-1 (ET-1), atrial natriuretic peptide (ANP), vasopressin, renin, and catecholamine (epinephrine, norepinephrine) plasma levels were measured before start of CVVH (= "baseline") (in the non-CVVH patients: admission to intensive care unit) and during the next 5 days. Various hemodynamic parameters were additionally monitored. MAP, HR, PAP, CI, and right ventricular hemodynamics (RVEF, RVEDV, RVESV) remained almost unchanged in the CVVH patients and were without differences to the non-CVVH group within the entire investigation period. PCWP and RAP were higher in the CVVH patients already at baseline (RAP, 17.8 +/- 4.0 mmHg; PCWP, 22.1 +/- 4.5 mmHg) (p < .02) and remained elevated in the further course of the investigation. Renin plasma level was higher already at baseline in the CVVH patients (907 +/- 184 pg/ml) (p < .05) and further increased during CVVH (to 1453 +/- 186 pg/mL). Vasopressin increased only in the CVVH group (from 3.80 +/- .66 to 11.85 +/- 1.05 pg/mL) (p < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Kidney Injury; Atrial Natriuretic Factor; Blood Circulation; Blood Pressure; Creatinine; Dopamine; Endothelins; Epinephrine; Female; Hemodynamics; Hemofiltration; Humans; Lactates; Lactic Acid; Male; Middle Aged; Norepinephrine; Renin; Sepsis; Time Factors; Vascular Resistance; Vasopressins; Wounds and Injuries

Previous studies have shown that common bile duct ligation in the rabbit is followed by a reduction of the extracellular water compartment. To further elucidate the mechanisms leading to volume depletion in this model, water and sodium balances and changes in plasma concentrations of atrial natriuretic peptide (ANP), vasopressin (ADH), plasma renin activity (PRA) and aldosterone (Ald) were investigated during the first 4 days after common bile duct ligation (group OJ,) or sham operation (group SO). Water and chow intakes were lower in group OJ (148 +/- 30 versus 226 +/- 40 mL/4 days; p = 0.004 and 12 +/- 9 versus 171 +/- 40 g/4 days; p = 0.0001). There were no differences in urine output. Sodium urinary losses were marginally higher in group OJ (12.4 +/- 7 versus 6.7 +/- 5 mEq/4 days; p = 0.06). Water balance was lower in group OJ (-50 +/- 56 versus 101 +/- 71 mL/4 days; p = 0.0001). At 24 hours, plasma ANP (41 +/- 7 versus 10.7 +/- 1 fmol/mL, p = 0.0001), ADH (21.8 +/- 7 versus 12.3 +/- 6 pg/mL, p = 0.008) and Ald (14.5 +/- 5 versus 3.7 +/- 3 ng/dL, p = 0.001) were higher in group OJ. These alterations persisted 72 hours after bile duct ligation, when a concomitant increase in PRA (10.7 +/- 5 versus 3 +/- 1.6 ng/dL, p = 0.006) was also observed. A group of pair-fed pair-watered sham-operated controls (group SO2, n = 13) showed a metabolic profile similar to group OJ but a low ANP concentration. Multiple venous sampling in five rabbits 24 hours after bile duct ligation showed the highest plasma levels of ANP in the aorta and infrarenal vena cava. These results suggest that common bile duct ligation in the rabbit is followed by marked hypodipsia and hypophagia, possibly mediated by ANP, leading to isotonic volume depletion and secondary activation of the water and sodium retaining hormones.

Topics: Acute Kidney Injury; Aldosterone; Animals; Atrial Natriuretic Factor; Cholestasis; Common Bile Duct; Ligation; Male; Natriuresis; Rabbits; Renin; Time Factors; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

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

Changes in blood plasma content of hormones which are observed in the different periods of hemorrhagic fever and the attendant renal syndrome are directed to the maintenance of significantly deranged water-electrolyte homeostasis. Adequate secretion of vasopressin and aldosterone in response to the changes in sodium concentration and plasma osmolality point to the absence of significant functional disorders of the corresponding glands. Pronounced hypernatremia in fatal cases is evidence of the deranged processes of osmoregulation associated primarily with kidney areactivity to vasopressin and prognostically is an unfavourable sign. The presence of pituitary necrosis in deceased subjects does not rule out the role of vasopressin deficiency in the pathogenesis of pronounced hypernatremia.

Topics: Acute Kidney Injury; Adolescent; Adult; Aldosterone; Female; Hemorrhagic Fever with Renal Syndrome; Humans; Hypernatremia; Hyponatremia; Male; Middle Aged; Nephrotic Syndrome; Osmotic Pressure; Renin; Vasopressins

Topics: Acute Kidney Injury; Adult; Aged; Diagnosis, Differential; Humans; Hypothalamic Diseases; Kidney Function Tests; Middle Aged; Osmolar Concentration; Plasma; Reference Values; Urine; Vasopressins

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

Topics: Acute Kidney Injury; Adult; Humans; Hypoaldosteronism; Immersion; Middle Aged; Renin; Vasopressins

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

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

Topics: Acute Kidney Injury; Antibody Formation; Blood Coagulation; Blood Pressure; Calcium; Catecholamines; Complement Activation; Extracorporeal Circulation; Hemodynamics; Hemolysis; Humans; Immunity, Cellular; Intracranial Embolism and Thrombosis; Leukocytes; Potassium; Pulmonary Circulation; Thrombocytopenia; Vasopressins

Myoglobinuria and acute renal failure were observed in two patients with vasopressin-treated gastrointestinal hemorrhage. Because there were no other obvious causes of renal failure in either patient, we propose that skeletal muscle ischemia developed during vasopressin infusion, followed by release of myoglobin and renal damage. This association should be considered in the period after vasopressin-treated gastrointestinal hemorrhage.

Topics: Acute Kidney Injury; Aged; Female; Gastrointestinal Hemorrhage; Humans; Infusions, Parenteral; Ischemia; Male; Middle Aged; Muscles; Myoglobinuria; Rhabdomyolysis; Vasopressins

The effects of chronic gentamicin administration on renal function was studied in dogs receiving 4 mg/kg i.m. of gentamicin b.i.d. for 28 days. Administration of gentamicin resulted in a bimodal change in renal function. A decrease in urine osmolality was first noted on day 6 and declined progressively throughout the study. This decrease in urinary concentrating ability was preceded by a steady rise in urinary prostaglandin E2 (PGE) excretion and followed by a rise in plasma renin activity (PRA). Prior to an increase in azotemia, urinary PGE decreased precipitously while PRA continued to rise throughout the remainder of the study. The precipitous decrease in GFR was accompanied by a significant increase in FENa to seven times control. These studies suggest a dual effect of chronic gentamicin administration on renal function: (1) an early effect manifested by stimulation of urinary prostaglandin production with a concomitant loss of urinary concentrating ability and mild prerenal azotemia, and (2) a late effect, preceded by a decrease in urinary prostaglandin excretion while PRA continues to increase, and manifested by increase fractional excretion of sodium and progressive azotemia.

Topics: Acute Kidney Injury; Animals; Dogs; Female; Gentamicins; Kidney Concentrating Ability; Prostaglandins; Prostaglandins E; Renin; Time Factors; Urodynamics; Vasopressins

Topics: Acute Kidney Injury; Dopamine; Drug Interactions; Graft Survival; Humans; Kidney; Kidney Transplantation; Vasopressins

Circulatory shock mechanisms that may result in the acute renal failure (ARF) syndrome are summarized. Both circulatory and neurohumoral mechanisms leading to the shock state and ARF are emphasized. Release of vasoactive hormones, with a review of vasodilators and vasoconstrictors, is discussed in terms of release mechanisms, onset of release, magnitude and duration of plasma elevation, and the basal plasma level of each. Hemodynamic diagnoses in shock in both the classical low cardiac output and the early sepsis high cardiac output syndromes are commented upon with emphasis on the importance of early diagnosis and adequate measurements of the circulatory state for optimum therapy. The septic hyperdynamic syndrome is reviewed with particular regard to changes in the renal circulation and function. Mechanisms of lactic acidemia in the hyperdynamic syndrome in the presence of adequate nutrient tissue flow are discussed. Elevations of vasoactive hormones and their relationship to the early shock state are mentioned. Their elevations in late shock are reviewed with critical comments given as to the possible interactions and importance of the vasodilator and vasoconstrictor actions on organ function and survival. Blood pressure alone is not a good indicator of progress in the management of septic shock.

Topics: Acute Kidney Injury; Angiotensin II; Animals; Blood Pressure; Endorphins; Epoprostenol; Hemodynamics; Histamine; Hormones; Humans; Shock, Septic; Thromboxanes; Vasoconstriction; Vasodilation; Vasopressins

The present studies were carried out to delineate the mechanism of the polyuric state and renal concentration defect seen after gentamicin. Gentamicin was given at a dosage of 100 mg/kg/day subcutaneously for either 4 or 5 days to Sprague-Dawley rats and resulted in a reversible, polyuric form of acute renal failure. This nonoliguric acute renal failure was accompanied by significant polydipsia and a renal concentrating defect 11 days after gentamicin. To assess the role of polydipsia in the polyuria and renal concentrating abnormality, water intake was restricted in gentamicin-treated animals to match intake of control animals. Elimination of the polydipsia failed to eliminate the polyuria and to improve the renal concentrating abnormality. Postdehydration plasma vasopressin levels were higher in gentamicin-treated than control animals, suggesting that the renal concentrating defect was nephrogenic in origin. Daily urinary prostaglandin E2 excretion was comparable in gentamicin-treated and control animals. However, indomethacin failed to improve urinary concentrating ability, suggesting that the renal concentrating defect was prostaglandin E2 independent. Finally, depressed postdehydration inner medullary tonicity was found in gentamicin-treated animals In summary, gentamicin administration in the rat was associated with a reversible polyuric form of acute renal failure and a renal concentrating defect. This concentration defect was nephrogenic in origin, independent of polydipsia and prostaglandin E2, and was associated with a decrease in inner medullary tonicity.

Topics: Acute Kidney Injury; Animals; Dinoprostone; Gentamicins; Kidney Concentrating Ability; Kidney Medulla; Male; Polyuria; Prostaglandins E; Rats; Rats, Inbred Strains; Vasopressins; Water Deprivation

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: Acute Kidney Injury; Diagnosis, Differential; Humans; Hypoxia; Pulmonary Edema; Urethral Obstruction; Vasopressins

Topics: Acute Kidney Injury; Angiotensin II; Humans; Ischemia; Kidney; Kidney Tubular Necrosis, Acute; Kidney Tubules; Oliguria; Prostaglandins; Renin; Vasopressins

Topics: Acute Kidney Injury; Animals; Blood Volume; Ischemia; Kidney; Nephrectomy; Rats; Uremia; Vasopressins

Clonidine, an antihypertensive drug that inhibits renin release and causes a water diuresis in normal animals, was tested for its ability to reduce the severity of post-ischemic acute renal failure produced in rabbits by clamping the left renal pedicle for 1 hour and removing the opposite kidney. Clonidine significantly lessened renal failure when given during, or 1 hours after, the ischemic insult in dehydrated rabbits. It was also effective when given during the ischemic insult in vasopressin-treated water-drinking rabbits but not in control water-drinking rabbits. In vasopressin-treated rabbits, clonidine lessened renal failure observed 2 days after the ischemic insult despite the fact that in the immediate postischemic period it lowered total renal blood flow, produced hypotension, and did not bring about lower plasma renin levels. Clonidine treatment resulted in less outer medullary microvascular damage (demonstrated by colloidal carbon staining), higher outer medullary blood flow 1 to 2 hours after unclamping, fewer casts, and higher creatinine clearance and free water clearance/creatinine clearance 4 to 6 hours after unclamping compared with controls. The effect of clonidine was unrelated to plasma renin activity. Clonidine did not alter plasma vasopressin concentration. Demeclocycline and lithium, two agents that blunt renal responsiveness to vasopressin, had a beneficial effect in dehydrated animals similar to that of clonidine, but the angiotensin II antagonist saralasin and the angiotensin converting enzyme inhibitor SQ20881 did not. Normal rabbits given a large dose of vasopressin in oil plus clonidine had significantly greater urine output and free water clearance and lower urine osmolality than did rabbits given vasopressin in oil alone. These results suggest that clonidine may be beneficial because it prevents ischemic microvascular injury in the renal outer medulla, an effect that may decrease tubular obstruction by lessening desquamation of damaged tubular cells or cell constituents into the tubular lumen. Clonidine may also decrease formation of obstructive hyaline casts in collecting ducts by blunting the kidney's response to vasopressin and increasing tubular fluid flow rate.

Topics: Acute Kidney Injury; Animals; Clonidine; Creatinine; Disease Models, Animal; Diuresis; Female; Ischemia; Kidney; Microcirculation; Nephrectomy; Rabbits; Regional Blood Flow; Vasopressins

Rational intraoperative fluid therapy is based on an understanding of the pathophysiology of severe trauma and surgery. Fluids of suitable compositions are administered in sufficient quantities to form part of the daily maintenance requirement and also to replace blood and ECF lost during surgery.

Topics: Acute Kidney Injury; Adrenal Cortex Hormones; Blood Transfusion; Extracellular Space; Humans; Infusions, Parenteral; Kallikreins; Kidney; Oliguria; Postoperative Complications; Renin; Shock; Sodium; Surgical Procedures, Operative; Vasopressins; Water-Electrolyte Balance

Studies on the vasopressor role of the antidiuretic hormone arginine-vasopressin (AVP) in DOC hypertension, in two-kidney Goldblatt hypertension, and in spontaneous hypertension of rats, and during acute blood pressure elevation after intracerebroventricular injection of angiotensin II and in glycerol-induced acute renal failure of rats are reviewed. For the measurement of plasma AVP a radioimmunoassay has been developed. For this assay, a series of criteria has been met which allows the conclusion that, in plasma of rats, the antibody measures AVP only. For the blockade of vasopressor effects of AVP a specific antiserum has been used. On the basis of a series of control studies it has been concluded, but not proven that the antiserum lowers blood pressure exclusively by blockade of AVP. It could be shown that in the various animal models of hypertension and of acute blood pressure elevation AVP exerts systemic vasoconstriction when its plasma concentrations are elevated. In those models where the renin-angiotensin system played no role in blood pressure control, the height of blood pressure was closely related to the plasma AVP concentrations. When this relationship was compared with that obtained after the i.v. infusion or injection of AVP, a marked shift to the left became apparent. Hence, sensitization to the vasopressor effect of AVP had occurred, the factor of sensitization amounting to more than 1,000. It is concluded that AVP is not only an antidiuretic hormone but also a vasopressor hormone, and that any systemic vasopressor effect of AVP requires a mechanism of sensitization.

Topics: Acute Kidney Injury; Angiotensin II; Animals; Arginine Vasopressin; Blood Pressure; Hypertension; Hypertension, Renal; Immune Sera; Injections, Intraventricular; Radioimmunoassay; Rats; Vasopressins

Topics: Acute Kidney Injury; Angiotensinogen; Animals; Arginine Vasopressin; Blood Pressure; Glycerol; Hematocrit; Immune Sera; Male; Osmolar Concentration; Rats; Renin; Saralasin; Urea; Vasopressins

Topics: Acute Kidney Injury; Aldosterone; Animals; Anuria; Burns; Diabetes Insipidus; Disease Models, Animal; Diuresis; Diuretics; Furosemide; Kidney; Male; Mineralocorticoid Receptor Antagonists; Rats; Shock, Traumatic; Sodium; Sodium Chloride; Time Factors; Urea; Vasopressins; Water

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Anuria; Body Weight; Child; Child, Preschool; Creatinine; Diuresis; Female; Glomerular Filtration Rate; Humans; Kidney Concentrating Ability; Male; Middle Aged; Natriuresis; Nephrons; Osmolar Concentration; Vasopressins; Water-Electrolyte Balance

Topics: Acute Kidney Injury; Calcitonin; Calcium; Diet; Diuretics; Glomerular Filtration Rate; Glucocorticoids; Growth Hormone; Humans; Hyperparathyroidism; Hypoparathyroidism; Kidney; Kidney Concentrating Ability; Magnesium; Natriuresis; Parathyroid Hormone; Phosphates; Thyroxine; Vasopressins; Vitamin D

Topics: Acute Kidney Injury; Furosemide; Humans; Kidney; Kidney Medulla; Oxygen; Vasopressins; Water

Topics: Acute Kidney Injury; Angiography; Animals; Diatrizoate; Diuresis; Dogs; Female; Graft Rejection; Ischemia; Kidney; Kidney Concentrating Ability; Kidney Transplantation; Transplantation Immunology; Urography; Vasopressins

Topics: Acute Kidney Injury; Adipose Tissue; Animals; Fluorides; Humans; Kidney Tubules; Methoxyflurane; Muscle Relaxants, Central; Nitrous Oxide; Preanesthetic Medication; Rats; Vasopressins

Topics: Acute Kidney Injury; Adolescent; Amino Acids; Ammonia; Anti-Bacterial Agents; Arginine; Aspartic Acid; Coenzyme A; Diet Therapy; Exchange Transfusion, Whole Blood; Glutamates; Hepatic Encephalopathy; Humans; Malates; Male; NAD; Ornithine; Prednisone; Prognosis; Renal Dialysis; Thiamine Pyrophosphate; Thioctic Acid; Vasopressins

Topics: Acute Kidney Injury; Anesthesia; Blood Pressure; Glomerular Filtration Rate; Hemorrhage; Hepatic Artery; Humans; Hypotension; Kidney; Liver Circulation; Sympathetic Nervous System; Urine; Vascular Resistance; Vasopressins

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

Topics: Acute Kidney Injury; Adult; Aged; Female; Glomerular Filtration Rate; Humans; Hypercalcemia; Kidney; Kidney Concentrating Ability; Kidney Tubules; Male; Middle Aged; Osmolar Concentration; Pyelonephritis; Sodium; Vasopressins

Comprehensive one-day renal function tests in 20 patients with a history of analgesic abuse showed varying degrees of chronic renal failure in all. There was no evidence of a selective defect in proximal tubular function, while a defective concentrating mechanism, usually considered necessary for the diagnosis of analgesic-induced renal damage, could be demonstrated in only 16 patients. A urinary acidification defect associated with a concentrating defect was found in nine cases and was thought to reflect specific collecting duct dysfunction. Urinary ammonium excretion was reduced in 13 subjects, owing to a reduced number of functioning nephrons or inadequate acidification, or both. Low citrate excretion was frequently encountered, and this, as well as defective urinary acidification, may play some part in predisposing patients with analgesic nephropathy to intrarenal calcification and progressive renal failure.

Topics: Acid-Base Equilibrium; Acute Kidney Injury; Adult; Aged; Analgesics; Citrates; Creatinine; Female; Glomerular Filtration Rate; Humans; Kidney Concentrating Ability; Kidney Function Tests; Male; Middle Aged; Substance-Related Disorders; Vasopressins

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Anuria; Glucose Tolerance Test; Humans; Middle Aged; Peritoneal Dialysis; Uremia; 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