Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe two patients who developed acute renal failure secondary to severe pericardial effusion. In one patient, the pericardial effusion was due to coxsackievirus infection, and in the other patient, it was due to lung cancer. One patient was in cardiac tamponade, and the other was not yet in tamponade, as per echocardiographic criteria. Kidney function was relatively normal in both patients before the pericarditis episodes. In both patients, pericardiocentesis caused immediate massive diuresis with quick recovery of renal function back to baseline. In the first patient, blood urea nitrogen and serum creatinine decreased from 82 mg/dL and 7.6 mg/dL to 71 mg/dL and 4.6 mg/dL in the next 48 hours, then to 23 mg/dL and 1.3 mg/dL 5 days after the pericardiocentesis. In the second patient, blood urea nitrogen and serum creatinine decreased from 109 mg/dL and 2.9 mg/dL to 40 mg/dL and 0.9 mg/dL in the next 48 hours and 17 mg/dL and 0.7 mg/dL 3 days after release of tamponade. Pericardial effusion can affect renal hemodynamics in many different ways, including increased atrial natriuretic peptide secretion, increased renal efferent nerve activity, and increased secretion of renin and vasopressin. Although pericardial effusion is a complication of uremia, acute renal failure per se can occur in nonuremic cases of pericardial effusion. Two cases of acute renal failure resulting from pericardial effusion were reported in the literature in the past. Pericardial effusion should be included in the broad list of prerenal causes of acute renal failure.
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PMID:Pericardial effusion leading to acute renal failure: two case reports and discussion of pathophysiology. 1232 21

We report a child with diabetes insipidus and hypodipsia associated with holoprosencephaly. A two-year-old girl with the history of several admittances to hospital during and after the newborn period with hypernatremic dehydration, acute renal failure and convulsions is presented. The patient had hypodipsia, hypernatremia, microcephaly, failure to thrive, and unilateral cleft lip and palate. Magnetic resonance imaging revealed lobar type holoprosencephaly. Increased plasma osmolality and decreased urinary osmolality were detected. Her urine ADH level was 10 ng/day. Plasma osmolality levels returned to normal after hydration and administration of a vasopressin analogue. These findings suggest that in children with hypernatremia-hypodipsia syndrome, the possibility of cerebral malformations should always be kept in mind.
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PMID:Hypodipsia-hypernatremia syndrome associated with holoprosencephaly in a child: a case report. 1240 44

Based on the progress made during the last few years in understanding the pathophysiology of acute renal failure, a plethora of therapeutic drug and nondrug interventions have been developed and tested in animal and human forms of this disease. The first part of this article focuses on the role of volume expansion and vasopressors in the prevention and treatment of acute renal failure in the critically ill. From all prophylactic measures that have been proposed, volume expansion, or at least correction of volume depletion, remains the most efficient and most evidence-based intervention in these patients. Norepinephrine is, out of all the vasopressors, probably the most appropriate to use in cases of hypotension, provided circulating volume is adequate. In hypotensive septic patients, vasopressin has been shown to be useful. Direct renal vasodilating substances, the most popular still being low-dose dopamine, have never been proved to be useful in carefully performed prospective trials. Moreover dopamine especially is associated with a number of side effects and complications. From the agents acting on tubular factors, the diuretic mannitol and loop diuretics are the most prescribed. Only in specific situations such as rhabdomyolysis and kidney transplant surgery has it been shown that mannitol was able to prevent acute renal failure. The loop diuretics are able, after establishing adequate circulating volume, to promote diuresis in some forms of oliguric acute renal failure; however, some recent papers have shown that the administration of loop diuretics may actually be associated with increased mortality and delayed recovery of renal function. The last few years have seen a number of trials with acetylcysteine in the prevention of mainly radiocontrast nephropathy. Although the results are still conflicting, the majority indicates that acetylcysteine, when applied together with adequate volume expansion, may be a useful drug to incorporate in the standard treatment procedures in patients at risk for acute renal failure. Interventions to stimulate the recovery process of the damaged kidney with growth factors, although theoretically sound, have thus far not led to successful results.
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PMID:Prevention and nondialytic treatment of acute renal failure. 1463 67

DEFINITION OF HYPOURICEMIA: Hypouricemia (serum uric acid less than 120 micro mol/l) is a biological abnormality often discovered accidentally and with a low prevalence depending on its permanent or transitory nature ranging from 0.15 to 3.38%. NEW PHYSIOLOGICAL CONCEPTS OF ITS PATHOGENESIS: Recently, our knowledge of the physiopathological mechanisms of hypouricemia has been emphasized by the identification of three systems of renal and extra-renal uric acid transport: a Cl/urate (URAT1) transporter, a multispecific organic anion transporter (OAT) and a urate transporter/channel. ETIOLOGY AND COMPLICATIONS OF HYPOURICEMIA: Through questioning, drugs and toxics (allopurinol.) are generally rapidly recognized as responsible for half of the hypouricemia encountered. It can be concomitant to a known disease: severe liver disease, neoplasia, diabetes, AIDS, syndrome of inappropriate antidiuretic hormone secretion. Hypouricemia can also be isolated and justifies the measurement of uric acid clearance, the normality or reduction of which orients towards a deficiency in xanthine-oxydase, the increase in which suggests an abnormality in uric acid transport in the proximal tubule (Fanconi syndrome, primary hereditary anomaly of tubular uric acid transport). Hypouricemia does not appear to expose the patient to any danger, but the onset of nephrolithiasis or acute renal failure secondary to the combination of severe hypouricemia and oxidant stress is always possible.
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PMID:[Hypouricemia, an old subject and new concepts]. 1523 14

The mechanism behind iodinated radiocontrast nephropathy remains elusive. Direct oxidative damage is the prevailing hypothesis, but the apparent protective effect of iodine against oxidation contradicts this view. We propose that autonomic dysfunction participates in the pathogenesis of radiocontrast nephropathy and may account for other contrast-associated reactions previously attributed to allergy. Iodine, through its effects on thyroid function and chemoreceptor response to metabolic acidosis, may induce hyperadrenergia and consequently diminish renovascular flow and urine output. The renal response to adrenergia likely served an adaptive function during prehistoric evolution when trauma was a dominant source of hypovolemia and adrenergia, but the response may behave maladaptively today as evolutionarily nai ve triggers for adrenergia have emerged. Autonomic dysfunction can further impair renal function by deranging renovascular autoregulation and inducing oxidative reperfusion injury as a secondary phenomenon. Many other causes of acute renal failure such as drug toxicity, surgery, hospitalization, and diabetes may operate through hyperadrenergia, impaired renovascular autoregulation, and oxidative reperfusion injury. Dialysis, a volume reduction therapy for renal failure, can counterintuitively worsen renal dysfunction by exacerbating adrenergia, which may explain its association with accelerated atherosclerosis, inflammation, and cancer. Other examples of vicious cycles that perpetuate renal dysfunction may include renal artery stenosis, carotid stenosis, and atherosclerosis as well as the cardio-renal, hepato-renal, and pulmonary-renal syndromes. The benefits of hydration and bicarbonate in protecting renal function may operate in part through baroreceptor- and chemoreceptor-mediated reduction of sympathovagal ratio, respectively. New treatment paradigms for renal failure including pharmacologic and electro-mechanical therapies are envisioned based on autonomic remodeling, reduced sympathovagal ratio, and neuromodulation of pathways typically associated with trauma such as renin, angiotensin, vasopressin, and aldosterone.
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PMID:Contrast nephropathy may be partly mediated by autonomic dysfunction: renal failure considered as a modern maladaptation of the prehistoric trauma response. 1633 Jan 57

The management of children with end-stage chronic liver disease and acute liver failure mandates a multidisciplinary approach and intense monitoring. In recent years, considerable progress has been made in developing specific and supportive medical measures, but studies and publications have mainly concerned adult patients. Therapeutic approaches to complications of end-stage chronic liver disease and acute liver failure (e.g. refractory ascites, hepatorenal syndrome, encephalopathy, and cerebral edema) that may be applied to children are reviewed in this article.Mild-to-moderate ascites should be managed by modest salt restriction and oral diuretic therapy in the first instance. Large volume paracentesis associated with colloid volume expansion and diuretic therapy may be effective for acute relief. Treatment of hepatorenal syndrome type 1 with vasopressin analogs (terlipressin) is recommended prior to liver transplantation in order to improve renal function. Prevention and treatment of chronic hepatic encephalopathy are directed primarily at controlling the events that may precipitate hepatic encephalopathy and at reducing ammonia generation and increasing its detoxification or removal. In addition to reduction of gut ammonia production using non-absorbable disaccharides such as lactulose and/or antibacterials such as neomycin, sodium benzoate may be used on a long-term basis to prevent, stabilize, or improve hepatic encephalopathy. The management of hepatic encephalopathy in acute liver failure is considerably more unsatisfactory; treatment is aimed at preventing brain edema and intracranial hypertension. Extracorporeal liver support devices are now used commonly in critically ill children with acute renal failure, advanced hepatic encephalopathy, cerebral edema, intracranial hypertension, and severe coagulopathy. Continuous renal replacement therapy could potentially help support patients until liver transplantation is performed or liver regeneration occurs. The Molecular Adsorbent Recirculating System (MARS or albumin dialysis) is the liver support system most frequently used worldwide in adults and appears to offer distinct advantages over hepatocyte-based systems. There are no specific medical therapies or devices that can correct all of the functions of the liver. Apart from a few metabolic diseases presenting with severe liver dysfunction for which specific medical therapies may preclude the need for liver transplantation, liver transplantation still remains the only definitive therapy in most instances of end-stage chronic liver disease and acute liver failure. Future research should focus on gaining a better understanding of the mechanisms responsible for liver cell death and liver regeneration, as well as developments in hepatocyte transplantation and liver-directed gene therapy.
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PMID:New management options for end-stage chronic liver disease and acute liver failure: potential for pediatric patients. 1649 8

The kidney is a remarkable organ whose functions include maintaining fluid and electrolyte balance, excreting metabolic waste products, and controlling vascular tone. Blood flow within the kidney is very heterogeneous, which places the metabolically active medulla at high risk for ischemic injury. A number of mediators play a role in the modulation of renal blood flow, including angiotensin II, dopamine, vasopressin, prostaglandins, atrial natriuretic peptide, endothelin, and nitric oxide. Early markers of renal injury elicit strong interest, although currently there is no reliable marker available. Surgery causes the release of catecholamines, renin, angiotensin, and AVP that lead to a redistribution of renal blood flow and a decrease in GFR. Additionally, general anesthesia often results in some degree of hypotension and depressed cardiac output, which further reduces renal perfusion and potentially jeopardizes renal function. A careful anesthetic plan is imperative in the patient with renal insufficiency or failure because acute renal failure in the perioperative period is associated with a high morbidity and mortality. Factors including advanced age, diabetes, underlying renal insufficiency, and heart failure place a patient at high risk for developing acute renal failure. It is imperative to maintain euvolemia, normotension, and cardiac output, and to avoid nephrotoxic agents to optimize renal blood flow and renal perfusion as the best prevention of renal dysfunction. Further studies are needed to establish if any therapies exist to prevent or treat renal dysfunction effectively.
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PMID:Renal disease: the anesthesiologist's perspective. 1724 Jun 5

Acute renal failure during human sepsis is often nonoliguric. To study the underlying mechanisms, renal function was assessed in endotoxic and control male Wistar rats during and after saline loading and treatment with the selective V2 receptor agonist desmopressin. Escherichia coli endotoxin (dose, 8 mg/kg) was administered from time (t)=0 to t=60 min; saline loading (rate, 5 mL/100 g per hour) was administered from t=0 to t=120 min. Thereafter, half of each group received desmopressin (dose, 10 microg) for 1 h. The inner medullary (IM) osmolality, hematocrit, plasma, and urinary concentrations of sodium, potassium, urea, and osmolality were measured; then, aquaporin 2 (AQP2) immunohistochemistry was performed. Plasma vasopressin concentrations were measured at t=180 min. Saline loading increased urine volume in all rats. In the endotoxic group, mean arterial pressure decreased when saline loading was stopped. Despite increased hematocrit and vasopressin levels (>16 pg/mL), the endotoxin group had a low IM osmolality (mean +/- SEM, 412+/-0.04 mOsm/kg H2O) in comparison with the control group (mean +/- SEM, 1,094+/-0.17 mOsm/kg H2O) and was not able to either decrease urine volume or raise urine osmolality. Desmopressin treatment in endotoxin-treated rats maintained mean arterial pressure, increased sodium reabsorption, IM osmolality, and urine osmolality, and decreased urine flow. The AQP2 intensity decreased in the endotoxin group, and the apical localization disappeared; both were not affected by desmopressin. Our results indicate that endotoxemia in rats acutely diminishes renal urinary concentration capacity and is associated with a decreased IM osmolality and diminished apical AQP2 localization. These findings may help to explain nonoliguric acute renal failure in human septic shock.
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PMID:Mechanisms of the urinary concentration defect and effect of desmopressin during endotoxemia in rats. 1769 23

Hepatorenal syndrome is a form of acute or sub-acute renal failure which develops in patients with chronic liver disease. In contrast to other forms of acute renal failure it may be reversible using pharmacological agents. The pathogenesis involves splanchnic vasodilatation and intense renal vasoconstriction. Increasing intravascular volume and prolonged treatment with vasoconstrictor drugs reverses renal failure in a significant proportion of patients. Agents currently used include the vasopressin analogues terlipressin and the alpha1-adrenoceptor agonist midodrine. The somatostatin analogue octreotide has been used in combination therapy but is ineffective as monotherapy. Intravenous albumin is an important adjunctive treatment both in the prevention and treatment of hepatorenal syndrome. Increasing intravascular volume using TIPS (transjugular intrahepatic stent shunt) is effective in some patients and may be useful in maintaining patients who have initially responded to pharmacological therapy. Despite improvements in survival, long term prognosis is still poor and generally depends on the degree of reversibility of the underlying liver disease or access to liver transplantation.
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PMID:Management of hepatorenal syndrome. 1853 34

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.
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PMID:Inhibition of NF-kappaB ameliorates sepsis-induced downregulation of aquaporin-2/V2 receptor expression and acute renal failure in vivo. 1982 75


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