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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In almost all cases of acute renal failure associated with cholestatic jaundice, the occurrence of renal failure is preceded by episodes of shock, hypotension, sepsis, or surgical intervention. The pathologic finding is usually that of acute tubular necrosis. A patient with obstructive jaundice developed renal failure; the clinical and pathologic features were consistent with those found in the hepatorenal syndrome. No episodes of shock or sepsis preceded the onset of that renal failure. At autopsy, the findings were normal.
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PMID:Hepatorenal syndrome associated with obstructive jaundice. 406 31

The association between obstructive jaundice and postoperative acute renal failure has been originally described more than eight decades ago and is now a well-established clinical phenomenon. Acute renal failure occurs in 8 to 10% of patients requiring surgery for relief of obstructive jaundice and contributes to eventual mortality in 70 to 80% of those who develop it. A major factor that may underlie the susceptibility to renal failure in patients with obstructive jaundice is cardiovascular instability manifested as systemic hypotension and defective vascular reactivity. This article outlines the scope of the clinical association between jaundice and renal failure and reviews the clinical and experimental studies that have contributed to our understanding of the underlying pathophysiologic mechanisms for this phenomenon. A growing body of evidence emanating from these studies indicates that bile constituents (e.g., bile acids, bilirubin, cholesterol) do not exert a direct nephrotoxic effect. Rather, the retention of bile during cholestatic jaundice has deleterious effects on cardiovascular function and on blood volume. This, in turn, sensitizes the kidney to prerenal failure and acute tubular necrosis in postsurgical patients with obstructive jaundice. The institution of prophylactic measures based on the appreciation of these underlying pathogenic mechanisms may result in an improvement in the overall prognosis of jaundiced patients undergoing surgery.
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PMID:Systemic hypotension and renal failure in obstructive jaundice-mechanistic and therapeutic aspects. 762 83

Acute renal failure in liver disease includes prerenal renal failure, acute tubular necrosis (ATN) and hepatorenal syndrome (HRS). Patients with liver cirrhosis are susceptible to prerenal renal failure because of gastrointestinal bleeding, diuretics and paracentesis etc. ATN is more common in patients with obstructive jaundice but it also develops as a result of prolonged prerenal renal failure. HRS is a functional form of oliguric acute renal failure, occurring in patients with advanced liver disease in the absence of known cause of renal failure. Intrarenal vasoconstriction, attributable to a decrease in effective arterial blood volume, induced by peripheral arterial vasodilation, is proposed to play a causative role. Central hemodynamic monitoring is useful to distinguish HRS from other reversible conditions with renal failure in liver disease.
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PMID:[Renal damage in liver cirrhosis: pathophysiology and management]. 811 86

Surgery in patients with surgical obstructive jaundice is known to be associated with increased risk of post-operative acute renal failure. A prospective study was carried out to evaluate the renal function in patients with obstructive jaundice. Renal functions of thirty two patients with jaundice secondary to mechanical obstruction of the biliary tract were evaluated pre-operatively and 7 days after surgical biliary decompression. Although no significant difference was seen in the mean values of pre and post operative renal function variables, two patients had overt renal failure, one with pre-operative cholangitis and acute tubular necrosis and another with carcinoma of the pancreas and postoperative acute renal failure. The overall satisfactory outcome in our obstructive jaundice patients may be related to pre-operative and intraoperative preparation with intravenous fluids and mannitol. It is concluded that patients with obstructive jaundice can be satisfactorily treated with special preoperative care including good hydration and mannitol therapy during anaesthesia and surgery.
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PMID:Renal functions in obstructive jaundice: a pre and post operative assessment. 822 98

Following studies showing an association between helminth infections and protection from cerebral malaria, we compared 22 patients with malaria-associated acute renal failure with 157 patients with moderately severe malaria. Helminths were associated with protection from renal failure (adjusted odds ratio [AOR], 0.16 [0.03-0.85], P = 0.03). Helminth-infected controls were less likely to have jaundice (AOR, 0.39 [0.16-0.96], P = 0.04) or to have peripheral mature schizonts (AOR, 0.2 [0.07-0.62], P = 0.005) than controls without helminths. This suggested that preexisting helminth infections may have been protective by influencing sequestration and obstructive jaundice, 2 possible determinants of acute tubular necrosis.
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PMID:Helminth infections are associated with protection from malaria-related acute renal failure and jaundice in Thailand. 1179 82

The two most widely used experimental models of advanced liver disease are the administration of carbon tetrachloride, and common bile duct ligation (BDL), however, neither has been systematically evaluated as a model of hepatorenal syndrome (HRS). The BDL model in rats, studied at diverse time points, induced a progressive renal dysfunction without structural changes in the kidney. The authors concluded that BDL is a good model for further studies of HRS and its treatment. However, the renal impairment observed at the acute phase of the BDL model is based on a different pathophysiology than that of HRS. Specifically, in acute obstructive jaundice, cholemia predominates over parenchymal liver disease (reversible at this stage without portal hypertension or cirrhosis) and independently induces negative inotropic and chronotropic effects on the heart, impaired sympathetic vasoconstriction response and profound natriuresis and diuresis that might lead to volume depletion. In addition, systemic endotoxemia contributes to the prerenal etiology of renal impairment and promotes direct nephrotoxicity and acute tubular necrosis. On the other hand, the renal failure observed in the chronic BDL model (with development of biliary cirrhosis, portal hypertension and ascites) shares pathophysiological similarities with HRS, but the accordance of the chronic BDL model to the diagnostic criteria of HRS (e.g. absence of spontaneous bacterial peritonitis, no renal function improvement after plasma volume expansion) should have been confirmed. In conclusion, we think that the BDL model is not suitable for the study of the natural history of HRS, but the chronic BDL model might be valid for the study of established HRS and its potential therapies.
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PMID:Bile duct ligation in rats: a reliable model of hepatorenal syndrome? 1868 Feb 30