Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. Rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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PMID:Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study. 714 28

Acetaminophen is the most commonly reported drug overdose in the United States. Acute renal failure occurs in less than 2% of all acetaminophen poisonings and 10% of severely poisoned patients. At the therapeutic dosages, acetaminophen can be toxic to the kidneys in patients who are glutathione depleted (chronic alcohol ingestion, starvation, or fasting) or who take drugs that stimulate the P-450 microsomal oxidase enzymes (anticonvulsants). Acute renal failure due to acetaminophen manifests as acute tubular necrosis (ATN). ATN can occur alone or in combination with hepatic necrosis. The azotemia of acetaminophen toxicity is typically reversible, although it may worsen over 7 to 10 days before the recovery of renal function occurs. In severe overdoses, renal failure coincides with hepatic encephalopathy and dialysis may be required. Recognition of acetaminophen nephropathy requires the following: (1) a thorough drug history, including over-the-counter medications such as Tylenol or Nyquil; (2) knowledge of the risk factors that lessen its margin of safety at therapeutic ingestions, i.e., alcoholism; and (3) consideration of acetaminophen in the differential diagnosis of patients who present with combined hepatic dysfunction and ATN.
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PMID:Acute renal failure due to acetaminophen ingestion: a case report and review of the literature. 757 69

Spontaneous bacterial peritonitis (SBP), refractory ascites, hepatorenal syndrome (HRS), hyponatremia and hepatic encephalopathy are complications which frequently happen during a clinical course of decompensated cirrhosis. Splanchnic and peripheral vasodilatation, increased intrarenal vasoconstriction and impaired cardiac responsive function are pathological changes causing systemic and hemodynamic derangement. Extreme renal vasoconstriction leads to severe reduction of renal blood flow and glomerular filtration rate, which finally evolves into the clinical feature of HRS. Clinical manifestations of type 1 and type 2 HRS come to medical attention differently. Patients with type 1 HRS present as acute kidney injury whereas those with type 2 HRS will have refractory ascites as the leading problem. Prompt diagnosis of type 1 HRS can halt the progression of HRS to acute tubular necrosis if the combined treatment of albumin infusion and vasoconstrictors is started timely. HRS reversal was seen in 34%-60% of patients, followed with decreasing mortality. Baseline serum levels of creatinine less than 5 mg/dL, bilirubin less than 10 mg/dL, and increased mean arterial pressure of over 5 mmHg by day 3 of the combined treatment of vasoconstrictor and albumin are the predictors of good response. Type 1 HRS can be prevented in some conditions such as albumin infusion in SBP, prophylactic antibiotics for upper gastrointestinal hemorrhage, albumin replacement after large volume paracentesis in cirrhotic patients with massive ascites. The benefit of albumin infusion in infection with primary source other than SBP requires more studies.
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PMID:Current position of vasoconstrictor and albumin infusion for type 1 hepatorenal syndrome. 2626 32