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)

A 42-year-old female was admitted to a hospital, because of acute hepatitis A. Laboratory data were GOT 8210mU/ml. GPT 4650mU/ml, LDH 11860mU/ml, total bilirubin 4.7mg/dl, BUN 19.5mg/dl and creatinine 1.9mg/dl. Urinalysis showed proteinuria 3+ and occult blood 1+. Soon after admission, she suffered from anuric acute renal failure and was transferred to our hospital for hemodialysis. Her urine-volume was under 20 ml per day. Urinalysis showed proteinuria 4+, occult blood 1+ and casts. Laboratory data showed BUN 58.2mg/dl and creatinine 8.5mg/dl. She was treated by hemodialysis for 35 days, before recovering from renal failure. However, her renal function did not recover perfectly and her 24-hour creatinine clearance remained at 50ml/min after 6 months. Renal biopsy was performed on the 17th day after admission. Examination by light microscopy revealed the findings of acute tubular necrosis and examination by immunofluorescence antibody method was negative. Urinalysis of 8 patients with acute hepatitis A showed that all patients had proteinuria at the onset. Patients with acute hepatitis A have symptoms of appetite-loss, nausea, vomiting and/or diarrhea. These symptoms cause hypovolemia, and hepatic dysfunction causes discontrol of vasoactive hormones, which gives rise to disturbance of renal circulation. Subsequently, acute tubular necrosis and acute renal failure occur.
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PMID:[A case of acute hepatitis A associated with acute renal failure from the onset]. 823 Aug 22

Nonfulminant hepatitis A viral infection has rarely been associated with renal abnormalities, most commonly microscopic hematuria and minimal proteinuria. An unusual case is presented of a 37-yr-old female with serologically proven acute hepatitis A infection complicated by acute oliguric renal failure. The patient recovered, and laboratory tests returned to normal 1 month after initial hospitalization. Renal biopsy revealed acute tubular necrosis; dialysis was not necessary. The relevant world literature is reviewed.
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PMID:Acute renal failure associated with nonfulminant hepatitis A viral infection. 885 78

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
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PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78

Acute renal failure has rarely been reported in association with acute hepatitis A infection. The commonest form of renal injury in such patients has been found to be acute tubular necrosis. We report two cases of hepatitis A infection in which acute renal failure occurred very early in the course of the illness and had a clinical presentation and recovery pattern suggestive of acute tubular necrosis. In both patients, the clinical course of renal dysfunction was almost parallel to the course of hepatic dysfunction. Patient 1 needed dialysis, whereas patient 2 did not need dialysis and had a very rapid recovery from renal function in spite of having more severe azotaemia. Patient 2 was administered acetylcysteine in high doses for suspected fulminant hepatic failure. A potential benefit of a high dose of acetylcysteine in recovery of renal function from acute tubular necrosis is postulated.
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PMID:Acute renal tubular injury with acute hepatitis A infection: is it just a coincidence? 1499 9

Hepatitis A is generally regarded as a mild, self-limiting disease of the liver. Acute renal failure has rarely been reported in association with non-fulminant acute hepatitis A. Acute tubular necrosis is the most common form of renal injury in such patients. We recently experienced two cases of hepatitis A in which acute renal failure occurred early in the course of the illness and had a clinical course suggestive of acute tubular necrosis. In both patients, the clinical course of renal dysfunction was almost parallel to that of hepatic dysfunction. Hemodialysis was performed in patient 1 because of severe uremia despite maintaining urine output more than 2,000 mL per day. On the other hand, hemodialysis was not performed in patient 2 who showed a rapid recovery of renal dysfunction. The renal biopsy of patient 1 demonstrated typical findings of acute tubular necrosis on microscopy.
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PMID:[Two cases of acute renal failure associated with non-fulminant acute hepatitis A]. 1718 26

Although most cases of immunoglobulin A (IgA) nephropathy are idiopathic, several diseases are associated with IgA nephropathy. Of these, chronic liver disease resulting from hepatitis B or C virus infection has been reported as a secondary cause of IgA nephropathy. Recently, hepatitis A virus (HAV)-associated kidney disease has received attention because acute kidney injury can occur as a complication of HAV infection, generally caused by acute tubular necrosis or interstitial nephritis. However, unlike IgA nephropathy related to hepatitis B or C, HAV-associated IgA nephropathy is extremely rare and long-term outcomes have not been reported yet. We describe a case of spontaneous remission of IgA nephropathy associated with serologically documented HAV infection. The patient presented with microhematuria and moderate proteinuria, but acute kidney injury did not occur during active hepatic injury. Kidney biopsy specimens clearly showed mesangial IgA deposits with intact tubules and interstitium. Serum liver enzyme levels returned to reference values 1 month after the onset of acute hepatitis, but urinary protein excretion remained increased. Approximately 1 year later, urinary abnormalities were resolved and a second biopsy showed no mesangial IgA deposits. These findings suggest that IgA nephropathy can transiently accompany HAV infection, but may not progress to chronic glomerulonephritis after recovery from HAV.
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PMID:Spontaneous remission of IgA nephropathy associated with resolution of hepatitis A. 2093 22

Hepatitis A is usually a benign self-limiting disease with few or no extrahepatic manifestations. Acute hepatitis A causing severe renal dysfunction is not very common, although described. Patients developing renal dysfunction post hepatitis A infection usually have prerenal acute kidney injury (AKI) or acute tubular necrosis due to vomiting, diarrhea, and poor fluid replacement. However, if renal dysfunction persists, other causes need to be evaluated. The term cholemic nephrosis or more specifically bile cast nephropathy has been described in the setting of cholestatic jaundice and decompensated liver failure where bilirubin levels reach above 20 mg/dL. Herein, we describe the clinical course of a patient who developed acute hepatitis A with severe liver dysfunction and subsequently AKI which persisted for six weeks. Renal biopsy showed the evidence of bile cast nephropathy. After six weeks of hemodialysis, urine output improved. He slowly recovered both hepatic and renal functions.
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PMID:Bile cast nephropathy causing acute kidney injury in a patient with nonfulminant acute hepatitis A. 3058 86