| Abstract|| |
A nine-year-old male child with acute renal failure complicating serologically proven non-fulminating hepatitis A virus infection is being reported. This is rare complication. The patient required dialysis for two weeks and recovered completely with the return of his laboratory tests back to normal.
Keywords: Hepatitis A, Renal failure, Peritoneal dialysis.
|How to cite this article:|
Hazza I. Acute Renal Failure Associated with Nonfulminating Hepatitis A; A Case Report. Saudi J Kidney Dis Transpl 1999;10:506-8
|How to cite this URL:|
Hazza I. Acute Renal Failure Associated with Nonfulminating Hepatitis A; A Case Report. Saudi J Kidney Dis Transpl [serial online] 1999 [cited 2020 Jun 3];10:506-8. Available from: http://www.sjkdt.org/text.asp?1999/10/4/506/37210
| Introduction|| |
The association of hepatitis B and C viruses with renal diseases has been firmly established. , Renal failure has been described most often as a complication of fulminant hepatitis. Non-fulminating hepatitis A viral infection has rarely been associated with renal abnormalities and acute renal failure.
In this report, we describe a child who developed acute renal failure as a complication of non-fulminating a viral infection and required peritoneal dialysis for two weeks before he recovered completely.
A Medline search revealed relevant articles in English and Japanese literatures and to our knowledge this is the third case to be reported in children.
| Case Report|| |
A nine-year-old male child was referred to our hospital with acute renal failure. He was admitted to another hospital two days earlier with anorexia, epigastric pain and yellowish discoloration of the sclera. He developed oliguria with perioribital edema and his creatinine rose to 300 µmol/L and blood urea to 16 mmol/L.
One the day of admission the patients's initial biochemical investigations revealed a blood urea nitrogen level of 19 mmol/L, creatinine 425 µmol/L, white blood cell count 37000 cells, hemoglobin level, 116g/L and platelets 370,000/µL. The blood film showed over 50% of atypical lymphocytes, with neutrophilic leucocytosis suggesting viral infection. Serum potassium (K) was 5 mmol/L, serum sodium (Na) 122 mmol/L, total serum bilirubin 200 µmol/L, ALT 1021 U/L, SAT 1024 U/L, prothrombin time (PT) 15/13 sec and activated thromboplastin time (APTT) 36/42 sec. Urinary sodium was 70 mmol/L. Urinalysis demonstrated 10-15 RBC's/hpf, +3 albumin, with gramular casts.
Two days later, the patients became almost anutic. At this stage his physical examination revealed a blood pressure of 110/60, deep jaundice but without signs of hepatic encephalopathy. The patient had generalized edema, ascitis and hypatomegaly with a 14 cm-liver span.
Repeated biochemical investigations showed serum creatinine level of 900 µmol/L, blood urea 41.3 mmol/L, total bilirubin 390 µmol/L, PT 15/13 sec., APTT 44 sec., serum Na 125 mmol/L, K 5.1 mmol/L, blood glucose 112 mg/dl. Hepatitis B surface antigen an antihepatitis C antibody were negative, while antihepatitis A IgM was positive. Blood cultures wee negative and blood complement level was normal. Kidney biopsy was not performed.
The child was started on peritoneal dialysis. Anuria persisted for 10 days then he started to urinate. After he was dialyzed for two weeks, dialysis was discontinued and one week later he was discharged home.
One month later his follow up biochemistry returned completely to normal with creatinine level of 80 µmol/L, urea 4 mmol/L and normal liver function tests.
| Discussion|| |
In the absence of fulminating disease acute renal failure is a rare complication of hepatitis A infection.  Non-fulminating hepatic A has rarely been associated with acute renal failure especially in children. Reviewing the literature disclosed only 21 reported cases of which two cases were reported in children. , while the other reported cases were almost exclusively in adult patients. 
Faust and Pimstone in their review of literature revealed 17 previous reports of renal failure associated with hepatitis A infection. Nineteen of 20 cases complicated by renal impairment were in the setting of non-fulminating disease. 
In our case renal failure was well documented and advanced with almost complete anuria which lasted for two weeks and necessitated the establishment of peritoneal dialysis. There was a complete recovery of both renal and hepatic dysfunction over a six-week period.
The mechanism of viral hepatitis induced renal dysfunction in the setting of acute fulminant hepatitis has been related to endotoxemia which may lead to impairment of renal perfusion by increasing renal vascular resistance.
An immune complex mediated glomerulonephritis was published in one previous report,  and acute tubular necrosis was presumed to be the etiology in other cases., In our case the absence of liver failure, and the absence of clinical evidence of hepatic encephalopathy argued against hepatorenal syndrome. The absence of severe hypertension, hematuria and the presence of high urinary sodium were in favor of acute tubular necrosis.
| References|| |
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Pediatric Department, King Hussein Medical Center, P.O. box 143924, Amman