Non-oliguric acute renal failure associated with hepatitis E.

A 34-year-old female was referred to our unit with acute hepatitis. From September 1994 until May 1995 she travelled through Thailand, Malaysia, Singapore, Introduction Nepal, India, and Bhutan. Before leaving The Netherlands she received immunoglobin for hepatitis A prophylaxis. During her travels she used mefloquine Hepatitis E usually presents as a self-limiting, acute as malaria prophylaxis, and oral anticonceptives. She icteric disease similar to hepatitis A [1]. Jaundice is suffered some short periods of self-limiting diarrhoea. usually accompanied by malaise, anorexia, abdominal In India, a few weeks before her return, she once drank discomfort and liver enlargement. The hepatitis E virus water from a river. There was no history of unprotected is enterically transmitted and frequently spread by sexual intercourse. fecally contaminated drinking water. Five weeks after her return she was admitted to a Hepatitis E is endemic in developing countries of local hospital with fever, nausea, vomiting, muscle the Indian subcontinent, Asia, Africa and South pains, and diffuse abdominal pains. The next day she America [1,2]. The infection is recognized as a significwas transferred to our hospital because of serious liver ant health problem in these areas and so far outbreaks failure, possibly requiring liver transplantation. have been described and serologically confirmed in 29 At admission physical examination revealed an countries [2]. icteric young female with grade 1 encephalopathy. Hepatitis E is rare in the so-called developed counTemperature was 34.9°C, blood pressure 140/80 mmHg tries and mostly restricted to immigrants from endemic and the central venous pressure was normal. We found areas or travellers returning from endemic areas [2]. diffuse tenderness of the abdomen, a palpable liver Also in the Netherlands most cases of hepatitis E are and spleen, but no ascites. described in immigrants and visitors of third world countries [3 ]. Although in general hepatitis E runs a Laboratory test results at admission were as follows: benign course, death may follow. In endemic areas the Hb 13,4 g/dl, leucocytes 11.7×109/l, platelets case-fatality rate is estimated to be 0.5–4%, although 108×1012/l, Na 133 mmol/l, K 4.2 mmol/l, urea in pregnant women these rates are much higher i.e. 7.9 mmol/l, creatinine 179 mmol/l, uric acid 10–40% [1,2]. Death is most often due to acute liver 0.40 mmol/l, APh 170 U/l, LDH 15495 U/l, ASAT failure with resulting coma and bleeding. Renal failure 9766 U/l, ALAT 7712 U/l, gamma GT 41 U/l, bilirubin however may be of additional importance. 125 mmol/l, albumin 33 g/l, pH 7.39, bicarbonate Renal failure in liver disease is most often caused 17.5 mmol/l, lactate 2.8 mmol/l, ammonia 102 mmol/l. by hepato-renal syndrome or acute tubular necrosis Prothrombin time 25 s prolonged, APTT 10 s pro[4,5]. Other causes of renal failure in viral hepatitis longed, fibrinogen 2.5 g/l, anti-thrombin III 64%,and are acute glomerulonephritis as seen in hepatitis B [6], coagulation factor V 18%. and interstitial nephritis, which has been reported in Urine analysis showed many erythrocytes, 0–5 leucohepatitis A [7]. Renal failure complicating hepatitis E cytes and many granular casts per high powered field. has, to our knowledge, never been described. We Urine sodium was low: 12 mmol/l; there was no describe a patient with fulminant hepatitis E, who proteinuria. developed an acute non-oliguric renal failure. Serologic tests for hepatitis B, hepatitis C, Epstein–Barr virus, cytomegalovirus, human immunedeficiency virus, herpes viruses, leptospirosis, Q fever, toxoplasma and schistosoma were negative. There were Correspondence and offprint requests to: E. A. M. Verschuuren, no serological features of auto-immune hepatitis. Department of Internal Medicine, University Hospital, PO Box 30 001, 9700 RB Groningen, The Netherlands. However IgM antibodies against hepatitis E virus were