Acute glomerulonephritis in hepatitis A virus infection: a rare presentation

Introduction

The most common cause of acute glomerulonephritis (AGN) in tropical countries is post-streptococcal, although viruses have also been implicated. ¹ Hepatitis A virus (HAV) as a cause of AGN has rarely been reported in the paediatric population. ^2–4

Case history

An eight-year-old boy presented with fever, cough and coryza that had persisted for three days. He had gross haematuria and a decreased urine output. There was no history of abdominal trauma, burning micturition, increased frequency of urination, swelling over the body, sore throat, pyoderma or bleeding. An examination revealed a well-nourished child with a mild pallor. He was hypertensive with a blood pressure of 132/100 mmHg. Systemic examinations were normal. Investigations revealed a haemoglobin of 9.1 g/dL, total leukocyte count of 11,000/mm³ and a platelet count of 10,800/mm³. A peripheral smear did not reveal any haemolysis or malarial parasites. His blood urea was 29 mg/dL, serum creatinine-0.6 mg/dL, serum sodium-134 mEq/L and serum potassium-3.6mEq/L. Urinary proteins were absent and, on microscopy, dysmorphic red blood cells were seen. The antistreptolysin O titres were <200 IU/L and C-reactive protein (CRP) was negative. Serum C3 was 63 mg/dL (normal = 90–180 mg/dL). Urine and blood cultures revealed no organisms.

The boy was administered intravenous crystalline penicillin, frusemide and amlodipine. By the fourth day he became normotensive and his urinary output increased but haematuria persisted. He developed jaundice on the fifth day. Liver function tests revealed a total protein of 4.5 g/dL, albumin 2.4 g/dL, globulin 2.7 g/dL, total bilirubin 5.1 mg/dL with a direct fraction of 3 mg/dL, serum glutamic pyruvic transaminase (SGPT) 1974 U/L and alkaline phosphatase 216 U/L. Immunoglobulin M (IgM) for HAV was positive. The hepatitis B surface antigen, anti-hepatitis C virus, anti-hepatitis E virus antibodies were nonreactive. Abdominal sonography revealed hepatomegaly, renal size and texture were normal.

The jaundice subsided over the next week. Liver function tests revealed a total protein of 5.7 g/dL, albumin 3 g/dL, albumin: globulin 1.3:1 and SGPT 159 U/L. There were no dysmorphic red blood cells in the urine. On follow-up the boy was normotensive and a urine examination did not reveal any abnormality.

Discussion

Viral hepatitis is associated with various extra hepatic manifestations. ⁵ They can be seen in both acute and chronic liver disease and may precede or follow overt liver disease. Glomerulonephritis is the most common cause of acute and chronic renal disease. Recently glomerulopathy has been associated with bacterial, viral and other infections. ¹ Although there are many reports about viral infections including the hepatitis B virus, hepatitis C virus, cytomegalovirus, varicella, Ebstein-Barr virus, coxsackie, rubella, mumps, and oncoviruses preceding AGN, HAV associated with AGN has rarely been reported in the paediatric population. ^2–4 Facts supporting association of HAV infection and AGN in our patient were: absence of prior renal disease; absence of any systemic disease; absence of elevated antistrptolysin-O and C-reactive protein, presence of anti HAV IgM, presence of dysmorphic red blood cells in the urine and hypocomplementaemia and a normal coagulation profile. Mathur et al. ⁴ published a case report with a similar association of AGN with HAV infection in a seven-year-old boy who had mesangial proliferative glomerulonephritis, nephrotic syndrome and acute renal failure with HAV infection.

Demircin et al. ² reported AGN and HAV infection in two Turkish children. Merium et al. ³ also reported a four-year-old boy who had AGN and renal insufficiency, with HAV infection developing later. The clinical findings of our patient resemble this report as manifestations of HAV infection developed later in the course of AGN.

The mechanism of glomerular injury with viral infections include the formation of immune complexes with subsequent deposition in the glomerular structures or a direct cytopathogenic effect of the viruses on the glomerular cells. ⁶ In our patient an immune complex type of glomerulonephritis was presumed due to documented hypocomplementaemia. A biopsy was not carried out as it was seen as an invasive procedure and the parents' consent could not be obtained. Our patient recovered uneventfully.

This case highlights the fact that AGN can be caused by HAV infection and that we should be aware of the possibility of glomerular involvement in HAV infection. Renal function should be closely monitored during the course of an HAV infection. Research needs to be carried out to determine the exact mechanism and prognosis of renal disease in this infection.