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Editor,—Renal disease occurring in HIV infected individuals is well described.1, 2 HIV associated nephropathy (HIVAN) is the predominant renal lesion in black patients, whereas immune complex and membranous nephropathy occur more commonly in white patients.1 Improvements in renal function have been described with highly active antiretroviral therapy (HAART) when the underlying renal lesion is HIVAN or membranous nephropathy.3–5 We report here an HIV infected patient in whom renal disease caused by hepatitis B induced membranoproliferative glomerulonephritis improved with HAART.
A 34 year old white homosexual man was found to be HIV-1 antibody positive in August 2000 after he presented with biopsy proved Kaposi's sarcoma. At this time he also reported 2 months of fatigue and frothy urine. In the past he had been found to be hepatitis BeAg positive in 1996. Examination revealed multiple cutaneous Kaposi's sarcoma, BP = 170/100, no peripheral oedema, and scanty retinal haemorrhages on funduscopy. Investigations showed blood urea = 9.2 (normal = 2.8–7.6) mmol/l, serum creatinine = 178 (normal = 80–133) μmol/l, normal serum, potassium, and sodium. Liver function tests were normal apart from a serum albumin of 29 (normal = 35–50) g/l. The haemoglobin was 9.3 g/dl and white blood cell and platelet counts were normal. The CD4 count was 110 cells ×106/l and HIV viral load was 47 500 copies/ml. Complement C3 was 0.56 (normal = 0.9–1.8) g/l, C4 was 0.07 (normal = 0.1—0.4) g/l. Immunoglobulin quantification showed normal IgA, IgG = 23.2 (normal = 7.0—16.0) mg/l and IgM = 4.4 (normal = 0.4—2.3) g/l. Hepatitis B serology showed HbeAg+ and HbsAg+ (titre 1:3200). Urinalysis showed blood +++ and ++++ protein. Urine protein = 5.8 g/24 hours and creatinine clearance = 66 ml/min. Ultrasound examination showed normal sized kidneys. Histology of a renal biopsy showed membranoproliferative glomerulonephritis. Staining showed marked deposits of hepatitis B core and surface antigens (fig 1).
The patient was managed conservatively. HAART was commenced with efavirenz, didanosine, and stavudine and hypertension was treated with ramipril. After 8 weeks of HAART the CD4 count was 140 cells ×106/l and viral load was 100 copies/ml. The serum creatinine returned to normal and there was no persistent proteinuria.
This case illustrates the importance of considering non-HIV associated pathology in the HIV infected patient presenting with renal disease. It also shows the value of renal biopsy in identifying the precise cause of the presentation. This patient demonstrates that non-HIV hepatitis B associated renal disease may improve with HAART. The exact mechanism for this remains unclear.