Hippokratia 2002, 6(4):171-176
Gr Miserlis, G Vergoulas, M Leontsini, A Papagiannis, V Papanikolaou, D Gakis, D Takoudas, A Antoniadis
Abstract
In renal transplantation, chronic allograft nephropathy is the leading cause of long term graft losses, transplant glomerulopathy being its glomerular form. Differential diagnosis from recurrent or de novo glomerulonephritis should be enstablished. Whether hepatitis C virus is associated with glomerular damage in renal allograft recipients, as in native kidneys, is not known. The aim of this case report was to show the clinical course of a HCV-positive kidney graft recipient who four and a half years posttransplantation presented de novo allograft glomerulonephritis. He was a 45-year-old male kidney graft recipient who presented to the Outpatient Department of Organ Transplant Unit at Hippokratio General Hospital of Thessaloniki on 1999, for further clinical and laboratory evaluation because of bilateral lower extremity edema, proteinuria (24h urine protein: 1,5 g) and mild hypertension. He was a healthy hepatitis C carrier who had received a kidney allograft from his 42-years-old sister on 1995 and no specific treatment was given to him for the positive HCV test before kidney transplantation. He had repeated episodes of acute tonsillitis while he was six years old and he presented rheumatic fever symptoms at age of eight. Aortic and mitral valve deficiency were added at age of fifteen and proteinuria, microscopic hematuria and mild elevation of serum creatinine (Scr: 1,8 mg/dl) at age thirty two. He had two replacements of aortic valve while he was thirty three and thirty eight years old and one of mitral valve at age of thirty eight. The renal function deteriorated gradually and he commenced hemodialysis treatment at age of forty four. He became HCV-positive during the renal replacement treatment. On 13th post-transplant day he was discharged with normal kidney graft function. One month after renal transplantation he presented acute bronchitis which was treated successfully with antibiotics and concomitant reduction of immunosuppression, while four months later he was admitted to our department with acute cholecystitis due to chololethiasis. Sixteen months after kidney transplantation he underwent laparoscopic cholecystectomy but two months later the clinical and laboratory evaluation at the Outpatient Department revealed mild elevation of blood pressure (BP: 140/95 mmHg), microscopic hematuria of upper urinary system origin and microalbuminuria (24h urine protein: 150 mg). The kidney and the liver function tests remained within normal limits during the 2nd, 3rd and 4th post-transplantation year. Proteinuria of nephrotic type (24h urine protein: 1,5 g) and edema of the lower extremities were added to the clinical syndrome, four and a half years post-transplantation. The circulating immune complexes (CICs) were found above normal limits (CIC:75 ng/ml, normal range: 0,5-15 ng/ml) while at the same period the blood viral load of HCV by polymerase chain reaction ( HCV-RNA PCR) was greater than 106 copies/ml. Renal graft biopsy demonstrated de novo stage II membranous glomerulonephritis with mild arteriosclerosis. Valsartan was added to the treatment in order to reduce proteinuria and stabilize blood pressure and allograft function. Eight years after kidney transplantation there is no impairment either of kidney or liver function, his 24h urine protein is 750 mg, he has negative HCV-RNA PCR and normal serum concentrations of CICs. In conclusion, we have shown that in renal allograft recipients with a past rheumatic fever history, HCV infection may be rarely associated with de novo membranous glomerulonephritis. In this group of patients the angiotensin II type I receptor antagonists may play a useful role for the treatment of proteinuria and hypertension.