INTRODUCTION
The development of acute renal failure (ARF) in patients with nephrotic syndrome is rare and usually associated to minimal changes nephropathy.1 The pathogenesis is not clear and several mechanisms have been implicated.2, 3 The increase in the pressure within the tubules and the Bowman¿s space can play a role. This is due both to interstitial edema and to intratubular obstruction because of accumulation of proteins4 and cellular detritus.5 Hypovolemia is another mechanism implicated and is related to hypoalbuminemia and to the excessive use of diuretics.
CASE REPORT
A 36 year-old male is presented with a history of nephrotic syndrome in complete remission since 2000.
In 2004 he was evaluated in the Emergency Room because of edemas. The laboratory findings revealed mild renal function impairment and mild proteinuria. Diuretics were prescribed and the patient was referred to the outpatient clinic. Eight days later he was again evaluated because of increasing edemas and he was admitted to the hospital. The following laboratory findings were obtained: urea 71, Cr 1.15, cholesterol 423, triglycerides 254 mg/dL; total proteins 4.32, albumin 2.22g/dL; proteinuria 3.1 g/12-hours. A new renal biopsy was performed and the patient was discharged.
A week later the patients was again admitted with anasarca and oligo-anuria. Serum level of urea was 287 and creatinine was 4.1 mg/dL. Severe hypoalbuminemia was detected that prompted the administration of albumin. The urine analysis revealed Na < 10 mEq/L and Cr > 130 mg/dL, which supported the diagnosis of prerrenal renal failure. Diuretics were withdrawn. The patient developed anuria and a central catheter was placed to initiate hemodialysis. Renal biopsy (fig. 1) showed 8 glomeruli with mild sclerosis and capillary collapse within the vascular pole and others with capsular adhesions or capillary lumen collapse. The interstitium and the tubules were normal. The immunofluorescence pattern was granular mesangial IgM+ and C3 ++. Adiagnosis of focal and segmentary glomerulosclerosis (FSGS) was made and three boluses of steroids were administrated followed by oral prednisone and cyclophosphamide. When the patient was discharged he was in anuria and required periodic hemodialysis.
Two days later the patient was again admitted to the hospital to evaluate renal function because he referred increasing diuresis that reached 7 L/day. On day 9 of hospital stay the laboratory parameters were as follows: urea 32, Cr 0.8 mg/dL; proteinuria 2.5 g/24h; CrCl 156 mL/min.
After 10 months of periodic follow up, the proteinuria was negative and therefore treatment with steroids and cyclophosphamide could be discontinued. The patient remained asymptomatic, with no signs of nephropathy relapse.
DISCUSSION
Some cases of ARF remission without steroidal administration have been reported.7 However the treatment with high doses of prednisone (1 mg/kg/day) is considered necessary in case of nephrotic syndrome associated to FSGS and can induce complete remission in 35-45% of the patients.8 The effect of steroids on glomerular filtrate in ARF associated to nephrotic syndrome is unknown, but they may prevent the tubular reabsorption of sodium and allow the complete recovery of filtration fraction9, 10 as proteinuria decreases. The judicious use of diuretics should maintain the diuresis, avoiding a misbalance of pressures within the glomeruli and the potential progression to anuria. Ultrafiltration hemodialysis is indicated in case of nephrotic syndrome due to FSGS with ARF, which presents with oligo-anuria and accumulation of nitrogen products. At the same time, steroidal treatment should be initiated or their dose increased. The resolution of ARF is in this way to be expected, which may occur in a few weeks or months5, 11 or dramatically, as it happened in the reported case.
