CLINICOPATHOLOGICAL STUDY IN IDIOPATHIC NEPHROTIC SYNDROME-ASSOCIATED WITH AZOTEMIA

초록

Nephrotic syndrome is clinically characterized by heavy proteinuria, hypoalbumin- emia, generalized edema, and hyperlipidemia. The natural disease course and prognosis are variable according to renal pathologic findings, so renal biopsy is essential in the treatment of patients. The phenomenon of azotemia in nephrotic syndrome associated with normal renal structure was first described in detail by Chamberlain et al in 1966. The pathophysiologic mechanisms of azotemia in nephrotic syndrome are supposed to be intravascular volume depletion, renal vein thrombosis, acute interstitial nephritis and acute tubular injury due to renal ischemia, but the exact role of these factors was controversial. We examined the clinical features of azotemia and evaluated the renal pathologic findings in these patients. The results were as follows: (1) The study population consisted of a renal dysfunction group (7 cases) and a normal renal function group (31 cases). The mean age and male to female ratio of each group were: 35 years, 6:1 and 32 years, 23:8, respectively. (2) The mean serum BUN level was 43 20 mg/dl, creatinine 2.36 1.00 mg/dl, blood pressure 136/89 mm Hg in the patient group associated with azotemia. (3) The mean serum albumin concentration and urine protein excretion were, respectively, 2.24 0.83 g/dl, 8.67 8.11 g/day in the azotemic patients group, and these values were not statistically significant different from those in the normal renal function group. (4) Azotemia was documented an average of 12 days after onset of nephrotic syndrome and persisted for 3 weeks in the 7 patients in whom recovery of renal function occurred. (5) Of the renal pathologic findings in the azotemic group, the most common findings were minimal change disease in 4 cases, membranoproliferative glomerulonephritis in 2 cases, and focal segmental glomerulosclerosis in 1 case. These results suggested that minimal change disease was the most common pathologic finding in the patients with azotemia. The 24 hour urine protein excretion was not correlated with the development of azotemia and their clinical course was similar to that of the patients with acute tubular necrosis.