Reversible Renal Failure in Minimal-Change Nephrotic Syndrome

Abstract

Renal failure as it occurs in the course of chronic glomerular diseases is generally slowly progressive and irreversible and is caused by anatomic obliteration of the glomerular filtering bed by proliferation of endothelial and epithelial cells, by thickening of capillary walls, by sclerosis resulting from primary glomerular damage, or by ischemic changes related to intrarenal vascular disease. In the absence of a structural basis for glomerular obliteration in minimal-change nephrotic syndrome (MCNS), functional deterioration would not be expected to occur. However, acute renal failure in patients with the nephrotic syndrome and minimal glomerular changes has been reported by a number of observers since 1958^1–14 in a total of approximately 50 patients. Deterioration of renal function in this group of patients has generally been attributed to presumed hypovolemia secondary to hypoalbuminemia with resultant renal vasoconstriction with or without ischemic acute tubular necrosis. A minority of observers have proposed causative roles for tubular obstruction by proteinaceous casts or increased intrarenal pressure related to interstitial edema.