Minimal-change nephropathy proteinuria

Pathogenesis of foot process fusion in various human glomerulopathies may be different. On one hand, in membranous nephropathy, foot process fusion may be the consequence of complement-induced podocyte damage (Cl 1) on the other hand, in minimal change disease, proteinuria may be caused by direct damage to the slit diaphragm with consequent foot process fusion. In any case, foot process fusion results in the formation of large pores and proteinuria. 

Proximal renal tubnlar proteinuria is a possible complication in patients treated with high doses of mesalazine, and it is clearly important to monitor renal function in these patients (SEDA-22, 394) (75). Two studies in 21 (76) and 95 (77) patients with ulcerative colitis and Crohn s disease have shown that proteinuria of tubular marker proteins is common and is related to disease activity rather than to treatment with mesalazine. Thus, tubular proteins are not useful predictors of an adverse renal response to the drug. Nephrotic syndrome with minimal change nephropathy has been described with sulfasalazine and mesalazine (SEDA-16, 427). 

Interferon Proteinuria in up to 5 to 20% patients Rarely nephritic syndrome or/and acute renal failure (acute interstitial nephrotoxicity and minimal change nephropathy ... 

The presenting clinical features in nephrotic adults with minimal-change nephropathy can be indistinguishable from that of FSGS, and renal biopsy is therefore critical in the treatment of adults with nephrotic syndrome. FSGS is two to four times more common in black patients than in white patients. They tend to present with proteinuria more frequently in the nephrotic range and are more likely to experience a rapid decline in renal function. 

A 50-year-old man with pancolitis, who was taking sulfasalazine 1 g bd, developed the nephrotic syndrome, with peripheral and eyelid edema, dyspnea, proteinuria, hypoalbumine-mia, hypercholesterolemia, and a raised eryth-roc5rte sedimentation rate, but the serum urea and creatinine concentrations were normal. A renal biopsy showed changes consistent with minimal change nephropathy, probably caused by sulfasalazine, which was withdrawn. Oral methylprednisolone was introduced, and within 1 week the edema disappeared, the proteinuria resolved, and the other laboratory tests began to normalize. He remained asymptomatic after withdrawal of methylprednisolone. 

Nephrotic syndrome. Patients with minimal change disease respond well to daily or alternate day therapy. With a total of prednisolone 60 mg/d, 90% of those who will lose their proteinuria will have done so within 4-6 weeks, and the dose is tapered off over 3-4 months. Longer courses only induce adverse effects. Relapses are common (50%) and it is then necessary to find a minimum dose of steroid that will keep the patient well. If a steroid is for any reason undesirable, cyclophosphamide or chlorambucil may be substituted. Membranous nephropathy may respond to high dose corticosteroid with or without chlorambucil. 

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