A 7-year-old boy has become less active over the past 10 days. On physical examination, the boy has facial puffiness. Urinalysis shows no blood, glucose, or ketones, and microscopic examination shows no casts or crystals. The serum creatinine level is normal. A 24-hour urine collection yields 3.8 g of protein. He improves after corticosteroid therapy. He has two more episodes of proteinuria over the next 4 years, both of which respond to corticosteroid therapy. What is the most likely mechanism causing his disease?
Steroid-responsive proteinuria in a child is typical of minimal change disease, in which the kidney looks normal by light microscopy, but the fusion of foot processes is visible with electron microscopy. The most likely cause of foot process fusion is a primary injury to visceral epithelial cells caused by T cell-derived cytokines. Acute cellular renal transplant rejection is mediated by T cell injury with tubulitis. IgA nephropathy with mesangial IgA deposition and consequent glomerular injury causes recurrent gross or microscopic hematuria and, far less commonly, nephrotic syndrome. Immune complex deposition in membranous nephropathy can cause nephrotic syndrome, but is less common in children than in adults and is not steroid responsive. Certain verocytotoxin- producing Escherichia coli strains can cause hemolytic uremic syndrome by injury to capillary endothelium.
Cytokine-mediated visceral epithelial cell injury
Cytotoxic T cell-mediated tubular epithelial cell injury
IgA-mediated mesangial cell injury
Immune complex-mediated glomerular injury
Kidney