Expression of the polymeric immunoglobulin receptor and excretion of secretory IgA in the postischemic kidney

The humoral mucosal immune response of the kidney involves the transport of secretory IgA (S-IgA) through renal epithelial cells by the polymeric immu noglobulin receptor (pIgR). The pIgR is cleaved and released as free secret ory component (FSC) or attached to IgA (S-IgA). We examined the effects of an ischemic model of acute renal failure (ARF) on the expression of pIgR an d the secretion of FSC and S-IgA in the urine. Kidney pIgR mRNA levels decr eased in ischemic animals by 55% at 4 h and by 85% at 72 h compared with co ntrols. pIgR protein expression in the medullary thick ascending limb (TAL) decreased within 24 h and was nearly undetectable by 72 h. Urinary S-IgA a nd FSC concentrations decreased by 60% between days 3 and 6. pIgR mRNA and pIgR protein in the kidney returned to similar to 90% of control levels and urinary FSC and S-IgA concentrations returned to similar to 55% of control levels by day 7. We demonstrate that ischemic ARF decreases renal mucosal S-IgA transport in vivo and may contribute to the increased incidence of ur inary tract infections.