Occupational exposure to lead: Effects on renal function

Abstract

Although nephrotoxicity is common following exposure to lead, the dose-response relationship in adults with occupational exposure is not well understood because information is lacking on early nephrotoxic effects. By the time serum urea nitrogen and creatinine levels are elevated, renal damage may be advanced and not fully reversible. Detailed investigations of renal glomerular and tubular function were performed in six adults with occupational exposure to lead. In all patients, the serum creatinine and urea nitrogen concentrations were within the normal range. GFR was decreased in all but two. Glucose reabsorptive capacity (Tm(G)) was decreased in all, and this decrease was disproportionately greater than expected from the reduced GFR in all but one. Normal values for renal plasma flow (RPF) were observed in four of the six, and for p-aminohippurate (PAH) secretory capacity (Tm(PAH)) in all but one. Bicarbonate reabsorptive capacity (Tm(HCO3)) and urinary excretion of β2-microglobulin were normal in all. Routine clinical laboratory tests are insensitive for the detection of early renal effects of heavy metal exposure. Measurement of renal tubular reabsorptive capacity for glucose appears to be a sensitive method for the early detection of renal effect of lead.