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 (TmG) 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 (RFP) were observed in four of the six, and for rho-aminohippurate (PAH) secretory capacity (TmPAh) in all but one. Bicarbonate reabsorptive capacity (TmHCO3) and urinary excretion of beta2-microglobulin were normal in all. Routine clinical laboratory tests are insensitive for the detection of early renal effects of heavy metal exposure. Measurements of renal tubular reabsorptive capacity for glucose appears to be a sensitive method for the early detection of renal effect of lead.

Lead Nephropathy - A Preventable Cause of Renal Failure

“…The organo-Iead compounds in petrol, although associated with significant neurological effects, are not associated with renal impairment. Adults at highest risk of lead intoxication are those exposed to lead fumes or dust in industry (1,2,12) and as little as 3 months exposure may cause pathological renal lesions (3). In children, direct ingestion of lead accounts for most of the lead intoxication.…”

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

“…Data points indicating proteinuria refer to total urinary protein, urinary albumin, or urinary LMW protein (e.g., 2μG or RBP). Indices of impaired transport include clearance or transport maxima for organic anions (e.g., p-aminohippurate, urate) or glucose (Biagini et al 1977;Hong et al 1980;Wedeen et al 1975). A few studies have provided histo pathological confirmation of proximal tubular injury (Biagini et al 1977;Wedeen et al 1975Wedeen et al , 1979.…”

Dugway Proving Ground: Closure Plan Module 2, for SWMUs 20, 164, 166 and 170

“…Chronic nephropathy, indicated by nuclear inclusion bodies, mitochondrial changes, interstitial fibrosis and glomerular changes, have been associated with prolonged (greater than 10 years) occupational exposures and blood lead levels greater than 40-60 gg/dl (Lilis, et al, 1968;Cramer, et al, 1974;Biagini, et al, 1977;Wedeen, et al, 1975Wedeen, et al, , 1979Buchet, et al, 1980;Hong, et al, 1980). …”