Lead nephropathy occupational

Baker EL, GoyerRA, Fowler BA, etal. 1980. Occupational lead nephropathy and renal cancer. Am J IndMed 1 138-148. 

Wedeen RP, Mallik DK. Batuman V. 1979. Detection and treatment of occupational lead nephropathy. Arch Intern Med 139 53-57. 

The increase in urinary N-acetyl- -D-glucosamini-dase (NAG) with increasing blood lead concentrations reflects the proximal tubule dysfunction seen in acute lead nephropathy rather than the chronic interstitial nephritis associated with occupational lead exposure [35, 36]. NAG excretion correlates positively with the blood lead concentration but not with the bone lead concentration [37]. Eicosanoid excretion in lead workers is similar to that in patients with essential... 

In contrast to the reabsorptive defect of acute lead nephropathy, saturnine gout is characterized by renal retention of uric acid [18]. The clearance (Cp ) and maximal secretion rate (Tmp ) for p-aminohippurate (PAH) have been found to be variable in patients with occupational lead nephropathy. 

Although chelation therapy effectively reverses acute lead nephropathy and the preclinical renal dysfunction of occupational lead nephropathy, there is no evidence that such therapy reverses established interstitial nephritis due to lead. The partial remissions achieved among moonshiners and symptomatic lead workers may represent reversal of acute poisoning superimposed on chronic lead nephropathy. No improvement in renal function can be expected once ad-... 

Wedeen RP, Maesaka JK, Weiner B, Lipat GA, Lyons MM, Vitale LF, Joselow NM. Occupational lead nephropathy. Am J Med 1975 59 630-641. 

Selevan SG, Landrigan PJ, Stern FB, Jones JH. Mortality of lead smelter workers. Am J Epidemiol 1985 122 673-683. Wedeen RP, Mallik DK, Batuman V. Detection and treatment of occupational lead nephropathy. Arch Intern Med 1979 139 53-57. 

Chronic lead nephropathy in the occupational setting has been noted for many years, but the lead dosimetry in early studies was generally poorly characterized (Eimnerson 1973 Cramer et al. 1974 Wedeen et al. 1975). Most of the occupational studies have been small and have failed to consider other important confounders of the association between lead exposure and renal function adequately. In addition, the healthy-woiker effecf which is probably pronounced in industries in which health surveillance is required, may bias possible associations toward the null (Ekong et al. 2006). 

More recent evidence in the occupational and environmental health literature identifies two general forms of nephropathological and nephrotoxicolo-gical responses to lead in lead workers and others. Acute nephrotoxic effects of lead present clinically and functionally with a different array of signs and symptoms than the chronic lead nephropathy syndrome, as discussed below. 

CHRONIC LEAD NEPHROPATHY IN ADULTS WITH OCCUPATIONAL EXPOSURES... 

TABLE 15.3 Illustrative Studies of Chronic Lead Nephropathy in Workers with High Occupational Lead Exposures ... 

In a study of 102 cases of occupational lead poisoning, 17 cases of clinically verified chronic nephropathy were found (Lilis et al. 1968). Endogenous creatinine clearance was <80 pg/dL. The mean PbB level for the entire study population was 80 pg/dL (range, 42-141 pg/dL). Nephropathy was more common among those exposed to lead for more than 10 years than among those exposed for less than 10 years. 

Taken together, these studies provide some evidence for the association of chronic nephropathy in occupationally exposed workers with PbB levels ranging from 60 to >100 pg/dL. It should be noted, however, that PbB levels measured at the time of renal function testing may not fully reflect the exposure history that contributed to the development of chronic nephropathy in lead workers. 

Lilis R. 1981. Long-term occupational lead exposure, chronic nephropathy, and renal cancer A case report. Am J Ind Med 2 293-297. 

This chapter describes the acute and chronic nephrotoxic effects of lead in human populations. These effects have long been recognized in chronic adult occupational lead exposures and in nonoccupational adult exposures arising from dietary Pb intakes, producing disorders such as gouty nephropathy. In acute childhood Pb exposure, severe kidney effects in the form of Fanconi syndrome were identified in the early pediatric literature. The syndrome often co-occurred with acute encephalopathy. 

Lead exposures in diverse human populations produce both acute and chronic nephrotoxic effects. The chronic kidney disease association with occupational Pb exposures in the clinical literature, dating to the nineteenth century, was typically characterized as a glomerulonephritic disease histo-pathologically. This traced to the absence of evaluation of the temporal course of Pb-induced nephropathy, particularly the acute effects. 

Examination of Pb mobilization data through provocative chelation or chelation therapy plumburesis (Chisolm et al., 1976 Emmerson, 1963) showed large bone Pb stores in the Queensland young adults, while bone Pb concentrations in these nephropathy patients years after the lead paint exposures were also quite high. The mean bone Pb content reported by Inglis et al. (1978) for such patients rivals that reported for individuals with high occupational Pb exposures. 

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