Environmental and industrial lead exposures continue to pose major pub
lic health problems in children and in adults. Acute exposure to high
concentrations of lead can result in proximal tubular damage with char
acteristic histologic features and manifested by glycosuria and aminoa
ciduria. Chronic occupational exposure to lead, or consumption of illi
cit alcohol adulterated with lead, has also been Linked to a high inci
dence of renal dysfunction, which is characterized by glomerular and t
ubulointerstitial changes resulting in chronic renal failure, hyperten
sion, hyperuricemia, and gout. A high incidence of nephropathy was rep
orted during the early part of this century from Queensland, Australia
, in persons with a history of childhood lead poisoning. No such seque
la has been found in studies of three cohorts of lead-poisoned childre
n from the United States. Studies in individuals with low-level lead e
xposure have shown a correlation between blood lead levels and serum c
reatinine or creatinine clearance. Chronic low-level exposure to lead
is also associated with increased urinary excretion of low molecular w
eight proteins and lysosomal enzymes. The relationship between renal d
ysfunction detected by these sensitive tests and the future developmen
t of chronic renal disease remains uncertain. Epidemiologic studies ha
ve shown an association between blood lead levels and blood pressure,
and hypertension is a cardinal feature of lead nephropathy. Evidence f
or increased body lead burden is a prerequisite for the diagnosis of l
ead nephropathy. Blood lead levels are a poor indicator of body lead b
urden and reflect recent exposure. The EDTA lead mobilization test has
been used extensively in the past to assess body lead burden. It is n
ow replaced by the less invasive in vivo X-ray fluorescence for determ
ination of bone lead content.