An elegant retrospective description of an epidemic of chronic renal failure occurring in patients with histories of untreated childhood lead poisoning in Queensland, Australia established beyond reasonable doubt the existence of lead nephropathy. However, a retrospective uncontrolled report from Boston in 1963 refuted the claim that there are serious renal consequences of untreated childhood lead poisoning. We conducted a controlled prospective, longitudinal study to examine the effects of childhood lead poisoning on renal function 17 to 23 years after chelation therapy. The present study reports the results of renal functional tests in a unique cohort of study subjects (N = 62) with significant lead poisoning (initial PbB > 100 micrograms/dl) diagnosed and treated between 1966 and 1972 and their age-matched control siblings (N = 19; initial PbB < 40 micrograms/dl). During the past nine years serial determinations of renal function on all study subjects and control siblings were obtained. Mean values of systolic and diastolic blood pressures, serum creatinine, serum beta 2-microglobulin, fractional excretion beta 2-microglobulin, urinary protein:creatinine ratio, serum phosphate, tubular reabsorption of phosphate, serum uric acid, and urinary specific gravity were similar in study subjects compared with sibling controls. The frequency of abnormal values for these tests was similar in the two groups. Multiple linear regression analyses failed to demonstrate a significant influence of the presence of plumbism or initial PbB on serum creatinine or systolic or diastolic blood pressure. A modest increase in serum creatinine values was observed over a nine year period in four of 62 study subjects (1.4, 1.4, 1.5, 1.6 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)

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