CHRONIC LEAD NEPHROPATHY

SUMMARY In view of the evidence for the existence of a form of chronic renal disease due to renal damage by lead in childhood, the requirements for a clinical diagnosis of chronic lead nephropathy were considered. The chief difficulty in confirming such a diagnosis during life was that of finding evidence of excessive past lead absorption. To this end, the effect of a standardized infusion of calcium EDTA upon the excretion of lead in the urine in various groups of patients was investigated. In 19 control subjects with normal renal function, the increase in the urinary excretion of lead due to the calcium EDTA (the EDTA lead excretion) varied up to about 0·6 mg. In 22 subjects with renal insufficiency of varying degrees attributable to childhood lead poisoning, the EDTA lead excretion was always above this figure, as it was also found to be in patients with significant industrial lead exposure. In 19 out of 23 patients with renal disease attributable to causes other than lead, the EDTA lead excretion was comparable with that of the control group with normal renal function. The results in the other four patients in this group were considered in detail, and it was suggested that they had suffered excessive past lead absorption which was ætiologically unrelated to their renal disease. In patients with chronic lead nephropathy, a significant correlation was also demonstrated between the EDTA lead excretion and both the plasma creatinine level and the plasma carbon dioxide content. The results in individual patients also suggested that the amount of lead excreted after the infusion of calcium EDTA increased with increasing renal failure, probably owing in part to the associated disorder of bone metabolism. A group of patients with renal disease in whom the nature of the renal disease was not readily apparent were investigated by this calcium EDTA technique. It was shown that, of those whose EDTA lead excretion exceeded 0·6 mg., evidence of excessive past lead absorption likely to be ætiologically related to the renal disease could be demonstrated in 12 out of 16 patients. In the other four patients, the lead content of bone was at the upper limit of normal, but, even at autopsy, the role of lead in the ætiology of the renal disease in these patients could not be determined with any certainty. The chief toxic effect of the calcium EDTA to be noted was the development of postural hypotension in patients with severe renal disease, especially in those already receiving hypotensive agents. Gout was found to occur in half the patients with chronic lead nephropathy, but to occur infrequently in patients with chronic renal disease not due to lead or to primary gout. Therefore, a patient with chronic renal disease who develops an acute attack of gouty arthritis should be investigated to determine whether the underlying renal disease is chronic lead nephropathy.