No abstract

Aluminum levels were measured in a variety of tissues obtained from 36 control subjects, 30 nondialyzed uremic patients, 57 dialyzed uremic patients dying of a variety of different causes, and 38 dialyzed uremic patients dying of dialysis encephalopathy. The low aluminum levels consistently found in the control tissues support the fact that in health aluminum is largely excluded from the body. However, this ability to prevent aluminum accumulation is overcome with renal failure. Bone and liver aluminum levels were found to be significantly increased in 82% and 56% respectively in nondialyzed uremic patients and in 100% of the tissues examined from dialyzed uremic patients. In patients dying of dialysis encephalopathy, tissue aluminum levels were not only the highest but also affected in a different manner than that found in other dialyzed patients. It is suggested that dialysis encephalopathy occurs as a result of such rapid aluminum loading during dialysis that bone's ability to sequester this element is overcome, and it is shunted to liver and brain with resulting toxicity.

EDTA (calcium disodium edetate) lead mobilization and x-ray fluorescence (XRF) finger bone lead tests were done in 42 patients with chronic renal failure and without persisting lead intoxication. Nineteen of 23 patients with gout and 8 of 19 without gout had positive EDTA lead mobilization tests. Those patients with gout excreted significantly more excess lead chelate than those without gout. In the gout group 17 patients denied any childhood or industrial exposure to lead. They had a greater number of positive tests and excreted significantly more excess lead chelate than 14 patients with neither gout nor lead exposure. These results confirm that gout in the presence of chronic renal failure is a useful marker of chronic lead poisoning. Of 27 patients with positive lead mobilization tests, only 13 had elevated XRF finger bone lead concentrations (sensitivity 48%). Three of 15 patients with negative lead mobilization tests had elevated XRF finger bone lead concentrations (specificity 80%). Although the XRF finger bone lead test is a convenient noninvasive addition to the diagnostic evaluation of patients with chronic renal failure and gout, its application is limited due to the lack of sensitivity of the method.

Urinary excretion of lead (Pb) was measured in the basal state and following the infusion of EDTA (1 g of calcium disodium edetate) in healthy German controls and in patients with chronic renal failure with and without gout. When evaluated with Zeeman-compensated atomic absorption spectroscopy using the L’vov platform and urine pretreated with nitric acid and Triton X-100, the control basal Pb excretion (median 28, range 11–19 nmol Pb/24 h) and the postinfusion Pb increment (306, range 131–1,587 nmol/4 days/1.73 m²) were considerably lower than most values reported previously in the literature. Elevated Pb body burden was found in 7 of 8 patients who developed gout in the course of renal failure, but only in 2 of 8 patients who had gout prior to development of renal failure; this confirms that appearance of gout in patients with renal failure points to prior Pb exposure. In 7 of 19 nongouty patients with impaired renal function secondary to known renal diseases, urinary Pb excretion was above the 95th percentile of normal. All these patients had occupational Pb exposure. The high prevalence of elevated Pb body burden in patients with renal failure of known cause may not be coincidental and raises the possibility that Pb adversely affects the course of renal disease.