Chronic Lead Nephropathy with Excessive Body Lead Burden

A 50-yr-old man, a secondary lead smelting worker, was examined because of persistent renal insufficiency and intermittent gouty arthritis. Four yr earlier, his serum creatinine had fluctuated between 2.1 and 2.5 mg/dl, and creatinine clearance and serum uric acid levels were 40 to 54 ml/min/1.73 m and 9.9 to 12.3 mg/dl, respectively. He had worked intermittently at several lead-smelting plants for approximately 17 yr between 1968 and 1994. Air lead monitoring in 1993–94 at his work site showed it in excess of the threshold limit value (TLV) for lead in Korea (0.05 mg/m). The man was completely removed from further exposure after he was diagnosed as having lead poisoning by a regular special health examination in September 1994. We had examined his health condition by regular health check-up annually since 1988, but no specific symptoms and abnormal screening findings related to renal function were observed until 1994. He presented with fatigue, dizziness, numbness, facial edema, and polyarthralgia for several years before admission. However, he denied headache, wrist drops, and abdominal pain. The remainder of his medical and familial histories were non-contributory. On physical examination, his blood pressure was 120/80 mmHg, and other vital signs were normal. He had a slightly pale face, mild edema on both legs, and reddish nodules on the left ankle and great toe. Results of laboratory studies showed the following values: normocytic normochromic anemia (hemoglobin, 10.7 g/dl) with basophilic stippling of erythrocytes; albumin, 4.2 mg/dl; total cholesterol, 225 mg/dl; sodium, 140 mEq/L; potassium, 5.0 mEq/L; C3, 140 mg/dl; C4, 50 mg/dl; IgG/IgA/IgM, 1,520/220/165 mg/dl; blood lead, 62.0 μg/dl; and zinc protoporphyrin, 218 μg/dl. Renal sonography revealed bilateral normalsized kidneys. Renal biopsy showed focal moderate atrophy or loss of proximal tubules with prominent interstitial fibrosis. Also, 22% of glomeruli showed global sclerosis and arterioles exhibited patchy hyaline deposits (Fig. 1-A). An ultra-structural study revealed an absence of immune complex depositions. The schedule of the lead mobilization test (LMT) is summarized in Table 2. Baseline urinary excretion of lead was 106 μg/d, and after the first LMT with an intravenous infusion of 1 g calcium disodium ethylenediamine tetraacetic acid (CaEDTA), urine lead increased to 3,934 μg/d (Table 1). Cortical bone lead was assessed (in units of μg Pb/g bone mineral) after 30 min of measurement at the left mid-tibia shaft using Cd K-shell X-ray fluorescence (K-XRF) . Tibial bone lead level was 337 μg Pb/g bone mineral. At present, after treatment with 50 g CaEDTA over 11 months, serum creatinine has fallen to less than 2.0 mg/dl (about 1.5 to 1.9 mg/dl) and CaEDTA chelatable lead has decreased to 3,028 μg/d. However, blood lead has been sustained at a high level (59.3 μg/dl).