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Gordon Research Institute
Garry F. Gordon, MD, DO, MD(H), President 600 N Beeline Hwy, Suite B, Payson, AZ 85541 OFFICE: (928) 472-4263 FAX: (928) 474-3819 www.gordonresearch.com Click here to e-mail Dr. Gordon |
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Original Paper Elevated Lead Burden in Chinese Patients
without Occupational lead Exposure Ja-Liang Lin (a) . . . . . . . . . . . . . . . . . . . . . . . . . .
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Abstract Studies were conducted in 10 healthy Chinese Controls, 10 patients with chronic renal failure without gout, 8 patients with gout complicated with chronic renal failure who subsequently developed gout. All the subjects had no history of occupational or accidental lead exposure. Total body lead burden was assessed by 24-hour urine collection measurements over a 72-hour period after intravenous administration of 1g of calcium disodium EDTA. The postinfusion urinary lead excretion of the healthy controls (90.2, range 57.2-161.5 ug/3 days/1.75m2) was higher than the values recently reported for healthy German controls. Similar to earlier studies, we failed to find elevated urinary lead excretion in patients with chronic renal failure without gout. Nevertheless, the EDTA mobilization test identified 2 patients with occult plumbism in this group of patients. Our study also clearly demonstrated that 4 of 6 patients with renal failure who developed gout de novo had underlying plumbism. The high prevalence of increased lead body burden in patients with chronic renal failure, in particular those associated with out, indicates that lead may contribute to a significant portion of chronic renal disease in our patients. In addition, our data suggest that chronic low-level environmental lead exposure may subtly affect renal function. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Introduction
A causal relationship between gout and renal disease has been recognized since antiquity. However, this relationship had largely been forgotten or disclaimed by the turn of the 19th century. In the late 1960s the well-known epidemiological observations in Queensland [1] and the moonshine whisky belt of the USA [2] provided the most concrete confirmation and reawakened interest in this field. Until recently, its pathomechanism has not been clearly elucidated. The high prevalence of gout in uremic populations with saturnism is remarkable. Emmerson [1] suggested that patients with renal failure who developed gout when serum creatinine had already been elevated almost invariably had underlying chronic saturnism. In addition he also stressed the diagnostic importance of the temporal relationship between the onset of gout and the occurrence of renal failure. . . . the once well-recognized chronic lead nephropathy has virtually disappeared in the western world because of improvements of industrial hygiene . . . _________________________________________ |
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