genitourinary disorders
Heavy Metal Nephropathy
Lead nephropathy
Chronic tubulointerstitial nephritis results as lead accumulates in proximal tubular cells. Short-term lead exposurecauses proximal tubular dysfunction, including decreased urate secretion and hyperuricemia (urate is the substrate for saturnine gout), aminoaciduria, and renal glucosuria. Chronic lead exposure(ie, for 5 to≥30 years) causes progressive tubular atrophy and interstitial fibrosis, with renal insufficiency, hypertension, and gout. However, chronic low-level exposure may cause renal insufficiency and hypertension independent of tubulointerstitial disease. The following groups are at highest risk: Children exposed to lead paint dust or chips Welders Battery workers Drinkers of high-proof distilled (moonshine) alcohol Exposed children may develop nephropathy during adulthood. Common findings include a bland urinary sediment and hyperuricemia disproportionate to the degree of renal insufficiency: Serum urate>9 mg/dL (535.4 micromol/L) with serum creatinine<1.5 mg/dL (132.6 micromol/L) Serum urate>10 mg/dL (594.9 micromol/L) with serum creatinine 1.5 to 2 mg/dL (132.6 micromol/L to 176.8 micromol/L) Serum urate>12 mg/dL (713.8 micromol/L) with serum creatinine>2 mg/dL (176.8 micromol/L) Diagnosis is usually made by measuring whole blood lead levels. X-ray fluorescence may also be used to detect increased bone lead concentrations, but its use is largely limited to research settings. Treatment with Treatment can stabilize renal function, but recovery may be incomplete. 