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MERCURY 113<br />

Renal Effects<br />

2. HEALTH EFFECTS<br />

Inorganic Mercury. The kidney appears to be the critical organ of toxicity <strong>for</strong> the ingestion of mercuric<br />

salts. Renal effects in humans have been observed following acute oral exposure to inorganic mercury.<br />

Acute renal failure has been observed in a number of case studies of mercuric chloride ingestion (Afonso<br />

<strong>and</strong> deAlvarez 1960; Murphy et al. 1979; Samuels et al. 1982). An autopsy of a 35-year-old man who<br />

ingested a lethal dose of mercuric chloride <strong>and</strong> exhibited acute renal failure showed pale <strong>and</strong> swollen<br />

kidneys (Murphy et al. 1979). A case study reported acute renal failure characterized by oliguria,<br />

proteinuria, hematuria, <strong>and</strong> granular casts in a woman who ingested 30 mg Hg/kg as mercuric chloride<br />

(Afonso <strong>and</strong> deAlvarez 1960). Another case study reported a dramatic increase in urinary protein secretion<br />

by a patient who ingested a single dose of 15.8 mg Hg/kg as mercuric chloride (assuming a body weight of<br />

70 kg) (Pesce et al. 1977). The authors of the report surmised that the increased excretion of both albumin<br />

<strong>and</strong> β2-microglobulin was indicative of mercury-induced tubular <strong>and</strong> glomerular pathology. Acute renal<br />

failure that persisted <strong>for</strong> 10 days was also observed in a 19-month-old child who ingested an unknown<br />

amount of powdered mercuric chloride (Samuels et al. 1982). Decreased urine was observed in a<br />

22-year-old who attempted suicide by ingesting approximately 20 mg Hg/kg (Chugh et al. 1978).<br />

Myoglobin <strong>and</strong> pigmented casts were observed in the urine, <strong>and</strong> the authors suggested that these<br />

observations, in combination with a highly elevated level of serum creatine phosphokinase, indicated that<br />

rhabdomyolysis may have contributed to the renal failure.<br />

Ingestion of mercurous chloride has also resulted in renal toxicity in humans. Decreased urinary output <strong>and</strong><br />

edema were observed in a 60-year-old woman who ingested an unspecified amount of mercurous chloride<br />

in a Chinese medicine (Kang-Yum <strong>and</strong> Oransky 1992). Renal failure was a contributing factor in the death<br />

of this woman. Renal failure also developed in two female patients who chronically ingested a mercurous<br />

chloride-containing laxative (Davis et al. 1974).<br />

Renal toxicity has been observed in Fischer 344 rats <strong>and</strong> B6C3F 1 mice following acute-, intermediate-, <strong>and</strong><br />

chronic-duration exposures to mercuric chloride (Dieter et al. 1992; NTP 1993). In the 14-day study,<br />

male <strong>and</strong> female rats were exposed by gavage to 0.93–14.8 mg Hg/kg/day as mercuric chloride <strong>for</strong> 5<br />

days a week. There was a significant increase in the absolute <strong>and</strong> relative kidney weights of males beginning<br />

at the 1.9-mg/kg/day dose level. An increased incidence of tubular necrosis was observed in rats exposed to<br />

at least 3.7 mg/kg/day; severity progressed with increasing dose levels. Increases in urinary levels of<br />

alkaline phosphatase, AST, <strong>and</strong> LDH were also observed at 3.7 mg Hg/kg/day; at 7.4 mg Hg/kg/day,

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