Kidney urinalysis

Exposure of rats to sodium dichromate at 0.4 mg chromium(VI)/m3 for 90 days did not cause abnormalities, as indicated by histopathological examination of the kidneys. Serum levels of creatinine and urea and urine levels of protein were also normal (Glaser et al. 1985, 1990). Furthermore, no renal effects were observed in rats exposed to 0.1 mg chromium/m3 as sodium dichromate (chromium(VI)) or as a 3 2 mixture of chromium(VI) trioxide and chromium(III) oxide for 18 months, based on histological examination of the kidneys, urinalysis, and blood chemistry (Glaser et al. 1986, 1988). Rats exposed to 15.5 mg chromium(IV)/m3 as chromium dioxide for 2 years showed no histological evidence of kidney damage or impairment of kidney function, as measured by routine urinalysis. Serum levels of blood urea nitrogen, creatinine, and bilirubin were also normal (Lee et al. 1989). 

Urinalysis. Urine is collected at various times and examined with respect to its volume, specific gravity, and the presence of abnormal constituents. The results may indicate kidney damage or suggest tissue injury at other sites (77). 

Animal data suggest that renal and liver effects may occur in humans exposed to high doses of hexachloroethane. Kidney and liver effects are not specific to hexachloroethane. Lesions of the kidney (nephropathy, linear mineralization, and hyperplasia) were reported at 10 mg/kg/day or greater in male rats (NTP 1989). Urinalysis also revealed granular and cellular casts in rats exposed to hexachloroethane (47 mg/kg/day or greater) for 13 weeks (NTP 1989). Because other compounds cause similar effects and because some of these effects are unique to male rats, they are not valuable as biomarkers for human hexachloroethane exposure. 

Renal Effects. Clinical chemistry, urinalysis, and histological examination of kidneys revealed no renal effects in rats exposed intermittently to <3.7 mg/m for 3 weeks (Thyssen 1980) or to <1.4 mg/m for 13 weeks (Shiotsuka 1989). 

The answer is D. The patient s symptoms are consistent with a kidney stone, which is confirmed by the radiographic finding. The etiology of the stone is indicated by the urinalysis data, which suggest cystinuria. The cells of this patient s renal proximal tubules would be deficient in a transporter responsible for the reabsorptive uptake of cystine and the basic amino acids, arginine, lysine, and ornithine. Failure of the tubules to reabsorb these amino acids from the ultrafiltrate causes them to be excreted at high concentration in the urine. 

Hepatic dysfunction and urinary abnormalities were seen In some subjects after CS exposure at Edgewood. Little is known of the effects of CS on the kidneys and liver. The small proportion of subjects who had abnormal urinalysis (7 of 50 14Z) and high transaminase (3 of 50 6Z) Indicates Idiosyncratic reactions, If the abnormalities were indeed due to CS exposure. The most likely course of idiosyncratic drug-induced, nonfulmlnant hepatitis is complete recovery after removal of the agent. Recurrence of hepatic reactions would be expected on re-exposure to CS If the original transaminase Increases were due to CS. 

In the Hazleton Labs (1968) 4-week study, no treatment-related histopathological effects on the kidney were found in rats exposed to 37 ppm. Because the histological examination was performed on only 30% of the treated and control rats, however, the possibility exists that renal lesions were missed. The 37 ppm concentration can be considered an intermediate duration NOAEL for kidney effects, however, because no exposure-related renal effects were detected upon urinalysis and histological examination of rats and rabbits that were exposed to isophorone in air at a concentration of 250 ppm for 18 months (Dutertre-Catella 1976). The NOAELs of 37 ppm for intermediate duration and 250 ppm for chronic exposure are presented in Table 2-1 and Figure 2-1. 

Intermediate-duration gavage exposure to a higher FireMaster FF-1 dose of 30 mg/kg/day for 4.5 weeks caused dilation of Bowman s capsule with serous fluid in rats observed for 60 days posttreatment (Gupta and Moore 1979) however, rats that were similarly treated (< 30 mg/kg/day for 30 days) but observed longer (90 days posttreatment) had normal kidney histology, urinalysis values, and BUN (Gupta et al. 

In the case of most chemicals, urine analysis provides less precise information than blood serum analysis about the donor s instantaneous state of health. This is because the chemicals build up over time as filtered by the kidney and are diluted by variable amounts of water in the bladder depending upon the donor s hydration state. However, the easy availability of urine, compared with blood, means that repeated urinalysis can monitor a person s state of health with little pain or disruption. As noted above, another major use of urine analysis is the detection of breakdown products from medications or illegal drugs. 

Renal Effects. Acute nephritis with albuminuria and oliguria, polyuria, and nitrogen retention were observed in individuals after application of a salve that contained potassium chromate. These effects disappeared in individuals who survived. Autopsy of people who died revealed hyperemia and tubular necrosis (Brieger 1920). Acute nephritis with polyuria and proteinuria were also described in a man who was admitted to a hospital with skin ulcers on both hands due to dermal exposure to ammonium dichromate in a planographic printing establishment where he had worked for a few months (Smith 1931). A 49-year-old man with an inoperable carcinoma of the face was treated with chromic acid crystals. Severe nephritis occurred after treatment with the chromium(VI) compound. Urinalysis revealed marked protein in the urine. Death resulted 4 weeks after exposure. A postmortem examination of the kidneys revealed extensive destruction of the tubular epithelium (Major 1922). 

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