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Chronic tubular proteinuria

RBP has been found in relatively large amounts in the urine from patients with tubular proteinuria (Peterson and Berggard, 1971). Much is known about urinary protein excretion of Japanese patients with chronic cadmium poisoning (Kanai-er al., 1972a,b). These patients manifest tubular proteinuria and the excretion of considerable amounts of low-molecular-weight proteins, including RBP. The urinary excretion of RBP has been induced in a rabbit (Muto et al., 1976) and in a rhesus monkey (Nomiyama et al., 1981) by chronic poisoning with cadmium. Studies of the role of the kidney in RBP metabolism have also been carried out in rats with various kinds of experimentally induced renal lesions (Peterson et al., 1974). These various reported observations are all consistent with the above postulated role of the kidney in RBP metabolism. [Pg.60]

After chronic exposure, cadmium accumulates in the human body and causes kidney diseases, especially lesions of proximal tubular cells. A tubular proteinuria causes an increase in urinary excretion of microproteins. Excretions of retinol binding protein (RBP), (32-microglobulin ((32-M), and a 1-microglobulin are validated biomarkers for analyzing cadmium effects. For this purpose, immunological procedures such as ELISA, and radio- and latex-immunoassays are used. [Pg.87]

Once absorbed, Cd is very poorly excreted, mainly in urine and feces. In humans the amount excreted daily in urine represents only about 0.005-0.015% of the total body burden [39,96]. The mean concentration of urinary Cd in people not exposed to high Cd levels is 0.5-2.0 pg/L [23] and increases with age [97-99] and body burden [2,100,101]. Smokers have higher urinary excretion than non-smokers [97,99]. Increased urinary Cd excretion occurs when tubular proteinuria develops [100,102]. Most of the Cd in urine is transported bound to MT. Tohyama et al. [103] found good correlation between urinary MT and Cd in the general population as well as in smokers [104]. Roels et al. [105] confirmed this correlation in Cd workers. Over a range of doses, an increase in urinary excretion of Cd is associated with an increase of Cd in the renal cortex [106-108]. Chronic studies on several mammalian species have shown that urinary excretion of Cd increases slowly for a considerable time but, as kidney dysfunction develops, a sharp increase in excretion occurs [5,106,107,109]. This leads to a decrease in renal and liver Cd concentrations [5,106]. [Pg.425]

Genitourinary Renal papillary necrosis, hematuria, hyposthenuria, proteinuria, nephritic syndrome, tubular dysfunction, chronic renal failure, impotence... [Pg.1860]

Adefovir dipivoxil canses dose-related nephrotoxicity and tubular dysfunction, manifested by azotemia and hypophosphatemia, acidosis, glycosnria, and proteinuria that usually are reversible months after discontinuation. The lower dose (10 mg/day) nsed in chronic HBV infection patients has been associated with a few adverse events (e.g., headache, abdominal discomfort, diarrhea, and asthenia) and negligible renal toxicity compared with a threefold higher dose. [Pg.47]

Proteinuria, hematuria, and acute tubular necrosis have been reported in severely intoxicated patients. Gouty nephropathy may occur in chronically treated patients. Azoospermia has been reported with chronic use. [Pg.169]

Rosuvastatin (crestor) is available in doses ranging between 5 and 40 mg. It has a t of 20—30 hours and may be taken at any time of day. Since experience with rosuvastatin is more limited, treatment should be initiated with 5-10 mg daily, increasing stepwise if needed. If the combination of gemfibrozil with rosuvastatin is used, the dose of rosuvastatin should not exceed 10 mg. Rosuvastatin at a dose of 80 mg (dose not approved by the FDA) was noted to cause proteinuria and hematuria and isolated cases of renal failure. Other statins have also been observed to cause proteinuria, apparently by inhibiting tubular protein reabsorption. Whether statin-induced proteinuria is harmful or beneficial, especially in patients with chronic kidney disease, remains to be determined. [Pg.615]


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