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Cadmium is an inessential trace metal which accumulates in human tissues from contamination of food, water or air. The kidney is the critical organ following long-term, low-level absorption either by inhalation or ingestion; accumulation occurring in tubular epithelium in the form of a cadmium-metallothionein complex, giving rise to tubular dysfunction. In a group of 12 cadmium workers some of whom were followed for up to 16 years, tubular proteinuria, renal glycosuria, aminoaciduria, hypercalciuria and defects of concentration and acidification have been observed. Two men became recurrent renal stone formers and 1 man, who had nephrocalcinosis when first seen, later developed vitamin D-resistant osteomalacia. Renal tubular dysfunction following cadmium exposure may continue symptom-free for long intervals, but in a proportion of cases serious clinical effects may eventually develop.
There are currently no reliable early markers of renal tubular damage. Since aminoaciduria is an accompanying feature of this condition, the usefulness of increased urinary amino acid excretion as a marker was investigated by inducing renal tubular necrosis in male Wistar rats by the administration of gentamicin (40 mg/kg/d) for 14 d. Plasma amino acids, urea, creatinine, protein and electrolytes, and urine amino acids, protein and N-acetylglucosaminidase (a lysosomal enzyme) were measured over a 20 d period. Amino acid excretion increased dramatically within 24 h of the initial dose for 14 of the 16 amino acids measured. The conventional renal disease markers listed above did not increase until after day 7. Glomerular damage caused by puromycin aminonucleoside did not induce aminoaciduria until marked proteinuria occurred (day 9), and even then amino acid excretion was much less than that caused by gentamicin. To distinguish whether the gentamicin-induced aminoaciduria was a consequence of tubular damage or inhibition of amino acid transport, isolated rat kidneys were perfused with a Krebs-Henseleit albumin buffer with and without gentamicin for 20 min, during which time urinary amino acids were quantitated. Gentamicin did not inhibit amino acid reabsorption. Thus, it appears that in the rat-gentamicin model of acute renal failure, urinary amino acids are early markers of renal tubular damage.
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Two siblings of Turkish-Assyrian extraction, whose parents were first cousins, had poor appetite, slow weight gain and retarded psychomotor development. When given milk the galactose concentration in blood increased. An oral galactose load showed a markedly reduced capacity to metabolize galactose. Fanconi syndrome was present as in classical galactosemia. A galactose-free diet reduced the aminoaciduria but did not normalize the renal tubular function nor the children's general condition. Galactokinase and galactose-1-phosphate uridyltransferase activities in red blood cells were normal. The physical appearance of the children (sparse subcutaneous fat, thin extremities and distended abdomen) and the results of vitamin A and xylose absorption tests, were in accordance with a malabsorption condition. Glucose, however, seemed to be absorbed normally from the gut. There was no evidence of primary liver disease. Since the condition did not normalize with a galactose-free diet, an enzyme defect of galactose metabolism is unlikely. Instead, a more general transport defect with autosomal recessive inheritance is proposed.
Renal damage induced by cadmium (Cd) results in a proximal renal tubular dysfunction, characterized by low-molecular weight (LMW) proteinuria, renal glucosuria, generalized aminoaciduria and decreased renal tubular reabsorption of uric acid and phosphate. Since LMW proteinuria is thought to be one of the earliest adverse health effects caused by Cd, the prevention of the progress of LMW proteinuria is important to avoid further deteriorations in the health condition. Follow-up studies on residents in Cd-polluted areas and Cd-exposed workers have indicated that Cd-induced LMW proteinuria is generally irreversible and progressive even after the cessation or reduction of exposure. The intensity of exposure and the body burden of Cd before the reduction of exposure may influence the prognosis of Cd-induced LMW proteinuria. Several studies have reported a gradual decline in the glomerular filtration rate even after the reduction of Cd exposure. Cohort studies performed in Cd-polluted areas of Japan showed that renal tubular dysfunction and a decreased glomerular filtration rate were strongly associated with increased risk of mortality. However, the results also suggested that overall mortality rates in Cd-polluted areas were not necessarily increased, because of the low mortality among those with urinary beta 2-microglobulin concentrations < 1,000 micrograms/g creatinine. At present, incidence data are too limited to draw a conclusion regarding the cancer risk among residents in Cd-polluted areas.
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