Some effects of uranyl acetate on proximal tubular function in rabbit kidney

Chronic Ingestion of Uranium in Drinking Water: A Study of Kidney Bioeffects in Humans

“…The glucose, creatinine, and total protein data taken together appear to suggest that at the levels of uranium intake observed in this study (2 to 410 fig/day among males and 2 to 570 fig/day for females), the segment of the nephron most at risk to injury is the proximal tubule rather than the glomerulus. This finding is in agreement with animal data obtained by previous investigators (Nomiyama and Foulkes, 1968;Haley et al, 1982;Diamond et al, 1989). Diamond and co-workers (1989) also found LDH to be a sensitive bioindicator of renal injury.…”

Uranyl Nitrate Acute Renal Failure in the Dog: Early Changes in Renal Function and Haemodynamics

“…This occurred without a measurable fall in filtration fraction and was not associated with significant alterations in blood pressure, respiratory rate, heart rate, cardiac output, packed red blood cell volume and plasma sodium or blood urea concentrations. This natriuresis occurred before significant histological damage (Flamenbaum et al, 1972), and confirms the inhibition of sodium reabsorption and of other renal tubular functions described by various investigators after uranium poisoning (Wills & Main, 1948;MacNider, 1944;Rothstein & Berke, 1949;Nomiyama & Foulkes, 1968). Uranyl nitrate has been shown to inhibit sodium transport in turtle bladder epithelium preparations, where haemodynamic considerations can be excluded (Schwartz & Flamenbaum, 1974).…”

In vitro Inhibition of Na-K-ATPase by Trace Metals: Relation to Renal and Cardiovascular Damage

“…Various of the potentially toxic trace metals may affect energy metabolism within the cell or inhibit the Na-K-ATPase enzyme which represents the biochem- ical correlate of the Na-K pump [8]. Many of the trace metals investigated in the present study accumulate pre ferentially in the kidney cortex, e.g., Cd [17], Cu [18], Hg [19], Ni [20], Pb [21], Ur [22,23], and may thereby cause metabolic a n d /o r morphological alterations at structures located within this region of the kidney. They may cause damage to mitochondria, e.g., Cd [17], Cu [24][25][26], Hg [19], Pb [27], Zn [28], or accumulate in ATPase-rich microsomes, e.g., Zn [29], Cu [30], Pb [31], and in the cyto-plasma, e.g.…”

“…Thus, the renal Fanconi syn drome [5,6], a generalized proximal tubular transport defect with proteinuria, glycosuria and aminoaciduria which may be associated with a variety of hereditary or acquired, most often metabolic diseases, may also result from acute or chronic heavy metal intoxications. Trace metals which have been incriminated as etiological in human proximal tubular transport defects or which are known to experimentally mimic this defect include Cd [1,17] as in battery workers [I], Cu [2,18] as in Wilson's disease [2], Pb [3,21] as in children chronically exposed to it [3], or Hg and Ur [4,5,19,23] as in miners [4]. More rarely, other metal ions such as vanadate [32], chromium [33], gold [34], and platinum [35] may cause tubular or glomerular damage.…”