A 43-year-old female patient with hypertension was diagnosed as having one-kidney renovascular hypertension with dysfunction of the contralateral kidney, and percutaneous transluminal renal angioplasty was carried out. Marked polyuria was observed during the 2- to 72-hour postoperative period. During the 12- to 18-hour period of polyuria, the urine volume was 8.9 liters/6 h, which was 62% of the glomerular filtration, and was accompanied by high fractional excretion of sodium and of potassium and a high urine β₂-microglobulin level. The mechanism of polyuria in this case is discussed.

The aim of the present study was to assess the effect of calcium infusion on segmental tubular reabsorption in humans using lithium clearance, along with creatinine and free water clearances during maximal water diuresis. In 8 healthy volunteers, a 20-min 5 mg/kg calcium infusion that increased serum calcium levels from 2.27 ± 0.07 to 2.87 ± 0.07 mmol/l (p < 0.01) was followed by a 60-min 3 mg/kg infusion for maintenance. During the experimental period, blood pressure did not change. Maximal urine flow increased from 15.6 ± 2.4 to 20.8 ± 2.8 ml/min (p < 0.01), while clearance of sodium increased from 1.5 ± 0.4 to 3.7 ± 0.9 ml/min (p < 0.001). Lithium clearance showed an increase of 7.4 ml/min, pointing to a suppression of proximal reabsorption. Free water clearance also increased from 11.5 ± 3.7 to 14.4 ± 3.9 ml/min, indicating an increase in TALH reabsorption which was attributed to increased sodium and water reaching this segment. Time control studies showed no significant changes in the parameters measured except for potassium excretion. Potassium excretion during calcium infusion was somewhat lower than during the control studies. The data support the view that an increase in serum calcium concentration leads to a decrease in proximal tubular reabsorption as indicated by lithium clearance while a decrease in reabsorption in the collecting duct could well add to the diuretic properties of calcium.

Phosphate depletion (PD) causes a rise in basal level of cytosolic calcium ([Ca2+]i) of pancreatic islets, a decrease in their basal and stimulated ATP content, a reduction in the maximum velocity (Vmax) of Ca2+ adenosine triphosphatase (ATPase) and Na(+)-K+ ATPase, impaired glucose-induced calcium signal and decreased glucose-induced insulin secretion. The sequence of events that lead to these derangements during the evolution of PD are not defined. The present study examined this issue by measuring the metabolic and functional profile of pancreatic islets weekly during the evolution of PD over a period of 6 weeks, and whether phosphate repletion reverses these abnormalities. The results show that initial abnormalities are a rise in Vmax of Ca2+ ATPase and modest rise in basal [Ca2+]i. This was followed by a fall in basal and stimulated ATP content. With the fall in ATP content, the Vmax of Ca2+ ATPase and Na(+)-K+ ATPase decreases and the rise in [Ca2+]i becomes more pronounced. A decrease in glucose-induced insulin secretion becomes evident with the fall in ATP, the decrease in glucose-induced calcium signal, and/or delta[Ca2+]i/basal[Ca2+]i. All functional and metabolic derangements of the pancreatic islets returned to normal after phosphate repletion. Taken together, our data are consistent with the notion that PD is associated with an initial increase in calcium influx into the islets. This is followed by modest but significant rise in [Ca2+]i which, in turn, would inhibit mitochondrial oxidation and ATP generation leading to a decrease in ATP content. The latter compromises the activity of Ca2+ ATPase and Na(+)-K+ ATPase which are involved, directly or indirectly, in calcium extrusion out of the islets. The increased influx of calcium combined with decreased calcium extrusion is followed by a further rise in basal levels of [Ca2+]i. This sequence of events continues until a steady state is reached and is characterized by reduced basal and stimulated ATP content, reduced Vmax of Ca2+ ATPase and Na(+)-K+ ATPase and elevated basal level of [Ca2+]i. Phosphate repletion reverses all these abnormalities.

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