The mechanism of hypercalciuria in streptozotocin-induced diabetic rats.

Metabolic studies were performed in streptozotocin-induced diabetic (D) rats and normal control (C) rats to assess the role of hyperphagia in the hypercalciuria of diabetes. Urinary calcium excretion (UCaV) was significantly higher in D v C rats fed ad libitum. When D rats were pair-fed (calorie and mineral restriction) with C rats, UCaV declined but remained significantly higher than in C rats. When D rats were allowed their usual increased calorie intake but restricted to C rat mineral consumption, UCaV remained elevated. These findings suggested a tubular reabsorptive defect. In vivo microinjection studies were then performed to identify the site(s) of the tubular reabsorptive defect. Using 1.0 mmol/L Ca in the injectate, 45Ca recovery in the urine (CaR%) was significantly higher in D rats after intratubular injections into early and late proximal tubules and late distal but not early distal tubules. An additional load-dependent defect was revealed in the terminal nephron when the Ca concentration of the injectate was increased to 1.8 mmol/L. After early distal injection, CaR% was significantly increased in D v C rats. Infusion of PTH into thyroparathyroidectomized C and D rats enhanced Ca absorption to a similar degree but did not correct the reabsorptive defect in D rats. These results argue against a lack of end-organ responsiveness to PTH in diabetes or a low serum PTH level as the cause of the hypercalciuria. We conclude that hyperphagia contributes to the hypercalciuria of diabetes in the absence of increased Ca intake. Also, two tubular reabsorptive defects exist: one in the loop of Henle; the other, load-dependent in the terminal nephron.(ABSTRACT TRUNCATED AT 250 WORDS)

Microinjection study of renal calcium absorption in the phosphate-depleted rat.

Tracer microinjection studies were performed in chronically phosphate-depleted (CPD) and phosphate-supplemented (PS) rats in order to determine the site of the defect in calcium absorption which developed in CPD. Calcium recovery in the final urine was significantly higher in CPD than in PS rats after microinjections into the early and the late proximal tubules. However, there was no significant difference in the urinary recovery between the two groups after injection into the early and late distal convoluted tubules. The difference in calcium recovery in late proximal studies persisted during PTH infusion. This indicates that there is a defect in calcium absorption in phosphate-depleted rats between late proximal and early distal tubules, which is not correctable with PTH infusion.

Lactic acidosis and hypoglycemia: experimental evidence to show lactate prevents insulin induced seizures in rats.

A 52-year-old man with lactic acidosis and severe hypoglycemia was fully conscious and alert with a blood sugar of 8 mgs%. We believe normal level of consciousness was maintained due to the presence of hyperlactatemia. We show experimental evidence to suggest that lactate prevents the development of insulin-induced seizures in rats.

Position-related false-positive renal imaging.

A case report of false-positive renal imaging due to anterior displacement of the upper pole of the left kidney with the patient in the prone position is presented. False imaging can be avoided by imaging the kidneys with the patient in the supine position and with the detector behind the patient.

Charcoal hemoperfusion for chronic renal failure.

16 patients with end-stage renal disease were treated with a fixed-bed, uncoated-charcoal hemoperfusion device, used either alone or in series with a hemodialyzer. 3 patients had one of their thrice weekly dialyses replaced by one 3 hour combined treatment for up to 6 months, and 3 patients had 150-min combined treatments thrice weekly for up to 5 months. The procedure was well tolerated. Transient hypotension occurred and interfered with fluid removal by ultrafiltration. Platelet counts were reduced, but there was no clinical bleeding. Pretreatment of the device with albumin provided no advantage over heparinized saline, and dextran caused a more severe reduction in the platelet count. The changes in platelets, white blood cells, and hematocrit were transient and noncumulative. Considerable amounts of creatinine and uric acid were removed. Regular charcoal hemoperfusion appears to be safe, and long-term studies of clinical efficacy are indicated.