Renal handling of phosphate following release of ureteral obstruction.

The handling of phosphate by the kidney following release of unilateral ureteral obstruction (UUO) was investigated in intact and thyroparathyroidectomized (TPTX) dogs, and compared to that in the kidney following unilateral release of bilateral ureteral obstruction (BUO). By contrast to the kidney after release of BUO, the kidney following release of UUO showed a much lower fractional excretion (FE) of phosphate in TPTX animals (BUO 21.5 +/- 6.8%; UUO 1.3 +/- 0.5%) and a blunted phosphaturic response to PTH (BUO delta + 25.8%; UUO delta + 2.6%). Administration of cyclic AMP, prostaglandin synthetase inhibitors and ammonium chloride failed to correct the hypophosphaturia or the blunted response to PTH. Raising the filtered load of phosphate, however, raised the FE of phosphate in TPTX dogs in the kidney after release of UUO to levels comparable to those in BUO (BUO 21.5 +/- 6.8%; UUO 21.8 +/- 5.1%) and restored the responsiveness to PTH (BUO 49.0 +/- 8.2%; UUO 39.7 +/- 10%). When reabsorptive capacity (RC) was calculated during stepwise increments of serum phosphate, an additional difference was identified between the kidney after release of UUO on the one hand, and the control kidney and the kidney after release of BUO on the other: RC for phosphate was 294 +/- 66 micrograms/min . kg in UUO, 130 +/- 16 micrograms/min . kg in control, and 62 +/- 19 micrograms/min . kg in BUO. It is concluded that, in addition to the role of reduced filtered load of phosphate, an increased capacity to reabsorb phosphate is responsible in part for the hypophosphaturia observed in the kidney following release of UUO.

Lead poisoning from a gunshot wound. Report of a case and review of the literature.

A man was hospitalized on three occasions for symptoms of lead intoxication 20 to 25 years after a gunshot wound that resulted in retention of a lead bullet in his hip joint. The potential for lead toxicity as a complication of a lead missile injury appears to be related to (1) the surface area of lead exposed for dissolution, (2) the location of the lead projectile, and (3) the length of time during which body tissues are exposed to absorbable lead. Cases of lead poisoning of immediate onset resulting from lead shot have been reported in Europe, but all documented cases of ammunition-related plumbism reported in the United States have involved synovial fluid dissolution of a single lead bullet over many years. The solvent characteristics of synovial fluid and associated local arthritis are apparently important factors in the dissolution and absorption of lead from projectiles located in joints. Awareness that lead intoxication can be a complication of retained lead projectiles should allow rapid institution of appropriate diagnostic and therapeutic modalities when such a clinical situation arises.

Failure of histidine supplementation to improve anemia in chronic dialysis patients.

Failure of histidien supplementation to improve anemia in chronic dialysis patients was seen in six patients after a study period of 8 weeks. Serum amino acid levels were elevated to normal by supplementation with 1 g of oral histidine/day in all patients. There was no significant change in serum iron or transferrin levels, hematocrit, or red cell mass in five of the six patients. Histidine supplementation may raise serum amino acid levels, but does not cause any increase in red cell mass or improve the anemia in patients on chronic dialysis who are ingesting adequate dietary protein.

Comparison of inulin, iothalamate, and 99mTc-DTPA for measurement of glomerular filtration rate.

Clearances of inulin, 125I-iothalamate, and 99mTc-Sn-DTPA were measured simultaneously in five mongrel dogs exhibiting a wide range of glomerular filtration rates (GFR). Standard constant-infusion inulin clearance was compared to radionuclide clearances after subcutaneous injection of the emitters mixed with aqueous epinephrine. All three substances were found to have virtually identical clearances. The accuracy, accessibility, low cost, low radiation hazard, and short half-life of 99mTc-Sn-DTPA make it an excellent substance for measuring GFR. The subcutaneous technique offers an accuracy comparable to the more difficult constant-infusion method.

Effects of volume expansion, purified parathyroid extract, and calcium on renal bicarbonate absorption in the dog.

The role of parathyroid hormone (PTH) and of Ca(++) in the regulation of bicarbonate absorption (RHCO(3)) and its response to extracellular volume expansion (VE) was studied in HCO(3) (-)-loaded dogs.VE lowered RHCO(3) in both intact (from 24.8 to 22.0 mmol/liter GFR, P < 0.01) and thyroparathyroid-ectomized (TPTX) (from 24.5 to 18.0 mmol/liter GFR, P < 0.001) dogs; glomerular filtration rate (GFR) and filtered HCO(3) (-) did not change. Both groups showed a significant increase in the fractional excretion of sodium (C(Na) x 100/GFR), calcium (C(Ca) x 100/GFR), and chloride (C(Cl) x 100/GFR) and a decrease in phosphorus reabsorption. Fractional clearance of phosphate (C(P) x 100/GFR) rose in both groups but did not achieve significance. Infusion of purified parathyroid extract (PTE) decreased RHCO(3) in intact dogs (from 24.6 to 22.5 mmol/liter GFR, P < 0.025) and in TPTX dogs (from 26.9 to 22.6 mmol/liter GFR, P < 0.05). No change was noted in GFR, renal blood flow (RBF), filtered HCO(3) (-), or fractional excretion of sodium, calcium, or chloride in either group. There was a significant increase in fractional phosphorus clearance and a decrease in phosphorus reabsorption in each group. Infusion of Ca(++) raised ultrafilterable Ca(++) from 5.7 to 7.9 mg/100 ml in intact and from 4.9 to 7.2 mg/100 ml in TPTX dogs; RHCO(3) increased in intact (from 22.9 to 26.9 mmol/liter GFR, P < 0.025) and in TPTX dogs (from 26.6 to 28.6 mmol/liter GFR, P < 0.05). The GFR, RBF, and the fractional excretion of sodium, chloride, and calcium did not change in either group. The reabsorbed phosphate increased in both groups, and fractional phosphorus clearance fell in the intact group but did not change significantly in the TPTX group. Superimposition of PTE on hypercalcemia in TPTX dogs resulted in a decrease in RHCO(3) (from 27.3 to 23.9 mmol/liter GFR, P < 0.001), which was accompanied by an increase in the fractional excretion of phosphate and a decrease in the reabsorbed phosphate. In this group of TPTX dogs hypercalcemia caused a drop in RBF from 135.6 to 105.8 ml/min with no change in GFR. The RBF returned to control value with PTE infusion. IT IS CONCLUDED THAT: (a) the lowering of RHCO(3) by VE is not dependent solely on stimulation of PTH by the lowered Ca(++), (b) PTE acts directly on the renal tubules to lower RHCO(3), (c) Ca(++) enhances RHCO(3) and this effect is exerted in the absence of PTH and calcitonin, (d) neither the effects of Ca(++) nor of PTH appear to be mediated by altered hemodynamics, although this cannot be excluded in Ca(++)-infused TPTX dogs, (e) Ca(++) enhanced phosphate reabsorption in the absence of PTH; this may be a specific effect of hypercalcemia on phosphate reabsorption or the nonspecific consequence of the rise in serum phosphorus.