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P Borensztein

Publications and source records attributed to P Borensztein.

27 records · Page 2Linked to original sources
PubMed1991

[Distal tubular acidosis. Recent data].

Tubular acidosis is diagnosed when hyperchloremic acidosis is associated with inappropriate NH4 excretion (less than or equal to 40 mmol/24 hours). Urinary pH is variable because it depends on the secretion of H+ into the collecting duct and is inversely correlated with the amount of ammonia available in the urine. Administration of NaHCO3 for diagnostic purpose allows to eliminate proximal tubular acidosis and to measure the elevation of urinary PCO2 reflecting the secretion of H+ in the collecting duct. Hypokalemia points towards distal tubular acidosis, either by defect of H(+)-ATPases pumps, or by the incapacity to create a normal gradient of H+. In contrast hyperkalemia suggests distal tubular acidosis associated either with hypoaldosteronism or with diminution of trans-epithelial voltage or with pseudohypoaldosteronism. The incidence of distal tubular acidosis with hyperkalemia is increasing whereas distal tubular acidosis with hypokalemia remain rare.

Acidosis, Renal Tubular↗
PubMed1991

[Should the parathyroid function be evaluated in a patient with calcium kidney stones? If so, when and why?].

About 7% of patients with calcium urolithiasis suffer from primary hyperparathyroidism. A systematic search for this diagnosis is therefore mandatory in such patients. Because hypercalcemia is often discrete or intermittent, determinations of calcium levels should be repeated at least thrice. Measurement of ionized calcium levels improves the detection of hypercalcemia. The biological diagnosis is based on the presence of hypercalcemia together with an increased plasma level of 1-84 intact parathormone (PTH). A PTH value still in the normal range but inappropriately elevated in the context of hypercalcemia could be sufficient for the diagnosis of primary hyperparathyroidism.

Calcium↗
PubMed1990

[Renal regulation of the acid-base equilibrium].

The kidney controls extracellular bicarbonate concentration and the pH of the body by modulating neat acid excretion (ammonium plus titratable acidity minus bicarbonate) according to the systemic acid-base balance. Proton, bicarbonate and phosphate transport and ammonium synthesis in the proximal tubules change in a homeostatic manner. The intercalycial A (proton secreting) and B cells (bicarbonate secreting) of the distal tubule and cortical collecting ducts have a high capacity of adaptation. The wide ascending branch of the loop of Henle also plays an important role in the bicarbonate and ammonium transport. Recent data suggest a pluri-hormonal regulation of urinary acidification. Therefore, the precision of the renal response to metabolic acidosis depends on the coordinated regulation of different segments of the nephron by the parathyroid hormone, aldosterone and the glucocorticosteroids.

Acid-Base Equilibrium↗
PubMed1990

[Renal acidosis].

Normal adults with normal protein intakes have a urinary NH4 excretion of 40 to 50 mmol/24 hours and a variable urinary pH. In cases of metabolic acidosis a urinary pH less than 5.5 suggests an extra-renal origin whilst a urinary pH greater than 5.5 is in favour of renal acidosis, but there are many exceptions to this rule. On the other hand, urinary NH4 excretion is always greater than 70 mmol/24 hours in the first case and less than 40-50 mmol/24 hours in the second; and the use of the urinary anionic gap (Na + K - Cl), negative in the first case and positive in the second, enables the two situations to be distinguished. The acidosis of nephron reduction is easily recognised in cases of severe renal failure with an increase in unmeasured plasma anions whilst tubular acidoses are accompanied by a hyperchloremia. Measurement of fractional HCO3 excretion after an oral loading dose of NaHCO3, preferably by TmCHO3 with respect to GFR, distinguishes proximal tubular acidosis (low TmHCO3) from distal tubular acidosis (normal or high TmHCO3). In the latter case, the presence of hypokalemia suggests a distal tubular acidosis either due to deficiency of the H(+)-ATPase pumps (absence of increased urinary pCO2 after oral loading dose of NaHCO3) or to the inability of the kidney to maintain a normal H+ gradient (normal increase of urinary pCO2. The presence of hyperkalemia suggests diseases associated with hypoaldosteronism (low or inappropriate serum aldosterone concentrations), abnormal transepithelial voltages or with a pseudo-hypoaldosteronism syndrome (high plasma aldosterone concentration). The prevalence of distal tubular acidosis with hyperkalemia is on the increase whilst tubular acidosis with hypokalemia remains rare.

Acid-Base Equilibrium↗
PubMed1990

Acute metabolic acidosis enhances circulating parathyroid hormone, which contributes to the renal response against acidosis in the rat.

Acute PTH administration enhances final urine acidification in the rat. HCl was infused during 3 h in rats to determine the parathyroid and renal responses to acute metabolic acidosis. Serum immunoreactive PTH (iPTH) concentration significantly increased and nephrogenous adenosine 3H,5H-cyclic monophosphate tended to increase during HCl loading in intact and adrenalectomized (ADX) rats despite significant increments in plasma ionized calcium. Strong linear relationships existed between serum iPTH concentration and arterial bicarbonate or proton concentration (P less than 0.0001). Serum iPth concentration and NcAMP remained stable in intact time-control rats and decreased in CaCl2-infused, nonacidotic animals. Urinary acidification was markedly reduced in parathyroidectomized (PTX) as compared with intact rats during both basal and acidosis states; human PTH-(1-34) infusion in PTX rats restored in a dose-dependent manner the ability of the kidney to acidify the urine and excrete net acid. Acidosis-induced increase in urinary net acid excretion was observed in intact, PTX, and ADX, but not in ADX-thyroparathyroidectomized rats. We conclude that (a) acute metabolic acidosis enhances circulating PTH activity, and (b) PTH markedly contributes to the renal response against acute metabolic acidosis by enhancing urinary acidification.

Acidosis↗
PubMed1989

Determinants of parathormone secretion in primary hyperparathyroidism.

We studied the effects of acute modifications in plasma calcium on parathormone (PTH) secretion in 23 patients with primary hyperparathyroidism (PHPT). In 12 patients, PTH hypersecretion was autonomous, and basal plasma calcium concentration was positively correlated with maximal serum PTH(1-84) reached during Na2EDTA infusions. In 11 patients, PTH hypersecretion remained suppressible, but with elevated set point value, and basal plasma calcium concentration was positively correlated with set point. Thus, the degree of hypercalcemia seems mainly determined by the magnitude of maximal PTH secretion and set point error in autonomous and suppressible PHPT, respectively. We have previously suggested that high serum calcitriol levels might chronically inhibit PTH hypersecretion in PHPT. We showed that hyperparathyroid patients with renal stone presentation exhibited an abnormally high value of circulating calcitriol and a moderately elevated PTH activity, while patients with severe bone disease presentation displayed a low to normal calcitriol value and a dramatically increased PTH activity. The hypothesis was supported by a recent study from our Unit in one hyperparathyroid patient with severe bone disease and normal serum calcitriol level. Increment of serum calcitriol after daily intravenous Rocaltrol for 5 days directly suppressed PTH hypersecretion without change in plasma ionized calcium.

Calcitriol↗
PubMed1989

Marked direct suppression of primary hyperparathyroidism with osteitis fibrosa cystica by intravenous administration of 1,25-dihydroxycholecalciferol.

A marked direct suppression of primary hyperparathyroidism with osteitis fibrosa cystica has been achieved by the intravenous administration of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. In a recent survey of 306 patients with primary hyperparathyroidism (PHPT), we hypothesized that the far higher degree of parathyroid hormone (PTH) hypersecretion in PHPT with osteitis fibrosa cystica than in PHPT without overt bone disease might be due to the absence of suppression of hormonal hypersecretion by the low-to-normal circulating 1,25(OH)2D reflecting a relative vitamin D deficiency. To test this hypothesis, a patient having hypercalcemic PHPT with florid osteitis fibrosa cystica and normal serum 1,25(OH)2D was given increasing daily doses of intravenous calcitriol (0.5-2 micrograms) for several days. Doubling the level of circulating 1,25(OH)2D from 48 to 100-114 pg/ml was accompanied by a marked decline (46%) in serum iPTH(1-84), without a change in the serum calcium concentration. A lowered set point of parathyroid cells for calcium, and a diminished maximum secretory rate of PTH, may contribute to the marked suppression of PHPT.

Calcitriol↗
PubMed1989

Effects of citrate on urinary calcium excretion.

Thyroparathyroidectomized rats were studied during control, citrate infusion, and recovery periods to analyze the effects of citrate on urinary calcium excretion. The rats were infused with human PTH-(1-34) at a constant rate throughout the experiments that produced physiologic circulating PTH activity. Ultrafiltrable calcium was measured with a micropartition system while maintaining constant the pH and PCO2 of the sample. The plasma acid-base status, filtered load of calcium, and urinary sodium excretion rate did not vary during citrate infusion. The urinary calcium excretion rate increased from 71 +/- 9 nmol/min/g kidney during control period to 122 +/- 22 nmol/min/g kidney (p less than 0.05) during citrate infusion, and then returned below control levels during recovery period. A strong positive linear relationship was observed between the urinary excretion rates of calcium and citrate (r = 0.88; p less than 0.001). We conclude that tubular fluid citrate inhibits renal calcium reabsorption probably by forming calcium-citrate complexes.

Animals↗