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Biomedical subjects

M M Popovtzer

Publications and source records attributed to M M Popovtzer.

At least 145 records · Page 8Linked to original sources
PubMed1977

Furosemide-induced reduction in ionized calcium in hypoparathyroid patients.

Six hypoparathyroid patients were treated with oral furosemide for 4 days. All six had a significant decrease in serum ionized calcium level from the control period (4.05 +/- 0.31 mg/dl) to the furosemide period (3.46 +/- 0.26 mg/dl, P less than 0.005). In five patients, the decrease in serum ionized calcium concentration occurred in association with an increase in urinary calcium excretion. Although serum immunoreactive parathyroid hormone level increased in five patients, it was insufficient to return serum ionized calcium to control levels. Changes in serum phosphorus, magnesium, or pH could not account for the observed decrease in serum ionized calcium concentration. It is necessary to monitor serum ionized calcium level in hypoparathyroid patients during furosemide therapy.

Adult↗
PubMed1977

Dopamine-related polyuria in patients with gram-negative infection.

Two patients developed polyuria with natriuresis while receiving intravenous dopamine hydrochloride for the treatment of hypotension. Both patients had Gram-negative pneumonia and both had evidence of extracellular volume depletion that was considered to be a result of the dopamine-induced polyuria. Following restoration of extracellular volume and withdrawal of dopamine therapy, both patients became normotensive and required no vasopressors. The diuretic action of dopamine, which persisted despite the severe intravascular volume contraction and perpetuated the hypotensive state in these two patients, is not well understood. The Gram-negative infection could play an important role possibly by enhancing the effect of dopamine on the renal vasculature.

Aged↗
PubMed1976

Effects of alternating phosphorus and calcium infusions on osteoporosis.

The osteoblastic effect of inorganic phosphorus and the inhibitory action of calcium on parathyroid hormone secretion formed the basis for a therapeutic trial in which both elements were given intravenously in an alternating sequence for one year to five patients with severe osteoporosis. During treatment, calcium and phosphorus balances were positive, and serum phosphorus concentrations decreased. Iliac crest bone biopsy specimens obtained one year after beginning treatment demonstrated an increase in the thickness of cortical bone. All patients experienced lasting relief of bone pain, and the rate of spontaneous fractures decreased from at least one fracture per year to none following the beginning of treatment. These findings suggest that long-term treatment with alternating phosphorus and calcium infusions may result in lasting relief of symptomatic osteoporosis. It is proposed that the observed improvement reflects an increase in bone mass resulting from enhanced bone formation.

Aged↗
PubMed1975

Secondary hyperparathyroidism. Conservative management in patients with renal insufficiency.

In three patients with advanced renal disease (inulin clearance, 4.6 to 9.1 ml/min) and systemic manifestations of secondary hyperparathyroidism, concentrations of serum calcium and phosphorus were maintained within our normal limits (9 and 3.5 mg/100 ml, respectively) with phosphate-binding antacids and orally given calcium carbonate. The result was progressive disappearance of symptoms related to secondary hyperparathyroidism, healing of osteitis fibrosa, and normalization of serum concentrations of immunoreactive parathyroid hormone.

Administration, Oral↗
PubMed1975

Effect of Ca++ on renal handling of PO4 identical to: evidence for two reabsorptive mechanisms.

The effect of hypercalcemia on renal handling of phosphorus was studied in parathyroidectomized rats during 1) extracellular volume expansion with normal saline (0.1 mg/100 g per min) and 2) parathyroid extract infusion (1 U/100 g per h). Hypercalcemia (serum calcium 12-15 mg/100 ml) blunted the phosphaturic response to volume expansion, both when serum calcium was raised acutely during volume expansion and when volume expansion was induced in rats with sustained hypercalcemia. These changes were not associated with significant variations in glomerular filtration rate and serum concentration of phosphorus. Hypercalcemia failed to alter the phosphaturic response and the increase in urinary cyclic AMP excretion following both continuous infusion and a single injection of parathyroid extract. These results are consistent with two components of tubular reabsorption of phosphorus. The first is suppressed by extracellular volume expansion and stimulated by hypercalcemia. The second is suppressed by parathyroid hormone and is not affected by hypercalcemia.

Absorption↗
PubMed1975

Effect of 25(OH)vitamin D3 on urinary excretion of cyclic adenosine monophosphate.

To further evaluate the effect of 25(OH)vitamin D3 (25(OH)vit D3) on renal handling of phosphorus, fractional excretion of phosphorus (CP/CIn) and urinary excretion of cyclic AMP (UcAMP) were measured in the following groups of animals: 1) intact rats receiving intravenously 25(OH)vit D3. 2a) Parathyroidectomized (PTX) rats receiving a continuous infusion of parathyroid hormone (PTH). 2b) PTX rats undergoing continuous infusion of PTH and receiving intravenously 25(OH)vit D3. In group 1 a decrease in CP/CIn from a control value of 0.210 +/- 0.064 (kappa +/- SE) to 0.052 +/- 0.017 (P less than 0.001) during 25(OH)vit D3 infusion was associated with a corresponding decrease in UcAMP from 182 +/- 18 to 87 +/- 8 pmol/min (P less than 0.001). In group 2a an increase in CP/CIn from a control value of 0.031 +/- 0.014 to 0.365 +/- 0.017 during PTH infusion was associated with a corresponding increase in UcAMP from 76 +/- 17 to 330 +/- 51 pmol/min (P less than 0.001). In group 2b a decrease in CP/CIn from 0.365 +/- 0.017 to 0.256 +/- 0.011 (P less than 0.01) during 25(OH)vit D3 infusion was associated with a decrease in UcAMP from 356 +/- 63 to 191 +/- 33 pmol/min (P less than 0.01). These results indicate that the blunting of the phosphaturic response to PTH by 25(OH)vit D3 is associated with a decrease in UcAMP. This observation suggests that the mechanism underlying the enhanced tubular reabsorption of phosphorus is inhibition of the PTH-induced activation of adenylate cyclase in the kidney.

Absorption↗
PubMed1975

The acute effect of chlorothiazide on serum-ionized calcium. Evidence for a parathyroid hormone-dependent mechanism.

The acute effects of chlorothiazide (CTZ) on total (TSCA) and ionized (SCA-plus 2) serum calcium concentrations were studied in three groups of people: (a) eight subjects with normal parathyroid function; (b) six patients with hypoparathyroidism; and (c) two patients with hyperparathyroidism. Most subjects were studied on four occasions; at least 3 days intervened between studies on an individual subject. During each experiment the subject received an i.v. influsion of 5% dextrose in water at 1 ml/min from 8 a.m. to 4 p.m. Additions to the infusions were (a) none; (b) CTZ to deliver 3.33 mg/kg/h; (c) parathyroid extract to deliver 1 U/kg/h; or (d) both CTZ and parathyroid extract at the rates previously indicated. CTZ, when used, was added to the infusion at 10 a.m., parathyroid extract at 8 a.m. When CTZ was infused, the diuretic-induced losses of Na and water were replaced by i.v. infusion. In normal subjects 2 h after the start of CTZ infusion, there was a transient increase in SCA-plus 2 which coincided in time of day with a transient decrease in SCA-plus 2 in control experiments. At that time of day SCA-plus 2 was 4.18 plus or minus 0.12 mg/100 ml in control experiments and 4.56 plus or minus 0.08 in experiments with CTZ, P smaller than 0.025. The corresponding values for (TSCA) were 9.32 plus or minus 0.15 and 9.80 plus or minus 0.30, P smaller than 0.01. Such differences were not observed in the group with hypoparathyroidism. In the two patients with hyperparathyroidism, CTZ produced sustained increases in TSCA and SCA-plus 2. In normal subjects and those with hypoparathyroidism, CTZ plus parathyroid extract infusion resulted in sustained increases in both SCA-plus 2 and TSCA throughout the periods of observation when compared to experiments in which only parathyroid extract was infused, P smaller than 0.01 in all instances. The results suggest that the acute hypercalcemic action of CTZ requires the presence of circulating parathyroid hormone.

Adult↗
PubMed1975

Serious pulmonary hemorrhage, glomerulonephritis, and massive steroid therapy.

A patient suffered from acute glomerulonephritis with modest renal impairment and life-threatening pulmonary hemorrhage. The pulmonary hemorrhage caused severe hypoxia that necessitated artificial ventilation. As a last resort, 1 g/day of methylprednisolone was administered intravenously. Rapid cessation of pulmonary hemorrhage ensued with clearing of the lungs fields. We suggest that large doses of glucocorticosteroids should be administered to patients with life-threatening pulmonary hemorrhage before considering bilateral nephrectomy, especially if the renal function is still adequate. Bilateral nephrectomy is an irreversible approach and, as with massive doses of steroids, has yet to be proved to be a consistently effective mode of therapy.

Acute Disease↗
PubMed1975

Metabolic bone disease in chronic renal failure. II. Renal transplant patients.

Trabecular vertebral bone of renal transplant patients was quantitatively compared with bone from normal individuals and dialyzed and nondialyzed patienets with chronic renal failure reported in detail in an earlier study. Long- and short-term transplant patients have increased bone resorption and mineralization defects similar to renal osteodystrophy in dialyzed and nondialyzed patients. However, in transplant patients the magnitude of resorption is greater, and bone volume tends to decrease rather than increase. Resorptive activity in transplant patients is maximal during the first year after transplantation. Bone volume decreases continuously for at least 96 months after transplantation. Only decreased bone volume correlated with success or failure of the renal transplant. Morphologic findings in this study correlate with other clinical and morphologic data to suggest that reduction in bone volume in transplant patients results from a combination of persistent hyperparathyroidism and suppression of bone formation by steroid therapy.

Adult↗
PubMed1975

Metabolic bone disease in chronic renal failure. I. Dialyzed uremics.

Garner and ball's point counting technic was used to compare metabolic bone disease in dialyzed and nondialyzed uremic patients. Histologic measurements of bone from dialyzed and nondialyzed uremic patients dying between 1966 and 1971 showed that dialyzed patients have quantitatively more severe bone resorption, distortion of trabecular architecture and mineralization defects. Mineralization defects become more severe as the duration of dialysis increases but are not related to serum calcium and phosphorus levels. Bone volume in both groups is normal or increased and in dialysis patients increases in proportion to the elevation of serum phosphorus. Mean serum phosphorus and calcium levels, bone volume, and volume: surface ratios all decreased in dialysis patients between 1966 and 1971, while bone resorption and mineralization defects did not change. These results suggest that lowering of serum phosphorus without increasing serum calcium may aggrevate the uremic bone disease by reducing bone volume without improvement of mineralization and resorption defects.

Adult↗
PubMed1974

Halothane hepatitis with renal failure treated with hemodialysis and exchange transfusion.

A 38-year-old white female, hepatitis B antigen negative, developed fluminating hepatic failure associated with oliguria and severe azotemia after two halothane anesthesia and without exposure to other hepatotoxic drugs or blood transfusions. She was treated with multiple hemodialysis and exchange blood transfusion. The combined treatment corrected the uremic abnormalities and improved her level of consciousness. the liver and kidney function gradually improved, and she made a complete recovery, the first recorded with hepatic and renal failure under these postanesthetic conditions. Further evaluation of this combined treatment used for this patient is warranted.

Acute Kidney Injury↗
PubMed1974

The acute effect of 25-hydroxycholecalciferol on renal handling of phosphorus. Evidence for a parathyroid hormone-dependent mechanism.

The acute effect of i.v. and direct intrarenal arterial infusion of 25-hydroxycholecalciferol (25HCC) and 1,25-dihydroxycholecalciferol (1,25-DHCC) on renal handling of phosphorus was evaluated in the following groups of rats: (a) intact animals, (b) parathyroidectomized (PTX) hypocalcemic rats, (c) PTX rats in which normocalcemia was maintained with calcium supplements and (d) PTX animals in which urinary phosphorus was augmented by (i) i.v. sodium phosphate, (ii) expansion of the extracellular fluid volume with normal saline, and (iii) i.v. parathyroid hormone (PTH). Clearances of inulin (C(In)), phosphorus (C(P)), and fractional clearances of phosphorus (C(P)/C(In)) of the experimental groups were compared with those of the corresponding control groups, and the clearances of the infused kidneys with those of the contralateral kidneys. In intact animals, i.v. 25HCC decreased C(P)/C(In) from 0.29+/-0.04 (mean +/-SE) to 0.19+/-0.04, and i.v. 1,25-DHCC decreased C(P)/C(In) from 0.25+/-0.04 to 0.15+/-0.02. The intrarenal infusion of both 25HCC and 1,25DHCC into intact animals failed to produce a unilateral change; however, it decreased C(P)/C(In) bilaterally. i.v. and intrarenal infusions of 25HCC or 1,25DHCC in PTX hypocalcemic and normocalcemic rats, and i.v. infusions of 25HCC in PTX rats receiving either sodium phosphate or normal saline, all failed to produce significant changes in C(P)/C(In). In contrast, 24HCC given i.v. to PTX animals receiving exogenous PTH was associated with a significant fall in C(P)/C(In), from 0.34+/-0.08 to 0.13+/-0.02. These results indicate that 25HCC enhances tubular reabsorption of phosphorus in rats, only in the presence of either endogenous or exogenous circulating PTH, but not in its absence and thus imply a PTH-dependent mechanism of 25HCC action on the kidney. This effect does not appear to be related to the conversion of 25HCC into 1,25DHCC, since the latter fails to affect tubular reabsorption of phosphorus in PTX rats.

Animals↗