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Biomedical subjects

M M Popovtzer

Publications and source records attributed to M M Popovtzer.

At least 91 records · Page 5Linked to original sources
PubMed1987

Effect of bicarbonate and phosphate on renal phosphate leak in experimental Fanconi syndrome.

The role of acidosis in the renal phosphate leak in Fanconi syndrome (FS) was studied in maleate-induced FS in rats. Clearance studies were performed in the following groups: 1) intact rats served as control, 2) rats with maleate-induced FS, 3) rats with FS receiving intravenous bicarbonate (HCO3-), 4) intact rats receiving intravenous 0.03 N HCl (inducing acidosis similar to that of Group 2), 5) rats with FS receiving intravenous phosphate buffer and NaCl, and 6) rats with FS receiving intravenous phosphate buffer and bicarbonate similar to Group 3. In Group 2 serum pH and fractional excretion of phosphate (CP/GFR) averaged 7.31 +/- 0.08 (mean +/- SE) and 1.00 +/- 0.06, respectively, and differed significantly from Group 1, in which the corresponding values were 7.41 +/- 0.01 and 0.12 +/- 0.02, respectively. In Group 3, intravenous HCO3- corrected pH to 7.43 +/- 0.01 and reduced CP/GFR to 0.33 +/- 0.05, both results were different from the corresponding rates in Group 2 (P less than 0.0005). In Group 4, intravenous HCl reduced serum pH to 7.31 +/- 0.02 (P not significant as compared with Group 2) and increased CP/GFR to 0.186 +/- 0.030, the latter was higher than CP/GFR in control rats (P less than 0.01) but was lower than that in HCO3- -treated FS rats. In Group 5 serum pH was 7.31 +/- 0.021, similar to Group 2. CP/GFR was 0.84 +/- 0.031, significantly lower than in Group 2 (P less than 0.05). In Group 6 serum pH was 7.43 +/- 0.013 and CP/GFR was 0.86 +/- 0.044.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Enhanced glomerular filtration and Na+-K+-ATPase with furosemide administration.

To evaluate the effect of furosemide on kidney function, glomerular filtration rate (GFR), urinary Na excretion (UNaV), Na reabsorption (NAR), and Na+-K+-ATPase in isolated nephron segments were measured in 1) rats treated with furosemide 10 mg X 100 g-1 X 24 h-1 ip for 7 days, and 2) rats receiving an oral Na load for 12 days. In furosemide-treated rats, GFR rose from 0.61 +/- 0.03 (mean +/- SD) to 0.83 +/- 0.06 ml/min (P less than 0.01), UNaV rose from 904 +/- 71 to 1,402 +/- 85 mueq/day (P less than 0.001), and net NAR rose from 87.5 +/- 3.7 to 116.7 +/- 9.0 mueq/min (P less than 0.01). Na+-K+-ATPase remained unchanged in the proximal convoluted tubule (PCT), proximal straight tubule (PST), cortical thick ascending limb of Henle's loop (cTALH), and medullary thick ascending limb of Henle's loop (mTALH), but was increased in the distal convoluted tubule (DCT) and in cortical collecting duct (CCD) from 48.5 +/- 1.2 to 75.3 +/- 0.7 (P less than 0.001) and from 18.6 +/- 0.7 to 27.1 +/- 2.7 (P less than 0.02) X 10(-11) mol X mm-1 X min-1, respectively. In Na-loaded rats GFR rose from 0.61 +/- 0.04 to 0.86 +/- 0.03 ml/min (P less than 0.001), UNaV rose from 1,064 +/- 118 to 18,532 +/- 2,045 mueq/day (P less than 0.001), net NAR from 88.1 +/- 3.0 to 107.8 +/- 3.9 mueq/min and Na-K-ATPase in the mTALH rose from 40.3 +/- 1.4 to 56.2 +/- 2.11 (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

24,25(OH)2D3 enhances the calcemic effect of 1,25(OH)2D3 in PTX rats.

The effect of 24,25(OH)2D3 on 1,25(OH)2D3-induced hypercalcemia was studied in parathyroidectomized (PTX) rats for 10 days. Serum (S) and urinary Ca excretion (UCaV) were measured in (a) control rats, (b) rats receiving a daily sc injection of 54 ng 1,25(OH)2D3, (c) rats receiving 24,25(OH)2D3 in the same dose and same manner, and (d) rats receiving 1,25(OH)2D3 + 24,25(OH)2D3. Our results show that (i) 24,25(OH)2D3 alone does not increase SCa2+ in PTX rats, (ii) combined administration of 1,25(OH)2D3 + 24,25(OH)2D3 enhances the hypercalcemic response to 1,25(OH)2D3 without a parallel increase in UCaV, (iii) combined administration of 1,25(OH)2D3 + 24,25(OH)2D3 reduces the rise in urinary excretion of Ca2+ compared with that of rats receiving 1,25(OH)2D3 alone for 10 days, and (iv) these alterations are independent of parathyroid hormone.

24,25-Dihydroxyvitamin D 3↗
PubMed1987

24,25(OH)2D3 attenuates the calcemic effect of 1,25(OH)2D3 in rats with reduced renal mass.

The present study was undertaken to evaluate the effect of 24,25(OH)2D3 on serum calcium concentration in rats with reduced renal mass. Adult 5/6 nephrectomized male rats were divided into four groups: (i) control rats, (ii) rats treated with 1,25(OH)2D3, (iii) rats treated with 24,25(OH)2D3, and (iv) rats treated with 1,25(OH)2D3 and 24,25(OH)2D3. After 4 days, serum calcium in the 1,25(OH)2D3-treated group was 7.13 +/- 0.32 meq/liter (P less than 0.001 vs control). With the combination of 1,25(OH)2D3 and 24,25(OH)2D3 serum calcium was higher than that in control, 6.25 +/- 0.5 meq/liter (P less than 0.001 vs control), but lower than that in rats receiving 1,25(OH)2D3 alone (P less than 0.05). No change in serum calcium was seen in animals treated with 24,25(OH)2D3 alone. On the eighth day serum calcium in the 1,25(OH)2D3-treated group, 6.52 +/- 0.25, was higher than in the 1,25(OH)2D3 + 24,25(OH)2D3 group, 5.87 +/- 0.17 meq/liter, P less than 0.05, P less than 0.001 vs control. In both 1,25(OH)2D3- and 1,25(OH)2D3 + 24,25(OH)2D3-treated rats, hypercalciuria of similar magnitude occurred on the fourth and eighth day of treatment. No change in urinary calcium was seen in the control and 24,25(OH)2D3-treated rats. Thus, in 5/6 nephrectomized rats combined administration of 1,25(OH)2D3 and 24,25(OH)2D3 attenuates the calcemic response to 1,25(OH)2D3 without changes in urinary calcium excretion. These observations suggest that the effect of 24,25(OH)2D3 on serum calcium is different in 5/6 nephrectomized rats as compared to normal rats, in which an augmentation of serum calcium was observed following administration of both vitamin D metabolites. The effect of 24,25(OH)2D3 on serum calcium in rats with reduced renal mass may result from a direct effect of 24,25(OH)2D3 on the bone.

24,25-Dihydroxyvitamin D 3↗
PubMed1987

Renal biopsy in Fabry's disease eight years after successful renal transplantation.

Late graft histology after renal transplantation for Fabry's disease has only once been previously reported. Clinical data and kidney biopsy findings in a case of Fabry's disease before and eight years after successful kidney transplantation are presented. The graft maintains normal function. Graft histology in light microscopy showed no abnormalities reminiscent of the diseased native kidney. Electron microscopy revealed occasional small myelin figures which were present only in the vascular endothelium. Their significance and a review of conflicting reports and opinions from the literature are discussed.

Adult↗
PubMed1987

Renal handling of phosphate during extracellular volume expansion and parathyroid hormone administration.

To further examine the interaction between the phosphaturic effects of parathyroid hormone (PTH) and extracellular volume expansion (ECVE), clearance studies were performed in chronically and acutely parathyroidectomized (PTX) rats in three sets of experiments. In the first series, two groups of chronically PTX animals (groups 1 and 2) received a PTH infusion (2 U/h). In group 1 ECVE was superimposed on the PTH infusion, while the animals in group 2 received the hormone infusion alone. In the second series the following groups of chronically PTX rats were examined: volume expanded rats (groups 3 and 4) and control normovolemic rats (group 5). A PTH bolus (5 units) was added to group 3 while group 4 underwent volume expansion alone. The third series of experiments compared the response of acutely and chronically PTX rats given a submaximal dose of PTH (1 U/h) with additional ECVE (group 6) or undergoing submaximal ECVE with additional PTH (group 7). In the first set of experiments, the PTH-ECVE rats had a higher inulin clearance (CIn) and phosphate clearance (Cp) than the animals receiving the PTH alone. The maximal fractional excretion of phosphate (Cp/CIn) was similar in both groups. In the second set, GFR was similar in the normovolemic and the volume expanded animals. The two volume expanded groups had a higher Cp/CIn than the control normovolemic animals. The maximal Cp/CIn was 0.234 +/- 0.031 in the ECVE-PTH and 0.235 +/- 0.056 in the ECVE animals (p = NS). No significant difference could be detected during the whole experiment in any variable between the volume-expanded PTH-injected (ECVE-PTH) and ECVE only rats. Acutely and chronically PTX rats responded with a similar degree of phosphaturia after ECVE superimposed on PTH infusion or after PTH superimposed on ECVE. Acutely PTX rats, however, exhibited a significantly delayed response to exogenous PTH as compared to chronically PTX animals. There was no difference in the response to ECVE between the acute and chronically PTX rats. When chronically PTX rats were exposed to submaximal ECVE, the final Cp/CIn was less than after ECVE-PTH, PTH-ECVE or PTH. These findings show that in chronically PTX rats the phosphaturic response to PTX and ECVE is not additive under conditions of maximal stimulation by PTH or ECVE. Examination of acutely PTX animals and use of a different protocol of ECVE disclose a broader spectrum of phosphaturic responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Sodium handling by the Sabra hypertension prone (SBH) and resistant (SBN) rats.

The acute and chronic renal handling of salt was evaluated in age matched Sabra hypertension-prone (SBH) and hypertension-resistant (SBN) rats. Acute oral (4 ml/100 g) and intravenous (3.3 ml/100 g) isotonic saline loading in unanesthetized normotensive animals maintained on normal diet elicited a significantly lesser diuretic and natriuretic response in SBH than in SBN. Intermittent studies in metabolic cages in rats aged 5 to 21 weeks showed that both strains consumed similar amounts of salt but that SBH excreted significantly less urinary sodium than SBN (F = 40, p less than 0.001). Twenty four hour clearance studies showed a similar filtered sodium load in the two strains but a lower total and fractional sodium excretion in SBH, suggesting increased tubular reabsorption. Under conditions of water diuresis, free water clearance was similar in the two strains, suggesting the site for disparate tubular sodium handling to be distal to the thick medullary ascending limb of the loop of Henle. Acute oral saline loading and long term studies in metabolic cages in rats prepared with deoxycorticosterone-acetate (doca) and salt showed no significant differences in sodium excretion between hypertensive SBH and normotensive SBN. These findings indicate disparate renal sodium handling between SBH and SBN rats, already apparent before the onset of hypertension, which dissipates during doca-salt treatment.

Age Factors↗
PubMed1986

Progressive vascular calcification with necrosis of extremities in hemodialysis patients: a possible role of iron overload.

Progressive vascular calcification with ischemia and gangrene of the extremities occurs rarely in uremic patients, patients undergoing maintenance dialysis, and following renal transplantation. In this paper we present two additional patients on chronic hemodialysis who developed this syndrome in association with severe secondary hyperparathyroidism. Fulminant gangrene led to the death of the first patient, while in the second, multiple amputations had to be performed after parathyroidectomy. In both patients, evidence of iron overload due to multiple blood transfusions was present and iron was histologically demonstrated in a calcification area in one case. The possibility of iron overload as a "challenger" for systemic calciphylaxis is discussed.

Acute Disease↗
PubMed1986

Enhanced renal tubular ouabain-sensitive ATPase in streptozotocin diabetes mellitus.

The effect of streptozotocin-induced diabetes mellitus on rat renal ouabain-sensitive ATPase in six distinct nephron segments was studied. Twenty-four hours after administration of streptozotocin, blood glucose increased threefold (P less than 0.001), and glucosuria was evident. Aldosterone levels increased almost twofold (P less than 0.001). Ouabain-sensitive ATPase increased in the proximal segments PC (proximal convoluted tubule) and PS (proximal straight tubule) by 43 and 62%, respectively, (P less than 0.001) and CD (cortical collecting duct) ouabain-sensitive ATPase increased 77% (P less than 0.001). Ouabain-sensitive ATPase in the cortical (CTAL) and medullary (MTAL) thick ascending limbs of Henle's loop and in the DC (distal convoluted tubule) remained unchanged after 24 h of streptozotocin administration. Eight days after streptozotocin administration, when glomerular filtration rate (GFR) was already markedly elevated, ouabain-sensitive ATPase remained increased in the PC, PS, and CD but was significantly less compared with the activity after 24 h (P less than 0.05), whereas in the CTAL and MTAL a marked increase in ouabain-sensitive ATPase occurred by 54% in the CTAL and 65% in the MTAL (P less than 0.001). Aldosterone levels remained elevated compared with control but less than after 24 h. Pretreatment with deoxycorticosterone acetate abolished the increase in ouabain-sensitive ATPase in the CD. These findings show that streptozotocin-induced diabetes mellitus in the rat is associated with a substantial increase in ouabain-sensitive ATPase activity along most of the nephron. This increase in enzyme activity may represent a mechanism of physiological adaptation of the nephron to maintain electrolyte homeostasis in diabetes in face of the increased GFR and osmotic diuresis.

Aldosterone↗
PubMed1986

Combined cyclophosphamide and corticosteroid-induced remission in severe glomerulopathy associated with systemic vasculitis.

Three patients with systemic vasculitis and severe renal disease as major manifestations are reported. In 2 cases, rapidly progressive glomerulonephritis presented as oliguric renal failure. In the third case, the clinical picture was severe nephrotic syndrome with decreased renal function. Combined cyclophosphamide and corticosteroid treatment resulted in dramatic improvement of renal function and remission of nephrotic syndrome. In 2 cases, histological improvement was documented by repeated kidney biopsy. The optimal duration of cyclophosphamide therapy has to be determined.

Adult↗
PubMed1986

Regulation by vitamin D metabolites of parathyroid hormone gene transcription in vivo in the rat.

In vitro 1,25-dihydroxycholecalciferol (1,25(OH)2D3) decreased levels of preproparathyroid(preproPTH) hormone mRNA. We have now pursued these studies in vivo in the rat. Rats were administered vitamin D metabolites i.p. and the levels of preproPTH mRNA were determined in excised parathyroid-thyroid glands by blot hybridization. PreproPTH mRNA levels were less than 4% of basal at 48 h after 100 pmol 1,25(OH)2D3, with no increase in serum calcium. Gel blots showed that 1,25(OH)2D3 decreased preproPTH mRNA levels without any change in its size (833 basepair). Microdissected parathyroids after 1,25(OH)2D3 (100 pmol) showed mRNA levels for preproPTH were 40 +/- 8% of controls, but for beta-actin were 100% of controls. The relative potencies of vitamin D metabolites were: 1,25(OH)2D3 greater than 24,25(OH)2D3 greater than 25(OH)D3 greater than vitamin D3. In vitro nuclear transcription showed that 1,25(OH)2D3-treated (100 pmol) rats' PTH transcription was 10% of control, while beta-actin was 100%. These results show that 1,25(OH)2D3 regulates PTH gene transcription. PTH stimulates 1,25(OH)2D3 synthesis, which then inhibits PTH synthesis, thus completing an endocrinological feedback loop.

Animals↗
PubMed1986

Dietary calcium deprivation and secondary hyperparathyroidism in patients treated with chronic dialysis.

In 33 patients with end-stage renal disease undergoing chronic dialysis, serum parathyroid hormone (PTH) levels were correlated with serum concentrations and dietary intakes of calcium and phosphate. The average dietary calcium intake (549 +/- 54 mg/24 h) was lower than the recommended dietary allowance. There was a weak correlation between serum PTH and serum calcium concentrations (r = 0.39, p less than 0.03). There was also a significant negative exponential relationship between dietary calcium intake and serum PTH (y = 162e-0.0016x, r = 0.61, p less than 0.002). Likewise, when divided into low calcium (less than 500, 304 +/- 27 mg/24 h) and modest calcium (greater than 500, 809 +/- 56 mg/24 h) intake groups, in the low calcium-intake group, serum PTH (128 +/- 20 pg/ml) was more than 2-fold greater than that in the modest calcium-intake group (53 +/- 8 pg/ml, p less than 0.003). These results suggest that low dietary calcium intake may contribute to the occurrence of secondary hyperparathyroidism in patients with chronic renal failure undergoing chronic dialysis.

Adult↗
PubMed1986

Resorption of soft tissue calcification: a possible mechanism of hypercalcemia.

In rats with intact parathyroid glands and normal renal function, extraskeletal Ca3(PO4)2 deposits cause an increase in serum Ca2+ concentration from 4.39 +/- 0.07 to 5.24 +/- 0.13 mEq/l (p less than 0.001) and an increase in urinary excretion of calcium. In rats with acute renal failure and secondary hyperparathyroidism, Ca3(PO4)2 deposits potentiate the pre-existing elevation of serum calcium from 4.9 +/- 0.08 to 5.4 +/- 0.13 mEq/1 (p less than 0.01). In parathyroidectomized rats, Ca3(PO4)2 produce a significant increase in serum calcium from 3.39 +/- 0.07 to 4.19 +/- 0.2 mEq/1 (p less than 0.005). Induction of acute renal failure elevated the serum calcium concentration both in intact rats from 4.39 +/- 0.07 to 4.9 +/- 0.08 mEq/1 (p less than 0.01) and in parathyroidectomized rats from 3.39 +/- 0.07 to 3.85 +/- 0.15 mEq/1 (p less than 0.02). In parathyroidectomized rats with acute renal failure, Ca3(PO4)2 deposits cause an increase in serum Ca2+ concentration from 3.85 +/- 0.15 to 4.26 +/- 0.15 mEq/1 (p less than 0.05).

Acute Kidney Injury↗
PubMed1985

Parallel changes in red blood cell and renal Na-K-ATPase activity in adrenal and electrolyte disorders in the rat.

To compare the activity of Na-K-ATPase in the red blood cells (RBCs) and in renal tissue in disorders of Na+ metabolism, the following groups of rats were studied: 1) control, intact rats, 2) adrenalectomized (ADX) rats, 3) intact rats treated with DOCA, 4) ADX DOCA-treated rats, 5) intact salt-loaded rats, 6) ADX salt-loaded rats, 7) intact dexamethasone-treated rats (DEXA), and 8) ADX DEXA-treated rats. After adrenalectomy (group 2) serum Na+ decreased and serum K+ increased. Renal Na-K-ATPase in cortex, medulla and papilla of the control group was 44 +/- 2.7 mumol Pi/mg prot/h, 128.2 +/- 5.9 and 44 +/- 3.2 respectively and in group 2 the enzyme activity was 32.5 +/- 2.0 (P less than 0.005), 81.7 +/- 4.5 (P less than 0.001) and 23.6 +/- 1.9 (P less than 0.001) respectively. RBCs Na-K-ATPase of control animals was 2.82 +/- 0.19 mumol Pi/mg prot/h, while in group 2 the activity was 1.43 +/- 0.24 (P less than 0.001). DOCA treatment of ADX rats (group 4) normalized serum electrolytes and Na-K-ATPase activity in the renal cortex and papilla and in the RBCs. In the renal medulla the correction by DOCA was only partial. Salt loading of ADX rats (group 6) normalized serum electrolytes and Na-K-ATPase activity in the renal medulla and RBCs. Salt loading of normal rats increased RBC Na-K-ATPase to 3.72 +/- 0.36 (P less than 0.02) and medullary Na-K-ATPase to 185.6 +/- 9.8 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1985

Water handling by the sabra hypertension prone (SBH) and resistant (SBN) rats.

The renal handling of water by SBH and SBN rats was evaluated under basal conditions and following various intervention procedures. During 17 weeks of unrestricted water intake, SBH rats drank less water and excreted less urine with a higher osmolality than SBN. The differences in urine volume and osmolality persisted during 2 weeks of paired water intake. Acute water loading elicited comparable dilution of the urine in the two strains. Water deprivation for 48 h resulted in a marked rise in urine osmolality, which tended to be higher in SBN. Administration of exogenous vasopressin in water loaded animals caused a similar rise in urine osmolality. Papillary solute and urea content was higher in SBH than in SBN, but comparable in water loaded animals. The results show that although SBH differ from SBN rats in the handling of water under basal conditions, their renal diluting and concentrating capacity is comparable at extreme conditions. GFR and RBF were equal in both strains. The data suggest that SBH rats have increased renal water reabsorption as compared to SBN, which may be mediated by ADH, PG or other mechanisms. This characteristic may be related to their propensity to develop hypertension.

Animals↗