Hyporeninemic hypoaldosteronism in sickle cell disease.
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Adult↗
Biomedical subjects
N Brautbar
Publications and source records attributed to N Brautbar.
Intestinal absorption of calcium: role of dietary phosphate and vitamin D.
The intestinal absorption of calcium (Ca) has been shown to depend on vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], and dietary phosphorus (P) concentration. This study was designed to evaluate the role of dietary P independent of vitamin D3 or 1,25(OH)2D3. Vitamin D-deficient rats were studied during dietary P restriction and were compared with control groups raised on a normal-phosphorus diet (NP). Balance studies were sued. Net intestinal Ca absorption was significantly lower with dietary P restriction compared with the NP group. This malabsorption of Ca was corrected by the administration of either D3 for 1,25(OH)2D3, despite hypophosphatemia. Everted gut sacs showed a marked reduction in the uptake of 45Ca in the duodenum, jejunum, and ileum during dietary P restriction. We concluded that dietary P concentration plays a major role in intestinal Ca absorption in the vitamin D-deficient rats. These findings suggest an effect of the low-phosphate diet on the vitamin D-dependent, Ca-transport mechanism.
Animals↗
Prevention of hypoxemia during dialysis by the use of sequential isolated ultrafiltration-diffusion dialysis with bicarbonate dialyzate.
Previous studies have demonstrated that hypoxemia does not occur during isolated ultrafiltration, but does occur during diffusion dialysis with acetate, whether it is performed alone or following a period of isolated ultrafiltration. To determine if the substitution of bicarbonate for acetate in dialyzate could prevent hypoxemia, we studied the effect of sequential isolated ultrafiltration-diffusion dialysis with bicarbonate on arterial oxygen concentration. There was no significant change in pO2 during isolated ultrafiltration or the subsequent period of diffusion dialysis. In addition, excess body fluid could be removed and effective dialysis achieved without marked tachycardia or fluctuation in blood pressure. We conclude that sequential isolated ultrafiltration diffusion dialysis with bicarbonate is a safe and effective way of dialyzing patients without producing hypoxemia or cardiovascular instability.
Bicarbonates↗
Gut absorption of calcium: interactions between phosphate and vitamin D.
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Animals↗
The interrelationship between phosphate and magnesium metabolism.
a) It appears that the interrelationship between phosphate and magnesium metabolism is complicated and the mechanisms involved are not fully understood, b) the interaction between the homeostasis of these two ions is species dependent and its full expression is most evident in the rat, c) body depletion of either of these ions may result in marked changes in the blood levels, intestinal absorption, renal handling and body content of the other, d) hypermagnesemia causes hyperphosphatemia and decreased urinary excretion of phosphate, and e) the effects of hyperphosphatemia on magnesium are not elucidated as yet.
Animals↗
Role of growth hormone in experimental phosphorus deprivation in the rat.
The demands of growth are known to exacerbate the effect of phosphorus deprivation (PD). We examined whether changes associated with PD could be prevented in young rats in which growth and growth hormone (GH) were eliminated by hypophysectomy (HPX) and whether PD in normal intact rats (INT) was associated with increased secretion of GH. INT or thyroxine- and ACTH-replaced HPX rats were fed one of the three diets: 0.31% P (NP); 0.027% P (LP), and 0.31% P, pair-fed with LP-mates (NP-PF). The results indicate that HPX did not qualitatively alter several physiologic responses to PD: (a) serum and urinary phosphorus (P) decreased and urinary calcium (Ca) increased; (b) net intestinal Ca retention fell and duodenal sac uptake of 45Ca rose; and (c) external P balance was restored and duodenal sac uptake of 32P-phosphate increased. Only the hypercalcemia seen in INT, LP rats was prevented by HPX. In INT rats serum immunoassayable GH levels, measured in single samples, were not different between different dietary groups while pituitary bioassayable GH was reduced in both LP and NP-PF rats when compared to the NP rats. Thus, except for hypercalcemia, the physiologic responses associated with PD are not prevented by the elimination of growth and GH, and the development of these responses in INT rats was not associated with a consistent or specific alteration in GH secretion.
Animals↗
Effects of vitamin D and diet magnesium on magnesium metabolism.
Effects of 6-9 days of vitamin D3 (D3), 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], or 1,24,25-trihydroxyvitamin D3 [1,24,25(OH)3D3] on Mg metabolism were studied in vitamin D-deficient (-D) rats. Mg absorption expressed as percent intake increased with 1,25(OH)2D3 and 1,24,25(OH)3D3. Urinary Mg (UMg) increased with no change in serum Mg (SMg) or Mg balance. 1,25(OH)2D3 was threefold more potent than 1,24,25(OH)3D3 in raising serum Ca and Mg absorption. In a separate experiment in pair-fed rats given D3, 1,25-(OH)2D3, or 1,24,25(OH)3D3, the diet contained either 0.03 or 0.2% Mg; 1,25(OH)2D3 and D3 lowered SMg after 3 days; UMg increased after 24 h to remain elevated. D3 and 1,25(OH)2D3 augmented Mg absorption; feeding 0.2% Mg lowered Mg absorption in -D animals. All sterols augmented Mg absorption in -D rats; both the earlier action of 1,25(OH)2D3 and 1,24,25(OH)3D3 suggests that 1-hydroxylation is necessary. Suppressed Mg absorption with 0.2% Mg in -D rats suggests two transport processes, with one vitamin D dependent. Higher UMg with decreased SMg with 1,25(OH)2D3 suggests reduced tubular reabsorption.
Animals↗
Hemodialysis hypoxemia: evaluation of mechanisms utilizing sequential ultrafiltration-dialysis.
We studied the role of blood-dialyzer-membrane interactions in hemodialysis-induced hypoxemia by measuring PaO2 and white blood cell counts during isolated ultrafiltration (UF). These values were compared to those obtained from the same patients during subsequent hemodialysis (HD; utilizing the same dialyzer and membrane). Patients in the UF period displayed no hypoxemia, rather a slight increase in PaO2 (from 82.5 +/- 3.0 to 88.5 +/- 2.0 mm Hg, mean +/- SE, p greater than 0.05). In contrast, these patients displayed significant hypoxemia when HD was imposed (88.5 +/- 2.0-78.0 +/- 1.5 mm Hg, mean +/- SE, p less than 0.02). We suggest that the hypoxemia characteristic of HD initiation is not solely dependent on blood-dialyzer-membrane interactions, but also requires blood-dialysate interactions.
Adult↗
Effect of thiazides on the hypercalciuria of phosphate depletion.
The present investigation was carried out to examine the effect of thiazides on the hypercalciuria of phosphate depletion. Studies were done on 160 to 190 gm male rats, utilizing metabolic balance techniques. Animals were assigned to a phosphate-deficient diet and divided into a vehicle and thiazide-treated group. Both groups raised on a phosphate-deficient diet developed hypophosphatemia, hypercalciuria, and hypercalcemia; the latter was significantly greater in the thiazide-treated group. The magnitude of the hypercalciuria was significantly smaller in the thiazide-treated group. This occurred despite a significantly greater elevation in the concentration of serum calcium and its filtered load in the rats treated with the diuretic. Thiazides failed to produce natriuresis in the phosphate-deficient rats, suggesting a possible tubular resistance to the natriuretic action of the drug in phosphate depletion. Our data demonstrate that thiazide administration blunts the hypercalciuria of phosphate depletion. The results are consistent with the postulates that (1) phosphate depletion suppresses tubular calcium reabsorption at a site proximal to the segment where thiazides enhance calcium transport or (2) thiazide enhances calcium reabsorption at a terminal site in the nephron where a decrease in calcium transport may occur during phosphate depletion.
Animals↗
Normophosphatemic phosphate depletion in growing rat.
To study the influence of phosphate depletion (PD) on the serum, urinary, bone, and soft tissue phosphorus, we studied growing rats given a high-phosphorus (HP), normal-phosphorus (NP), or low-phosphorus (LP) diet. We obtained the following results. a) With an LP diet, animals did not grow but developed the characteristic biochemical changes of PD. b) The NP rats had an unexplained accelerated rate of growth, and developed all the biochemical changes of PD, although they were normophosphatemic. c) Bone P and Ca were significantly lower in the LP and NP rats compared to the HP rats, suggesting that minerals were mobilized from bone to support soft tissue P needs. d) Soft tissue P was not different in HP, NP, and LP rats, confirming previous observations that soft tissue P is maintained even in PD. We conclude that 1) the physiologic adaptation to PD may occur in growing rats on an apparently normal phosphorus diet when the metabolic demand is unusually high, e.g. accelerated growth; 2) the evolution of the biochemical parameters of PD in the face of normophosphatemia suggest a sensor mechanism sensitive to change in dietary P concentration.
Animals↗
Effect of phosphorus depletion on intestinal calcium and phosphorus absorption.
Intestinal calcium (Ca) hyperabsorption is a well-documented feature of experimental phosphorus depletion (PD). To further evaluate the effect of PD on Ca absorption we studied metabolic balance and in vitro everted duodenal sac uptake of Ca and phosphorus (P) in weanling male rats. Animals were assigned to three dietary groups: normal, 0.3% P ad libitum (NP); low, 0.03% P ad libitum (LP); and normal, 0.3% P but pair-fed with assigned LP mates (NP-PF). Results indicate that although PD led to an early but unsustained increase in 45Ca uptake by the everted duodenal sac in vitro, net intestinal Ca retention is consistently decreased in rats on the LP diet compared with rats eating either the NP or NP-PF diet. The reduction in net intestinal Ca absorption is reflected by an increase in fecal Ca, both in absolute quantities and in proportion to dietary Ca intake. The initial negative P balance after the initiation of the LP diet was promptly, albeit precariously, corrected. This was associated with a sustained increase in duodenal 32P uptake in vitro and virtual cessation of growth. Because the biosynthesis of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and its accumulation in intestinal mucosa have been reported to increase with PD, our study represents an example in which the physiological interrelationship between the activity of 1,25(OH)2D3 and intestinal Ca absorption may be dissociated.
Animals↗
Influence of dietary magnesium in experimental phosphate depletion: bone and soft tissue mineral changes.
We studied weanling rats fed 0.06% (group 1) and 0.10% (group II) magnesium (Mg) during phosphate depletion (PD) in order to evaluate the role of Mg in the bone, soft tissue, and serum changes of PD. The following results were obtained: 1) serum Mg remained stable in the face of a negative Mg balance; 2) the hypercalcemic and hypercalciuric response to PD was the same in both groups; 3) bone Mg content was decreased with PD in both groups and was associated with a significant decrease in bone calcium and phosphorus. We conclude that: 1) the hypomagnesemia of PD is dependent mainly on the dietary intake of Mg; 2) the hypercalcemia and hypercalciuria of PD are not caused by primary changes in Mg homeostasis; 3) low-dietary Mg during PD may cause a defect in soft tissue utilization of P in the growing rat.
Animals↗
Interaction of somatostatin with PTH and AVP: renal effects.
Six conscious intact dogs were studied to evaluate the interactions of somatostatin (SRIF) with exogenous antidiuretic hormone arginine vasopressin (AVP). SRIF administration caused a significant increase in free water clearance compared to a vehicle-treated group: -0.91 (+/- 0.41 SD) ml/min to 0.21 (+/- 0.32 SD) ml/min in the experimental group (P less than 0.01) versus 0.21 (+/- 0.81 SD) ml/min to -0.21 (+/- 0.68 SD) ml/min in the control (P greater than 0.5). Six conscious, thyroparathyroidectomized dogs were studied to test the interaction of SRIF and parathyroid extract (PTE). There were no significant changes in the phosphaturic and hypocalciuric effects of PTE with SRIF administration. We conclude that acute systemic SRIF administration interferes with the antidiuretic action of AVP, probably at the renal-tubular level, but does not antagonize the renal actions of PTE.
Animals↗
Interactions between vitamin D deficiency and phosphorus depletion in the rat.
To evaluate the role of vitamin D in the physiologic response to phosphorus depletion (P depleton) and the response to vitamin D administration in P depletion, we studied vitamin D-deficient (-D) rats, fed either a normal or low phosphorus diet and then injected intraperitoneally on alternate days with replacement vitamin D(3), 1.25 mug qod (D(3)); 1.25-dihydroxy-vitamin D(3)[1,25(OH)(2)D(3)] in physiologic, 54 ng qod (LD), and pharmacologic doses, 400 ng qod (HD); or vehicle alone (-D). The following results were obtained: (a) With P depletion, urinary excretion of inorganic phosphorus (Pi) fell to almost undetectable levels in -D rats, and two physiologic features of P depletion a calcemic effect and hypercalciuria, ensued. (b) With administration of vitamin D(3) or 1,25(OH)(2)D(3) in either doses to P-depleted rats, the renal retention of Pi was unaltered despite a significant elevation of serum Pi. (c) The calcemic response to P depletion was accentuated by vitamin D sterols, and the hypercalciuria of P depletion was reduced by 1,25(OH)(2)D(3), HD > LD > D(3). (d) In -D animals receiving normal Pi (+P), D(3), and 1,25(OH)(2)D(3), both LD and HD produced a significant calcemic and phosphatemic effect. (e) Urinary Pi excretion in +P animals was reduced slightly by vitamin D(3) whereas 1,25(OH)(2)D(3), both LD and HD, lowered urinary Pi markedly despite an increased serum Pi. (f) The serial values of serum Ca and Pi and urinary Ca in PD rats and the sequential values for urinary and serum Pi in +P rats indicated more rapid effects of 1,25(OH)(2)D(3), both HD and LD, compared with D(3). We conclude that: (a) The renal adaptation and physiologic response to PD does not require the presence of vitamin D. (b) 1,25(OH)(2)D(3) may directly enhance the renal tubular reabsorption of Pi even as serum Pi rises. (c) A hypocalciuric action of 1,25(OH)(2)D(3) in rats on low phosphorus diet could be direct or occur as a consequence of an increase in serum Pi produced by 1,25(OH)(2)D(3). The different sequential renal response to D(3) compared with 1,25-(OH)(2)D(3) raises the possibility that other natural forms of vitamin D(3) [i.e., 25(OH)D(3), 24,25(OH)(2)D(3), etc.] which may be present in vitamin D-fed rats but not those given only 1,25(OH)(2)D(3), could modify the actions of 1,25(OH)(2)D(3).
Animals↗
Disordered divalent ion metabolism in kidney disease: comments on pathogenesis and treatment.
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Calcitonin↗
Retroperitoneal bleeding hemodialysis patients. A cause for morbidity and mortality.
Retroperitoneal bleeding in hemodialysis patients has been rearely reported. The diagnosis of this entity in the nondialysis patient is difficult, and factors such as chronic anemia and hypotensive episodes during hemodialysis are adding difficulty to the early diagnosis and therapeutic approach. A patient receiving long-term hemodialysis anticoagulation therapy had retroperitoneal bleeding and died without having his condition diagnosed: the retroperitoneal bleeding was masked by other events occurring during hemodialysis.
Adult↗
The biochemical indices of experimental phosphorus depletion (PD): a re-examination of their physiological implications.
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Animals↗
Familial hyperkalemia, hypertension, and hyporeninemia with normal aldosterone levels. A tubular defect in potassium handling.
A 52-year-old man had hypertension, persistent hyperkalemia, and hyperchloremic metabolic acidosis; renal and adrenal functions were normal. Four other members of the family have the same findings. The patient's plasma aldosterone (PA) level was within normal range, though plasma renin activity (PRA) was undetectable. The ability to conserve sodium with increased endogenous aldosterone levels, and the inability to increase potassium excretion while exogenous mineralocorticoid (fludrocortisone acetate) was administered, indicated a distal tubular defect in potassium handling. Effective reduction of the hyperkalemia by K+ -Na+ exchange resin also corrected the acidosis and the hyperchloremia, suggesting that hyperkalemia may cause metabolic acidosis.
Acidosis↗