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Z S Agus

Publications and source records attributed to Z S Agus.

At least 55 records · Page 3Linked to original sources
PubMed1978

Mechanism of lithium-induced hypercalciuria in rats.

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.

Animals↗
PubMed1978

Dissociation of tubular sites of action of saline, PTH and DbCAMP on renal phosphate reabsorption.

The effects of saline expansion, parathyroid hormone (PTH) administration and dibutyryl cyclic 3'5'-adenosine monophosphate (DbCAMP) infusion on renal phosphate reabsorption were examined in acutely thyroparathyroidectomized (TPTX), phosphate infused dogs by the recollection micropuncture technique. Saline expansion reduced whole kidney phosphate reabsorption from a mean of 66.1 to 50.4% of filtered load. This response was entirely accounted for by an inhibition of proximal tubular phosphate reabsorption which fell from a mean of 35 to 21% of the filtered phosphate load. Both PTH and DbCAMP produced a fall in whole kidney phosphate reabsorption comparable to saline. However, this effect was the sum of inhibition of both proximal tubular and distal nephron phosphate reabsorption. These studies demonstrate the important role of the distal nephron in modulating urinary phosphate excretion.

Animals↗
PubMed1977

Acute effects of bovine growth hormone on renal calcium and phosphate excretion.

To evaluate the acute effects of bovine growth hormone upon renal hemodynamics and urinary electrolyte excretion, clearance studies were performed in intact and thyroparathyroidectomized dogs, receiving either vehicle alone or bovine growth hormone. Growth hormone had no effect when compared to controls upon glomerular filtration rate, renal plasma flow, or clearance of sodium, calcium, and phosphate either in the presence or absence of parathyroid hormone. It is concluded that acute changes in circulating growth hormone levels do not play an important role in calcium and phosphate homeostasis. The data suggest that previously described antiphosphaturic and hypercalciuric actions of growth hormone are not due to direct acute renal tubular effects but may be the result of indirect effects of chronic growth hormone administration.

Animals↗
PubMed1977

The pathophysiology of acid-base changes in chronically phosphate-depleted rats: bone-kidney interactions.

Acid-base disturbances may develop secondary to the changes in renal tubular function and bone dynamics which attend phosphate depletion (PD). This work characterizes the acid-base status of rats fed a low phosphate diet. After 18 days, PD rats had marked calciuria (pair-fed controls: 0.3 +/- 0.2; PD 32.2 +/- 2.5 mueq/h; P less than 0.001), severe bicarbonaturia (controls: 0; PD 17.6 +/- 0.2 meq/h; P less than 0.001), and negative net acid excretion (controls: 44.5 +/- 2.9; PD: --6.6 +/- 2.5 meq/h; P less than 0.001), but plasma pH, HCO3, and PCO2 were equal in both groups. After 45 days, plasma HCO3 fell to 21.1 +/- 0.9 meq/liter in PD (controls: 23.6 +/- 0.5 meq/liter; P less than 0.05), while bicarbonaturia (controls: 0.4 +/- 0.2; PD: 3.8 +/- 1 mueq/h; P less than 0.02) and calciuria were present but diminished. These data suggested the coexistence of bone HCO3 mobilization and renal HCO3 wasting in PD. To test this thesis, bicarbonaturia was eliminated by nephrectomy. 24 h later plasma HCO3 was higher in PD rats (controls: 19.3 +/- 0.02; PD: 22.6 +/- 0.8 meq/liter; P less than 0.05), consistend with the presence of extrarenal HCO3 production. After inhibition of bone resorption with colchicine (1 mg/kg), plasma HCO3 decreased to 16.8 +/- 0.6 meq/liter in PD rats (controls): 26.4 +/- 1 meq/liter; P less than 0.001) while bicarbonaturia persisted. These data indicate that the plasma HCO3 in PD is the net result of renal HCO3 wasting and bone HCO3 mobilization. These combined effects maintain normal blood HCO3 initially (18 days) but with time (45 days), bone resorption diminishes and the acidifying renal tubular defect predominates.

Acid-Base Imbalance↗
PubMed1977

Renal tubular effects of chronic phosphate depletion.

The effects of chronic phosphate depletion on renal tubular function were evaluated by micropuncture and free water clearance studies in the dog. Proximal tubular punctures demonstrated that chronic hypophosphatemia led to a reduction in ratio of tubular fluid to plasma inulin in late superficial tubular from 1.59+/-0.08 in control animals to 1.29+/-0.06 in phosphate-depleted dogs, with proportional inhibition of calcium and sodium reabsorption. The chronic decrease in proximal tubular fluid reabsorption was confirmed by the analysis of sustained water diuresis in conscious, phosphate-depleted dogs, before and after repletion of body PO4 stores, and in control animals. Urine flow rate/100 ml glomerular filtration rate (V/GFR) was significantly higher in PO4 DEPLETION THAN CONTROL (15.8+/-1.1 VS. 10.7+/-0.82). In addition, acetazolamide infusion did not increase V/GFR in phosphate-depleted dogs (15.8+/-1.1 vs. 17.16+/-0.9), supporting the conclusion that inhibition of proximal tubular fluid reabsorption was responsible for the elevated urine flow rate. PO4 repletion over 5 days reduced V/GFR to 9.2+/-0.7 despite no change in urine osmolality and no change in GFR, further suggesting a specific reversible alteration in proximal tubular reabsorption in phosphate depletion. Although hypercalciuria was a constant finding in phosphate depletion (fractional excretion of calcium of 2.04+/-0.4% vs. 0.47+/-0.13% in controls), the enhanced distal delivery of calcium was not a crucial factor; acute phosphate infusion reduced urinary calcium excretion to control values without affecting the reduced proximal tubular reabsorption in either intact or thyroparathyroidectomized phosphate-depleted dogs the change in distal nephron calcium reabsorption was independent of parathyroid hormone (PTH) levels since infusion of PTH failed to alter urinary calcium excretion. We conclude that chronic phosphate depletion leads to a reversible, sustained inhibition in proximal tubular reabsorptive fuction as well as a specific decrease in distal nephron calcium reabsorption. This latter reabsorptive defect is sensitive to phosplate infusion but not corrected by PTH.

Acetazolamide↗
PubMed1977

Impaired renal tubular potassium secretion in systemic lupus erythematosus.

Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.

Acetazolamide↗
PubMed1977

Tubular effects of acute metabolic acidosis in the rat.

Micropuncture and clearance studies were performed to evaluate the effects of acute NH4Cl-induced metabolic acidosis. Studies were performed in four groups of rats: controls, urea-saline, saline, and NH4Cl. Acidosis (pH: 7.25 +/- 0.02[S.E.M.], HCO3- = 12.4 +/- 0.7 mEq/L) was associated with increased fractional sodium excretion, 9.13% +/- 0.52 and calcium excretion, 1.32% +/- 0.43, which was significantly greater than controls, 0.30% +/- 0.07 and 0.30% +/- 0.07; urea-saline, 0.54% +/- 0.1 and 0.54% +/- 0.13; saline, 0.71% +/- 0.17 and 0.47% +/- 0.09. In the proximal tubule, however, fractional reabsorption was less with saline, 41.5 +/- 1.7, than either urea-saline, 51.1 +/- 1.3, or the NH4Cl-infused group, 46.9 +/- 0.4. The data indicate that natriuresis of acute NH4Cl loading is associated with but cannot be accounted for by inhibition of proximal tubular reabsorption. The mechanism of inhibition of transport at sites beyond the proximal tubule is not clear but cannot be either volume expansion or increased solute load due to urea excretion.

Acidosis↗
PubMed1977

Transient diabetes insipidus with elevated serum osmolarity associated with 'benign' febrile illness.

A 38-year-old physician developed polyuria and hypodipsia four days after the onset of an upper respiratory tract infection. Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI). Skull roentgenograms, EEG, and lumbar puncture were normal. The polyuria and hypodipsia slowly resolved without treatment. Normal urinary concentration ability was achieved by the 48th day, but a residual elevation in serum osmolarity persisted for one year. Review of the literature failed to show previous documentation of transient DI with elevated serum osmolarity from an acute, febrile illness. The mechanism is speculative, but may be related to a subclinical encephalitis. The true frequency of this syndrome and its relationship to the frequent observation of transient polydipsia and polyuria in "benign" febrile illness remains to be determined.

Acute Disease↗
PubMed1976

The effects of glucose and insulin on renal electrolyte transport.

The effects of hyperglycemia and hyperinsulinemia on renal handling of sodium, calcium, and phosphate were studied in dogs employing the recollection micropuncture technique. Subthreshold sustained hyperglycemia resulted in an isonatric inhibition of proximal tubular sodium, fluid, calcium, and phosphate reabsorption by 8-14%. Fractional excretion of sodium and phosphate, however, fell (P is less than 0.01) indicating that the increased delivery of these ions was reabsorbed in portions of the nephron distal to the site of puncture and in addition net sodium and phosphate transport was enhanced resulting in a significant antinatriuresis and antiphosphaturia. The creation of a steady state plateau of hyperinsulinemia while maintaining the blood glucose concentration of euglycemic levels mimicked the effects of hyperglycemia on proximal tubular transport and fractional excretion of sodium and calcium. Tubular fluid to plasma insulin ratio fell, similar to the hyperglycemic studies. These results suggest that the effects of hyperglycemia on renal handling of sodium and calcium may be mediated through changes in plasma insulin concentration. In contrast to hyperglycemia, however, hyperinsulinemia cuased a significant fall in tubular fluid to plasma phosphate ratio with enhanced proximal tubular phosphate reabsorption (P is less than 0.02). This occurred concomitantly with a significant inhibition of proximal tubular sodium transport. These data indicate that insulin has a direct effect on proximal tubular phosphate reabsorption, and this effect of insulin is masked by the presence of increased amounts of unreabsorbed glucose in the tubule that ensues when hyperinsulinemia occurs secondary to hyperglycemia. Fractional excretion of phosphate fell significantly during insulin infusion but unlike the hyperglycemic studies, the fall in phosphate excretion could be entirely accounted for by enhanced proximal reabsorption.

Absorption↗
PubMed1976

Normal diluting capacity in hyponatremic patients. Reset osmostat or a variant of the syndrome of inappropriate antidiuretic hormone secretion.

Four patients with chronic illnesses and stable hyponatremia and plasma hypotonicity had normal urinary diluting capacity, with excretion of greater than 80% of a standard water load (20 ml/kg) within 4 hours and maintenance of a urine osmolality less than 100 mosmol/kg, during sustained water diuresis. Administration of a chronic salt load did not correct the hyponatremia. However, it was stabilized after treatment of the underlying medical condition. These subjects may represent a true resetting of the osmostat or a variant of the syndrome of inappropriate antidiuretic hormone secretion.

Aged↗
PubMed1976

Effectiveness of bumetanide in nephrotic syndrome: a double-blind crossover study with furosemide.

A double-blind crossover study was undertaken to delineate the renal tubular sites of action of bumetanide and to compare its effects upon electrolyte excretion to that of furosemide in six nephrotic patients with various degrees of renal insufficiency. Bumetanide was found to be a potent oral natriuretic agent without producing changes in either GFR or effective renal plasma flow. The natriuresis was associated with inhibition of proximal tubular transport as evidenced by an increased distal delivery (CH2O+CNA+K) and inhibition of sodium transport in the loop of Henle as shown by a fall in CH2O/CH2O+CC1 during sustained water diuresis and an unchanged TCH2O with continued hydropenia. The increases in free-water clearance induced by furosemide and bumetanide were equivalent, but bumetanide produced significantly higher flow rate, greater solute delivery from the proximal tubule, and a greater natriuresis. The data indicate that at the dosages used, bumetanide has a proportionately greater inhibitory effect than furosemide in both the proximal tubule and the ascending limb of the loop of Henle.

Adolescent↗