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Biomedical subjects

R M Friedler

Publications and source records attributed to R M Friedler.

At least 37 records · Page 2Linked to original sources
PubMed1977

Effect of phosphate depletion on renal tubular reabsorption of glucose.

The renal handling of glucose was evaluated in six dogs before and after chronic phosphate depletion of 51 to 112 days' duration. Phosphate depletion was produced by feeding the dogs with phosphate-restricted diet and administration of Al(OH)3. With phosphate depletion, serum phosphate fell from 3.5 +/- 0.36 (S.E.) to 0.5 +/- 0.19 mg./dl. Both TmG and TmG/GFR fell significantly during phosphate depletion. TmG/GFR was 4.0 +/- 0.41 mg./ml. before phosphate depletion and 2.9 +/- 0.19 mg./ml. after phosphate depletion. In four phosphate-depleted dogs TmG/GFR fell precipitously after glucose loading for more than 200 minutes, and practically all of the filtered glucose was excreted in the urine. It is possible that the levels of cytosolic adenine nucleotides which are required for energy of the renal cell may be reduced during phosphate depletion. This may underlie the fall in TmG and may explain the precipitous fall in TmG when the transport mechanism for glucose was operating at maximum capacity for a prolonged period of time.

Absorption↗
PubMed1977

Hyponatremia and hypernatremia.

The concentration of serum sodium is determined by the external balance of water. Hyponatremia occurs when total body water is in excess of sodium, and hypernatremia develops when body water is relatively decreased in relation to sodium. Both disorders may be present in patients with various disease states in which total body sodium is either decreased, normal or increased. The symptomatology in both disorders is related to the disturbance in central nervous system due to brain edema in patients with hyponatremia and brain dehydration, and cerebrovascular hemorrhages in patients with hypernatremia. The treatment of hypo and hypernatremia is achieved by correcting the abnormalities in body water content.

Adult↗
PubMed1976

Skeletal resistance to the calcemic action of parathyroid hormone in uremia: role of 1,25 (OH)2 D3.

Studies were carried out to investigate the role of 1,25(OH)2D3 in the skeletal resistance to the calcemic action of parathyroid hormone. The change in serum calcium after the intravenous infusion of 2 U of parathyroid extract (PTE)/kg body wt/hr for eight hours was evaluated in thyroparathyroidectomized (T-PTX) dogs before, and one, two and three days after, induction of uremia by bilateral ureteral ligation (11 dogs) or by bilateral nephrectomy (8 dogs). In another six nephrectomized and T-PTX dogs, 0.68 ug of 1, 25 (OH)2D3/day was given on the day of nephrectomy and for two days thereafter. Serum creatinine in each day of the study was not different among the three groups. The study also included the evaluation of the effect of sham operation (five dogs) and the administration of 1,25 (OH)2D3 to dogs with normal renal function (four dogs) on the calcemic response to PTE, as well as the reproducibility of such a response in the same animal. The results showed that 1) the calcemic response to PTE was markedly impaired after one day of bilateral ureteral ligation or nephrectomy, but the impairment was more severe after nephrectomy; 2) the calcemic response to PTE after two or three days of bilateral ureteral ligation was similar to that seen at one day after nephrectomy; 3) 1, 25 (OH)2D3 partially restored the calcemic response to PTE in the nephrectomized animals to levels similar to those seen after one day of bilateral ureteral ligation; 4) sham operation did not affect the response to PTE, and repeated infusion of PTE produced similar changes in the concentrations of serum calcium. The data indicate that (a) a deficiency of 1,25 (OH)2D3 is at least partly responsible for the skeletal resistance to the calcemic action of PTH in uremia; (b) uremia, per se, may also contribute to this phenomenon; and (c) the kidney after one day of complete bilateral ureteral ligation may still produce 1,25 (OH)2D3, but this ability is compromised after two days of ureteral obstruction.

Animals↗
PubMed1976

Sites of clearance of endogenous parathyroid hormone in the vitamin D-deficient dog.

The sites of clearance of endogenous parathyroid hormone (PTH) were studied in dogs who developed secondary hyperparathyroidism on a vitamin D-deficient diet. Simultaneous blood samples were obtained from the femoral artery, and the hepatic, renal, portal, and femoral veins. Radioimmunoassay of canine immunoreactive PTH (iPTH) in a heterologous bovine PTH (bPTH) system indicated that the kidney and liver extracted 49% and 46%, respectively, of the iPTH circulating through these organs. Characterization of the circulating iPTH in these animals was carried out by gel filtration and radioimmunoassay of the eluant fractions utilizing specific amino- and carboxyl-terminal antisera. The hormone in the peripheral circulation co-eluted with [125I]-iodobPTH and no fragments of iPTH were detected. Immunochemical differences between bovine and canine PTH were detected in the carboxyl-terminal region of the molecule. The results indicate that endogenous PTH in the vitamin D-deficient, hypocalcemic dog is cleared by the kidney and liver and that the predominant form of the hormone in this animal is similar to glandular bPTH 1-84.

Animals↗
PubMed1976

Acute renal failure due to nontraumatic rhabdomyolysis.

Twenty-one patients developed acute renal failure in association with nontraumatic rhabdomyolysis and myoglobinuria. The illness followed an overdose of ethanol, heroin, or other depressant drug in 18 patients. Lethargy or coma was present in 17 patients and muscle swelling in 11. Evidence of rhabdomyolysis included markedly elevated creatine phosphokinase, myoglobinuria, and aldolase in blood. Initial biochemical findings were similar to those of acute renal failure due to other causes, but the abnormalities were exaggerated. There was a disproportionate rise in serum creatinine concentration in relation to serum urea nitrogen concentration. Profound hyperuricemia was present in most patients. Transient hypercalcemia developed during the diuretic phase in 5 patients. One patient died. We conclude that nontraumatic myoglobinuria with acute renal failure is not infrequent and may occur after an overdose of ethanol or heroin. The disease has good prognosis despite severe hypercatbolism and untreated profound hyperuricemia.

Acidosis↗
PubMed1976

The high incidence of persistent secondary hyperparathyroidism after renal homotransplantation.

Sixty-eight patients were observed for a period of up to seven years after transplantation. Serum parathyroid hormone levels were measured in 41 patients; 17 patients had persistent hypercalcemia for a period of from one to seven years. Serum parathyroid hormone levels were elevated in seven of these 17 patients. Serum parathyroid hormone was elevated in 11 of the other 24 patients with normocalcemia. The function of the kidney was not affected either by the state of hypercalcemia or persistent hyperparathyroidism. Aseptic necrosis was significantly present in those of the hypercalcemic group. It is suggested that persistent hypercalcemia is an important precipitating, if not the main, cause of an aseptic necrotic condition of the bones.

Calcium↗
PubMed1975

Renal action of cholera toxin: I. Effects on urinary excretion of electrolytes and cyclic AMP.

The infusion of cholera toxin (CT), 4 mug/min, into one renal artery of normal and thyroparathyroidectomized (T-PTX) dogs produced ipsilateral increments in the excretion of Na, K, Ca, Mg and Cl. Phosphate excretion increased from both kidneys, but more from the infused kidney in intact dogs. Unilateral phosphaturia occurred in T-PTX dogs studied five or more days after T-PTX. The changes in electrolyte excretion appeared 40 to 80 min after initiation of CT infusion and the maximal effects were noted after 100 to 140 min. The effects of CT on electrolyte excretion could not be accounted for by changes in glomerular filtration rate or renal plasma flow. Urinary cyclic adenosine monophosphate (AMP) increased from both kidneys but slightly more from the infused kidney. Adenylate cyclase activity of cortex and outer medulla of the infused kidney was 109 to 142% higher than that of the control kidney. The results indicate that CT decreases the net transport of various electrolytes by the renal tubule. This effect is probably mediated by the activation of renal adenylate cyclase(s) sensitive to the enterotoxin.

Adenylyl Cyclases↗
PubMed1975

Renal action of cholera toxin: II. Effects on adenylate cyclase-cyclic AMP system.

The effects of cholera toxin (CT) on the adenylate cyclase-adenosine 3',5'-cyclic monophosphate (cAMP) system(s) in renal cortex were examined using the isolated renal cortical tubules of rat. Unlike parathyroid hormone, catecholamines or prostaglandins, CT had no immediate effects on cAMP production by the tubules or on adenylate cyclase activity. However, after 30 min of incubation at 37 C, cAMP production by the tubules started to rise and reached a plateau between 60 and 90 min. This rise in cAMP production was not abolished by protein synthesis inhibitors (actinomycin D and cycloheximide) nor by the inhibitors of prostaglandin synthesis (acetyl-salicylate and indomethacin). Repeated washings of the tubules exposed to the toxin for five minutes at 0 or 37 C did not abolish the effect of CT to stimulate cAMP production. Assays of adenylate cyclase activity using homogenates prepared from isolated tubules which were incubated for 60 min with CT revealed an increase in the basal adenylate cyclase activity without any change in NaF-sensitive enzyme activity. It is concluded that CT binds to renal tubule cells rapidly, possibly through energy-independent process. CT stimulates adenylate cyclase activity and increases cAMP production by the renal tubule cells after a latent period of 30 min. The stimulatory effects of CT are not due to new protein synthesis or prostaglandin formation.

Adenylyl Cyclases↗
PubMed1975

Relationship between the kidney and parathyroid hormone.

This report reviews the interrelationship between the activity of the parathyroid glands and renal function. Among the topics discussed are: effects of parathyroid hormone on various aspects of renal function such as: (1) glomerular filtration rate and renal blood flow; (2) renal handling of phosphorus, calcium, magnesium, sodium and potassium; (3) renal production of 1,25-dihydroxycholecalciferol; (4) renal handling of bicarbonate and acid-base metabolism, and (5) mechanism of action of parathyroid hormone on the renal cell. Further topics include: renal metabolism of parathyroid hormone; the kidney in hyperparathyroidism, and effects of renal failure on structure and function of the parathyroid glands.

Acid-Base Equilibrium↗
PubMed1973

Studies on mechanisms of hypocalcemia of magnesium depletion.

Studies were carried out to evaluate the mechanism of hypocalcemia in magnesium depletion. Day old chicks fed a magnesium deficient diet developed marked hypocalcemia, with a direct relation between serum calcium (y) and magnesium (x): y = 2.68 x + 4.24, r = 0.84 (both in mg/100 ml). Injections of parathyroid extract that increased serum calcium 2-3 mg/100 ml in normals had no effect in Mg-depleted birds. Very large dietary supplements of calcium or vitamin D(3) increased mean serum calcium only from 5.3 to 7.7 and 7.8 mg/100 ml, respectively, while a normal magnesium diet for 3 days increased calcium from 5.3 to 9.9 mg/100 ml despite absence of dietary calcium. Intestinal calcium transport, studied in vitro, and the calcium concentration of the carcass was significantly increased in magnesium-depleted chicks, making it unlikely that reduced intestinal absorption of calcium caused the hypocalcemia. In magnesium-deficient chicks, the bone content of magnesium was decreased by 74%, the calcium content was unchanged, and the cortical thickness of bone was markedly increased. After 3 days of magnesium-repletion, cortical thickness was reduced with increased endosteal resorption. There was an increase in unmineralized osteoid tissue in the magnesium-depleted chicks. Parathyroid gland size and histology did not differ in magnesium-depleted and control birds. The results suggest that hypocalcemia develops due to altered equilibrium of calcium between extracellular fluid and bone, favoring increased net movement into the latter. Failure of parathyroid gland function could also exist, and unresponsiveness to parathyroid hormone (PTH) may also contribute to the hypocalcemia. However, failure of PTH action is probably due to the presence of excess osteoid tissue rather than a primary event leading to hypocalcemia.

Animals↗