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Biomedical subjects

N Telfer

Publications and source records attributed to N Telfer.

At least 19 recordsLinked to original sources
PubMed1986

Hypocalcemia and hypercalcemia in patients with rhabdomyolysis with and without acute renal failure.

Patients with rhabdomyolysis (RBD) and acute renal failure (ARF) are hypocalcemic during the oliguric phase of ARF and over 30% develop hypercalcemia during the diuretic phase. The present study examined the factors underlying these derangements in calcium metabolism in 15 patients: 7 with RBD and ARF, 4 with RBD only, and 4 with ARF only. All patients had hypocalcemia on admission and the hypocalcemia was more pronounced in those with RBD and ARF. All patients with RBD independent of the presence or absence of ARF had calcium deposition in soft tissues as documented by technetium-99 scan. In 4 patients with RBD and ARF, hypercalcemia developed during the diuretic phase at a time when Serum PTH levels were undetectable. Only patients with RBD and ARF had a significant increase in serum levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D [1,25(OH)2D] during the diuretic phase and both the increments in and the levels of 1,25(OH)2D were significantly greater in those who were hypercalcemic. The data indicate that 1) hypocalcemia occurs in RBD independent of ARF and is most likely related to calcium deposition in injured tissues, and 2) elevation in serum levels of 1,25(OH)2D plays an important role in the genesis of hypercalcemia during the diuretic phase of patients with RBD and ARF. Our observations suggest that extrarenal production of 1,25(OH)2D may occur in these patients, and/or that the renal production of 1,25(OH)2D may not be so tightly controlled as it is in normal subjects.

Acute Kidney Injury↗
PubMed1985

Erythrocyte survival in chronic renal failure. Role of secondary hyperparathyroidism.

The human erythrocyte (RBC) is a target organ for parathyroid hormone (PTH) and the hormone increases RBC osmotic fragility and induces their hemolysis. The present study was undertaken to examine whether elevated blood levels of PTH affect RBC survival, and therefore whether PTH, being an extracorpuscular factor, is responsible for the shortened RBC survival in chronic renal failure. 51Cr-labeled RBC survival was elevated in six normal dogs, in six animals with chronic renal failure and secondary hyperparathyroidism (NPX), and in six thyroparathyroidectomized dogs (NPX-TPTX) with comparable degree and duration of chronic renal failure. In the normal dogs, 51Cr-labeled RBC survival ranged between 22 and 35 (25.6 +/- 1.9) d. In the NPX dogs, 51Cr-labeled RBC survival was shortened and the values ranged between 16 and 20 (18.4 +/- 0.6) d, a value significantly (P less than 0.01) lower than normal dogs. In NPX-TPTX dogs, 51Cr-labeled RBC survival ranged between 20 and 33 (25.2 +/- 1.8) d, a value not different from that in normal dogs but significantly higher (P less than 0.01) than that in NPX animals. Our data demonstrate that excess blood levels of PTH and not other consequences of the uremic state are responsible for the shortened RBC survival in chronic renal failure.

Animals↗
PubMed1981

Rubidium-86 uptake by red blood cells of breast cancer patients.

The red blood cell (RBC) uptake of rubidium-86 (Rb-86), a sensitive in vitro test of RBC membrane transport, was measured in 22 controls, 8 patients with benign breast lesions, and 30 stage I/II, 13 stage III/IV untreated breast cancers. Total Rb-86 transport was measured. Following ouabain block, passive transport was determined, allowing calculation of active Rb-86 uptake by difference. There was a significant decrease in total and passive uptake by RBCs from patients with breast cancer when compared to controls and those with benign lesions (total uptake 58.6 +/- 6.1% versus 63.6 +/- 3.9%, P less than 0.01; passive uptake 38.7 +/- 6.8% versus 42.7 +/- 4.6%, P less than 0.02). The Rb-86 uptake returned towards normal in successfully treated stages-II-to-IV patients. There were no correlations with the patient's age, hematocrit, or incubation hematocrit with RBC Rb-86 uptakes. Results from incubation in Krebs-Ringer solution were not consistent with a plasma blocking factor. The RBC potassium content was slightly increased in the cancer patients. This, along with decreased passive transport, eliminates the nonspecific malfunction of the Na-K-pump as an explanation, and suggests that the decreased uptake is a cancer-related phenomenon.

Adolescent↗
PubMed1981

Delayed hypercalcemia with acute renal failure associated with nontraumatic rhabdomyolysis.

Delayed hypercalcemia developed in two patients with acute renal failure and rhabdomyolysis. In patient 1, the hypercalcemia appeared 14 days after the beginning of the diuretic phase of the illness and was associated with severe diastolic hypertension and soft-tissue calcification, including the lungs and skeletal muscles. The blood levels of 25-hydroxyvitamin D (25OHD3) were elevated during the hypercalcemia and decreased to normal when the patient became normocalcemic. In patient 2, the hypercalcemia occurred 55 days after the start of the diuretic phase and at a time when renal function was normal.

25-Hydroxyvitamin D 2↗
PubMed1980

Role of sympathetic nerve inhibition and body sodium-volume state in the antihypertensive action of clonidine in essential hypertension.

A simultaneous analysis of the interrelationships between mean blood pressure (MBP), plasma catecholamines, plasma renin activity (PRA) and aldosterone, exchangeable body sodium, and blood volume was carried out before and after acute and chronic administration of clonidine in 15 patients with essential hypertension, in order to further elucidate the mechanism(s) of action of this drug. After a single oral dose of 200 microgram, clonidine produced a significant fall in MBP, heart rate, plasma norepinephrine (NE), PRA, and aldosterone. There were significant correlations (P < 0.01) between NE and MBP, but not between PRA or aldosterone and MBP both before and after the ingestion of clonidine. Furthermore, there was a significant correlation (P < 0.05) between the magnitude of fall of plasma NE and change in MBP. After 6 weeks of treatment, conidine at a dose of 960 +/- 80 microgram/day produced a significant decrement in MBP and NE, but not in PRA and aldosterone; with upright posture, the magnitude of the fall in MBP was significantly greater (P < 0.01), and the rise in plasma NE was significantly smaller (P < 0.01) after chronic clonidine treatment. There was also a significant fall (P < 0.01) in exchangeable sodium and plasma volume. The data provide evidence that inhibition of the sympathetic nervous system by clonidine plays a major role and that the decrease in exchangeable body sodium and blood volume after chronic treatment may contribute to the antihypertensive action of the drug.

Adult↗
PubMed1980

Comparison of adriamycin- and ouabain-induced cytotoxicity and inhibition of 86rubidium transport in wild-type and ouabain-resistant C3H/10T1/2 mouse fibroblasts.

Ouabain (OUA) inhibited 86Rb uptake (50% inhibitory concentration = 0.8 X 10(-4) M) over concentration ranges close to those at which it caused a reversible cytotoxicity (50% lethal dose = 2.5 X 10(-4) M) in growing wild-type C3H/10T1/2 cells. On the other hand, Adriamycin (ADM) inhibited 86Rb uptake (50% inhibitory concentration = 2 X 10(-3) M) but at concentrations 10(4)-fold higher than those causing irreversible cytotoxicity in growing wild-type cells (50% lethal dose = 3 X 10(-8) M). While OUA inhibited 86Rb uptake more in wild-type cells than in a OUA-resistant mutant, ADM inhibited 86Rb uptake to the same extent in confluent wild-type and OUA-resistant cells. Further, three OUA-resistant mutants were not cross-resistant to ADM- or daunomycin (DM)-induced cytotoxicity during log phase or to ADM-induced cytotoxicity at confluence. In addition, ADM, DM, or 5-iminodaunomycin did not displace the cardiac glycosides digoxin or digitoxin from their respective antibody complexes. The order of potency of anthracycline derivatives in inhibiting 86Rb uptake in confluent wild-type cells was the same as their order of inhibiting the growth of wild-type cells and in detaching confluent wild-type cells (DM > ADM > 5-iminodaunomycin) but did not correlate with their cardiotoxic potentials (ADM > DM > 5-iminodaunomycin). Therefore, in this model system, ADM cytotoxicity is mediated differently from OUA cytotoxicity. Further, we find no biological evidence consistent withADM binding to the OUA site on the cell surface (Na+-K+) adenosine triphosphatase and therefore no evidence in this model system that ADM cardiotoxicity could be a digitalis-type toxicity per se.

Animals↗
PubMed1978

Demonstration of traumatic hepato-pleural-cutaneous defect by 131I-rose bengal.

A 19-year-old man was shot in the right chest about 2 cm below the nipple; bloody fluid was drained through a chest tube. Two days later sero-sanguineous fluid tinged with bile was seen to drain from the wound site. 131I-rose bengal, injected intravenously, collected in the dome of the liver and drained into a collection bag placed over the wound site, thus identifying a hepato-pleural-cutaneous fistula, which was confirmed at surgery.

Adult↗
PubMed1978

Resolution of muscle calcification in rhabdomyolysis and acute renal failure.

We studied four patients with acute renal failure associated with nontraumatic rhabdomyolysis to evaluate the presence and progression of calcium deposits in damaged muscle tissue. Conventional and electron radiography and technetium-99m diphosphonate (TcDP) scans were done during the oliguric phase of acute renal failure and repeated after renal function returned to normal. Three patients showed deposits of calcium by conventional radiography and all by electron radiography and TcDP during the oliguric period. When the patients recovered renal function and muscle injuries healed, calcium deposits disappeared. The results show that calcium deposits in damaged muscle occur during the oliguric phase of acute renal failure due to rhabdomyolysis and the calcification disappears with recovery of renal failure; and TcDP scans are the most sensitive method of detecting calcium deposits in these patients.

Acute Kidney Injury↗
PubMed1977

Determination of the vascularity of the femoral head with technetium 99m-sulphur-colloid.

The results of technetium 99m-sulphur-colloid scans performed at the Los Angeles County-University of Southern California Medical Center and Rancho Los Amigos Hospital to assess the vascular status of the femoral head after sixty-five displaced and thirty undisplaced fractures of the neck of the femur and forty-four traumatic hip dislocations as well as in fifty patients with idiopathic ischemic necrosis of seventy femoral heads were evaluated by histological and clinical examination after follow-up of two years or more. The accuracy of the scan as corroborated by the histological findings and clinical results was 95 per cent. The method is safe, reliable, accurate, and simple in contrast to other methods which have disadvantages related primarily to technical complexities, difficulty in interpretation, and expense.

Biopsy↗
PubMed1976

Role of prostaglandins in the pathogenesis of Bartter's syndrome.

Increased renal prostaglandins activated by beta-catecholamines could produce renal tubular sodium wasting and angiotensin pressor resistance observed in Bartter's syndrome. We therefore measured plasma renin activity (PRA), aldosterone and prostaglandin A (PGA) by radioimmunoassay, and body composition by isotope dilution prior to and following beta-adrenergic blockade with propranolol (200 mg/day for 4 days) and prostaglandin synthesis inhibition by indomethacin (200 mg/day for 4 days) in a patient with Bartter's syndrome on a 250 meq sodium diet. After the administration of propranolol, body weight increased 3 kg, daily urine sodium decreased within 24 hours from 230 to 64 meq, and urine potassium from 102 to 45 meq, but PRA and the aldosterone level remained elevated. With the administration of indomethacin, body weight increased 5 kg, daily urinary sodium decreased within 24 hours to 11meq and urine potassium to 16 meq, PRA (normal less than 3 ng/100 ml/hour) decreased from 55 to 4.3 ng/ml/hour, plasma aldosterone (normal less than 8 ng/100 ml) from 74.1 to 3.6 ng/100 ml, and whole blood PGA (normal 546 +/- 307 pg/ml) decreased from 1,390 and 945 to 86 pg/ml. After the administration of propranolol or indomethacin, exchangeable sodium, total body water, extracellular volume and plasma volume all increased from less than to greater than predicted, and pressor resistance to angiotensin was normalized. These results suggest that Bartter's syndrome results from beta adrenergic and prostaglandin-mediated proximal tubular rejection of sodium leading to increased distal sodium-potassium exchange.

Adolescent↗
PubMed1975

Distribution of sodium and potassium in chronic obstructive pulmonary disease.

The body electrolyte composition of 34 patients with severe chronic obstructive pulmonary disease and without complications or medications known to influence body sodium or potassium was studied. Exchangeable sodium, exchangeable potassium, extracellular water, and total body water were measured using radioisotope dilution techniques. From these values and serum sodium and potassium levels, the intracellular water, intracellular concentrations of sodium and potassium, and factors to estimate lean body mass were calculated. Normal values were predicted for factors that vary with weight, age, and sex--exchangeable sodium, exchangeable potassium, total body water, extracellular water, intracellular water, and estimates of lean body mass--for each subject using regression equations that took into account the variables. For values that do not vary with weight or age--residual sodium and intracellular concentration of potassium--comparisons were made with values from our control subjects. The patients with chronic obstructive pulmonary disease showed a slower rate of potassium exchange than the control subjects, requiring at least 48 hours. There was also an increase in residual sodium composed of intracellular sodium and exchangeable bone sodium. The possibilities that the abnormalities could be ascribed to congestive heart failure, loss of lean tissue, or to a slowly functioning sodium pump were considered.

Adult↗