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Biomedical subjects

J P Rado

Publications and source records attributed to J P Rado.

13 recordsLinked to original sources
PubMed1981

Reversal of glucose-induced hyperkalemia by sodium restriction in normaldosteronemic diabetes: evidence for elevated mineralocorticoid threshold.

Acute glucose loading studies were performed on seven diabetic patients and 18 control subjects. In two normaldosteronemic insulin-dependent diabetic patients during high sodium intake and insulin withdrawal infusion of hypertonic glucose induced a paradoxical elevation of serum potassium levels, while no such abnormalities were found in two other diabetics despite of lower plasma aldosterone levels. Paradoxical glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained l glucose-induced hyperkalemia (PGIH) was abolished during insulin withdrawal by sodium restriction associated with a dramatic increase in plasma aldosterone. PGIH was elicited when given 100 g of glucose orally to further three patients with normaldosteronemic diabetes in whom a complete reversal of PGIH was obtained also by sodium restriction or by administering a large intravenous dose of desoxycorticosterone. These findings suggested an elevated mineralocorticoid threshold level for the normal cellular regulation of potassium distribution in normaldosteronemic diabetics with PGIH.

Aldosterone↗
PubMed1979

Efficacy, safety and hypothalamic-pituitary-adrenal axis function in patients with asthma treated with cloprednol.

Cloprednol was tested in 25 patients with chronic reversible bronchial obstruction, with respect to changes in hypothalamic-pituitary-adrenal (HPA) axis function and its efficacy on their clinical asthma. Patients were treated by a single morning dose for a 6-month period. The HPA axis function as estimated by fasting plasma cortisol levels did not show any significant changes, but adrenal response, assessed by ACTH stimulation test, was found slightly less at 6 months than at 3 months and at baseline. Pulmonary function tests--FEV1 and Raw--showed some improvement during the trial period. The score of respiratory complaints and symptoms, as well as the subjective status of the patients, showed a trend towards improvement. No significant side effects were observed.

Adrenal Cortex↗
PubMed1979

"Outpatient hyperkalemia" syndrome in renal and hypertensive patients with suppressed aldosterone production.

"Outpatient hyperkalemia" is a new clinical syndrome in which high serum potassium levels (SK) are found in the outpatient condition returning toward normal without any specific treatment after admission to the hospital. We report here of six patients with high blood pressure of various origin (chronic glomerulonephritis, interstitial nephritis, diabetic nephropathy, Gordon syndrome) in whom dietary and postural factors were found to be responsible for the outpatient hyperkalemia. The Na content of the "ad libitum" outpatient diet was definitely higher than that of the regular hospital diet. Increasing the Na intake from 120 mEq to 300 mEq induced a marked elevation of SK (from 5.21 +/- 0.16 to 6.34 +/- 0.40 mEq/l; p less than 0.001) in two hospitalized, recombent patients. On the other hand, Na restriction induced a dramatic improvement in hyperkalemia (from 5.89 +/- 0.11 mEq/l to 4.79 +/- 0.08 mEq/l:; p less than 0.001) in 4 patients in whom the effect was studied in the outpatient state. Although the mean plasma aldosterone (PA) was significantly lower in the patient group than in the healthy group, during normal Na intake there was a considerable overlap. A clearer distintion was made by using the new index of PA per SK ratio expressing the diminution in the apparently normal PA when related to the abnormally high SK. During high Na intake, PA was definitely suppressed and during Na restriction there was a dramatic relief from suppression. The present studies confirmed the previously described phenomenon of "upright hyperkalemia" which may have played an additional role in the development of outpatient elevation of SK. The knowledge of the clinical syndrome of "outpatient hyperkalemia" may be important to single out certain cases of easily correctable insufficient (suppressed) aldosterone production.

Adult↗
PubMed1977

Postural plasma aldosterone response in "upright hyperkalemia" associated with selective hypoaldosteronism.

Upright posture induced a consistent increase in serum K with a blunted plasma aldosterone response in four male renal patients with selective hypoaldosteronism. Dietary Na restriction induced a dramatic increase in the suppressed plasma aldosterone without returning the elevated serum K levels to normal and abolishing the postural serum K change. Therefore it is concluded that "upright hyperkalemia" may not be caused exclusively by suppression or/and inadequate postural response of aldosterone. Cellular disturbance in the regulation of K distribution might be an additional explantation for the aldosterone unresponsive postural K change.

Adult↗
PubMed1977

Effect of mineralocorticoids on the paradoxical glucose-induced hyperkalemia in nondiabetic patients with selective hypoaldosteronism.

Intravenous infusion of hypertonic glucose induced a transitory paradoxical serum potassium elevation in 3 nondiabetic patients with selective hypoaldosteronism. The abnormal serum potassium response developed in spite of a normal insulin release and was abolished by pharmacological doses of mineralocorticoids in two. It is apparent that in certain patients with aldosterone deficiency normal insulin production alone cannot reverse completely the hyperosmolality-induced transfer of potassium from the intracellular to the extracellular fluid.

Aldosterone↗
PubMed1976

Effect of 1-deamino-5-D-arginine vasopressin (DDAVP) on plasma cortisol (hydrocortisone).

The influence of 1-deamino-8-D-arginine vasopressin (DDAVP), the new antidiutetic polypeptide without any side effects on plasma cortisol, was investigated in 30 healthy persons. A dose of 4 mug DDAVP administered intravenously induced a rise in plasma cortisol (hydrocortisone) levels greater than 3.5 mug/100 ml in 12 out of 20 persons studied. In this group (group I), the average increase at 15 minutes was 6.92+/-1.74 mug/100 ml (P less than 0.005), while in the remaining eight persons (group II) plasma cortisol levels decreased according to the usual normal daily rhythm. DDAVP, 80 mug, administered intranasally had no demonstrable influence on physiologic plasma cortisol regulation. On the basis of the present findings with relatively low doses, pituitary responsiveness (ACTH release) might be expected to occur in a higher percentage of persons after giving high intravenous doses of DDAVP. Further efforts are necessary to develop a safe vasopressin test for clinical examination of adenohypophyseal function.

Administration, Intranasal↗