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Biomedical subjects

J P Radó

Publications and source records attributed to J P Radó.

At least 19 recordsLinked to original sources
PubMed1999

Patterns of potassium wasting in response to stepwise combinations of diuretics in nephrotic syndrome.

OBJECTIVE: To study the urinary potassium wasting patterns when the decreasing effectiveness of diuretics during repeated administrations are counterbalanced by stepwise increases of doses and combinations of them. PATIENTS: Eleven patients with renal edema. Seven patients suffered from advanced nephrotic syndrome and 4 patients were "forme fruste". METHODS: Urinary excretions and serum levels of potassium, sodium, creatinine, osmoles were determined; specific renal functions, glomerular filtration rate (GFR) fractional excretion of potassium (FE(K)), transtubular potassium gradient (TTKG) and free water reabsorption (TcH2O) were calculated. Nine different intervention-induced changes were followed daily: furosemide (FSD) alone, FSD with chlorthalidone (CTN), "low dose" and "high dose" potassium sparing drugs (PSD), FSD with CTN and "low dose" or "high dose" PSD, and "no drug" as well as "postdiuretic" periods with or without PSD. RESULTS: TTKG significantly decreased in response to FSD. It elevated during FSD with CTN, but remained lower than the baseline. The normal correlation between urinary potassium excretion (UKV) and TTKG became distorted under FSD. UKV and FE(K) were slightly increased by FSD and more markedly when given FSD together with CTN, probably because "distal volume flow" was elevated. In the "postdiuretic" periods TTKG increased, but this was reversed by PSD. In response to PSD, TTKG and UKV decreased, but both were elevated when combining with FSD + CTN. CONCLUSIONS: FSD caused relatively small potassium loss, because the enhanced "distal volume flow" was counterbalanced by a decrease of TTKG. FSD may have had a potassium secretion inhibitory influence as well. Potassium loss and TTKG were enhanced during coadministration of CTN, and decreased by PSD. "Postdiuretic rebound" increase of TTKG was reversed by PSD.

Aged↗
PubMed1998

High-dose phosphate treatment leads to hypokalemia in hypophosphatemic osteomalacia.

The mechanism of the decrease in plasma potassium induced by phosphate treatment was investigated in a 24-year-old hypertensive patient with hypophosphatemic osteomalacia, who was the youngest of four patients, belonging to a 23 number kindred of five generations. Parameters of potassium, sodium, calcium, and phosphate metabolism as well as specific renal functions have been studied in the basal state and during administration of graded doses of phosphate (500-6000 mg). Progressive hypokalemia developed during phosphate treatment. An inverse correlation was found between plasma potassium and doses of phosphate (plasma potassium = -0.2 g phosphate + 3.9 r = -0.49; p < 0.05; N = 21). A renal route of potassium loss was suspected, but could not be confirmed as potassium excretion did not increase although sodium excretion was augmented [basal sodium output: 56.7 mmol/24 h; phosphate treatment: 153 mmol/24 h (p < 0.05)]. Transtubular potassium gradient (TTKG) also decreased and an inverse correlation was found between TTKG and doses of phosphate (r = -0.37; p < 0.02; N = 38). Decrease of TTKG was possibly the result of suppressed K+ secretion. It was concluded that potassium loss occurred by a non-renal (intestinal) route in phosphate-induced hypokalemia. Although major hazards of treatment of hypophosphatemic osteomalacia with phosphate and calcitriol are secondary hyperparathyroidism and vitamin D intoxication, potassium loss also should be kept in mind.

Adult↗
PubMed1993

Metabolic bone disease (anticonvulsant osteomalacia) and renal tubular acidosis in tuberous sclerosis.

The characteristics triad of tuberous sclerosis-adenoma sebaceum, mental deficiency and epilepsy-associated with distal-type renal tubular acidosis was combined with anticonvulsant osteomalacia in a 41-year-old woman. In addition to the specific bone lesions of tuberous sclerosis, the bone disease was caused by an adverse effect of a drug and possibly also by the renal disorder leading to significant musculoskeletal disability. In response to calcium carbonicum and 1-25-dihydroxyvitamin D therapy the musculoskeletal disability healed and the abnormal biochemical markers of anticonvulsant osteomalacia disappeared. The present observation draws attention to the increased hazard threatening patients on chronic anticonvulsant therapy simultaneously suffering from renal diseases.

Acidosis, Renal Tubular↗
PubMed1990

Simultaneous occurrence of diabetes insipidus and ascites due to liver cirrhosis: clinical and pathophysiological studies.

Authors describe the simultaneous occurrence of ascites due to liver cirrhosis and diabetes insipidus in a patient with consistently normal urine volume. The diagnosis of diabetes insipidus has been proved by the water deprivation test combined with the administration of dDAVP as well as by serial determinations of plasma arginine vasopressin levels before and during infusion of hypertonic sodium chloride solution. Authors discuss the differential-diagnostic difficulties of the case and consider the mechanisms playing a role in the abolishment of diabetic polyuria by hepatic disease.

Aged↗
PubMed1989

Endocrinological aspects of potassium metabolism.

After reviewing the anatomy and physiology of potassium the endocrine regulation of the "external" and "internal" potassium balance is summarized. As the plasma potassium concentration has an extraordinary role in the maintenance of the activity of the living cell membrane, the review focuses on endocrine factors inducing hypokalaemia and hyperkalaemia. Modern research has revealed many renal and extrarenal influences and we have learned a lot concerning the development of plasma potassium changes. The renal and extrarenal mechanisms governing potassium homeostasis are regulated by precisely coordinated endocrine mediators. The most important hormones involved in the regulation of internal potassium balance are the catecholamines, insulin and aldosterone. Several drugs causing changes in the plasma potassium level exert their effect through the above mentioned hormones.

Aldosterone↗
PubMed1988

Successful treatment of hyperkalemic quadriplegia associated with spironolactone.

Hyperkalemic flaccid quadriplegia and cardiotoxic disturbances developed during antihypertensive therapy with spironolactone in a 76-year-old woman with chronic renal insufficiency. Hyperkalemia was successfully overcome and followed by the disappearance of all cardiac and muscular disorders. Progression of the renal disease leading to a decrease of creatinine clearance from 85 ml/min to 4.5 ml/min, during a three-year observation period per se had apparently no influence on the serum level of potassium. Our studies suggested that no primary insufficiency of the renin-aldosterone and glucocorticoid systems had been responsible for the hyperkalemia, therefore, it could be contributed entirely to the effect of spironolactone abolishing the K+ secreting capacity of the already decreased renal mass. Further studies revealed that blocking action of the drug on H+ secretion ("renal tubular acidosis") may also have had a role-in addition to the K+ retention-in the development of the spironolactone-induced hyperkalemia.

Acid-Base Equilibrium↗
PubMed1986

Interplay of various factors in glucose-induced hyperkalemia during captopril treatment.

The effect of angiotensin converting enzyme inhibition by captopril (CAP) on serum potassium (SK) changes was studied during a three-hour glucose tolerance test (GTT) in recumbent and upright positions in 16 patients with drug-resistant hypertension. An elevation of SK in the upright posture occurred in the course of GTT during CAP treatment in 50% of the patients (Group I) even without consistent changes in baseline SK. In Group II a qualitatively normal glucose-induced hypokalemic response was obtained. Aldosterone was suppressed by CAP, predominantly in the upright position in Group I due to the significant interaction between the drug and posture. Significant inverse correlations were found in Group I between glucose-induced serum potassium changes and basal glomerular filtration rate. A similar correlation was found also with serum insulin in the whole patient material. It was concluded that the interplay of various factors, CAP, upright posture and impaired renal functions resulting in suppression of aldosterone and insulin played a role in the paradoxical glucose-induced serum potassium elevation.

Adult↗
PubMed1984

Effect of body posture on the serum potassium response to glucose in healthy subjects, diabetics and hyperthyroid patients.

Administration of glucose induces normally a decrease in serum potassium, though exceptionally a paradoxcial increase (PGIH) may occur. The effect of posture on glucose-induced serum potassium changes in health and disease has not been previously studied. We have investigated the influence of changes in body posture on the different serum potassium responses to glucose in various groups of 47 subjects. We have found a smaller decrease in serum potassium in the upright position than in the recumbent one in 20 healthy subjects and in 12 non-insulin dependent diabetics, but no significant difference in hyperthyroidism. The variable effect of posture on glucose-induced insulin secretion in the various groups of subjects did not provide explanation for the postural inhibition of the normal serum potassium response to glucose. A tendency to PGIH was found in a small number of diabetics. Although PGIH was completely reversed by DOC the normal postural difference between serum potassium curves was uneffected. It was concluded that change in the body posture has a definite influence on the glucose-induced decrease in serum potassium in normal people and is not mediated by insulin and/or aldosterone; PGIH develops in the upright position more easily than recumbency; exact serum potassium changes after glucose loading can be explored only by adequate standardization and carrying out both recumbent and upright measurements.

Adult↗
PubMed1984

Prediction of hyperkalemia associated with prolonged treatment with captopril by glucose-induced acute serum potassium changes.

The effect on potassium levels of short-term (5-10 days) and "prolonged" (4 weeks) captopril therapy were compared. No consistent changes during short-term treatment were found and the elevations in serum potassium associated with prolonged treatment could not be predicted on the basis of short-term changes. However, a definite correlation was found between glucose-induced serum potassium alterations (in the course of glucose tolerance test) during short-term captopril administration and elevations in baseline serum potassium during prolonged treatment In the patients with glucose-induced paradoxical serum potassium elevations, baseline serum potassium levels increased more markedly during prolonged captopril therapy than in patients with the opposite glucose-induced changes.

Aldosterone↗
PubMed1982

Simultaneous occurrence of hyperkalemia due to aldosterone suppression and hyperfunctioning parathyroid adenoma.

The change of the pattern of clinical presentation of primary hyperparathyroidism in older patients is illustrated by a case history of a 61-year-old woman with multicystic kidney disease in whom a thiazide antihypertensive drug (clopamide) induced a very severe symptomatic hypercalcemia. Withdrawal of the drug was followed by a prolonged complete clinical remission, normocalcemia, normocalciuria, but consistently elevated parathormone levels. This "normocalcemic biochemical hyperparathyroidism" was complicated with hyperkalemia due to aldosterone suppression, a counterpart of the recently described association with hypokalemia due to primary hyperaldosteronism, necessitating further studies on the occurrence and significance of altered production of aldosterone in geriatric patients with primary hyperparathyroidism.

Acid-Base Equilibrium↗