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At least 757 records · Page 42Linked to original sources
PubMed1984

[Diuretics in cardiovascular pathology. Their clinical use in the light of recent pathogenetic studies].

The action of the most common diuretics is reviewed with emphasis on precise indications in the case of cardiac deficiency, arterial hypertension and certain forms of angina pectoris. These drugs are judged extremely useful if the necessary precautions are taken at all times. Disturbances to the water-electrolyte balance may however occur during treatment and changes in the magnesium electrolyte are described in the light of recent developments in our knowledge of the physiopathology of diuretics.

Angina Pectoris↗
PubMed1983

Acid-base disorders and the kidney.

In the normal human body, the extracellular fluid pH of 7.40 is closely protected. Any increase in acidity or alkalinity summons forth three lines of defense, starting immediately with the blood buffers, followed soon by the respiratory system's control of CO2, and finally purged by the renal excretion of the excess acid or base. The complex interrelated processes of the renal responses require a few days to accomplish maximum compensation. We have presented the fundamental principles governing maintenance of the acid-base equilibrium to provide a conceptual framework for understanding the clinical disorders of hydrogen ion metabolism. The somewhat elusive concepts of endogenous acid production and net acid balance have also been reviewed to help reveal the pathophysiology of metabolic acidosis caused by renal tubular acidosis, chronic renal failure, certain infant feedings, and total parenteral nutrition. The development and perpetuation of metabolic alkalosis in relationship to chloride and potassium deficiency have been examined. In the delineation of a clinical acid-base disorder, the clinician must bear in mind the continual interactions of electrolytes and hormonal systems and should be prepared to reevaluate frequently the elected therapy against the changing responses, based on a thorough understanding of physiology. The various types of renal tubular acidosis have manifold facets but the basic understanding of their pathophysiology begins with the concept of the "anion gap," a point of reference that can be used in the differential diagnosis and treatment. In this chapter a number of new causes of type IV renal tubular acidosis--currently considered to be the most common form of renal tubular acidosis--have been pointed out, along with special reference to the mineral, electrolyte, and aldosterone metabolism in the various acidoses and current means of reversing growth failure in the child, especially through bicarbonate treatment. The mechanism of metabolic acidosis in chronic renal failure including metabolic acidosis in children undergoing dialysis and in recipients of kidney transplantation, and its relationships to mineral and electrolyte metabolism have been presented. The pathophysiology of the acidosis related to certain infant formulas and the acidogenic properties of some amino acid solutions employed in total parenteral nutrition have been briefly reviewed. Finally, the metabolic alkalosis seen in a variety of chloride deficiency syndromes, such as Bartter's syndrome and dietary chloride deprivation, has been discussed and a rational approach to evaluation and treatment outlined.

Acid-Base Equilibrium↗
PubMed1982

Hypokalemia stimulates plasma epinephrine and norepinephrine in the rat.

We examined the effect of dietary potassium depletion on plasma and urinary catecholamines in the rat. Ingestion of a potassium deficient diet for 45 days increased plasma norepinephrine by 80% and plasma epinephrine by 270%. Urinary excretion of epinephrine, norepinephrine and dopamine were not significantly affected by hypokalemia. The results suggest that the increase in plasma catecholamines may be mediated "reflexly" by an accompanying increase in vasodilator agents or may represent a direct "stress" effect of hypokalemia on the release of epinephrine and norepinephrine.

Animals↗
PubMed1978

[Phaeochromocytoma with hypokalaemia (two cases) (author's transl)].

Two cases of phaeochromocytoma with hypokalaemia are reported. In the first, a carcinoma, hypokalaemia was potentially secondary to hyperreninaemia and hyperaldosteronism in association with probably paraneoplastic hypercorticism. The other was benign and the origin of isotopically demonstrated potassium deficiency was less clear, because hyperreninaemia, hyperaldosteronism and hypercortisolism were moderate.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Acute toxic nephropathies: clinical pathologic correlations.

Man's ever increasing exposure to numerous drugs and chemicals, which are the results of medical and industrial progress, produces a by-product of acute toxic nephropathies. These include acute toxic renal failure, drug-induced acute oliguric renal failure, acute hemorrhagic glomerulonephritis, nephrotic syndrome, tubular disturbances and potassium deficiency. In depth information is provided for the previously mentioned disorders.

Acute Kidney Injury↗
PubMedDate not supplied

Studies on renal function in healthy women with different degrees of induced potassium depletion. 1) Hormonal changes relevant to salt and water balance.

In healthy women we have studied the effects of potassium depletions of different degrees on the generation of some bioregulators of hydro-saline balance. The study has been performed on 20 women in normal potassium balance (N group) and 20 women submitted to potassium depletive treatment by dietary and pharmacological means. On the basis of different patterns of treatment we have obtained three groups i.e. KD1 (n = 8), KD2 (n = 6) and KD3 (n = 6) with potassium cumulative deficit of 160 +/- 43, 198 +/- 22 and 214 +/- 54 mmol, respectively. The renal function was assessed by the clearance method during induced hypotonic polyuria and subsequent moderate antidiuresis induced by low dose infusion of lysine-8-vasopressin. The urinary PGE2, 6-keto-PGF1 (6KPGF) and TxB2 were determined by the RIA method. Moreover, the basal PRA and urinary aldosterone were determined before the renal functional exploration. The data obtained in both KD2 and KD3 groups where renal hypokalemic dysfunctions occurred--indicate that hypokalemia stimulated renin secretion and inhibited the reactivity of renal prostanoid production to the polyuric stimulus. However, in the KD3 group--where the circulating levels of renin, and probably of angiotensin II were the highest--the hypokalemic depression of the synthesis of 6KPGF and TxB2 precursors was attenuated while the synthesis of PGE2 was still inhibited.

Adult↗
PubMed1993

Studies on renal function in healthy women with different degrees of induced potassium depletion. 2). Patterns of hypokalemic renal dysfunction.

In order to investigate the renal functional effects of potassium depletion (KD) we have submitted 20 healthy women to different potassium depletive treatments by dietary and pharmacological means. By changing these treatments we have obtained three KD groups with cumulative potassium deficit of 160 +/- 43 (KD1, n = 8), 198 +/- 22 (KD2, n = 6) and 214 +/- 54 mmol (KD3, n = 6). Another 20 subjects were also studied as controls in normal potassium balance (N group). In all subjects the renal function has been evaluated by clearance (cl.) technique both during induced hypotonic polyuria and subsequent moderate antidiuresis induced by low dose infusion of lysine-8-vasopressin (LVP). A renal dysfunction occurred in differences between these two groups, they have been pooled in a single KD2 + KD3 group. In this group as compared to N the following renal dysfunctions were observed during hypotonic polyuria: a) reduction in creatinine cl. (in absence of significant differences in mean arterial pressure); b) inhibition of the fractional reabsorption of chloride by diluting segments; c) depression of the diuretic response to water load. Moreover in KD the LVP was less effective in reducing the creatinine cl. while it became effective in reducing the fractional excretions of NaCl. These findings indicate that the degree of KD reached in the KD2 + KD3 group was adequate to induce a renal dysfunction similar to that occurring in conditions of chronic hypokalemia. It is probable that hypokalemia by itself along with changes of both prostaglandin and angiotensin renal systems are involved in this renal dysfunction.

Blood Pressure↗
PubMed1997

[Bone changes in ulcerative colitis].

One of the complications of ulcerative colitis with frequent relapses is mineral deficiency (potassium, calcium, magnesium and phosphorus). The objective of the present work is to examine the bone density and laboratory parameters of bone metabolism in 25 patients with a medium severe and severe form of ulcerative colitis. In patients with ulcerative colitis a significantly reduced bone density was found in the era of neck of the femur (p < 0.05), a a non-significantly reduction of the bone density in the era of the lumbar vertebrae and an elevated level of osteocalcin (p < 0.05). These findings indicate a higher prevalence of bone changes in patients with ulcerative colitis. Early detection of bone changes makes adequate prevention and treatment of bone complications possible.

Adult↗
PubMed1980

Effect of insulinopenia and adrenal hormone deficiency on acute potassium tolerance.

The ability to dispose of an acute intravenous potassium load was examined in glucocorticoid-replaced adrenalectomized rats and in rats made insulinopenic with somatostatin. Adrenalectomy resulted in a significantly greater rise in plasma potassium concentration compared with controls (1.46 +/- 0.11 vs. 0.92 +/- 0.05 mEq/liter, P less than 0.001) despite the excretion of an identical percentage (47%) of the administered potassium load in 2 hours. Somatostatin-induced insulinopenia (insulin levels decreased from 37 +/- 5 to 20 +/- 3 microU/ml) was also associated with a significantly greater increment in plasma potassium controls, despite the excretion of a similar amount (39%) of the administered potassium load. In animals with combined adrenal and insulin deficiency, the rise in plasma potassium concentration occurred earlier and remained elevated for a more prolonged period of time compared with animals with either adrenalectomy or insulinopenia alone. Conclusion. During acute potassium loading in the rat, insulin and adrenal hormones play an important role in maintaining normal potassium homeostasis, primarily by enhancing potassium uptake by external tissues.

Adrenalectomy↗
PubMed1985

Enhanced distal absorption of potassium by magnesium-deficient rats.

The effect of acute potassium infusion on renal tubular reabsorption of potassium by magnesium-deficient and pair-fed control rats has been studied by the recollection micropuncture method. During potassium chloride infusion, the amount of potassium remaining in the distal tubule is lower in magnesium-deficient than in pair-fed rats. This could be due to a reduction in potassium secretion or to an enhancement of potassium reabsorption. The present study demonstrates enhanced renal potassium retention in the magnesium-deficient rat, and is in contrast to previous reports of renal potassium wasting in this circumstance.

Absorption↗
PubMed1995

Growth hormone (GH) receptor and GH-binding protein deficiency in the growth failure of potassium-depleted rats.

Potassium (K+) deficiency is associated with growth retardation in both man and experimental animals. Growth hormone (GH) administration to such animals prevents, to some extent, weight loss and selective muscle atrophy, but does not affect tail and tibia length even with supraphysiological doses. The present study was undertaken to investigate the possible effect of K+ deficiency on the hepatic GH receptor and GH-binding protein (BP). Young female Wistar rats were maintained on K(+)-deficient fodder and distilled water, and compared with pair-fed and ad-libitum-fed control groups. After 15 days GH-BP and electrolytes were measured in sera, GH receptors were studied in liver membranes by 125I-labeled human GH binding and muscles were weighed and saved for electrolyte measurements. K(+)-deficient rats showed complete growth arrest compared with an intermediate weight gain of the pair-fed group. Serum K+ was very low, at 1.5 +/- 0.1 mmol/l, compared with the mean value of 5.3 mmol/l of control animals. Somatogenic and lactogenic receptors in liver membranes and serum GH-BP levels were significantly (P < 0.05) lower in K+ deficiency, as compared with their pair-fed controls. Liver GH receptors correlated significantly (P < 0.05) with serum GH-BP levels. The growth variables correlated positively with both hepatic somatogenic and lactogenic receptors and serum GH-BP levels, with correlation coefficients that were highest against serum GH-BP and lowest against liver lactogenic receptors. Serum and muscle K+ correlated significantly (P < 0.05) with both liver GH receptors and serum GH-BP, with correlation coefficients that were higher against serum GH-BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1953

The importance of potassium after operation.

A deficiency of potassium in a patient after operation is manifest clinically by anorexia, malaise, apathy, weakness, abdominal distention and hypochloremia. Many patients who have had a prolonged disturbance in nutrition may have a "subclinical" hypopotassemia. Prophylaxis by means of replacement of the potassium excreted daily in the urine is the ideal treatment. When the clinical picture of potassium deficit develops, the amount of the potassium ion needed for replacement should be calculated on the basis of the total amount of water in the body of the patient.

Acid-Base Imbalance↗