PLASMA ALDOSTERONE CONCENTRATION IN ANEPHRIC CHILDREN

1974 ◽  
Vol 75 (3) ◽  
pp. 561-568 ◽  
Author(s):  
M. Birkhäuser ◽  
C. Godard ◽  
C. Loirat ◽  
M. B. Vallotton
Keyword(s):  
Serum Sodium ◽  
Plasma Cortisol ◽  
Potassium Concentration ◽  
Extracellular Volume ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Volume Depletion ◽  
Plasma Aldosterone Concentration ◽  
Serum Potassium Concentration ◽  
Postural Changes

ABSTRACT The effect of extractive haemodialysis and of postural changes on the plasma aldosterone concentration has been studied in 5 anephric children. The plasma aldosterone concentration tended to be lower after haemodialysis in spite of the extracellular volume depletion induced. No regular response occurred after orthostatism. There was no correlation between the plasma aldosterone and the plasma cortisol or the serum sodium concentration. A weak positive correlation was found between the plasma aldosterone and serum potassium concentration, suggesting that potassium may play a major role in aldosterone regulation in the anephric state.

CHANGES IN PLASMA RENIN ACTIVITY AND PLASMA ALDOSTERONE IN THE INDUCED PARALYTIC ATTACK OF THYROTOXIC PERIODIC PARALYSIS

1976 ◽  
Vol 82 (3) ◽  
pp. 715-727 ◽  
Author(s):  
Ryoyu Takeda ◽  
Shinpei Morimoto ◽  
Kenzo Uchida ◽  
Isamu Miyamori
Keyword(s):  
Plasma Renin Activity ◽  
Serum Sodium ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Serum Sodium Concentration ◽  
Serum Potassium Concentration

ABSTRACT Changes in serum electrolytes, haematocrit, plasma renin activity and plasma aldosterone induced by glucose and insulin (GI) infusion were serially investigated in seven patients with periodic thyrotoxic paralysis. An attack which developed into complete quadriplegia was induced within 90 min after the beginning of the GI infusion in four out of seven patients. Only a slight paralysis of the legs was produced in another two patients and induction of an attack did not materialize in one. In four patients with complete quadriplegia, the mean values of serum sodium and potassium concentrations, haematocrit, plasma renin activity and plasma aldosterone slightly decreased immediately after the beginning of the GI infusion. Induction of a paralytic attack was not accompanied by any significant changes in serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone either 15 min before or after the onset of attack, while the serum potassium concentration progressively decreased, and an increase in plasma aldosterone associated with an increase of haematocrit and plasma renin activity reached a peak level at the stage of complete quadriplegia. On the other hand, in the three patients in whom an infusion produced slight or no paralysis of the legs, changes in the serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone were insignificant and the serum potassium concentration was slightly but insignificantly decreased. These results suggest that hyperaldosteronism may not be a trigger for the induced paralytic attack but a phenomenon secondary to volume depletion and a change in potassium homoeostasis induced by GI infusion.

Does a Reduction in Serum Sodium Concentration or Serum Potassium Concentration Increase the Prevalence of Exercise-Associated Muscle Cramps?

2016 ◽  
Vol 25 (3) ◽  
pp. 301-304 ◽  
Author(s):  
Donal Murray ◽  
Kevin C. Miller ◽  
Jeffrey E. Edwards
Keyword(s):  
Serum Sodium ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Clinical Scenario ◽  
Clinical Question ◽  
Muscle Cramps ◽  
Serum Potassium Concentration ◽  
Exercise Associated Muscle Cramps

Clinical Scenario:Although exercise-associated muscle cramps (EAMC) are common in ultradistance runners and athletes in general, their etiology remains unclear. EAMC are painful, sudden, involuntary contractions of skeletal muscle occurring during or after exercise and are recognized by visible bulging or knotting of the whole, or part of, a muscle. Many clinicians believe EAMC occur after an imbalance in electrolyte concentrations, specifically serum sodium concentration ([Na+]s) and serum potassium concentration ([K+]s). Studies that have established a link between EAMC occurrence and serum electrolyte concentrations after an athletic event are unhelpful.Focused Clinical Question:Are [Na+]s and [K+]s different in athletes who experience EAMC than noncrampers?

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

Adrenocortical hormone secretory response to chronic NH4Cl-induced metabolic acidosis

1987 ◽  
Vol 252 (4) ◽  
pp. E454-E460 ◽  
Author(s):  
M. Schambelan ◽  
A. Sebastian ◽  
B. A. Katuna ◽  
E. Arteaga
Keyword(s):  
Metabolic Acidosis ◽  
Urinary Excretion ◽  
Potassium Concentration ◽  
Control Period ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Hydrogen Ion Concentration ◽  
Adrenocortical Hormone

We examined the effect of chronic metabolic acidosis on adrenocortical hormone production by administering NH4Cl for 5 days to four normal subjects. Plasma aldosterone concentration, aldosterone secretion, and urinary excretion of aldosterone-18-glucuronide increased significantly, whereas there were no significant changes in the plasma concentrations of cortisol, corticosterone, or deoxycorticosterone, or in the urinary excretion of 17-hydroxycorticoids. By day 2, plasma renin activity (PRA) and concentration (PRC) were not significantly different from control, and the slope of the regression line relating plasma aldosterone concentration to PRA was significantly greater than the slope in the control period, i.e., the sensitivity of aldosterone secretion to renin stimulation was increased. By day 5, however, PRA and PRC were increased above control. Plasma potassium concentration did not change significantly. Thus chronic NH4Cl-induced acidosis induces a sustained stimulation of aldosterone secretion in the absence of a change in adrenocorticotropin-dependent adrenocortical hormone secretion. Factors other than an increase in renin secretion and plasma potassium concentration may be involved in at least the early phase of aldosterone stimulation, suggesting that plasma hydrogen ion concentration might be a separate regulator of aldosterone secretion.

scholarly journals Effect of single dose resin-cathartic therapy on serum potassium concentration in patients with end-stage renal disease.

1998 ◽  
Vol 9 (10) ◽  
pp. 1924-1930
Author(s):  
C Gruy-Kapral ◽  
M Emmett ◽  
C A Santa Ana ◽  
J L Porter ◽  
J S Fordtran ◽  
...  
Keyword(s):  
Renal Failure ◽  
Single Dose ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Extracellular Volume ◽  
Cation Exchange Resin ◽  
High Volume ◽  
Sodium Polystyrene Sulfonate ◽  
Serum Potassium Concentration ◽  
Average Serum

Hyperkalemia in patients with renal failure is frequently treated with a cation exchange resin (sodium polystyrene sulfonate, hereafter referred to as resin) in combination with a cathartic, but the effect of such therapy on serum potassium concentration has not been established. This study evaluates the effect of four single-dose resin-cathartic regimens and placebo on 5 different test days in six patients with chronic renal failure. Dietary intake was controlled. Fecal potassium output and serum potassium concentration were measured for 12 h. Phenolphthalein alone caused an average fecal potassium output of 54 mEq. The addition of resin caused an increase in insoluble potassium output but a decrease in soluble potassium output; therefore, there was no significant effect of resin on total potassium output. Sorbitol plus resin caused less potassium output than phenolphthalein plus resin. On placebo therapy, the average serum potassium concentration increased slightly (0.4 mEq/L) during the 12-h experiment. This rise was apparently abrogated by some of the regimens that included resin; this may have been due in part to extracellular volume expansion caused by absorption of sodium released from resin. Phenolphthalein regimens were associated with a slight rise in serum potassium concentrations (similar to placebo); this may have been due to extracellular volume contraction produced by high volume and sodium-rich diarrhea and acidosis secondary to bicarbonate losses. None of the regimens reduced serum potassium concentrations, compared with baseline levels. Because single-dose resin-cathartic therapy produces no or only trivial reductions in serum potassium concentration, and because this therapy is unpleasant and occasionally is associated with serious complications, this study questions the wisdom of its use in the management of acute hyperkalemic episodes.

Effect of Low Electrolyte Feeding on Development of Potassium Deficiency

1957 ◽  
Vol 191 (3) ◽  
pp. 610-614 ◽  
Author(s):  
Malcolm A. Holliday ◽  
William E. Segar
Keyword(s):  
Potassium Concentration ◽  
Sodium Intake ◽  
Extracellular Volume ◽  
Sodium Concentration ◽  
Potassium Deficiency ◽  
Electrolyte Composition ◽  
Urine Excretion ◽  
Deficient Diet ◽  
Sodium Potassium ◽  
Low Sodium

Rats fed a diet deficient in sodium, potassium and chloride were observed for 3, 6, 12, 28, 60 and 110 days. Urine excretion of these ions was observed during the initial adjustment to the diet. Serum and muscle electrolyte composition was determined at the end of each interval. Initially the loss of sodium and chloride constituted a loss of extracellular volume without change in concentration. The loss of potassium in this period resulted in a decrease in the intracellular concentration of potassium. Subsequent conservation of all three substances was very effective. No alkalosis developed during the first 28 days on the deficient diet despite an 18% reduction in muscle potassium concentration. A minimal increase in muscle sodium concentration was observed at this level of potassium deficiency. Evidence indicates that this minimal increase was not a function of the low sodium intake per se but rather was characteristic of the magnitude of potassium deficiency, since a similar minimal increase in muscle sodium occurs when an adequate sodium intake is provided.

Effects of routine heparin therapy on plasma aldosterone concentration

1991 ◽  
Vol 124 (3) ◽  
pp. 267-270 ◽  
Author(s):  
Yo Kageyama ◽  
Hiromichi Suzuki ◽  
Takao Saruta
Keyword(s):  
Plasma Cortisol ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Heparin Therapy ◽  
Plasma Aldosterone ◽  
The Other ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium ◽  
Aldosterone Production ◽  
Sodium And Potassium

Abstract. Changes in plasma aldosterone, plasma renin activity, plasma cortisol, serum sodium and potassium concentrations were studied in 9 patients with thromboembolic diseases treated with heparin. Heparin was administered at doses of 700-1000 units/h for 7-10 days. Plasma aldosterone decreased from 239±33 to 114±25 pmol/l during heparin therapy and returned to basal levels after discontinuation of the therapy. In addition, responses to a low sodium intake (3 g/day) and ACTH were examined in 5 patients during and 2 weeks after heparin therapy. The increase in plasma aldosterone caused by low sodium intake was significantly attenuated during heparin therapy (124±5% increase from baseline) as compared with that 2 weeks after heparin therapy (148±7%, p<0.05). On the other hand, ACTH stimulated plasma aldosterone similarly during and at 2 weeks after heparin therapy (increase from baseline: 190±20% vs 193±9%). These results suggest that heparin decreased plasma aldosterone owing to attenuation of the angiotensin Il-induced aldosterone production.

Patient with Bartter syndrome in whom chronic potassium depletion was considered one of the causes of hyponatremia

2021 ◽  
Vol 14 (3) ◽  
pp. e240898
Author(s):  
Katsunobu Yoshioka
Keyword(s):  
Potassium Concentration ◽  
Sodium Concentration ◽  
Bartter Syndrome ◽  
Potassium Depletion ◽  
C Reactive Protein ◽  
Laboratory Examination ◽  
Serum Potassium Concentration ◽  
Reactive Protein ◽  
General Fatigue ◽  
Electrolyte Replacement

A 53-year-old man was admitted to our hospital because of general fatigue and disorientation. He had been diagnosed with Bartter syndrome in his teens and had been taking potassium preparations since then. However, his serum potassium concentration (K+s) remained persistently low. Ten days before admission, he developed fever. He was diagnosed as having bronchitis and was treated with antibiotics. Although his fever subsided, general fatigue worsened. Laboratory examination showed hyponatraemia (127 mEq/L), while K+s was 2.3 mEq/L. C reactive protein was negative. On admission, laboratory examination revealed deterioration of hyponatraemia (125 mEq/L). Although his serum sodium concentration (Na+s) was refractory to electrolyte replacement, the level increased towards normal after spironolactone administration, following normalisation of K+s, suggesting that hyponatraemia was caused by K+ depletion. Physicians should be aware of the importance of the effects of exchangeable K+ (K+e) on Na+s.

Subcutaneous administration of desoxycorticosterone pivalate for the treatment of canine hypoadrenocorticism

1995 ◽  
Vol 31 (2) ◽  
pp. 151-155 ◽  
Author(s):  
MD McCabe ◽  
EC Feldman ◽  
RC Lynn ◽  
PH Kass
Keyword(s):  
Body Weight ◽  
Potassium Concentration ◽  
Subcutaneous Administration ◽  
Sodium Concentration ◽  
Serum Electrolyte ◽  
Serum Electrolytes ◽  
Serum Potassium Concentration ◽  
Median Serum ◽  
Previously Treated ◽  
Fludrocortisone Acetate

Twelve dogs with hypoadrenocorticism were treated with subcutaneous desoxycorticosterone pivalate (DOCP). Eight of these dogs were recently diagnosed and had not yet been treated. Four dogs previously had been diagnosed and treated (three with intramuscular DOCP, one with oral fludrocortisone acetate). History, physical examination, serum electrolytes, and blood urea nitrogen (BUN) were evaluated. Desoxycorticosterone pivalate (2.2 mg/kg body weight) was administered every 25 days. On day 0, recently diagnosed dogs had a median serum sodium concentration of 131.5 mEq/L, median serum potassium concentration of 6.6 mEq/L, and median BUN of 41.5 mg/dl. All subsequent median serum electrolyte and BUN concentrations were normal. All previously treated dogs had normal blood values which were maintained throughout the study.

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