Recurrent Hyperkalaemia due to Selective Aldosterone Deficiency: Correction by Angiotensin Infusion

Brown, J. J.; Chinn, R. H.; Fraser, Robert; Lever, A. F.; Morton, J. J.; Robertson, J. I. S.; Tree, M.; Waite, Marion; Park, D. M.

doi:10.1136/bmj.1.5854.650

Cited by 46 publications

(7 citation statements)

References 35 publications

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“…In addition, an infusion of catecholamines at a rate which has been shown to cause twofold or greater increases in circulating renin levels in normal subjects had no effects on plasma renin activity in these patients. These results are consistent with the concept that these patients had hypo aldosteronism secondary to failure of the renin-angiotensin system [8,33,36,42]. These data do not support the presence of primary adrenal dysfunction as the cause of the mineralocorticoid deficiency.…”

Section: Discussionsupporting

confidence: 80%

Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Weidmann¹,

Maxwell²,

Rowe³

et al. 1975

Nephron

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The relationship between plasma potassium concentration and the renin-angiotensin-aldosterone system was evaluated in ten patients with chronic renal failure (creatinine clearance 10–56 ml/min). Under basal conditions and following various stimulation maneuvers, normokalemic patients demonstrated normal plasma renin and aldosterone levels. Five of six patients with hyperkalemia had diminished function of the renin-angiotensin-aldosterone system; their ability to conserve sodium during salt depletion was less than that of normokalemic patients. The data suggest that the maintenance of plasma potassium levels in these patients is dependent on the presence of a normally functioning renin-angiotensin-aldosterone system; aldosterone activity may be an important determinant of sodium conservation in patients with renal failure.

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Section: Discussionsupporting

confidence: 80%

Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Weidmann¹,

Maxwell²,

Rowe³

et al. 1975

Nephron

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“…Support for this hypothesis was provided by Tuck et al (99), who found a diminished plasma renin response to isoproterenol in fi ve hyperkalemic diabetic patients with "hyporeninemic hypoaldosteronism" and evidence of autonomic and/or peripheral neuropathy. In contrast, several studies describe normal plasma and/or urinary catecholamines in patients with selective hypoaldosteronism (123)(124)(125)(126), and deChatel et al (98) found no relation between decreased plasma epinephrine levels and defects in the renin-aldosterone axis in 59 diabetics. In summary, it seems unlikely that decreased sympathetic nervous system activity and/or low circulating plasma epinephrine levels can explain the hyporeninemia in most diabetic subjects.…”

Section: Impaired Renin-aldosterone Axismentioning

confidence: 86%

Clinical Disorders of Hyperkalemia

DeFronzo¹,

BIa²,

Smith³

1982

Annu. Rev. Med.

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Potassium DistributionTotal body potassium in a healthy adult is approximately 50 meqlkg body weight or about 3500 meq for a 70-kg man (1, 2). Most of this is located within cells (Figure 1), primarily muscle, at a concentration of about 150 meq/L. Only 2% of total body potassium is located in the extracellular fl uid, normally at concentrations of 3.5 -5.0 meq/L. The maintenance of this high intracellular to extracellular K concentration depends upon the Na-K ATPase pump (3, 4) as well as other fac tors, including H+ balance, plasma tonicity, and plasma insulin, epinephrine, and aldosterone concentrations (5). The large difference in potassium concentration across the cell mem brane is critical for normal cell fu nction since it is the primary determinant of the resting membrane potential. Small changes in the intracellular/ex tracellular K ratio can severely disturb neuromuscular fu nction, particu larly of the heart. A gain (or loss) fr om the extracellular space of an amount of potassium equal to only I % of the total body K content (35 meq) can cause a 50% increase (or decrease) in plasma K concentration. Such a change would have pronounced effects on neuromuscular func ti on. Like wise, redistribution of a similar amount of potassium fr om the intracellular to extracellular (or vice versa) fluid compartmen t without net gain or loss of K fr om the body, would similarly affect neuromuscular excitability. Thus, it is important that both the total amount of potassium within the body and the distribution of potassium between intracellular and extracellu lar fl uid compartments be closely regulated.In healthy man, potassium enters only via the gastrointestinal tract. Approximately 100 meq of K is ingested per day and essentially all of this is absorbed fr om the stomach and upper gastrointestinal tract. Approxi-521 0066-4219/8 2/040 1-0521 $02.00 Annu. Rev. Med. 1982.33:521-554. Downloaded from www.annualreviews.org Access provided by Haifa University on 01/05/15. For personal use only.Quick links to online content Further ANNUAL REVIEWS

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“…3); that this correlation is looser than that observed in the control subjects could be due to the direct effect of hyperkalemia on aldosterone secretion [13,[34][35][36][37][38][39], Diabetic patients may show a series of factors which could negatively affect, either singly or jointly, renin secretion: (1) afferent arteriole hyalinization, which al ters the juxtaglomerular cells [40][41][42], (2) Autonomic neuropathy, leading to a decrease in renin synthesis [27,43], Diabetic patients exhibit a lesion in the afferent loop of the sympathetic nervous system [34, 44. 45], (3) In these patients there is a defect in the conversion of pro renin or 'big-renin' into active renin, leading to an accu mulation of the former in the plasma [3,26], (4) The expansion in cell volume that this kind of patient may display could be a factor in determining the hyporeni nemic state [46], (5) In recent years, considerable impor tance has been given to prostaglandins (PGs) as media tors in renin synthesis.…”

Section: Discussionmentioning

confidence: 87%

Hyporeninemic Hypoaldosteronism in Diabetic Patients with Chronic Renal Failure

Villoria

Núñez²,

Miralles³

et al. 1988

Am J Nephrol

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Plasma renin activity, plasma aldosterone levels and renal tubular capacity to excrete hydrogen ions were studied in 13 patients suffering from diabetes mellitus with a creatinine clearance of less than 40 ml/min. The results were compared with those obtained in a control group, in a group of nondiabetic subjects with chronic renal failure (CRF) and in a group of diabetic patients without CRF. Twelve of the thirteen diabetic patients with CRF had data characteristic of hyporeninemic hypoaldosteronism associated with type IV renal tubular acidosis. On comparing the results with those of the other two groups of patients, it was observed that the manifestations of the latter two groups considered separately were different from those of the problem group, although in the diabetic patients with normal glomerular filtration rate (GFR) hyporeninism but not hypoaldosteronism was present accompanied by a lower net acid excretion (p < 0.001) due to a lower excretion of NH₄ (p < 0.05) and titratable acid (p < 0.001) when the patients were challenged with an NH₄C1 overload. We believe that a conjunction of diabetes and renal failure is necessary for the diabetic patients with a decrease in GFR to show hyporeninemic hypoaldosteronism and type IV tubular acidosis.

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Recurrent Hyperkalaemia due to Selective Aldosterone Deficiency: Correction by Angiotensin Infusion

Cited by 46 publications

References 35 publications

Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Clinical Disorders of Hyperkalemia

Hyporeninemic Hypoaldosteronism in Diabetic Patients with Chronic Renal Failure

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