Aldosterone Deficiency in Chronic Renal Failure

Gerstein, Alan R.; Kleeman, C.R.; Gold, E.M.; Franklin, Stanley S.; Maxwell, M.H.; Gonick, Harvey C.; Feffer, Myra L.; Steinman, T.I.

doi:10.1159/000179620

Cited by 53 publications

(10 citation statements)

References 17 publications

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“…In a patient with chronic renal insufficiency (severe arterial and arteriolar nephro sclerosis at necropsy), the marked hyperkalemia could be explained by the simultaneously present hypoaldosteronism; the observed Na loss of this patient is at variance with our findings [14]. There is no evi dence suggesting a similar pathogenesis in the occasional hyperka lemia, reported by L ath em [20] and in the more frequently observed elevation of potassium concentration described by Carro l l and F a rb e r [5].…”

Section: Discussionsupporting

confidence: 64%

“…A participation of an extrarenal mechanism, however, is likely since potassium retention may occur with a normal serum K ( fig. 1) and the amount of K loss during DOCA treatment suggests a contribu tion from an intracellular source; G e r st e in et al [14] made similar observations. At the other end of the spectrum, namely excessive aldo sterone production (Conn's syndrome), a consistent finding is nega tive K balance and hypokalemia, which may be improved by the same maneuver of restricting sodium intake [22].…”

Section: Discussionmentioning

confidence: 69%

“…Conceivably, this mechanism may account for other cases of hyperkalemic pyelonephritis ; in this type of kidney disease, with recog nized early tubular involvement [12,18], renal dysfunction may facil itate the rise of serum K in absence o f aldosterone production. In a recent report G e r st e in et al [14] postulated a similar mechanism for the marked hyperkalemia (7.6-9.0 mEq/liter) o f a patient with severe renal insufficiency.…”

Section: Introductionmentioning

confidence: 92%

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Selective Aldosterone Deficiency in Chronic Pyelonephritis

Ah¹

1970

Nephron

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Serum K concentration is usually normal or moderately elevated in chronic renal insufficiency. Severe hyperkalemia, disproportionate to the degree of renal deficiency, has been frequently observed in chronic pyelonephritis; its pathogenesis is still unknown. Marked elevation of serum potassium was observed in a patient with chronic pyelonephritis and simultaneous selective deficiency of aldosterone. The hyperkalemia was corrected by mineralocorticoid replacement therapy. In some cases of chronic pyelonephritis selective aldosterone deficiency may be responsible for the marked hyperkalemia.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 69%

Section: Introductionmentioning

confidence: 92%

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Selective Aldosterone Deficiency in Chronic Pyelonephritis

Ah¹

1970

Nephron

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“…It has been suggested that a compensatory increase in aldosterone secretion [14,18,27] with resultant increased potassium excretion may permit the main tenance of normal plasma potassium levels in chronic renal failure [17,27], although others have reported normal aldosterone excretion rates [37], These…”

mentioning

confidence: 99%

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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“…Gastrointestinal potassium content is proportional to plasma aldosterone and colon potassium secretion adapts to potassium loads. Gerstein et al [9] demonstrated that the colon has secretory processes for potassium, and that this activity is up-regulated in response to potassium loads, aldosterone and during renal insufficiency. In addition, several studies have demonstrated that colonic excretion of potassium increases in chronic renal failure and may play an important role in extrarenal potassium regulation for such patients.…”

Section: Discussionmentioning

confidence: 99%

Effect of fludrocortisone acetate on reducing serum potassium levels in patients with end-stage renal disease undergoing haemodialysis

Kim

Chung

Yoon

et al. 2007

Nephrology Dialysis Transplantation

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Background. Hyperkalaemia is a commonly encountered problem in dialysis patients with end-stage renal disease (ESRD). The aim of the present study was to assess the effect of fludrocortisone acetate (FCA) on reducing serum potassium levels in haemodialysis (HD) patients with hyperkalaemia. Methods. Prospectively, 21 HD patients with hyperkalaemia were enrolled in this study. Patients were divided into two groups, including FCA (0.1 mg/d, n ¼ 13) administration or no treatment (control, n ¼ 8) for 10 months. No changes in dialysis or drug regimens were made during this period.Result. There were no significant differences in the baseline characteristics and biochemical parameters between the two groups (FCA therapy and control). At 10-months after FCA therapy, serum potassium levels were not significantly different between the treatment and control groups [median value (range): 5.2 (4.4-6.0) vs 5.8 (4.8-6.3) mEq/l, P ¼ 0.121]. However, using the Wilcoxon signed ranks test, serum potassium levels were significantly lower at the end of the 10 month time period after FCA therapy compared with serum potassium levels of the pre-treatment period [5.2 (4.4-6.0) vs 6.1 (5.3-6.8), P ¼ 0.01]. The biochemical values, including sodium, chloride, protein, albumin, blood nitrogen, creatinine, interdialytic weight change and blood pressure, did not show significant difference in comparisons between the two groups and pre-and post-FCA therapy period. Conclusions. FCA therapy appears to slightly decrease serum potassium value in hyperkalaemic HD patients. However, these results are insufficient to explain the effectiveness of FCA. Therefore, potentially large-scale studies with increased dose concentrations are needed to minimize the positive potassium balance in hyperkalaemic HD patients.

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Aldosterone Deficiency in Chronic Renal Failure

Cited by 53 publications

References 17 publications

Selective Aldosterone Deficiency in Chronic Pyelonephritis

Selective Aldosterone Deficiency in Chronic Pyelonephritis

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

Effect of fludrocortisone acetate on reducing serum potassium levels in patients with end-stage renal disease undergoing haemodialysis

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