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Mineralocorticoid-Resistant Renal Hyperkalemia Without Salt Wasting

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Mineralocorticoid-Resistant Renal Hyperkalemia Without Salt Wasting View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 19 (1981), pp. 716—727 Mineralocorticoid-resistant renal hyperkalemia without sal wasting (type II pseudohypoaldosteronism): Role of increased renal chloride reabsorption MORRIS SCHAMBELAN, ANTHONY SEBASTIAN, and FLOYD C. RECTOR, JR. Medical Service and Clinical Study Center, San Francisco General Hospital Medical Center, and the Department of Medicine, Cardiovascular Research Institute, and the General Clinical Research Center, University of California, San Francisco, California Mineralocorticoid-resistant renal hyperkalemia without salt Hyperkaliemie rénale resistant aux minéralocorticoides sans wasting (type II pseudohypoaldosteronism): Role of increased perte de sel (pseudohypoaldostéronisme de type II): Role de l'aug- renal chloride reabsorption. A rare syndrome has been described mentation iie Ia reabsorption de chlore. Un syndrome rare a été in which mineralocorticoid-resistant hyperkalemia of renal origin décrit dans lequel une hyperkaliemie d'origine rénale resistant occurs in the absence of glomerular insufficiency and renal aux minéralocorticoides survient en l'absence de diminution du sodium wasting and in which hyperchioremic acidosis, hyperten- debit de filtration glomerulaire et de perte rénale de sodium et sion, and hyporeninemia coexist. The primary abnormality has dans lequel une acidose hyperchioremique, une hypertension et been postulated to be a defect of the potassium secretory une hyporéninémie coexistent. L'anomalie primaire qui a été mechanism of the distal nephron. The present studies were postulée est un deficit du mécanisme de secretion de potassium carried out to investigate the mechanism of impaired renal du nephron distal. Ce travail a etC entrepris pour étudier le potassium secretion in a patient with this syndrome. When mécanisme de Ia modification de Ia secretion rénale de potassium dietary intake of sodium chloride was normal, renal clearance of chez un malade atteint de ce syndrome. Quand l'apport alimen- potassium was subnormal (CK/GFR =3.6 0.2%;normal taire de chlorure de sodium était normal, Ia clearance rCnale du subjects, 9.0 0.9%,N =4)despite high normal or supernor- potassium était inférieure ala normale (CK/GFR =3,6 0,2%; mal levels of plasma and urinary aldosterone. The fractional sujets normaux 9,0 0,9%,N =4)malgré des niveaux a Ia clearance of potassium remained subnormal (CK/GFR =5.1 limite supérieure ou franchement élevCs d'aldostérone plasmati- 0.2%)during superimposed chronic administration of superphys- que et urinaire. La clearance fractionnelle du potassium était iologic doses of mineralocorticoid hormone. Little increase in inférieur a Ia normale (CK/GFR =5,1 0,2%)au cours de renal potassium clearance occurred when the delivery of sodium l'administration de doses supra-physiologiques de minCralocorti- to distal nephron segments was increased further by the iv. coIdes. Une augmentation faible de Ia clearance du potassium a infusion of sodium chloride, despite experimentally sustained etC observée quand le debit de sodium aux segments distaux du hypermineralocorticoidism. But potassium clearance increased néphron a été encore augmenté, par l'administration intravein- greatly when delivery of sodium to the distal nephron was euse de chiorure de sodium, malgré l'hyerminéralocorticisme increased by infusion of nonchloride anions: sulfate (sodium experimentalement maintenu. La clearance du potassium, ce- sulfate infusion, low sodium chloride diet; CK/GFR =63.7 pendant, a considérablement augmenté quand le debit de sodium 0.4%)or bicarbonate (sodium bicarbonate plus acetazolamide au nCphron distal a Cte augmente par Ia perfusion d'anions infusion; CK/GFR =81.7 1.7%).These findings indicate that différents du chlore: sulfate (perfusion de sulfate de sodium, mineralocorticoid-resistant renal hyperkalemia in this patient régime pauvre en chlorure de sodium: CK/GFR =63,7+ 0,4%) cannot be attributed to the absence of a renal potassium secre- ou en bicarbonate (perfusion de bicarbonate de sodium et tory capability or to diminished delivery of sodium to distal perfusion d'acetazolamide: CK/GFR =83,7 1,7%).Ces nephron segments; instead it may be dependent on chloride constatations indiquent que l'hyperkaliémie rénale resistant aux delivery to the distal nephron. We suggest that the primary minéralocorticoldes chez ce malade ne peut être attribuée a abnormality in this syndrome increases the reabsorptive avidity l'absence de capacitC secréter le potassium ou a une diminution of the distal nephron for chloride, which (1) limits the sodium and du debit de sodium aux segments distaux. Par contre elle peut mineralocorticoid-dependent voltage driving force for potassium dépendre du debit de chiore au nephron distal. Nous suggerons and hydrogen ion secretion, resulting in hyperkalemia and acido- que l'anomalie initiale dans ce syndrome est une augmentation sis and (2) augments distal sodium chloride reabsorption result- de Ia capacité reabsorption du chlore par le nCphron distal qui (1) ing in hyperchloremia, volume expansion, hyporeninemia, and limite la force électro-motnce, dépendant du sodium et des hypertension. minéralocorticoldes, de secretion des ions hydrogene et potassi- um, ce qui a pour rCsultat l'hyperkaliemie et l'acidose et (2) augmente Ia reabsorption distale de chiorure de sodium ce qui a pour résultat l'hypercholorCmie, l'expansion volémique, l'hy- poréninemie et l'hypertension. Received for publication June 16, 1980 and in revised form September 17, 1980 Chronic hyperkalemia almost always reflects di- 0085-2538/81/0019-0716 $02.40 minished renal clearance of potassium such as that © 1981 by the International Society of Nephrology occurring in patients with advanced renal failure. 716 Type II pseudohypoaldosteronism 717 Chronic renal hyperkalemia can also occur in pa- mg/24 hr) were within normal limits. Plasma concentrations of cortisol (19.0 j.gIdl), testosterone (1314 ngldl), and adrenocorti- tients in whom the GFR is within the normal range cotropin (59 pg/mI) were also within normal limits. Urinary or only moderately reduced. In some of these excretion of aldosterone-•l8-glucuronide was 14.4 p.g/24 hr (nor- mal, 5 to 18). Plasma renin activity was undetectable (less than patients (Addison's disease, isolated hypoaldoste- 0.1 ng/ml/hr). At the completion of these studies, the patient was ronism), renal hyperkalemia can be attributed to a referred to the Clinical Study Center for further evaluation. deficiency of aldosterone [1—4], the major known The family medical history revealed that his mother had hypertension and bronchial asthma. His sister was hypertensive hormonal regulator of renal potassium transport 115, during pregnancy but is otherwise normotensive. Neither his 6].In these patients renal clearance of potassium is mother nor his sister has been noted to be hyperkalemic. His normalized by administration of exogenous mm- father has no known medical problems but was unavailable for eralocorticoid hormone in physiologic replacement examination. The patient smokes I pack of cigarettes per day and drinks an occasional beer. He admitted to a period of i.v. doses. In other patients with renal hyperkalemia, drug abuse in 1973 that included heroin and amphetamines. aldosterone deficiency is not present, and hyperka- The patient was well developed and slightly obese. Blood lemia persists despite administration of even super- pressure was 160/106mm Hg supine and 170/116 mm Hg upright. Mild arteriolar narrowing was noted on funduscopic examina- physiologic doses of mineralocorticoids. Such mm- tion, but the remainder of the physical examination revealed no eralocorticoid-resistant renal hyperkalemia occurs abnormalities. in two distinctly different clinical syndromes: (1) Hemoglobin was 13.8 g/dl, hematocrit 41.4%, white blood cell count 5,600/il with a normal differential, and platelet count of classic pseudohypoaldosteronism, characterized by 352,000/uI. Urine specific gravity was 1.027; urine protein, renal salt wasting and hypotension 117—91and(2) a glucose, and acetone were negative; the urinary sediment con- syndrome of chronic mineralocorticoid-resistant tained 1 to 2 white blood cells per high power field. Serum sodium concentration was 140, potassium 5.8, chloride 112 hyperkalemia unaccompanied by renal salt wasting mEq/liter; and total carbon dioxide, 22 mmoles/liter; blood urea or hypotension [10—181. We have designated these nitrogen was 16; and creatinine, 1.2 mg/dl. Serum concentrations syndromes as types I and II pseudohypoaldosteron- of calcium, phosphorus, uric acid, bilirubin, cholesterol, fasting glucose, glutamic-oxaloacetic transaminase, lactic dehydrogen- ism, respectively. The primary abnormality in type ase, creatine phosphokinase, and alkaline phosphatase were I pseudohypoaldosteronism has been postulated to within normal limits. A roentgenogram of the chest and electro- be a specific defect in the renal response to mm- cardiogram showed no abnormalities. On this and six subsequent admissions, the patient's disorder eralocorticoid hormone, which accounts for the was evaluated extensively. Hyperkalemia (serum potassium, 6.0 coexistence of salt wasting and potassium reten- 0.1mEq/liter, N =5)persisted over a period of years and was tion. The primary abnormality in type II pseudohy- partially ameliorated during treatment with hydrochlorothiazide, 50 mg daily (5.0 0.1mEq/liter, N =12,P <0.001)or poaldosteronism
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