Hyperkalemia and Hyporeninemic Hypoaldosteronism

DeFronzo, Ralph A.

doi:10.1007/978-1-4612-5465-2_10

Cited by 16 publications

(26 citation statements)

References 81 publications

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“…Mineralocorticoid replacement represents the most logical approach to therapy in these patients. 9 Theoretically, a higher dose of furosemide together with a high salt intake to prevent volume depletion may have corrected the hyperkalemia, although this was not tried in the present patient. Although a sufficient dose of calcium polystyrene sulfonate may have been effective in treating the hyperkalemia, the patient found it difficult to tolerate.…”

Section: Discussionmentioning

confidence: 78%

Lobenzarit disodium-induced hyperkalemia successfully treated with fludrocortisone acetate

Yoshida

Arakawa²,

Ishida³

et al. 2000

Clinical and Experimental Nephrology

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A 65-year-old woman was admitted to our hospital because of hyperkalemia and renal dysfunction. Three months after she had been treated with lobenzarit disodium, a disease-modifying anti-rheumatic drug, her serum potassium and blood urea nitrogen levels rose. Neither calcium polystyrene sulfonate nor furosemide was effective in treating the hyperkalemia. On admission, she did not show metabolic acidosis and her creatinine clearance was 41 ml/ min. Urinalysis results and urinary 2 -microglobulin and N-acetyl--D-glucosaminidase concentrations were normal. Her pituitary and adrenal functions and renin-aldosterone axis were also normal. A renal biopsy specimen demonstrated almost normal glomeruli and almost normal proximal tubules. On the other hand, the distal tubules demonstrated patchy atrophy with an increase in the interstitium and an infiltration of mononuclear cells. Fludrocortisone acetate, a synthetic mineralocorticoid, was effective in treating her hyperkalemia. The impaired responsiveness of the distal nephron to mineralocorticoid may have been the pathophysiological mechanism in this patient.

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Section: Discussionmentioning

confidence: 78%

Lobenzarit disodium-induced hyperkalemia successfully treated with fludrocortisone acetate

Yoshida

Arakawa²,

Ishida³

et al. 2000

Clinical and Experimental Nephrology

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“…In addition, aldosterone stimulates H + secretion in the distal tubule and the collecting duct [4]. Therefore, hypoaldosteronism induces hyperkalemia, and 50% of patients with HH showed hyperchloremic metabolic acidosis [4].…”

Section: Discussionmentioning

confidence: 99%

“…In renal diseases, structural damage of the JGA and volume expansion are thought to be the most likely causes of HH [4,11,14].…”

Section: Discussionmentioning

confidence: 99%

“…While most patients with HH have asymptomatic hyperkalemia, some patients show symptoms associated with hyperkalemia, such as muscle weakness or cardiac arrhythmias [1,4]. Major underlying disorders of HH are chronic renal diseases with mild or moderate renal dysfunction, including diabetic glomerulosclerosis, interstitial nephritis, hypertensive nephropathy, gouty nephropathy, glomerulonephritis, and analgesic nephropathy [4].…”

Section: Introductionmentioning

confidence: 99%

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Transient hyporeninemic hypoaldosteronism in acute glomerulonephritis

Watanabe

Nitta

2002

Pediatric Nephrology

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While hyporeninemic hypoaldosteronism (HH) has been well described in relation to chronic renal diseases, transient HH has rarely been reported. Here we present a 9-year-old boy with acute glomerulonephritis who developed hyperkalemia, which persisted for a period of 3 weeks despite normal values of creatinine clearance and an absence of acidosis. He was diagnosed as having HH because of low basal plasma renin activity and serum aldosterone level. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis. There were no apparent pathological changes in the juxtaglomerular apparatus (JGA). Rapid adrenocorticotropic hormone administration increased adequately both serum aldosterone and cortisol levels. Responses of both plasma renin activity and serum aldosterone level following the furosemide upright provocation were blunted in the hyperkalemic acute phase, but recovered in the normokalemic convalescent phase. Serum levels of human atrial natriuretic peptide were within normal range, both in the hyperkalemic and normokalemic phases. These results suggested that a transient dysfunction of the JGA, without volume expansion or structural damage of the JGA, caused HH in this patient.

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“…Since hyporenemic hypoaldosteronism can result in RTA and impaired potassium excretion [11], the integrity of the renin-aldosterone axis was examined in our patient. The results demonstrated normal values for PRA and plasma aldosterone level, thus excluding hypoaldosteronism as the cause of impaired urinary acidification.…”

Section: Discussionmentioning

confidence: 99%

Hyperkalemic distal renal tubular acidosis associated with Rett syndrome

2006

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Renal function was studied in a 7-year-old girl with Rett syndrome (RS) complicated by persistent hyperchloremic hyperkalemic metabolic acidosis. The acidosis was associated with a urine pH above 5.5, positive urinary anion gap and decreased potassium excretion. Plasma renin activity, aldosterone and cortisol levels were normal. Therapy with sodium bicarbonate failed to lower urine pH below 5.5 or increase potassium excretion. Hydrochlorothiazide administration resulted in a fall in urine pH below 5.5 and an increase in potassium excretion as a result of increased distal sodium delivery and increased sodium reabsorption in the distal nephron. We conclude that a voltage-dependent type of derangement in the distal nephron, rather than aldosterone deficiency, is responsible for the impairment in urinary acidification observed in this patient. Early detection of impaired renal acidification in RS may prevent or slow the progression of growth failure.

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Hyperkalemia and Hyporeninemic Hypoaldosteronism

Cited by 16 publications

References 81 publications

Lobenzarit disodium-induced hyperkalemia successfully treated with fludrocortisone acetate

Lobenzarit disodium-induced hyperkalemia successfully treated with fludrocortisone acetate

Transient hyporeninemic hypoaldosteronism in acute glomerulonephritis

Hyperkalemic distal renal tubular acidosis associated with Rett syndrome

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