Renal tubular disease with muscle paralysis and hypokalemia

Owen, Edward E.; Verner, John V.

doi:10.1016/0002-9343(60)90218-7

Cited by 40 publications

(10 citation statements)

References 38 publications

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“…Deficiencies in acid excretion in human patients attributable to hypercalcemia have been reported by Wrong and Davis (26) and by Fourman, McConkey and Smith (27). In addition, the syndrome of potassium-wasting coupled with renal tubular acidosis has been documented in patients after hyperthyroidism (2,28), sarcoidosis (29), hyperparathyroidism (30), and vitamin D intoxication (3). The present data support the hypothesis that under some circumstances the ability of the kidneys to conserve potassium and excrete acid may be substantially and selectively impaired by nephrocalcinosis acquired as a result of hypercalcemia and hypercalciuria.…”

Section: Discussionmentioning

confidence: 94%

Renal Potassium-Wasting Induced by Vitamin D*†

Ferris¹,

Levitin²,

Phillips³

et al. 1962

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 94%

Renal Potassium-Wasting Induced by Vitamin D*†

Ferris¹,

Levitin²,

Phillips³

et al. 1962

J. Clin. Invest.

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“…Chronic Potassium Deficiency Transient hypokalemic paralysis occasionally occurs in patients with chronic potassium deficiency, especially when associated with primary aldosteronism [11] or renal tubular acidosis [25]. The plasma potassium level tends to be low between attacks of paralysis and to fall to lower values during paralysis, which can be reversed by administration of potassium.…”

Section: Em Resting Membrane Potentialmentioning

confidence: 99%

Periodic paralysis and the sodium‐potassium pump

Layzer

1982

Annals of Neurology

116

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Analysis of the pathophysiology of hypokalemic paralysis, as it occurs in barium poisoning, chronic potassium deficiency, and thyrotoxicosis, suggests that these disorders may have a similar mechanism. An increased ratio of muscle sodium permeability to potassium permeability reduces the ionic diffusion potential, while the resting membrane potential is sustained by an increase of Na-K pump electrogenesis. The result is that potassium entry (the sum of active and passive influx) exceeds potassium efflux; this causes a large shift of extracellular potassium into muscle until the Na-K pump turns off, leading to depolarization and paralysis. The primary defect in familial hypokalemic periodic paralysis, as in the example of barium poisoning, may be a marked reduction of muscle permeability to potassium.

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“…The hypokalacmia should be corrected cautiously and sodium bicarbonate should also be administered to prevent a precipitous fall in serum bicarbonate on restoration of the body potassium [80,105]. Spironolac tone may help in the treatment of secondary hyperaldosteronism [42,47], The oedema which can develop in the period imme diately after stopping laxatives [38, 44, 5 1 ] is thought to be due to a large but transient sodium retention [106], due to the impaired ability of the kidney to excrete a sodium load in potassium deficiency [107] and can be helped by salt restriction.…”

Section: Managementmentioning

confidence: 99%