Renal Potassium-Wasting Induced by Vitamin D*†

Ferris, Thomas F.; Levitin, Howard; Phillips, Emmanuel T.; Epstein, Franklin H.

doi:10.1172/jci104583

Cited by 28 publications

(7 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some of the subjects represented by 0 were mildly alkalotic and were excreting significant amounts of urinary bicarbonate (27) ; the subj ects represented by + were moderately alkalotic and were excreting more than 50 mEq of urinary bicarbonate daily (22) ; the subjects represented by X were given large amounts of desoxycorticosterone after hypokalemia supervened (27 (14,36,37). Such an impairment could differ from that in the presently reported patients only in degree.…”

Section: Methodsmentioning

confidence: 70%

“…For a given degree of impaira mild impairment in renal conservation of potassium ment in renal conservation of potassium, potassium balmay not cause hypokalemia unless potassium intake is ance can occur at either normal or subnormal serum poreduced to low-normal or slightly subnormal levels (14, tassium concentrations depending on the potassium intake 36, 37). With a more severe impairment in renal con- (36,37).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Renal potassium wasting in renal tubular acidosis (RTA)

Sebastián¹,

McSherry²,

Morris³

1971

J. Clin. Invest.

127

View full text Add to dashboard Cite

A B S T R A C T In two patients with classic renal tubular acidosis (RTA) and in two patients with RTA associated with the Fanconi syndrome, renal potassium wasting persisted despite sustained correction of acidosis:(a) during moderate degrees of hypokalemia, daily urinary excretion of potassium exceeded 80 mEq in each patient; (b) during more severe degrees of hypokalemia, daily urinary excretion of potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of potassium are more than twice those observed in potassium-depleted normal subjects with even minimal degrees of hypokalemia. The persistence of renal potassium wasting may have resulted in part from hyperaldosteronism, since urinary aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their potassium depletion. The hyperaldosteronism persisted despite sustained correction of acidosis, a normal sodium intake, and no reduction in measured plasma volume, and was not associated with hypertension; its cause was not defined. In the two patients with classic RTA, neither renal potassium wasting nor hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H' -Na' exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during acidosis. The findings provide no support for the traditional view that renal potassium wasting in either classic RTA or RTA

show abstract

Section: Methodsmentioning

confidence: 70%

Section: Methodsmentioning

confidence: 99%

Renal potassium wasting in renal tubular acidosis (RTA)

Sebastián¹,

McSherry²,

Morris³

1971

J. Clin. Invest.

127

View full text Add to dashboard Cite

show abstract

“…The observed proportionality between GFR and the tubular capacity to excrete acid in these patients with pyelonephritis, renal infarction, and atrophy does not indicate that specific tubular defects may not occur in other forms of renal disease, as in renal tubular acidosis (20), hypercalcemic nephropathy (5,(21)(22)(23), or the kidney in gout (24).…”

Section: Resultsmentioning

confidence: 88%

The Excretion of Acid in Unilateral Renal Disease in Man*

Steinmetz¹,

Eisinger²,

Lowenstein³

1965

J. Clin. Invest.

View full text Add to dashboard Cite

“…[2], Based upon studies performed in rats [3], this defect has been ascribed mainly to impaired am monia excretion. While Heinemann [4] showed that hypercalcemia, irre spective of its origin, limits the renal excretion of hydrogen by reducing am monia output, he was unable to uncover the pathogenesis behind this defect.…”

Section: Introductionmentioning

confidence: 99%

The Effects of High Calcium Concentrations on Renal Ammoniagenesis by Rat Kidney Slices

Vavatsi-Manos¹,

Hg²

1976

Nephron

View full text Add to dashboard Cite

Deficiences in acid excretion during hypercalcemia have been reported, and this defect has been ascribed to a deficiency in ammonia excretion. Because no changes in urine pH and urine flow occurred to explain decreased ammonia excretion, this suggested to us that decreased excretion was secondary to decreased renal ammonia production. To test this hypothesis, we investigated the ability of kidney slices from rats to produce ammonia and glucose and to consume oxygen when incubated in varying concentrations of calcium. High medium concentrations of calcium (3 and 4 mM) decreased kidney slice ammoniagenesis from glutamine and glutamate and kidney slice oxygen consumption while not affecting gluconeogenesis. Based upon our findings, we propose that hypercalcemia decreases urine ammonia excretion by depressing renal ammonia production.

show abstract

Renal Potassium-Wasting Induced by Vitamin D*†

Cited by 28 publications

References 21 publications

Renal potassium wasting in renal tubular acidosis (RTA)

Renal potassium wasting in renal tubular acidosis (RTA)

The Excretion of Acid in Unilateral Renal Disease in Man*

The Effects of High Calcium Concentrations on Renal Ammoniagenesis by Rat Kidney Slices

Contact Info

Product

Resources

About