Fractional excretion of potassium in normal subjects and in patients with hypokalaemia

Elisaf, Moses; Siamopoulos, K. C.

doi:10.1136/pgmj.71.834.211

Cited by 90 publications

(82 citation statements)

References 5 publications

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“…In several cases, multiple plasma magnesium values were available; in these cases, to avoid bias, we quote the median value together with time-matched plasma calcium, phosphate, albumin, and, when available, PTH levels. Renal magnesium and calcium excretion were assessed in patients with hypomagnesemia, and hypermagnesuria was defined as a fractional magnesium excretion Ͼ4% 45,46 and hypocalciuria as a fractional calcium excretion Ͻ1%. 47 Statistical significance between parameters with discrete values was determined using Fisher exact test and Mann-Whitney U test.…”

Section: Cohort Detailsmentioning

confidence: 99%

HNF1B Mutations Associate with Hypomagnesemia and Renal Magnesium Wasting

Adalat

Woolf

Johnstone

et al. 2009

Journal of the American Society of Nephrology

240

238

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Mutations in hepatocyte nuclear factor 1B (HNF1B), which is a transcription factor expressed in tissues including renal epithelia, associate with abnormal renal development. While studying renal phenotypes of children with HNF1B mutations, we identified a teenager who presented with tetany and hypomagnesemia. We retrospectively reviewed radiographic and laboratory data for all patients from a single center who had been screened for an HNF1B mutation. We found heterozygous mutations in 21 (23%) of 91 cases of renal malformation. All mutation carriers had abnormal fetal renal ultrasonography. Plasma magnesium levels were available for 66 patients with chronic kidney disease (stages 1 to 3). Striking, 44% (eight of 18) of mutation carriers had hypomagnesemia (Ͻ1.58 mg/dl) compared with 2% (one of 48) of those without mutations (P Ͻ 0.0001). The median plasma magnesium was significantly lower among mutation carriers than those without mutations (1.68 versus 2.02 mg/dl; P Ͻ 0.0001). Because hypermagnesuria and hypocalciuria accompanied the hypomagnesemia, we analyzed genes associated with hypermagnesuria and detected highly conserved HNF1 recognition sites in FXYD2, a gene that can cause autosomal dominant hypomagnesemia and hypocalciuria when mutated. Using a luciferase reporter assay, we demonstrated HNF1B-mediated transactivation of FXYD2. These results extend the phenotype of HNF1B mutations to include hypomagnesemia. HNF1B regulates transcription of FXYD2, which participates in the tubular handling of Mg 2ϩ , thus describing a role for HNF1B not only in nephrogenesis but also in the maintenance of tubular function.

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Section: Cohort Detailsmentioning

confidence: 99%

HNF1B Mutations Associate with Hypomagnesemia and Renal Magnesium Wasting

Adalat

Woolf

Johnstone

et al. 2009

Journal of the American Society of Nephrology

240

238

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“…The urinary electrolyte values revealed sodium excretion was 402 mEq/L, chloride was 281 mEq/L and potassium was 41.8 mEq/L per 24 h. The urinary Ca/creatinine ratio was low at 0.04 mg/mg (N ≥ 0.2) [8]. The fraction excretion of potassium (FE K ) was 29.4% (N = 4-16%, mean value 8%) [9] and high transtubular potassium gradient (TTKG) suggested that renal potassium wasting was responsible for the hypokalemia [10]. This findings indicated that the patient might have had renal tubulopathy and prompted us to examine distal tubular function.…”

Section: Sinaga Et Almentioning

confidence: 97%

Gitelman Syndrome: An Important Cause of Severe Hypokalemia and Periodic Paralysis

Sinaga¹,

Naibaho²,

Sibuea³

2016

World J Nephrol Urol

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Gitelman syndrome is a relatively rare renal tubular disorder. Though it has been reported as a recessively inherited disorder, sporadic cases have also been reported. Traditionally, Gitelman syndrome is considered as benign or mild tubulopathy. We present the case of an 18-year-old male patient with severe hypokalemia and periodic paralysis. Subsequent laboratory investigation revealed renal wasting hypokalemia, metabolic alkalosis, secondary hyperaldosteronism, hypomagnesemia and hypocalciuria, indicating that the patient might have had a renal tubular disorder. The confirmation of Gitelman syndrome was determined by evaluating tubular function using thiazide and furosemide challenge test. Genetic study was bypassed due to our technical unavaibility. Treament included magnesium aspartate/potassium aspartate, potassium chloride tablets and potassium-sparing diuretic. We are presenting our case seeing that Gitelman syndrome is not a syndrome to be overlooked as it bears a risk of severe complications. Gitelman syndrome may present in adulthood and should be borne in mind in the diagnosis of hypokalemia.

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“…Dette betyr at s-magnesium ikke er en optimal prøve i vurdering av magnesiummangel. Magnesium i spoturin og estimering av fraksjonert magnesiumekskresjon i urin kan gi informasjon om årsak, mens døgnutskil-lelse av magnesium i urin, som er praktisk vanskelig å gjennomføre i sykehjem og heller ikke ble gjennomført i sykehus i vårt tilfelle, sannsynligvis er en bedre parameter for evaluering av hypomagnesemi (14,15).…”

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