Literature DB >> 19377223

Diagnosis of hypokalemia: a problem-solving approach to clinical cases.

Farahnak Assadi1.   

Abstract

In situations where the cause of hypokalemia is not obvious, measurement of urinary potassium excretion and blood pressure and assessment of acid-base balance are often helpful. A random urine potassium-creatinine ratio (K/C) less than 1.5 suggests poor intake, gastrointestinal losses, or a shift of potassium into cells. If hypokalemia is associated with paralysis, we should consider hyperthyroidism, familial or sporadic periodic paralysis. Metabolic acidosis with a urine K/C ratio less than 1.5 suggests lower gastrointestinal losses due to diarrhea or laxative abuse. Metabolic acidosis with K/C ratio of 1.5 higher is often due to diabetic ketoacidosis or type 1 or type 2 distal renal tubular acidosis. Metabolic alkalosis with a K/C ratio less than 1.5 and a normal blood pressure is often due to surreptitious vomiting. Metabolic alkalosis with a higher K/C ratio and a normal blood pressure suggests diuretic use, Bartter syndrome, or Gitelman syndrome. Metabolic alkalosis with a high urine K/C ratio and hypertension suggests primary hyperaldosteronism, Cushing syndrome, congenital adrenal hyperplasia, renal artery stenosis, apparent mineralocorticoid excess, or Liddle syndrome. Hypomagnesemia can lead to increased urinary potassium losses and hypokalemia. The differential rests upon measurement of blood magnesium, aldosterone and renin levels, diuretic screen in urine, response to spironolactone and amiloride, measurement of plasma cortisol level and the urinary cortisol-cortisone ratio, and genetic testing.

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Year:  2008        PMID: 19377223

Source DB:  PubMed          Journal:  Iran J Kidney Dis        ISSN: 1735-8582            Impact factor:   0.892


  12 in total

1.  Primary aldosteronism due to adrenocortical adenoma with concurrent ileum carcinoid tumor: case report.

Authors:  L Zinnamosca; L Petramala; D Cotesta; C Marinelli; S Sciomer; G Cavallaro; A Ciardi; R Massa; G De Toma; S Filetti; C Letizia
Journal:  Endocrine       Date:  2010-12       Impact factor: 3.633

2.  Severe hypokalaemia as a cause of acute transient quadriparesis.

Authors:  Martin Bell Lybecker; Henrik Bjørnsgaard Madsen; Jens Meldgaard Bruun
Journal:  BMJ Case Rep       Date:  2017-07-27

3.  Potassium Homeostasis, Oxidative Stress, and Human Disease.

Authors:  Udensi K Udensi; Paul B Tchounwou
Journal:  Int J Clin Exp Physiol       Date:  2017

4.  Gitelman or Bartter type 3 syndrome? A case of distal convoluted tubulopathy caused by CLCNKB gene mutation.

Authors:  António José Cruz; Alexandra Castro
Journal:  BMJ Case Rep       Date:  2013-01-22

5.  Type 3 renal tubular acidosis.

Authors:  R P Goswami; S Mondal; P S Karmakar; A Ghosh
Journal:  Indian J Nephrol       Date:  2012-11

6.  Uncommon dyselectrolytemia complicating Guillain-Barré syndrome.

Authors:  Aralikatte Onkarappa Saroja; Karkal Ravishankar Naik; Mallikarjun S Khanpet
Journal:  J Neurosci Rural Pract       Date:  2013-07

7.  Neuroblastoma accompanied by hyperaldosteronism.

Authors:  Kaan Gulleroglu; Umut Bayrakci; Sibel Tulgar Kinik; Nihal Uslu; Alev Ok Atilgan; Faik Sarialioglu; Esra Baskin
Journal:  J Renal Inj Prev       Date:  2014-07-01

8.  Rhabdomyolysis following severe hypokalemia caused by familial hypokalemic periodic paralysis.

Authors:  Young-Lee Jung; Jae-Young Kang
Journal:  World J Clin Cases       Date:  2017-02-16       Impact factor: 1.337

9.  Hypokalaemia: common things occur commonly - a retrospective survey.

Authors:  Alasdair Reid; Gareth Jones; Chris Isles
Journal:  JRSM Short Rep       Date:  2012-11-30

10.  Complete Hypokalemic Quadriparesis as a First Presentation of Sjögren Syndrome.

Authors:  Jason An; Branko Braam
Journal:  Can J Kidney Health Dis       Date:  2018-05-10
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