A Practical Approach for Pathophysiological Diagnosis of Refractory Hypokalemia


A Practical Approach for Pathophysiological Diagnosis of Refractory Hypokalemia


Mohamed Foda Hendi, Zeyad Faoor Alrais, Hesham El Kholy

Department of Intensive Care Medicine, Rashid Hospital, Dubai health Authority, Dubai, United Arab Emirates


Global Journal of Urology and Nephrology

Hypokalemia is a common finding in hospitalized patients. In most cases the cause will be obvious. However, in a subgroup of patients the cause is occasionally uncertain and establishing the diagnosis may present difficulties and can become a challenge.
In such cases, measurement of urinary indices e.g. trans-tubular potassium gradient [TTKG] and random urine potassium/creatinine concentrations along with blood acid/base parameters and assessment of urinary excretion of potassium, chloride, calcium and creatinine have been employed in the differential diagnosis.
TTKG and urine potassium/creatinine ratio are used as a rapid appropriate index of potassium excretion and to establish a proper diagnosis and management in this medical emergency. It helps to differentiate between hypokalemia caused by redistribution or renal potassium wasting.
Urinary chloride excretion and urinary calcium/creatinine ratio in conjunction with plasma acid/base values, aldosterone, renin and cortisol values are used for narrowing the differential diagnosis of refractory hypokalemia.
Conclusions: Calculating the trans-tubular potassium concentration gradient, urinary potassium/creatinine ratio, urinary chloride excretion and urinary calcium/creatinine ratio in conjunction with plasma acid/base values provided simple and reliable tests for differential diagnosis of causes of refractory hypokalemia and to provide a proper management in the intensive care unit and in the emergency until advanced further tests to be done.


Keywords: Refractory Hypokalaemia, Trans-tubular Potassium Concentration Gradient, Urinary Potassium-creatinine Ratio, Urinary Calcium-Creatinine Ratio, Bartter Syndrome, Gitelman Syndrome.

Free Full-text PDF


How to cite this article:
Mohamed Foda Hendi, Zeyad Faoor Alrais, Hesham El Kholy.A Practical Approach for Pathophysiological Diagnosis of Refractory Hypokalemia. Global Journal of Urology and Nephrology, 2018, 1:6. DOI:10.28933/gjun-2018-10-1508


References:
1. Joo KW, Chang SH, Lee JG, Na KY, Kim YS, et al. (2000) Transtubular potassium concentration gradient (TTKG) and urine ammonium in differential diagnosis of hypokalemia. J Nephrol 13: 120-125.
2. Reimann D, Gross P (1999) Chronic, diagnosis-resistant hypokalaemia. Nephrol Dial Transplant 14: 2957–2961.
3. Assadi F (2008) Diagnosis of hypokalemia: A problem-solving approach to clinical cases. Iran J Kidney Dis 2: 115-122.
4. Lin C, Piao X, Pan Q, Li J, Shan Z, et al. (2017) Spot urine potassium creatinine ratio is a good alternative marker for 24 hours urine potassium in differential diagnosis of hypokalemia. Med Sci Tech 58:137-144.
5. Lin S, Lin Y, Chen DT, Chu P, Hsu CW, et al. (2004) Laboratory tests to determine the cause of hypokalemia and paralysis. Arch Intern Med 164: 1561-1566.
6. Viera AJ, Wouk N (2015) Potassium disorders: Hypokalemia and hyperkalemia. Am Fam Physician 92: 487-495.
7. Choi MJ, Ziyadeh FN (2008) The utility of the transtubular potassium gradient in the evaluation of hyperkalemia. J Am Soc Nephrol 19:424-426.
8. Lin SH (2008) A practical and pathophysiologic approach to hypokalemia. Hong Kong J Nephrol 10: 14-26.
9. Ethier JH, Kamel KS, Magner PO, Lemann J, Halperin ML (1990) The transtubular potassium concentration in patients with hypokalemia and hyperkalemia. Am J Kidney Dis 15: 309-315.
10. Halperin ML (2017) Assessing the renal response in patients with potassium disorders: A shift in emphasis from the TTKG to the urine K+/creatinine ratio. Afr J Nephrol 20: 22-24.
11. Kamel KS, Halperin ML (2011) Intrarenal urea recycling leads to a higher rate of renal excretion of potassium: Hypothesis with clinical implications. Curr Opin Nephrol Hypertens 20: 547-554.
12. Colussi G (2002) Bartter syndrome type 3: An unusual cause of nephrolithiasis. Nephrol Dial Transplant 17: 521-523.
13. Lim S (2007) Approach to hypokalemia acta med indones-indones. J Intern Med 39: 56-64.
14. Palmer B, Clegg DJ (2016) Physiology and pathophysiology of potassium homeostasis. Adv Physiol Educ 40: 480-490.
15. Konrad M, Weber S (2003) Recent advances in molecular genetics of hereditary magnesium-losing disorders. J Am Soc Nephrol 14: 249-260.
16. Colussi G (2005) Bartter syndrome. Orphanet encyclopedia.
17. Soriano RJ (1998) Bartter and related syndromes: The puzzle is almost solved. Pediatr Nephrol 12: 315-327.
18. Fremont OT, Chan JCM (2012) Understanding Bartter syndrome and Gitelman syndrome. World J Pediatr 8: 25-30.
19. Vantyghem MC, Douillard C, Binaut R (1999) Bartter’s syndromes. Ann Endocrinol 60: 465-472.
20. Zelikovic I, Szargel R, Hawash A, Labay V, Hatib I, et al. (2003) A novel mutation in the chloride channel gene, CLCNKB, as a cause of Gitelman and Bartter syndromes. Intern Soc Nephrol 63: 24-32.
21. Blanchard A, Bockenhauer D, Bolignano D, Calo LA, Cosyns E, et al. (2017) Gitelman syndrome: Consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) controversies conference. Kidney Int 91: 24-33.
22. Foley KF, Boccuzzi L (2010) Urine calcium: Laboratory measurement and clinical utility. Lab Medicine 41: 683-686.
23. Cruz AJ, Castro A (2013) Gitelman or Bartter type 3 syndrome?: A case of distal convoluted tubulopathy caused by CLCNKB gene mutation. BMJ Case Rep 1: 1-4.