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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2010  |  Volume : 21  |  Issue : 6  |  Page : 1127-1128
Pregnancy predisposes to rhabdomyolysis due to hypokalemia


Department of Endocrinology, Medwin Hospital, Hyderabad, India

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Date of Web Publication4-Nov-2010
 

   Abstract 

Increased predilection for hypokalemia-induced rhabdomyolysis has been noted in pregnant women. We managed a woman with distal renal tubular acidosis (RTA) with persistent hypokalemia who presented with recurrent rhabdomyolysis in her consecutive pregnancies despite adequate potassium citrate therapy.

How to cite this article:
Muthukrishnan J, Harikumar K, Jha R, Modi K. Pregnancy predisposes to rhabdomyolysis due to hypokalemia. Saudi J Kidney Dis Transpl 2010;21:1127-8

How to cite this URL:
Muthukrishnan J, Harikumar K, Jha R, Modi K. Pregnancy predisposes to rhabdomyolysis due to hypokalemia. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2019 Nov 12];21:1127-8. Available from: http://www.sjkdt.org/text.asp?2010/21/6/1127/72304

   Introduction Top


Increased predilection for hypokalemia-in­duced rhabdomyolysis has been noted in preg­nant women. [1] There is a single report of four cases in literature with this problem occurring during pregnancy. We managed a female pa­tient with distal renal tubular acidosis (RTA) with persistent hypokalemia who presented with recurrent rhabdomyolysis in her conse­cutive pregnancies.


   Case History Top


A 22-year-old lady presented with sponta­neous abortion in the third month of gestation, preceded by complaints of painful cramps and proximal muscle weakness in both lower limbs of one weeks' duration. She had no history of diuretic intake, fever, rash or arthralgia. There was no histor of renal stones or similar illness in the family. She had had an uneventful preg­nancy five-years back. On evaluation, she had hypokalemia (3.0 mEq/L), markedly raised crea­tine phosphokinase (CPK) levels (10,200 IU/L) and normal anion gap metabolic acidosis (pH 7.1, S. HCO 3 15 mEq/L, PaCO 2 32 mmHg). Urine analysis was negative for urinary tract infection. Urine pH was 7.2 by pH meter. Plas­ma anion gap was 12, which was within nor­mal limits and urine anion gap was positive. Acid load test with ammonium chloride was not performed due to baseline metabolic aci­dosis. She was diagnosed as a case of distal RTA with hypokalemia causing rhabdomyo­lysis. Screening tests (anti-nuclear antibody profile) for underlying connective tissue di­sease as cause of distal RTA were inconclu­sive. She was advised potassium citrate solu­tion in the dose of 2 mEq/kg body weight and serial serum potassium estimation but was lost to follow-up. She presented again after two years with similar complaints of painful cramps and proximal muscle weakness in the ninth week of gestation. She had been regularly com­pliant with intake of potassium citrate solution in the intervening period and a few available follow-up reports of serum potassium were in the low normal range (3.4-3.6 mEq/L). During present hospitalization, she was normotensive, had hypokalemia (2.9 mEq/L), metabolic aci­dosis (arterial blood gas: pH 7.32, pCO 2 28.4 mmHg and HCO 3 14.5 mEq/L), increased plas­ma anion gap (23.2), positive urine anion gap, fasting urine pH 7.5, CPK 11,500 IU/L, blood urea 45 mg/dL and creatinine 0.8 mg/dL. Mid­stream urine was negative for urinary tract infection. Thyroid profile was normal. Distal RTA complicated by recurrent rhabdomyolysis was diagnosed. Widening of anion gap noted du-ring this episode was suspected to be due to superimposed lactic acidosis secondary to rhab­domyolysis. She was managed with intrave­nous saline with potassium followed by oral potassium citrate. She recovered with norma­lization of serum potassium and CPK and had an uneventful pregnancy.


   Discussion Top


Our patient with distal RTA who had been asymptomatic with persistently uncorrected hypokalemia, presented with two episodes of rhabdomyolysis during consecutive pregnan­cies. Pregnancy as a high-risk state for pre­dilection to hypokalemia-induced rhabdomyo­lysis has been noted earlier. [1] Distal RTA ma­nifests with hypokalemia, metabolic acidosis and inappropriately alkaline urine. Hypokalemia may be severe in some cases of distal RTA manifesting with muscle pain, cramps and weakness. Treatment involves life long pota­ssium and alkali supplements in the form of potassium citrate which helps in restoring nor­mal acid-base and potassium status.

Rhabdomyolysis is a rare manifestation of severe hypokalemia associated with distal RTA. Potassium plays a major role in regulating ske­letal muscle blood flow. [2] Local elevation in the potassium concentration during muscle activity causes vasodilatation, which enhances regional blood flow. [2] This cellular release of potassium is impaired in potassium depleted state leading to relative muscle ischemia mani­festing as muscle cramps and in severe hypo­kalemia as muscle necrosis and rhabdomyoly­sis. [2] In addition to hypoperfusion, hypokalemia­induced impairment in muscle metabolism may also contribute to muscle dysfunction. [3] The exact mechanism underlying the increased tendency to develop hypokalemia-induced muscle damage in pregnancy is un-clear at present. This case and similar earlier report underline the need to monitor closely for potassium levels during pregnancy in women with distal RTA and other hypokalemic states and avoid drugs that may worsen hypokalemia.

 
   References Top

1.Carminati G, Chena A, Orlando JM, et al. Distal renal tubular acidosis with rhabdo­myolysis as the presenting form in 4 pregnant women. Nefrologia 2001;21(2):204-8.  Back to cited text no. 1
    
2.Knochel JP, Schlein EM. On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest 1972;51:1750.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Knochel JP. Neuromuscular manifestations of electrolyte disorders. Am J Med 1982;72:521.  Back to cited text no. 3
[PUBMED]    

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Correspondence Address:
Jayaraman Muthukrishnan
Department of Endocrinology, Medwin Hospital, Hyderabad, 500001
India
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PMID: 21060186

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    Abstract
    Introduction
    Case History
    Discussion
    References
 

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