Year : 2010 | Volume
: 21 | Issue : 6 | Page : 1127--1128
Pregnancy predisposes to rhabdomyolysis due to hypokalemia
Jayaraman Muthukrishnan, KVS Harikumar, Ratan Jha, Kirtikumar Modi
Department of Endocrinology, Medwin Hospital, Hyderabad, India
Department of Endocrinology, Medwin Hospital, Hyderabad, 500001
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;21:1127-1128
|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 2021 Oct 18 ];21:1127-1128
Available from: https://www.sjkdt.org/text.asp?2010/21/6/1127/72304
Increased predilection for hypokalemia-induced rhabdomyolysis has been noted in pregnant women.  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.
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.
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.  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.  Local elevation in the potassium concentration during muscle activity causes vasodilatation, which enhances regional blood flow.  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.  In addition to hypoperfusion, hypokalemiainduced impairment in muscle metabolism may also contribute to muscle dysfunction.  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.
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