| Abstract|| |
Rhabdomyolysis is not an uncommon cause of acute renal failure (ARF). It is usually caused by severe traumatic crush injury, severe exercise, septicemia, drug abuse, alcoholic intoxication, heat stroke and myopathy. In this case, we present a patient who developed rhabdomyolysis after severe hypokalemia (serum potassium 1.9mmol/L). This is an unusual cause of rhabdomyolysis even though hypokalemia is a common medical problem. This patient developed acute oliguric renal failure that required daily hemodialysis for 12 days, before start of recovery. This case demonstrates that hypokalemia is a preventable cause of rhabdomyolysis and ARF.
|How to cite this article:|
Ghacha R, Sinha AK. Acute Renal Failure due to Rhabdomyolysis Caused by Hypokalemia. Saudi J Kidney Dis Transpl 2001;12:187-90
|How to cite this URL:|
Ghacha R, Sinha AK. Acute Renal Failure due to Rhabdomyolysis Caused by Hypokalemia. Saudi J Kidney Dis Transpl [serial online] 2001 [cited 2020 Jul 15];12:187-90. Available from: http://www.sjkdt.org/text.asp?2001/12/2/187/33811
| Introduction|| |
Rhabdomyolysis is a well-recognized etiology of acute oliguric renal failure. It is generally caused by trauma or direct compression , but can also be a result of non-traumatic causes  such as seizures, heat stroke and extreme exercise, drugs, toxins, infection, endocrinopathies and stings of insects. Hypokalemia is a very common medical problem, but it is rarely a cause of rhabdomyolysis.
The presentation of rhabdomyolysis includes myalgia with elevated serum muscle enzymes as well as pigmenturia due to myoglobinuria.  Myoglobin is a monomer and is not protein bound, so it is more rapidly filtered and excreted than creatine phosphokinase (CPK). It is, therefore at times, not unusual to find raised serum CPK levels in the absence of myoglobinuria. 
Acute renal failure (ARF) is a known complication of rhabdomyolysis. It is caused by a number of different reasons such as volume depletion, tubular obstruction and injury due to pigment casts, and free iron. , The degree of serum muscle enzyme elevation does not predict the development of acute renal failure in rhabdomyolysis. In one study, for example, 58% of patients who developed acute renal failure had peak CPK levels greater than 266 U/L compared to only 11% in those who did not develop acute renal failure. 
There are various cellular elements released in rhabdomyolysis which results in hyperphosphatemia, and hyperuricemia. , Hypocalcemia results from the deposition of calcium in the necrotic muscles. The fractional excretion of sodium is often less than 1%, a finding that may reflect tubular obstruction rather than tubular necrosis.  The plasma creatinine concentration rises more rapidly because of release of the preformed creatinine from muscle injury. 
The ARF usually recovers within 2-3 weeks. Treatment is most effective if begun early and the two major aspects that may minimize the severity of acute renal failure are hydration and alkaline-mannitol diuresis.  Dialysis is necessary once ARF is severe and may be required daily.
We report a patient who developed severe hypokalemia that was associated with rhabdomyolysis and acute oliguric renal failure.
| Case report|| |
A twenty-five years old man was admitted to our hospital with a complaint of profuse watery diarrhea and severe vomiting of about 4-5 hours duration. There was no associated abdominal pain. There was no history of trauma, seizures, heat exposure, severe exercise, drug intake, insect stings or infection. There was no history of any renal disease.
On physical examination the patient was drowsy, afebrile, with sunken eyes, feeble pulse and hypotension (lying BP 80/50 mm Hg). The abdominal examination was unremarkable.
The laboratory investigations on admission showed total leucocyte count 12000 cells/µL, Hemoglobin 120 g/L, Hematocrit 36%, blood urea nitrogen 16 mmol/L, serum creatinine 88 µmol/L, potassium 3.5 mmol/L, sodium 139 mmol/L. Liver function tests and urinalysis were within normal limits. The stool culture revealed Vibrio cholerae.
The patient continued to have loose watery motions. A central venous pressure line was inserted to monitor fluid and hydration status. Intravenous fluid was administered to keep the patient euvolumic and hemodynamically stable. Blood pressure was normalized. However, the serum potassium fell gradually to 1.9 mmol/L and urine output diminished with a rise in blood urea nitrogen to 60mmol/L, serum creatinine 848 µmol/L, phosphate 3.8 mmol/L, uric acid 773 mmol/L, serum CPK 4265U/L, serum glutamic oxaloacetic transaminase (SGOT) 972 U/L and serum lactic dehydroginase (LDH) 2100 U/L. The serum calcium fell to 1.75 mmol/L. Arterial blood gases showed pH 7.24, PCO2 26, HCO 3 11.8 mmol/L and anion gap was 48 mmol/L. Urine was dark in color with positive blood on the dipstick test, and urinalysis showed only 2-3 red blood cells/high power field.
Accordingly, the patient was diagnosed to have rhabdomyolysis secondary to hypokalemia with acute oliguric renal failure. The patient was started on KCL infusion, doxycycline along with sodium bicarbonate infusion. However, his renal function continued to deteriorate and hemodialysis was started and continued daily for 12 days in order to control his hypercatabolic state. He received 1530 mmols of potassium infusion from day two to day seven, [Figure - 1].
Eventually, the renal functions started to improve gradually along with SGOT, LDH, and CPK and with normalization of serum potassium concentration. The patient did not develop muscle weakness at any stage of illness. He was discharged three weeks following his admission in a stable general condition and normal renal function.
| Discussion|| |
Acute renal failure secondary to rhabdomyolysis is well recognized. The frequency of rhabdomyolysis is increasing due to multiple causes such as crush injuries, heat stroke, prolonged convulsions, drugs (alcohol, colchicine, HMG Co-A reductase inhibitors) and sepsis.  Rhabdomyolysis secondary to hypokalemia has been reported. ,,, In our patient, the etiology of rhabdomyolysis was most likely due to hypokalemia.
The mechanism of rhabdomyolysis due to hypokalemia is not known. ,,, It is postulated that during exercise, there is normally an increase in muscle perfusion, which is mediated in part by the release of potassium from skeletal muscle. The cellular release of potassium is impaired by potassium depletion that results in a decrease of blood flow to the muscles and rhabdomyolysis. 
Hypokalemia is a very common electrolyte abnormality encountered in medical practice that can lead to cardiac arrhythmias, muscular weakness including periodic paralysis, paralytic ileus and metabolic alkalosis but rarely rhabdomyolysis. Our patient required 1530 mmols of potassium infusion from day two to day seven before the serum potassium concentration reached to normal, reflecting the severity of potassium depletion. Nevertheless, our patient did not develop muscle weakness at any stage of the illness.
Early hydration and alkalanization of urine can achieve prevention of rhabdomyolysis and ARF. In spite of good hydration, our patient developed ARF, which could be partly due to continued fluid and electrolyte loss from gastroenteritis, even though his fluid replacement was well monitored by the central venous line.
ARF due to rhabdomyolysis leads to disproportionate degree of hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia, metabolic acidosis and elevated serum creatinine. In our patient hyperkalemia and severe metabolic acidosis did not occur because of the severe co-existing hypokalemia.
The cause of ARF in our case could be attributed to hypovolemia and acute tubular necrosis; however, the ARF was sustained by the rhabdomyolysis that was secondary to the persistent hypokalemia.
In conclusion, this case demonstrates that hypokalemia is a preventable cause of rhabdomyolysis and ARF.
| References|| |
|1.||Bywaters EG, Beall D. Crush injuries with impairment of renal function. Br Med J 1941;1:427. |
|2.||Better OS. The crush syndrome revisited (1940-1990). Nephron 1990;55(2):97-103. |
|3.||Grossman RA, Hamilton RW, Morse BM, Penn AS, Goldberg. Nontraumatic rhab-domyolysis and acute renal failure. N Engl J Med 1974;291:807-11. |
|4.||Knochel JP. Rhabdomyolysis and myo-globinuria. Annu Rev Med 1982;33:435-43. [PUBMED] [FULLTEXT]|
|5.||Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine-Baltimore 1982;61:141-52. [PUBMED] |
|6.||Odeh M. The role of reperfusioninduced injury in the pathogenesis of the crush syndrome. N Engl J Med 1991;324:1417-22. [PUBMED] |
|7.||Zager RA, Burkhast KM, Conrad DS, Gmur DJ. Iron, heme oxygenase, and glutathione: effects on myohemoglobinuric proximal tubular injury. Kidney Int 1995;48:1624-34. |
|8.||Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med 1988;148:1553-7. [PUBMED] |
|9.||Corwin HL, Schreiber MJ, Fang LS. Low fractional excretion of sodium. Occurrence with hemoglobinuric-and myoglobinuric-induced acute renal failure. Arch Intern Med 1984;144:981-2. |
|10.||Oh MS. Does serum creatinine rise faster in rhabdomyolysis? Nephron 1993;63:255-7. [PUBMED] |
|11.||Zager RA. Combined mannitol and desfer-roxamine therapy for myohemoglobinuric renal injury and oxidant tubular stress. Mechanistic and therapeutic implications. J Clin Invest 1992;90:711-9. |
|12.||Prendergast BD, George CF. Drug induced rhabdomyolysis-mechanism and manage-ment. Postgrad Med J 1993;69:333-6. [PUBMED] |
|13.||Hanip MR, Cheong IK, Chin GL, Khalid BA. Rhabdomyolysis associated with hypokalemic periodic paralysis of renal tubular acidosis. Singapore Med J 1990; 31(2):159-61. |
|14.||Malickova K, Merta M, Zabka J, et al. Renal failure caused by rhabdomyolysis induced by hypokalemia in Conn's syndrome. Cas-Lek-Cesk 1996;135(4):117-9. |
|15.||Williams SG, Davidson AG, Glynn MJ. Hypokalaemic rhabdomyolysis: an unusual presentation of coeliac disease. Eur J Gastroenterol Hepatol 1995;7(2):183-4. |
|16.||Luchon L, Meyrier A, Paillard F. Hypo-kalemia without arterial hypertension by licorice poisoning. Nephrologie 1993;14(4): 177-81. |
|17.||Knochel JP, Schlein EM. On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest 1972;5:1750-8. |
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