Table of Contents  
CASE REPORT
Year : 2014  |  Volume : 7  |  Issue : 5  |  Page : 679-682  

Exercise-induced rhabdomyolysis with acute kidney injury: A case report with review of literature


1 Department of Emergency Medicine, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pimpri, Maharashtra, India
2 Deparment of Orthopedics, Aditya Birla Memorial Hospital, Thergaon, Chinchwad, Pune, Maharashtra, India
3 Department of Nephrology, Aditya Birla Memorial Hospital, Thergaon, Chinchwad, Pune, Maharashtra, India

Date of Web Publication10-Sep-2014

Correspondence Address:
Varsha S Shinde
Department of Emergency Medicine, Padmashree Dr. D.Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pimpri, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.140498

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  Abstract 

Exercise-induced rhabdomyolysis is a medical condition that results from muscle injury. Renal failure is the most serious complication of rhabdomyolysis, but is rare. We report a case of acute kidney injury following heavy exercise in a healthy, young adult.

Keywords: Acute kidney injury, exercise, myoglobin, rhabdomyolysis


How to cite this article:
Shinde VS, Shinde SR, Mali M. Exercise-induced rhabdomyolysis with acute kidney injury: A case report with review of literature. Med J DY Patil Univ 2014;7:679-82

How to cite this URL:
Shinde VS, Shinde SR, Mali M. Exercise-induced rhabdomyolysis with acute kidney injury: A case report with review of literature. Med J DY Patil Univ [serial online] 2014 [cited 2020 Aug 8];7:679-82. Available from: http://www.mjdrdypu.org/text.asp?2014/7/5/679/140498


  Introduction Top


Strenuous exercise can result in damage to skeletal muscle cells, a process known as exertional rhabdomyolysis. In most cases, this damage is resolved without consequences. Cases of exercise-induced rhabdomyolysis have been reported in unfit individuals or those attempting exhaustive exercise such as marathon running or weight lifting. [1],[2],[3],[4],[5],[6],[7] Exertional rhabdomyolysis cases mostly involve individuals who are inexperienced exercisers, dehydrated and uneducated in fitness. [8] Case reports show that rhabdomyolysis can develop in individuals who are physically fit, exercise-trained and healthy, due to overexertion under the guidance of a trainer. [9] Exertional rhabdomyolysis, localized to one muscle have been reported in biceps, [10] triceps, [2] soleus, [11] and adductor magnus. [12] Renal failure is the most serious complication of rhabdomyolysis, but is apparently rarer when the rhabdomyolysis is caused by exercise. We describe a case of a 20-year-old healthy student who developed acute kidney injury (AKI) following strenuous exercise in gym.


  Case Report Top


A 20-year-old healthy male presented with the complaints of pain in paraumbilical region, pain in the arm and leg muscles, vomiting and dark colored urine since 2 days. There was history of heavy physical exercise in the gymnasium 3 days ago when he joined gym for physical training. He was not doing regular exercise before this episode. He was very enthusiastic to start exercise. He did three rounds of squats 20 each, then push-ups three rounds of 15 each. Then he was introduced to weight training exercises of lower body such as leg press, leg curl, leg extension, and adduction-abduction. He did them for about 40 min. Then he did cardio for 15 min in the form of static cycling. Then before cooling down he did 20 crunches (abdominals). He had a lot of muscle pain postexercise, which he ignored for sometime. He went to see a doctor when he started getting dark colored urine after 24 h. He was admitted there for about 6 h, given nonsteroidal antiinflammatory drugs (NSAID) injection for muscle pain and some intravenous (IV) fluids. He was not on any medications or any performance enhancing substances. He was not doing any exercise for previous 2 years as he was busy in studies. There was no history of similar attack in the past. His urine output dropped and blood investigations showed higher creatinine; hence, he was shifted to tertiary care private hospital in Intensive Care Unit (ICU).

His vitals were normal. There was superficial tenderness in the anterior abdominal wall. Surgical reference was done, there was no deep tenderness. Ultrasonography was requested. Patient was dehydrated. Examination showed tenderness and swelling in both arms and thighs muscle groups. Movements were painful. There was no ecchymosis and no sensory or motor deficit of the limbs. Distal pulsations were normal. His laboratory parameters were: Hb 15.5 g/dL, total leukocyte count 8100, platelets 1.88 K. Urine analysis showed albumin 4s+, red blood cell 3-4, pus cells 1-2, granular casts 6-8/HPF. Creatinine phosphokinase 32,000, lactate dehydrogenase (LDH) 11,890, uric acid 10.8, serum sodium 131 mEq/L, potassium 4.2 mEq/L blood urea nitrogen 35 mg/dL and serum creatinine 4.9 mg/dL. On admission, there was metabolic acidosis pH 7.27/pCO 2 28/HCO 3 14. Myoglobin levels were not assessed. The blood chemistry results for the days after exertion are shown in [Table 1]. Ultrasound abdomen (ultrasonography) showed bilateral increased renal cortical echogenicity with loss of corticomedullary differentiation. Rest of the study within normal limits. Magnetic resonance imaging of the leg or paraumbilical muscles was not undertaken due to cost constrains.
Table 1: Blood chemistry results

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Echocardiogram showed normal functioning heart. A diagnosis of AKI secondary to rhabdomyolysis was done. Patient was treated with crystalloids at 150-200 mL/h after a fluid bolus. Furosemide infusion at 20 mg/h, injection sodabicarb 50 mL 8 hourly. His urine output was monitored hourly and was 75-100 mL/h. Fluids were titrated accordingly. He did not require renal replacement therapy. His renal functions were monitored daily. By the 3 rd day, his brown colored urine (myoglobinuria) was clearing to normal. He remained hemodynamically stable. Furosemide infusion was changed to fixed dose of 40 mg/6 hourly. His muscle swelling subsided on day 6. His creatinine gradually dropped to 2.8 mg/dL on 8 th day. He was shifted to ward on the 7 th day. The IV infusions were stopped. He received at least 3 L of oral fluids and rest in the ward. He made uneventful recovery and was discharged on day 9 th . Follow-up at 1-month showed normal renal parameters, normal creatine kinase and ultrasonography.


  Discussion Top


In this case, our young patient presented with classic signs of rhabdomyolysis. He is healthy and this is the first time of hospitalization for him. He is not on any performance enhancing drugs. He did strenuous exercise on the very 1 st day of gym in his youthful enthusiasm. He sought medical treatment after 24 h. He received nonsteroidal, antiinflammatory injection for his severe musculoskeletal pain. He did not hydrate himself well after exercise. He was dehydrated. Excessive eccentric exercise of leg, arm and abdominal muscles posed him to land into rhabdomyolysis. All these factors that is, eccentric muscle damage, late treatment, dehydration, and nephrotoxic insult by NSAIDs must have caused the renal insufficiency with which he presented.

Eccentric muscle damage response can be more stressed in individuals that are susceptible toward exertional rhabdomyolysis (high responders). [12] Squats, push-ups, static cycling with resistance done on machine are the examples of eccentric exercise he did.

Most reports show that patients in whom AKI developed had a longer delay in receiving supportive therapy than did patients in whom AKI did not develop. [13] The same is observed in our patient. Therefore, early, aggressive volume repletion is crucial in patients with crush syndrome. [14] Rapid fluid resuscitation and continued vigilance in ICU prevented further complications in our patient.

Myoglobinuria doesn't occur without rhabdomyolysis. Myoglobin is rapidly and unpredictably cleared by hepatic metabolism. Therefore, tests for myoglobin in plasma or urine are not a sensitive diagnostic procedure. It is also readily filtered by glomeruli. Water is progressively reabsorbed and the concentration of myoglobin rises proportionately, until it precipitates and causes obstructive cast formation and thus AKI. [15] Release of myoglobin is often associated with an increase in levels of creatine kinase (CK), aldolase, LDH, serum glutamic-pyruvic transaminase, and other enzymes. Because overall degradation and removal of CK is slow, its concentration remains elevated much longer and in a more consistent manner than that of myoglobin. Consequently, CK is more reliable than myoglobin in assessing the presence and intensity of damage to the muscle. [15]

There is no defined threshold value of serum CK above which the risk of AKI is markedly increased. The risk of AKI in rhabdomyolysis is usually low when CK levels at admission are <15000-20,000 U/L. [16] Although AKI may be associated with CK values as low as 5000 U/L, this usually occurs when coexisting conditions such as sepsis, dehydration, and acidosis are present. [15] Our patient had CK of 32,000 on admission.

The true incidence of AKI in rhabdomyolysis is difficult to establish owing to varying definitions and clinical scenarios. The reported incidence ranges from 13% to approximately 50%. [17] Sinert et al. have reported 0% incidence of acute renal failure in exercise-induced rhabdomyolysis without nephrotoxic co-factors. [18]

Acute kidney injury associated with rhabdomyolysis often leads to a more rapid increase in plasma creatinine than do other forms of AKI [19] as seen in our patient. Similarly, a low ratio of blood urea nitrogen to creatinine is often seen in patients with rhabdomyolysis. Rhabdomyolysis induced AKI frequently causes oliguria and occasionally causes anuria. [19]

In a review of 97 adult patients who presented to the emergency department with single episode of rhabdomyolysis, the most common triggers were cocaine use; exercise and immobilization. [20] The causes of rhabdomyolysis are drug [8],[21] alcohol abuse, use of statins, [22] intense eccentric exercise, [23] crush trauma and high-intensity exercise in heat stress conditions. Defects in fatty acid β-oxidation are the most common metabolic myopathy to cause recurrent exercise-induced rhabdomyolysis. [24]

The classic triad of presentation, muscle aches, weakness and dark urine, is seen in <10% of patients. [19] AKI associated with myoglobinuria is the most serious complication of both traumatic and nontraumatic rhabdomyolysis and it may be life-threatening. [19] AKI associated with rhabdomyolysis represents about 7-10% of all cases of AKI in United States. [25]

The true incidence of AKI in rhabdomyolysis is difficult to establish owing to varying definitions and clinical scenarios. The reported incidence ranges from 13% to approximately 50%. [17] Sinert et al. have reported 0% incidence of acute renal failure in exercise-induced rhabdomyolysis without nephrotoxic co-factors. [18]

The outcome of rhabdomyolysis is usually good provided that there is no renal failure. Nevertheless, mortality data vary widely according to the study population, setting, the number and severity of coexisting conditions. Among patients in ICU, the mortality has been reported to be 59% when AKI is present and 22% when it is not present. [16] Long-term survival among patients with rhabdomyolysis and AKI is reported to be close to 80% and the majority of patients recover renal function.

Most reports show that patients in whom AKI developed had a longer delay in receiving supportive therapy than did patients in whom AKI did not develop. [13] The same is observed in our patient. Therefore, early, aggressive volume repletion is crucial in patients with crush syndrome. [14]

Curry et al. recommended rapid correction of the fluid deficit with IV crystalloids followed by infusion of 2.5 mL/kg/h, with the goal of maintaining a minimum urine output of 2 mL/kg/h. [26] Until date, no prospective controlled studies have demonstrated benefit from alkalinization of the urine or forced diuresis with mannitol or loop diuretics. [27]


  Conclusion Top


Gymming is common and becoming popular in urban populations to keep fit. The purpose of this article is also to increase awareness of possibility of rhabdomyolysis and AKI requiring ICU admission especially in unconditioned, healthy subjects. This serious complication can be prevented by undertaking the exercise gradually. If it occurs, early, aggressive fluid resuscitation is the key management. Seeking medical help early and avoiding further nephrotoxic insult by commonly used NSAIDs is important.

 
  References Top

1.Aizawa H, Morita K, Minami H, Sasaki N, Tobise K. Exertional rhabdomyolysis as a result of strenuous military training. J Neurol Sci 1995;132:239-40.  Back to cited text no. 1
    
2.Goubier JN, Hoffman OS, Oberlin C. Exertion induced rhabdomyolysis of the long head of the triceps. Br J Sports Med 2002;36:150-1.  Back to cited text no. 2
    
3.Granata A, Lo Piccolo G, Ruffo C, Vittoria S, Stalteri A. Rhabdomyolysis after body building exercise. Nephron 2002;91:354-5.  Back to cited text no. 3
    
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6.Gagliano M, Corona D, Giuffrida G, Giaquinta A, Tallarita T, Zerbo D, et al. Low-intensity body building exercise induced rhabdomyolysis: A case report. Cases J 2009;2:7.  Back to cited text no. 6
    
7.Clarkson PM. Case report of exertional rhabdomyolysis in a 12-year-old boy. Med Sci Sports Exerc 2006;38:197-200.  Back to cited text no. 7
    
8.Sandhu RS, Como JJ, Scalea TS, Betts JM. Renal failure and exercise-induced rhabdomyolysis in patients taking performance-enhancing compounds. J Trauma 2002;53:761-3.  Back to cited text no. 8
    
9.Springer BL, Clarkson PM, Two cases of exertional rhabdomyolysis precipitated by personal trainers. Med Sci Sports Exerc 2003;35:1499-502.  Back to cited text no. 9
    
10.Bolgiano EB. Acute rhabdomyolysis due to body building exercise. Report of a case. J Sports Med Phys Fitness 1994;34:76-8.  Back to cited text no. 10
    
11.Watanabe N, Inaoka T, Shuke N, Takahashi K, Aburano T, Chisato N, et al. Acute rhabdomyolysis of the soleus muscle induced by a lightning strike: Magnetic resonance and scintigraphic findings. Skeletal Radiol 2007;36:671-5.  Back to cited text no. 11
    
12.Saka T. Exertional rhabdomyolysis of the bilateral adductor magnus. J Sports Sci Med 2007;6:568-71.  Back to cited text no. 12
    
13.Sever MS, Vanholder R, Lameire N. Management of crush-related injuries after disasters. N Engl J Med 2006;354:1052-63.  Back to cited text no. 13
    
14.Gunal AI, Celiker H, Dogukan A, Ozalp G, Kirciman E, Simsekli H, et al. Early and vigorous fluid resuscitation prevents acute renal failure in the crush victims of catastrophic earthquakes. J Am Soc Nephrol 2004;15:1862-7.  Back to cited text no. 14
    
15.Vanholder R, Sever MS, Erek E, Lameire N. Rhabdomyolysis. J Am Soc Nephrol 2000;11:1553-61.  Back to cited text no. 15
    
16.de Meijer AR, Fikkers BG, de Keijzer MH, van Engelen BG, Drenth JP. Serum creatine kinase as predictor of clinical course in rhabdomyolysis: A 5-year intensive care survey. Intensive Care Med 2003;29:1121-5.  Back to cited text no. 16
    
17.Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: An evaluation of 475 hospitalized patients. Medicine (Baltimore) 2005;84:377-85.  Back to cited text no. 17
    
18.Sinert R, Kohl L, Rainone T, Scalea T. Exercise-induced rhabdomyolysis. Ann Emerg Med 1994;23:1301-6.  Back to cited text no. 18
    
19.Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361:62-72.  Back to cited text no. 19
    
20.Fernandez WG, Hung O, Bruno GR, Galea S, Chiang WK. Factors predictive of acute renal failure and need for hemodialysis among ED patients with rhabdomyolysis. Am J Emerg Med 2005;23:1-7.  Back to cited text no. 20
    
21.Braseth NR, Allison EJ Jr, Gough JE. Exertional rhabdomyolysis in a body builder abusing anabolic androgenic steroids. Eur J Emerg Med 2001;8:155-7.  Back to cited text no. 21
    
22.Thompson PD, Clarkson P, Karas RH. Statin-associated myopathy. JAMA 2003;289:1681-90.  Back to cited text no. 22
    
23.Clarkson PM, Sayers SP. Etiology of exercise-induced muscle damage. Can J Sport Sci 1999;24:234-48.  Back to cited text no. 23
    
24.Hannah-Shmouni F, McLeod K, Sirrs S. Recurrent exercise-induced rhabdomyolysis. CMAJ 2012;184:426-30.  Back to cited text no. 24
    
25.Bagley WH, Yang H, Shah KH. Rhabdomyolysis. Intern Emerg Med 2007;2:210-8.  Back to cited text no. 25
    
26.Curry SC, Chang D, Connor D. Drug-and toxin-induced rhabdomyolysis. Ann Emerg Med 1989;18:1068-84.  Back to cited text no. 26
    
27.Kellum JA, Cerda J, Kaplan LJ, Nadim MK, Palevsky PM. Fluids for prevention and management of acute kidney injury. Int J Artif Organs 2008;31:96-110.  Back to cited text no. 27
    



 
 
    Tables

  [Table 1]


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