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Saudi Journal of Kidney Diseases and Transplantation
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ARTICLE Table of Contents   
Year : 1998  |  Volume : 9  |  Issue : 3  |  Page : 273-284
Rhabdomyolysis and Myoglobin-induced Acute Renal Failure


Department of Internal Medicine, Security Forces Hospital, Riyadh, Saudi Arabia

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How to cite this article:
Malik GH. Rhabdomyolysis and Myoglobin-induced Acute Renal Failure. Saudi J Kidney Dis Transpl 1998;9:273-84

How to cite this URL:
Malik GH. Rhabdomyolysis and Myoglobin-induced Acute Renal Failure. Saudi J Kidney Dis Transpl [serial online] 1998 [cited 2019 May 21];9:273-84. Available from: http://www.sjkdt.org/text.asp?1998/9/3/273/39270

   Introduction Top


In 1812, Larrey, the great military surgeon of the Napoleonic Army first described muscle necrosis in comatose subjects. He reported on skin and muscle necrosis in comatose soldiers Ipeisoned by carbon monoxide [1] . Traumatic .muscle destruction was described by the German Von Colmers in the casualties of the, 199l Messina earthquake [2] . Acute renal failure (ARF) associated with traumatic rhabdomyolysis in war injuries was reported by Frankenthal in 1916 [3] . Minawi in 1923 described further cases of muscle crush injury and renal failure and raised the possibility that the muscle damage somehow contributed to the renal failure [4] . In 1941, Bywaters and Beall described in detail the pathophysio­logical mechanisms of ARF due to rhabdomyolysis following crush injuries in victims of bombing raids in World War II [5] .


   Physiologic Anatomy of Skeletal Muscle Top


Approximately 600 skeletal muscles of the human body form 40 to 45 percent of its weight. Each muscle is composed of numerous muscle fibers ranging from 10 to 80 micrometers in diameter. In most muscles, the fibers extend the entire length of the muscle, each being innervated by only one nerve ending located near the middle of the fiber [6],[7],[8] . The cell membrane of the muscle fiber is the Sarcolemma, which is a true cell membrane. Surrounding individual muscle fibers is connective tissue called the endomysium, which contains small blood vessels and nerves. Groups of muscle fibers are bound together by denser layers of collagenous and elastic fibers (Perimysium) and finally the connective tissue binds the fascicles into definite muscle. At the ends of the elongated muscles, the connective tissue forms tendons, which are inserted into the bone [6],[7],[8] .

Each muscle fiber contains hundreds to thousands of myofibrils containing myosin and act in filaments, which are large polymerized protein molecules responsible for muscle contraction. The myofibrils are suspended inside the muscle fiber in a matrix called Sarcoplasm which is composed of the usual intracellular constituents: potassium, magnesium, phosphate, protein and enzymes. The presence of a large number of mitochondria is indicative of a great need for a large amount of adenosine triphosphate (ATP) formed by mitochondria and needed for muscle contraction. ATP provides the energy for the active transport of calcium into the Sarcoplasm, and both contraction and relaxation of muscle require ATP. All muscle fibers are metabolically similar and are of two types. Slow-fibers: are characterized by .oxidative metabolism with abundant numbers of mitochondria and a high myoglobin content (red fibers). Fast-fibers: are predominantly glycolytic with relatively few mitochondria and scanty myoglobin content (white fibers).

The slow fibers are thus utilized for prolonged sustained contractions and the fast fibers are used in sudden forceful contractions. 95% of glycogen as a source of energy is stored in skeletal muscle [6],[7],[8] .


   Etiopathogenesis of Rhabdomyolysis Top


Rhabdomyolysis is defined as injury to skeletal muscle cells of such severity that their contents are released into the circulation. Myoglobinuria is a consequence of rhabdo­myolysis. The causes of rhabdomyolysis are given in [Table - 1]. ARF occurs in about 30% of patients with rhabdomyolysis [9] .


   A. Traumatic Rhabdomyolysis Top



   The Crush Syndrome Top


The crush injuries leading to myoglobinuria and ARF were extensively studied in the victims of World War II. The patients studied had been buried beneath falling debris. They all died of uremia and post­mortem examination showed extensive skeletal muscle necrosis and specific pigment nephropathy [5],[10],[11],[12] . Further reports described the victims of bombing of Beirut barracks in 1983 [13] and those of the Armenian earthquake in 1988 where 600 patients developed myoglobinuric ARF [14] . Crush injury of the muscle leads to a series of consequences. The intracellular concentration of water, sodium, chloride and calcium is increased partly by the external pressure or tension on the muscle and partly by the impairment of activity of a sodium potassium adenosine triphosphatase in the damaged muscle. When the muscles are released from the crushing object; the impeded circulation restarts leading to further loss of water and electrolytes into the damaged muscle. Also, it is during this time that myoglobin gains access to the circulation [15],[16],[17],[18],[19] .


   Physical Torture Top


ARF due to rhabdomyolysis and myoglo­binuria following physical torture involving beating of skeletal muscles akin to crush injuries was first reported by our group from Kashmir (India) in 1993 [20],[21] . Emphasis has been put on considering the possibility of ARF rather than concentrating on surface injuries in a physically tortured person. Further reports of ARF due to physical torture also came from Israel wherein the condition has been described as pseudo-crush syndrome [22] and from Pakistan [23] . In these studies, the muscles were physically crushed during interrogation by the Police forces by blunt trauma using sticks, buts of guns, iron rods, leather belts and electric shocks leading to rhabdomyolysis. Myoglobinuria and "forced dehydration" during torture were considered as patho­genetic mechanisms of ARF in these studies [21],[22] .


   Prolonged Muscle Activity Top


Myoglobinuric ARF may follow any event involving violent and unaccustomed muscular activity [24],[25],[26] . The condition is characterized by pain, swelling and tenderness due to skeletal muscle necrosis associated with the passage of dark colored urine and renal failure [27] . Status epilepticus [28] , Status asthmaticus [29] , prolonged labor during pregnancy [30] and high voltage electric shock [31] have all resulted in ARF due to rhabdomyolysis. ARF, usually non-oliguric type, as a result of rhabdomyolysis and myoglobinuria has been described in tetanus [32] .


   B. Non-traumatic Rhabdomyolysis Top



   Arterial Embolization Top


ARF due to myoglobinemia and myoglobinuria following arterial emboli occluding major blood vessels to the lower limbs has been reported [33],[34] .

Rhabdomyolysis and ARF in patients undergoing cardiopulmonary bypass surgery have been described [35] . Release of myo­globin into the systemic circulation follow the restoration of blood flow to an ischemic muscle. Cases of ARF due to myoglobinuria have also been described in sickle cell disease [36],[37] .


   Metabolic Disorders Top


Hypokalemia as a cause of rhabdomyolysis has been described in a number of reports [38],[39],[40],[41],[42],[43],[44]. It has been suggested that arteriolar dilatation in the skeletal muscle occurs due to the release of potassium from the contracting muscle into the interstitial fluid. This leads to increase in blood flow to the muscle during exercise [45] . Knochel and Schlein demonstrated that electrically stimulated muscular exercise in potassium depleted dogs results in myonecrosis [38] . The authors suggested that potassium deficiency prevents the increase in muscle blood flow that would normally occur during exercise, thus resulting in rhabdo­myolysis. So a combination of potassium depletion and exercise is detrimental to skeletal muscle metabolism. Hypophos­phatemia may lead to cellular injury due to severe depletion of ATP content of the muscle [46] . A decrease in intracellular inorganic phosphorus concentration may interfere with the regeneration of ATP from ADP. Serum inorganic phosphorus levels of about 0.48 mmol/L (1.5 mg/dl) has been suggested as a crucial minimum [27] .


   Muscle Diseases Top


Various hereditary muscle disorders associated with rhabdomyolysis and ARF include glycogen storage diseases marked by lack of phosphorylase (McArdle's disease), phosphofructokinase (Tarui's disease) or the muscle lipid metabolic disorder due to absence of carnitine palmityl transferase. Abnormalities in glycogen or lipid meta­bolism result in a block of anaerobic glycosis that predisposes to the loss of integrity of the sarcolemmal membrane and the liberation of myoglobin following exercise [47],[48],[49],[50] . Rhabdomyolysis and ARF have also been reported in association with other muscle diseases like polymyositis [51] , dermatomyositis [52] and tropical pyomyositis [53] . Muscle diseases can lead to acute episodes of muscle necrosis when there is further stress by exercise or an inter-current infection [54] .


   Toxins and Drugs Top


Alcohol is a common cause of rhabdo­myolysis [55],[56],[57],[58] which is due to multiple factors. Stupor or coma due to alcohol or any other drug can cause myonecrosis if the muscles are compressed by the body's own weight for long periods [59],[60] . Alcoholic myopathy, sometimes with ARF, may occur due to altered cell membrane permeability [61],[62],[63],[64],[65] .

Alcohol abuse also causes phosphate depletion, which causes rhabdomyolysis. Myoglobinuria is found in 50 percent of these patients, half of them develop ARF and mortality may reach up to 50 percent due to hyperkalemia. Hypokalemia and hypomagnesemia, both common in alcoholics, may potentiate alcoholic myopathy [38],[66] .

Heroin addicts may develop myoglobinuria and ARF as a result of multiple factors like muscle damage resulting from coma, direct toxic effects of heroin or one of its contami­nants or as a result of tetanus secondary to the use of contaminated needles used for intravenous drug use [67],[68],[69] .

Cocaine has been reported as a cause of myoglobinuria induced ARF and the mechanisms of rhabdomyolysis suggested are abnormal postures and vasoconstriction by cocaine, causing ischemia of muscles and renal vasoconstriction leading to tubular injury [70],[71] .

Phenylcyclidine, a hallucinogenic agent may produce rhabdomyolysis by inducing tremors, posturing and seizures [72],[73] . Pentamidine [74] , Paraphenylenediamine [75] , Terbutaline overdose [76] high dose haloperidol [77] , Doxepine and nitrazem [78] , Lovastatin [79] have been reported as causes of rhabdomyolysis and acute renal failure.


   Infections and Envenomation Top


Some of the viral infections reported as causes of myoglobinuria and ARF are influenza, echovirus 9 and Varicella zoster infection [80],[81],[82],[83] . Direct invasion of muscle fibers has been postulated as one of the mechanisms of myoglobinuria [81] .

Some of the bacterial infections reported as causes of rhabdomyolysis and ARF are Legionnaire's disease,  Salmonella More Details and  Brucella More Details [84],[85],[86] .

Myonecrosis, myoglobinuria and ARF are induced by envenomation by snakebites [87] and honeybee stings [88] .


   Prolonged Coma Top


Prolonged coma induced by alcohol, narcotics and other sedatives has been reported to cause rhabdomyolysis due to pressure­induced myonecrosis in a prolonged immobilized state [57],[60] . Due to prolonged pressure there is an interference with the local blood supply causing loss of integrity of the sarcolemmal membrane and release of myoglobin.


   Heat Stroke and Malignant Hypothermia Top


Rhabdomyolysis and acute renal failure has been reported in exertion as well as classical heat stroke [89],[90],[91] . Heat stress leads to rhabdomyolysis by interfering with glycolysis. Hypokalemia, which occurs in heat stroke, also plays an important role in causing rhabdomyolysis since potassium is necessary for maintaining muscle cell membrane potential [92] . Potassium deficiency also interferes with glycogen synthesis [93] .


   Carbon Monoxide Poisoning Top


Carbon monoxide poisoning by causing hypoxia because of formation of monoxy­hemoglobin leads to rhabdomyolysis [87] .

Hypothyroidism causes elevated creatine phosphokinase and, sometimes, frank rhabdomyolysis [87] .


   Pathophysiology of Myoglobin-induced ARF Top


Myoglobin, a heme pigment with a molecular weight of approximately 17800 is present in the sarcoplasm of striated skeletal and cardiac muscle. It is released into the blood stream by any process that causes destruction of skeletal muscle. Due to its relatively small size, myoglobin is readily filterable and is excreted in urine at a serum concentration of less than 15 mg per decimeter which requires damage to about 200 gm of muscle [94].

A large number of Marine recruits have been shown to develop myoglobinemia and other evidences of exertion rhabdomyolysis without significant clinical symptoms [95] . Moreover, myoglobinuria is common, following exercise in patients with here­ditary or progressive muscle disease but ARF is unusual [96] . These studies indicate that myoglobinuria alone may not be sufficient to induce ARF. Bywaters and Beall, however, suggested that myoglobin and other muscle constituents impair renal function [5] . In their experimental studies it was recognized that hypovolemia and aciduria are two critical factors which predispose to myoglobinuric ARF [10],[11] . Infusion of saline and bicarbonate solutions early during rhabdomyolysis has prevented development of ARF, favoring this postulation [97] .

It has been postulated that at the nephronal level three basic mechanisms underlie heme protein toxicity: renal vasoconstriction, intrarenal cast formation and direct heme­protein induced nephrotoxicity [98] . Renal hypoperfusion and vasoconstriction occur due to different mechanisms. Fluid third­spacing leading to hypovolemia is an important factor for causing hypoperfusion. As much as 18 liters of fluid may extra­vagate into damaged limbs [13] . Myoglobin is a potent inhibitor of the vasodilator nitric oxide and may trigger intrarenal vaso­constriction and ischemia in patients with borderline renal hypoperfusion [99] . Besides, severe muscular injury can, for unknown reasons, activate the endotoxincytokine cascade, thus eliciting renal vaso­constriction [100] .

Once the myoglobin molecule is filtered by the glomerulus it enters the proximal tubular cells and is taken up by lysomes at acid pH. The heme pigment then splits into its globulin and ferrihemate components. Ferrihemate is transported out of the tubular cell at the expense of ATP. The tubular cell, thus is injured due to renal ischemia, hypoxia and a critical reduction of ATP stores [87] .

Distal nephron pigment casts thought to cause tubular obstruction have been noted in different studies. The heme protein cast formation is determined by the heme protein concentration in. the distal tubule and the urinary pH, aciduria being an important determinant of pigment induced ARF [101],[102],[103] .

In addition to the vasomotor, nephrotoxic and obstructive agents noted above as pathogenic in myoglobin induced ARF, other factors released into circulation by rhabdomyolysis appear to be operative in humans [104] . Hyperphosphatemia can markedly potentiate ischemic and nephrotoxic renal damage [105] . Hyperuricemia contributes to intratubular obstruction and also increases heme protein associated ischemic tubular damage [106] . The formation of thrombi in the glomerular capillary tufts due to disseminated intravascular coagulation can be triggered in rhabdomyolysis [20] . These factors may independently or together cause impairment of renal function particularly during hemodynamic shock.


   Clinical Features and Diagnosis of Myo­globinuric ARF Top


The ARF following rhabdomyolysis takes the usual course but has distinctive clinical features. The diagnosis in the first instance lies on a good index of clinical suspicion. Localized rhabdomyolysis is clinically obvious by swollen, painful and tender muscles [54] . As a result of muscle damage, many substances are released into the circulation and the biochemical findings in acute rhabdomyolysis are as follows [107] .

  1. Elevation of serum creatine phosphokinase (CK) aldolase and lactic dehydrogenase.
  2. Heme pigment (myoglobin) in urine
  3. Hyperkalemia
  4. Hypocalcemia
  5. Hyperphosphatemia
  6. Hyperuricemia
  7. High creatinine: blood urea nitrogen
  8. (BUN) ratio
  9. Disseminated intravascular coagulation
  10. Hypoalbuminemia


The CK-MM isoform is present in the skeletal muscle and its raised serum level is the most sensitive test to confirm the diagnosis of rhabdomyolysis. The serum levels depend upon the severity of rhabdo­myolysis and may range from thousands to 1,000,000 IU/L or even higher. Without ongoing muscle necrosis the CK levels peak at 12-36 hours. Measurement of other muscle enzymes such as aldolase, lactic dehydrogenase or transaminases provides no additional useful information in clinical practice [87] .

Myoglobin is lightly bound to a2- globulin and is quickly cleared from plasma by excretion in urine. From the clinical point of view, dark urine and pink serum are indicative of hemolysis whereas dark urine and clear serum suggest rhabdomyolysis [108] . In marathon runners Schiff et al showed that although 89% gave no history of pigmenturia, myoglobin was present in the blood of 25 out of 44 runners [109] . Specific radio-immunoassays are used to distinguish myoglobin and hemoglobin in urine. A simple laboratory test may be used to, distinguish the two pigments [54] . To 5ml of urine, 2.8 grams of Ammonium sulfate is added and the mixture is allowed to stand for 5 minutes and then filtered. Hemoglobinuria is indicated by a colored precipitate whereas colored supernatant indicates the presence of myoglobin. The test can be very useful in situations where both hemoglobinuria and myoglobinuria are simultaneously present as in cases of physical torture [21] .

The presence of pigmented granular casts in urine sediment is characteristic of rhabdomyolysis [110] . All ten cases in our study of ARF following physical torture showed the presence of pigment casts [20].

ARF due to rhabdomyolysis is associated with severe hypocalcemia in the oliguric phase and hypercalcemia in the recovery phase. Hypocalcemia occurs even without ARF due to calcium deposition in the injured muscle, and mobilization of this calcium in the diuretic phase causes hyper­calcemia [111] Once ARF is established, hypocalcemia is a consequence of hyper­phosphatemia and partly due to reduced 1,25 dihydroxycholecalciferol (l,25-DHCC) levels. Hypercalcemia in the recovery phase is associated with raised levels of 1, 25­DHCC, which plays contributory role in its etiology [108] .

A transient elevation of ratio of serum creatinine to BUN, which usually is 1:10 is commonly seen in acute rhabdomyolysis. The large quantity of creatine phosphate released from damaged muscle is spon­taneously dehydrated to creatinine leading to the rise in this ratio. Hyperuricemia is caused by release of purenes from damaged muscle. These purenes are converted to uric acid in liver. Hypoalbuminemia results from the leakage of plasma components due to capillary damage [87] .

Disseminated intravascular coagulation is a usual occurrence, noted usually on the 3rd to the 5th day. Lactic acidosis is a common feature in rhabdomyolysis due to muscle glycogen metabolism, and results from hypoxemia, volume depletion and decreased intestinal blood flow [107] .


   Prevention and Treatment of ARF Associated with Rhabdomyolysis Top


From studies on rhabdomyolysis Better and Stein concluded that hyperkalemia, hyperphosphatemia, hypocalcemia and metabolic acidosis appear before azotemia [17] . They suggested that early aggressive volume replacement and forced alkaline­diuresis therapy may protect the kidney against ARF. Isotonic saline solution should be infused at a rate of 1.5 liters per hour as soon as a trapped person's limb has been freed. This is followed by a forced alkaline diuresis using hypotonic sodium chloride, to which 40 mmol of sodium bicarbonate and 10 grams of 20% mannitol are added to each liter. A young adult may need up to 12 liters per day. This regimen will protect against the nephrotoxicity of myoglobin and urate and also control hyperkalemia and acidosis. Calcium infusion should be avoided as treatment of Ihyperkalemia unless there is danger of hyperkalemic cardiac arrhythmias [19] . Moreover, its administration will correct hypocalcemia temporarily and most infused calcium will get deposited in the traumatized muscles, thus aggravating rhabdomyolysis and causing metastatic calcification [112] . This will also increase the problem of hypercalcemia during the diuretic phase of recovery. Delaying volume expansion to six hours or more resulted in ARF in all the seven cases of traumatic rhabdomyolysis studied by Reis and Michaelson [113] . In contrast none of the seven cases with almost similar injuries in another study developed ARF when intravenous saline therapy was started immediately at the site of catastrophe [98] .

Dialysis may be needed for severe metabolic disturbances like hyperkalemia in the oliguric phase and hypercalcemia in the diuretic phase [114] . Nine out of our 10 cases of ARF following physical torture needed dialysis and recovered in 14-30 (mean 18) days [20] .

Development of compartment syndromes may lead to persistent rhabdomyolysis and delay the recovery from ARF.

Fasciotomy may be needed to reduce tissue damage and also avoid unnecessary amputations.

However, Better and Stein have urged conservative management because of the risk of infections in open wounds, which may become uncontrollable [17] . They suggested measurement of intra-compart­mental pressure by manometry. If the pressure is very high, surgical exploration should be undertaken. Rainford and Stevens, however, recommend surgical exploration in all doubtful cases [108] .

Myoglobin, because of its size, is poorly removed by either hemofiltration or peritoneal dialysis [115] . However, even in the presence of severe ARF, circulating myoglobin levels fall probably because of hepatic and splenic uptake [115] . There are no data indicating a role for removal of heme proteins by extracorporeal methods like plasmapheresis [101] .


   Prognosis Top


The prognosis for recovery of renal function is excellent. The mortality from the crush syndrome' is 60-70% usually due to sepsis and adult respiratory distress syndrome (54), In our study of 10 cases of ARF following physical torture all recovered [20] whereas 5 out of 34 (15%) in another study died, predominantly (4 out of 5) due to sepsis [21] ,


   Acknowledgment Top


I greatly appreciate the secretarial assistance of Sita J. Benedicto in the preparation of this manuscript and Alice Haddadin for literature search.

 
   References Top

1.Howse AJ, Seddon H. Ischemic contracture of muscle associated with carbon monoxide and barbiturate poisoning. Br Med J 1966; 1(5481):192-5.  Back to cited text no. 1    
2.Bywaters EG. 50 years on: the crush syndrome. BMJ 1990;301:1412-5.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Frankenthal L. Uber Verschuttungen. Virchows Arch 1916;222:332.  Back to cited text no. 3    
4.Better OS. History of the crush syndrome: from the earthquakes of Messina, Sicily 1909 to Spitak, Armenia 1988. Am J NephroI1997;17:392-4.  Back to cited text no. 4    
5.Bywaters EG, BeaU D. Crush injuries with impairment of renal function. Br Med J 1941;1:427-32.  Back to cited text no. 5    
6.West JB. Excitation and contraction of skeletal muscle. In: Best JB, Tay10r (eds). Physiological Basis of Medical Practice, Williams & Wi1kins. Baltimore 1985;96­-101.  Back to cited text no. 6    
7.Ganong WF (ed). Excitable tissue: muscle. In: Review of Medical Physiology, Appe1ton and Lange: Prentice Hall International (UK) Limited, London 1993;56-60.  Back to cited text no. 7    
8.Guyton AC, Hall JE. Contraction of skeletal muscle. In: Textbook of Medical Physiology. WB Saunders Company. Philadelphia 1996; 73-81.  Back to cited text no. 8    
9.Gabow PA, KaehnyWD, KeUeher SP. The spectrum of rhabdomyo1ysis. Medicine Baltimore 1982;61: 141-52.  Back to cited text no. 9    
10.Bywaters EG, Popjak G. Experimental crushing injury: Peripheral circulatory collapse and other effects of muscle necrosis in the rabbit. Surg Gynecol Ob stet 1942;75:612-27.  Back to cited text no. 10    
11.Bywaters EG, Stead JK. The production of renal failure following injection of solutions containing myohaemoglobin. QJ Exp Physiol 1944;33:53-70.  Back to cited text no. 11    
12.Bywaters EG. Ischemic muscle necrosis. JAMA 1944;124:1103-9.  Back to cited text no. 12    
13.Better OS. The crush syndrome revisited (1940 - 1990). Nephron 1990;55:97-103.  Back to cited text no. 13    
14.Collins AJ. Kidney dialysis treatment for victims of the Armenian Earthquake. N 1. Engl J Med 1989;320:1291-2.  Back to cited text no. 14    
15.Guharay F, Sachs F. Stretch activated single ion channel currents in tissue cultured embryonic chick skeletal muscle. J Physiol Lond 1984;352:685-701.  Back to cited text no. 15    
16.Christens en O. Mediation of cell volume regulation by Ca++ influx through stretch­activated channels. Nature 1987;330:66-8.  Back to cited text no. 16    
17.Better OS, Stein JR. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 1990;322:825-9.  Back to cited text no. 17    
18.Knochel JP. Rhabdomyolysis and myoglo­binuria. In: Suki WN, Eknoyan G (eds). The kidney in systemic disease. John Wiley, New York 1981;263-84.  Back to cited text no. 18    
19.Knochel JP. Serum calcium derangements in rhabdomyolysis. N Engl J Med 1981; 305:161-3.  Back to cited text no. 19    
20.Malik GH, Sirwal lA, Reshi AR, Najar MS, Tanvir M, Altaf M. Acute renal failure following physical torture. Nephron 1993; 63: 434-7.  Back to cited text no. 20    
21.Malik GH, Reshi AR, Najar MS, Ahmad A, Masood T. Further observations on acute renal failure following physical torture. Nephro1 Dial Transplant 1995;10:198-202.  Back to cited text no. 21    
22.Bloom AI, Zarnir G, Maggia M, Friedlaender M, Gimmon Z, Rivkind A. Torture Rhabdomyorhexis- a pseudo-crush syndrome. J Trauma 1995;38(2):252-4.  Back to cited text no. 22    
23.Naqvi R, Akhtar F, Yazdani I, et al. Acute renal failure due to traumatic rhabdo­myolysis. J Pak Med Assoc 1995;45(3):59­-61.  Back to cited text no. 23    
24.Hamilton RW, Gardner LB, Penn AS, Goldberg M. Acute tubular necrosis caused by exercise-induced myoglobinuria. Ann Intern Med 1972;77:77-82.  Back to cited text no. 24    
25.Jackson Rc. Exercise induced renal failure and muscle damage. Proc R Soc Med 1970; 63:566-70.  Back to cited text no. 25    
26.Melamed I, Romen Y, Keren G, Epstein Y, Dolev E. March myoglobinemia: a hazard to renal function. Arch Intern Med 1982;142:1277-9.  Back to cited text no. 26    
27.Dubrow A, Flamenbaum W. In: acute renal failure (2nd ed). Brenner BM and Lazarus JM (eds) Churchill Livingstone, New York 1988;p280-284.  Back to cited text no. 27    
28.Singhal PC, Chugh KS, Gulati OR. Myoglobinuria and renal failure after status epilepticus. Neurology (NY) 1978;28:200­-1.  Back to cited text no. 28    
29.Chugh KS, Singhal PC, Khatri GK. Rhabdomyolysis and renal failure following status astlunaticus. Chest 1978;73:879-80.  Back to cited text no. 29    
30.Singhal PC, Muthusethupathi MA, Chugh KS. Case report: rhabdomyolysis and post pactum renal failure. Int J Gynaecol Obstet 1977;15:250-2.  Back to cited text no. 30    
31.Glassock RJ. Hematuria and pigmenturia. In: Massry SG; Glassock RJ (eds). Textbook of Nephrology, Baltimore, Williams & Wilkins 1983;p422.  Back to cited text no. 31    
32.Martinelli R, Matos CM, Rocha H. Tetanus as a cause of acute renal failure: possible role of rhabdomyolysis. Rev Sac Bras Med Trop 1993;26:1-4.  Back to cited text no. 32    
33.Haimovici H. Arterial embolism, myoglobinuria and acute tubular necrosis. Arch Surg 970;100:639-45.  Back to cited text no. 33    
34.Haapanen E, Partanen J, Pellinen TJ. Acute renal failure following non­traumatic rhabdomyo1ysis.Scand J Uro1 Nephro1 1988; 22(4):305-8.  Back to cited text no. 34    
35.Maccario M, Fumagalli C, Oottori V, et al. The association between rhabdomyo1ysis and acute renal failure in patients undergoing cardiopulmonary bypass. J Cardiovasc Surg Torino 1996;37:153-9.  Back to cited text no. 35    
36.Koppes GM, Oaly JJ, Coltman CAJr, Butkus DE. Exertion induced rhabdomyo1ysis with acute renal failure and disseminated intravascular coagulation in sickle cell trait. Am J Med 1977;63:313­-7.  Back to cited text no. 36    
37.Devereux S, Know1es SM. Rhabdomyo1ysis and acute renal failure in sickle cell anaemia. Br Med J Clin Res Ed 1985; 290:1707.  Back to cited text no. 37    
38.Knochel JP, Schlein EM. On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest 1972;51:1750-8.  Back to cited text no. 38    
39.Nadel SM, Jackson JW, P1oth DW. Hypoka1emic rhabdomyo1ysis and acute renal failure. Occurrence following total parenteral nutrition. JAMA 1979;241:2294-6.  Back to cited text no. 39    
40.Van-Horn RG, Drori JB, Schwartz FD. Hypokalemic myopathy and elevation of serum enzymes. Arch Neurol1970;22:335-41.  Back to cited text no. 40    
41.Gross EG, Dexter ID, Roth RG. Hypokalemic myopathy with myoglobinuria associated with licorice ingestion. NEnglJMed 1966;274:602-6.  Back to cited text no. 41    
42.Mitchell AB, Duogastrone-induced hypokalemic nephropathy and myopathy with myoglobinuria. Postgrad Med J 1971; 47:807-13.  Back to cited text no. 42    
43.Tsapas G, Magoula I, Garyfullos A, Concouris L. Rhabdomyo1ysis and acute renal failure associated with pyloric stenosis. Am J Kid Dis 1987;10:373-5.  Back to cited text no. 43    
44.Saito T, Tsuboi Y, Fujisawa G, et al. An autopsy case of licorice-induced hypokalemic rhabdomyolysis associated with acute renal failure: special reference to profound calcium deposition in skeletal and cardiac muscle. Nippon Jinzo Gakkai Shi 1994;36:1308-14.  Back to cited text no. 44    
45.Dawes GS. The vasodilator action of potassium. J Physio1 Lond 1941;99:224.  Back to cited text no. 45    
46.Farber E. ATP and cell integrity. Fed Proc 1973;32:1534-9.  Back to cited text no. 46    
47.Stam:os GE, Crouch TT, Woon WG, Shanna IN. Acute renal failure in McArdle's disease. Soutth Med J 1979;72:77.  Back to cited text no. 47    
48.Chiado Fiat L, Mongini T, Doriguzzi C, Maniscalco M, Pahnucci L. Clinical spectrum of McArdle disease: three cases with unusual expression. Eur Neurol 1993;33: 208-11.  Back to cited text no. 48    
49.Layzer RB, Rowland LP, Ranney HM. Muscle phosphofructokinase deficiency. Arch NeuroI1967;17:512-23.  Back to cited text no. 49    
50.Reza MJ, Kar NC, Pearson CM, Katk RA. Recurrent myoglobinuria due to muscle carnitine palmityl transferase deficiency. Ann Intern Med 1978;88:610-5.  Back to cited text no. 50    
51.Kagen Ll. Myoglobinemia and myoglobinuria in patients with myositis. Arthritis Rheum 971;14:457-64.  Back to cited text no. 51    
52.Kessler E, Weinberger I, Rosenfeld JB. Myoglobinuric acute renal failure in a case of dermatomyositis. Isr J Med Sci 1972; 8:978-83.  Back to cited text no. 52    
53.Armstrong JH. Tropical pyomyositis and myoglobinuria. Arch Intern Med 1978;138:1145-6.  Back to cited text no. 53    
54.Swenny P, Farrington K, Moorhead JF. Pigment nephropathy: rhabdomyolysis and hemolysis. In: The kidney and its disorders. Blackwell Scientific Publications. Oxford 1989;348-58.  Back to cited text no. 54    
55.Haapanen E, Pellinen TJ, Partanen J. Acute renal failure caused by alcohol-induced rhabdomyolysis. Nephron 1984;36:191-3.  Back to cited text no. 55    
56.Klinkerfuss G, Bleisch V, Dioso MM, Perkoff GT. A spectrum of myopathy associated with alcoholism. H. Light and electron microscopic observations. Ann Intern Med 1967;67:493.  Back to cited text no. 56    
57.Koffler A, Friedler RM, Massry SG. Acute renal failure due to nontraumatic rhabdo­myolysis. Ann Intern Med 1976;85:23-8.  Back to cited text no. 57    
58.Perkoff GT, Dioso MM, Bleisch V, Klinkerfuss G. A spectrum of myopathy associated with alcoholism. Clinical and laboratory features. Ann Intern Med 1967; 67:481-92.  Back to cited text no. 58    
59.Cadnapaphornchai P, Taher S, McDonald FD. Acute drug associated rhabdomyolysis: an examination of its diverse renal mani­festations and complications. Am J Med Sci 1980;280:66- 72.  Back to cited text no. 59    
60.Penn AS, Rowland LP, Fraser DW. Drugs, coma and myoglobinuria. Arch Neurol 1972; 26:336-43.  Back to cited text no. 60    
61.Saltissi D, Parfrey PS, Curtis JR, et al. Rhabdomyolysis and acute renal failure in chronic alcoholics with myopathy, unrelated to acute alcoholic ingestion. Clin Nephrol 1984;21: 294-300.  Back to cited text no. 61    
62.Heil R, Lundmark C, Fahlgren H, Orell S. Acute muscular syndrome in chronic alcoholism. ActaMedScand 1962;17:585.  Back to cited text no. 62    
63.Schneider R. Acute alcoholic myopathy with myoglobinuria. South Med J 1970; 63 :485-9.  Back to cited text no. 63    
64.Pittman JG, Decker JW. Acute and chronic myopathy associated with alcoholism. Neurology (NY) 1971;21:293-6.  Back to cited text no. 64    
65.Fujie M, Furuya M, Yanagisawa H, et al. A case of alcoholic myopathy associated with acute renal failure due to myoglobinuria. Nippon Naika Gakkai Zasshi 1985;74:7869.  Back to cited text no. 65    
66.Knochel JP, Barcenas C, Cotton JR, Fuller TJ, Haller R, Carter NW. Hypophosphatemia and rhabdomyolysis. J Clin Invest 1978;62:1240-6.  Back to cited text no. 66    
67.Richter RW, Challenor YE, Pearson J, Kagen LJ, Hamilton LL, Rarnsey WH. Acute myoglobinuria associated with heroin addiction. JAMA 1971;216:1172-6.  Back to cited text no. 67    
68.Sreepada Rao TK, Nicastri AD, Friedman EA Renal consequences of narcotic abuse. Adv Nephrol Necker Hosp 1977;7:261-90.  Back to cited text no. 68    
69.Chan P, Lin TH, Luo JP, Deng JF. Acute heroin intoxication with complications of acute pulmonary edema, acute renal failure, rhabdomyolysis and lumbosacral plexitis: a case report. Chung Hua I Hsueh Tsa Chih Taipei 1995;55:397-400.  Back to cited text no. 69    
70.Roth D, Alaroon FJ, Fernandez JA, Preston RA, Bourgoignice n. Acute rhabdomyolysis associated with cocaine intoxication. N Bngl J Med 1988;319:673-7.  Back to cited text no. 70    
71.Singhal P, Horowitz B, Quinones MC, Sommer M, Faulkner M, Grosser M. Acute renal failure following cocaine abuse. Nephron 1989;52:76-8.  Back to cited text no. 71    
72.Cogen FC, Rigg G, Simmons JL, Domino EF. Phencyclidine associated acute rhabdo­myolysis. Ann Intern Med 1978;88:210-2.  Back to cited text no. 72    
73.Hoogwerf B, Kern J, Bullock M, Comty CM. Phencyclidine-induced rhabdomyolysis and acute renal failure. Clin Toxicol 1979; 14:47-53.  Back to cited text no. 73    
74.Sensakovic JW, Suarez M, Perez G, Johnson ES, Smith LG. Pentamidine treatment of Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome: association with acute renal failure and myoglobinuria. Arch Intern Med 1985; 145:2247.  Back to cited text no. 74    
75.Averbukh Z, Modai D, Leonov Y, et al. Rhabdomyolysis and acute renal failure induced by paraphenylenediamine. Hum Toxicol1989; 8(5):345-8.  Back to cited text no. 75    
76.Blake PG, Ryan F. Rhabdomyolysis and acute renal failure afterterbutaline overdose. Nephron 1989;53(1):76-7.  Back to cited text no. 76    
77.Marsh SI, Dolson GM. Rhabdomyolysis and acute renal failure during high dose haloperidol therapy. Ren Fail1995; 17:47-58.  Back to cited text no. 77    
78.Hojgaard AD, Andersen PT, Moller PI. Rhabdomyolysis and acute renal failure following an overdose of doxepine and nitrazepam. Acta Med Scand 1988;223:79-­82.  Back to cited text no. 78    
79.Femandez Zatarain G, Navarro V, Garcia H, Villatoro J, Calvo C. Rhabdomyolysis and acute renal failure associated with lovastatin. Nephron 1994;66:483-4.  Back to cited text no. 79    
80.Morgensen JL. Myoglobinuria and renal failure associated with influenza. Ann Intern Med 1974;80:362-3.  Back to cited text no. 80    
81.Cunningham E, Kohli R, Venuto Rc. Influenza-associated myog10binuric renal failure. JAMA 1979;242:2428-9.  Back to cited text no. 81    
82.Tanaka T, Takada T, Takagi D, Takeyama N, Kitazawa Y. Acute renal failure due to rhabdomyolysis associated with echovirus 9 infection: a case report and review of literature. Jpn J Med 1989;28:237-42.  Back to cited text no. 82    
83.Roberts DE. Varicella Zoster infection, massive rhabdomyolysis, myoglobinuria, and renal failure. J Am Board Fam Pract 1995;8:52-4.  Back to cited text no. 83    
84.Hall SL, Wasserman M, Dall L, Schubert T. Acute renal failure secondary to myoglobinuria associated with Legionnaires' disease. Chest 1983:84:633-5.  Back to cited text no. 84    
85.Lagarde C, Peyronnet P, Denis F, Benzakour M, Leroux Robert C. Salmonella bonariensis salmonellosis, rhabdomyo1ysis, ani acute renal failure. Nephron 1989; 53:179-80.  Back to cited text no. 85    
86.Wasserheit IN, Dugdale DC, Agosti JM. Rhabdomyolysis and acute renal failure: a new presentation of acute brucellosis. J Infect Dis 1984; 150:782-3.  Back to cited text no. 86    
87.Knockel JP. Pigment nephropathy. In: primer on kidney diseases, Greenberg A. (ed). Academic Press New York 1998;273­-6.  Back to cited text no. 87    
88.SeTt M, Tetiker T, Paydas S. Rhabdo­myo1ysis and acute renal failure due to honeybee stings as an uncommon cause. Nephron 1993; 65:647.  Back to cited text no. 88    
89.Vertel RM, Knochel JP. Acute renal failure due to heat injury. An analysis often cases. associated with a high incidence of myoglobinuria. AmJ Med 1967;43:435-51.  Back to cited text no. 89    
90.Shieh SD, Lin YF, Lin SH, Lu KC. A prospective study of calcium metabolism in exertional heat stroke with rhabdomyolysis and acute renal fui1ure. Nephron 1995;1 :428-32.  Back to cited text no. 90    
91.Tan W, Herzlich BC, Funaro R, et al. Rhabdomyolysis and myoglobinuric acute renal failure associated with classic heat stroke. South Med J 1995;88:1065-8.  Back to cited text no. 91    
92.Bilbrey GL, Herbin L, Carter NW, Knochel JP. Skeletal muscle resting membrane potential in potassium deficiency. J Clin Invest 1973;52:3011-8.  Back to cited text no. 92    
93.Knochel JP. Clinical effects of potassium deficiency on skeletal muscle. In: Potassium in cardiovascular and renal medicine. Whelton P, Whelton A, Walker W (eds). New York, Marcel Dekker 1986;97-109.  Back to cited text no. 93    
94.Rowland LP, Penn AS. Myoglobinuria. Med Clin North Am 1972;56:1233-56.  Back to cited text no. 94    
95.Olerud JE, Homer LD, Carroll HW. Incidence of acute exertional rhabdomyolysis. Serum myoglobin and enzyme levels as indicators of muscle injury. Arch Intern Med 1976; 136:692-7.  Back to cited text no. 95    
96.Grunfeld JP, GaneralD, ChanardJ, Fardeau M, Dreyfus JC. Acute renal failure in McArdle's disease. Report of two cases. N Engl J Med 1972;286:1237-41.  Back to cited text no. 96    
97.Ron D, Taitelman U, Michaelson M, Bar­Joseph G, Bursztein S, Better OS. Prevention of acute renal failure in traumatic rhabdomyolysis. Arch Intern Med 1984;144:277-80.  Back to cited text no. 97    
98.Zager RA. Heme protein ischemic interactions at the vascular, intraluminal and renal tubular cell levels: implications for therapy of myoglobin-induced renal injury. Ren FaiI1992;l4:341-4.  Back to cited text no. 98    
99.Brady HR, Brenner BM. Acute renal failure; in Harrison's Principles of Internal Medicine 14th Edition, McGraw Hill, New York 1998:507.  Back to cited text no. 99    
100.Badr KF, Kelley YE, Rennke HG, Brenner BM. Roles for thromboxane Az and 1eukotrienes in endotoxin-induced acute renal failure. Kidney Int 1986;30:474-80.  Back to cited text no. 100    
101.Zager RA. Rhabdomyolysis and myohemoglobinuric acute renal failure. Kidney Int 1996;49:314-26.  Back to cited text no. 101    
102.Cushner HM, Bames JL, Stein JH, Reineck HJ. Role of volume depletion in the glycerol model of acute renal failure. Am J Physio1 1986;250:F315-21.  Back to cited text no. 102    
103.Zager RA. Studies of mechanisms and protective maneuvers in myog1obinuric acute renal injury. Lab Invest 1989;60:619­-29.  Back to cited text no. 103    
104.Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med 1988;148:1553-7.  Back to cited text no. 104    
105.Zager RA. Hyperphosphatemia: a factor that provokes severe experimental acute renal failure. J Lab Clin Med 1982; 100:230-9.  Back to cited text no. 105    
106.Zager RA. Organic anion infusions exacerbate experimental acute renal failure. Am J physio11983;244:F48-55.  Back to cited text no. 106    
107.Knochel JP. Catastrophic medical events with exhaustive exercise: "White Collar rhabdomyolysis". Kidney Int 1990;38:709-­19.  Back to cited text no. 107    
108.Rainford DJ, Stevens PE. Acute renal failure from tubular injury. In: Cameron S, Davison AM, Grunfeld JP, Kerr D, Ritz E, (eds), Oxford Textbook of Clinical Nephrology. Oxford University Press. Oxford 1992;1006-14.  Back to cited text no. 108    
109.Schiff HB, MacSearraigh ET, Kallmeyer Je. Myoglobinuria, rhabdomyolysis and marathon running. QJMed 1978;47:463-72.  Back to cited text no. 109    
110.Rose BD. Acute renal failure prerenal disease versus acute tubular necrosis. In: Pathophysiology of renal disease; McGraw Hill Book Company. New York 1987:92.  Back to cited text no. 110    
111.Akmal M., Bishop JE, Telfer N, Norman A W, Massry SG. Hypocalcemia and hypercalcemia in patients with rhabdomyolysis with and without renal failure. J Clin Endocrinol Metab 1986; 63:137- 42.  Back to cited text no. 111    
112.Meroney WH, Amey GK, Se_ WE, Balch HH. The acute calcification of traumatized muscle, with particular reference to acute post-traumatic renal insufficiency. J Clin Invest 1957)6:825-32.  Back to cited text no. 112    
113.Reis ND, Michaelson M. Crush injury to the lower limbs: treatment of the local _ury. J Bone Joint Surg Am 1986;68:414-8.  Back to cited text no. 113    
114.Rainford DJ. Pigment nephropathy. In: acute renal failure. Rainford DJ and Sweny P (eds). Farrand Press, London 1990;129-­44.  Back to cited text no. 114    
115.Wakabayashi Y, Kikuno T, Ohwada T, Kikawada R. Rapid fall in blood myoglobin in massive rhabdomyolysis and acute renal failure. Intensive Care Med 1994 ;20: 109-­12.  Back to cited text no. 115    

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Ghulam Hassan Malik
Department of Internal Medicine, Security Forces Hospital, P.O. Box 3643, Riyadh 11481
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    Introduction
    Physiologic Anat...
    Etiopathogenesis...
    A. Traumatic Rha...
    The Crush Syndrome
    Physical Torture
    Prolonged Muscle...
    B. Non-traumatic...
    Arterial Emboliz...
    Metabolic Disorders
    Muscle Diseases
    Toxins and Drugs
    Infections and E...
    Prolonged Coma
    Heat Stroke and ...
    Carbon Monoxide ...
    Pathophysiology ...
    Clinical Feature...
    Prevention and T...
    Prognosis
    Acknowledgment
    References
    Article Tables
 

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