Acute Myoglobinuric Renal Failure Research Articles

Some Kinetic Considerations in High Cut‐Off Hemodiafiltration for Acute Myoglobinuric Renal Failure

The kinetics of myoglobin in severe rhabdomyolysis and dialysis-dependent myoglobinuric acute kidney injury (Mb-AKI) is still not well elucidated, and more detailed knowledge could improve the now empiric use of rapid extracorporeal myoglobin removal by high cut-off (HCO) hemodialysis treatments. Eighteen adult patients with severe dialysis-dependent Mb-AKI (median serum concentration of myoglobin 57.4 mg/L) participated in the prospective clinical study, assessing myoglobin kinetics during HCO hemodiafiltration (HCO HDF). High initial serum concentrations of myoglobin (median 57.4 mg/L), together with protracted myoglobin appearance in the blood, indicated a large accumulation of myoglobin in body fluids. Extra-renal endogenous metabolic myoglobin clearance was delayed, with a slow exponential fall in serum myoglobin (t½ 35 h). A mean myoglobin clearance of 90-94 mL/min, a reduction ratio of 80%, and a rapid exponential fall (t½ 1 h) in serum and dialysate myoglobin were achieved by HCO HDF. Half of the cumulative myoglobin removal was accomplished in 3-5 h, with an additional removal of 7% each hour thereafter. A 2.4-fold rebound in serum myoglobin followed the HCO procedures. Large amounts of myoglobin are released into the circulation, and its endogenous metabolic clearance in dialysis-dependent Mb-AKI is slow. Owing to its rapid and highly efficient myoglobin elimination, HCO HDF may represent a valuable tool in the initial management of severe Mb-AKI, with a potential for earlier application in the future.

A Case of Cocaine-Induced Myopathy

A Case of Cocaine-Induced Myopathy

Sickle Cell Trait and Fatal Rhabdomyolysis in Football Training

We report the athletic, the clinical, and the pathological details of a case of fatal rhabdomyolysis during training in a college football player with sickle cell trait (SCT) who collapsed minutes after running 16 successive sprints of 100 yd each. The player, 19 yr old, African American, was apparently healthy when he took the field for the conditioning run. No exertional heat illness was present. After collapsing on-field, the player soon went into coma and developed fulminant rhabdomyolysis, profound lactic acidosis, acute myoglobinuric renal failure, refractory hyperkalemia, and disseminated intravascular coagulation. Despite intensive care in the hospital, he died about 15 h after admission, likely from a hyperkalemic cardiac arrhythmia; the terminal rhythm was pulseless electrical activity. The forensic autopsy confirmed that the cause of death was acute exertional rhabdomyolysis associated with SCT. Counting this case, at least 15 college football players with SCT have died from complications of exertional sickling, as have younger football players and other athletes. In SCT, maximal, sustained exercise evokes four forces that can foster sickling: hypoxemia, acidosis, hyperthermia, and red cell dehydration. The setting, the clinical and laboratory features, and the clinicopathological correlation here suggest that the fulminant rhabdomyolysis and its fatal sequelae were from exertional sickling. These data suggest that screening and simple precautions for SCT may be warranted to prevent tragedies like this and enable all athletes with SCT to thrive in their sports.

Rhabdomyolysis and Acute Myoglobinuric Renal Failure in a Patient With Bilateral Pheochromocytoma Following Open Pyelolithotomy

Rhabdomyolysis is an unusual manifestation of pheochromocytoma. Early diagnosis and prompt management are crucial, as it may have life-threatening consequences. This is the case of a 19-year-old man with bilateral pheochromocytoma complicated with rhabdomyolysis and acute myoglobinuric renal failure after surgery for nephrolithiasis. A massive catecholamine release during the procedure manifested itself as a hypertensive crisis, producing severe vasoconstriction and thereby provoking ischemia of the patient's muscle tissue. This insult resulted in rhabdomyolysis and acute myoglobinuric renal failure. After making sure that all necessary medical precautions were performed, including blood pressure stabilization with alpha receptor blockade and adequate fluid replacement, the patient successfully underwent a bilateral cortex-sparing medullar adrenalectomy. The operation specimen was reported as pheochromocytoma.

Mechanical muscle-crush injury and acute muscle-crush compartment syndrome

An extensive muscle-crush injury culminating in a crush syndrome is often lethal unless treated actively and promptly. The causes of death in crush syndrome include hypovolaemic shock, hyperkalaemia, hypocalcaemia, metabolic acidosis, acute myoglobinuric renal failure and the acute muscle-crush

Rhabdomyolysis and myoglobinuria

Rhabdomyolysis is a disorder characterized by acute damage of the sarcolemma of the skeletal muscle leading to release of potentially toxic muscle cell components into the circulation, most notably creatine phosphokinase (CK) and myoglobin, and is frequently accompanied by myoglobinuria. Therefore, the term myoglobinuria is often used interchangeably with the term rhabdomyolysis. This disorder may result in potential life-threatening complications such as acute myoglobinuric renal failure, hyperkalemia and cardiac arrest, disseminated intravascular coagulation, and compartment syndrome. The condition is etiologically heterogeneous and may result from a large variety of diseases affecting muscle membranes, membrane ion channels, and muscle energy supply including acquired causes (e.g., exertion, crush injury and trauma, alcoholism, drugs, and toxins) and hereditary causes (e.g., disorders of carbohydrate metabolism, disorders of lipid metabolism, or diseases of the muscle associated with malignant hyperthermia). In many patients with idiopathic recurrent rhabdomyolysis, specific inherited metabolic defects have not been recognized up to now.

Rescue and Salvage of Casualties Suffering from the Crush Syndrome after Mass Disasters

Extensive muscle crush injury culminating in the crush syndrome (CS) is often lethal unless promptly and vigorously treated. The causes of death in the CS are extreme hypovolemic shock, hyperkalemia, hypocalcemia, metabolic acidosis, acute myoglobinuric renal failure, and the compartment syndrome. Treatment consists of early massive volume replacement, preferably administered in the field, followed by forced alkaline solute (mannitol) diuresis. With this regimen, it is possible to increase substantially the survival of lives and limbs and to prevent acute myoglobinuric renal failure in patients suffering from the CS. Preliminary experience suggests that intravenous hypertonic mannitol is protective also to the injured muscle and can be used as a noninvasive adjunct in the management of compartment syndrome in humans. Moreover, by preserving muscular integrity, mannitol can conceivably reduce sarcolemmal leakage of the nephrotoxic myoglobin urate and phosphate and thus further defend kidney function. Furthermore, mannitol reduces the plasma pool of these nephrotoxic metabolites by increasing urinary elimination.

Myoglobin Clearance during Continuous Veno-Venous Hemofiltration with or without Dialysis

The management of acute myoglobinuric renal failure, the major complication of rhabdomyolysis, continues to be a treatment dilemma for the clinician as limited therapeutic options are available. Previously, we have demonstrated that continuous arteriovenous hemofiltration (CAVH) is an effective technique for removing myoglobin in an animal model. In the present study, swine were administered four grams of equine myoglobin intravenously and underwent the continuous veno-venous hemofiltration (CVVH) procedure for six hours each. Animals were studied in each of the following groups: CVVH at a pump rate 100 ml/minute, CVVH at a pump rate 200 ml/minute and CVVH at a pump rate 100 ml/minute plus dialysis at a dialysate flow rate of one Liter/h. Once the filtering process was initiated there was a rapid and sustained production of ultrafiltrate in all groups. The amount of myoglobin excreted in the ultrafiltrate over the six-hour filtering period was 688, 948 and 570 mg which corresponded to 17, 24 and 14 percent of the administered dose, respectively, for the three treatments. In comparison to previous CAVH experiments, CVVH removed more circulating myoglobin and the addition of the dialysis component did not appear to improve removal. Based on these findings, it appears that the CVVH hemofiltration system is a viable option for the removal of systemic myoglobin.

Evaluation of Myoglobin Clearance during Continuous Hemofiltration in a Swine Model of Acute Renal Failure

Rhabdomyolysis is characterized by extensive damage of striated muscle, while the major complication of this disease is the development of acute myoglobinuric renal failure. Although first described more than five decades ago very little has changed with regard to the management of this entity as conventional hemodialysis has not been shown to effect myoglobin elimination. However, continuous arteriovenous hemofiltration (CAVH) offers an alternative to conventional hemodialysis as this procedure is more effective particularly for removing larger molecular weight substances such as myoglobin. We studied the effect of CAVH on myoglobin clearance in an animal model of acute myoglobinuric renal failure. Swine (n = 6) were given 4 grams of equine myoglobin intravenously and underwent the CAVH procedure for six hours each. Once the filtering process was initiated there was a rapid and sustained production of ultrafiltrate. The clearance of myoglobin via the hemofilter was 2.05 +/- 1.48 L/day. The amount of myoglobin excreted in the ultrafiltrate over the six hour filtering period was 410 +/- 234 mg which accounts for 10.27 +/- 5.85 percent of the administered dose. Based on these findings, it appears that the hemofiltration system is a viable option for the removal of myoglobin from the systemic circulation.

Unusual pattern of reversible renal hyperechogenicity associated with acute myoglobinuric renal failure

Unusual pattern of reversible renal hyperechogenicity associated with acute myoglobinuric renal failure

Rhabdomyolysis: a neglected priority in the early management of severe limb trauma

Potentially dangerous muscle damage is often overlooked in the salvage of severely injured limbs. Muscle damage may be due to direct injury with crush, laceration or contusion. This may be complicated by ischaemia through prolonged compression at the time of injury or later as a result of raised compartmental pressure. The result of muscle damage, irrespective of cause, is rhabdomyolysis, in which alteration of the cell membrane occurs with release of intracellular contents. The systemic effect of rhabdomyolysis can vary from transient mild hyperkalaemia, hypocalcaemia, myoglobinaemia and elevated creatinine phosphokinase to the lifethreatening crush syndrome with hypovolaemic shock, cardiac arrhythmias and acute myoglobinuric renal failure. The local effect is increased capillary permeability resulting in accumulation of tissue fluid and raised compartment pressure. Rhabdomyolysis may therefore cause compartment syndrome; however, the converse is true, with prolonged compartment syndrome small vessel thrombosis may cause cellular death with subsequent rhabdomyolysis despite axial vessel patency (Kitka et al., 1987). The crush syndrome was first described in air raid victims trapped under falling masonry (Bywaters and Beall, 1941); however, it may be encountered in peacetime as is illustrated by the following three cases.

Acute Myoglobinuric Renal Failure in a Patient With IgA Nephropathy

. A 36-year-old black man presented on a Friday evening with a I-week history of right-sided abdominal tenderness, chills, and dark urine. He had been treated by his family physician with oral tetracycline 100 mg once daily for 3 days, without benefit, and came to the hospital complaining of oliguria. Physical examination was not contributory, and urinalysis by a resident was reported as showing 3 giL of proteinuria, many red blood cells per high-power field, and several red blood cell casts. Serum creatinine was 314 /Lmol/L (3.6 mg/dL). There was a vague history of dark urine for a few days approximately 6 months earlier. A clinical diagnosis of rapidly progressive glomerulonephritis was made, with a concern that the lesion was superimposed on underlying 19A nephropathy, in view of the previous history of an episode of dark urine. Methyl prednisolone I g/d intravenously was administered for 3 days, and renal biopsy was planned for the following Monday. The serum creatinine increased to 750 /Lmol/L (8.5 mg/dL) and the potassium to 6.7 mmol/L. Hemodialysis three times weekly was initiated. Antineutrophil cytoplasmic antibodies were reported as absent, but on Monday morning the creatinine kinase was > 33,000 U/L (normal < 200 U/L). Hypocalcemia (1.23 mmol/L [4.93 mg/dL]) and hyperphosphatemia (5.28 mmol/ L [16.4 mg/dL]) were present. Myoglobin was detected in urine obtained 3 days after admission. Steroid therapy was discontinued. On further questioning, the patient admitted to some muscle tenderness and stiffness diffusely, but there was no weakness. The patient also confessed to drinking an unspecified volume of beer just before the illness started. Renal biopsy was obtained. Subsequently the patient's renal function returned to normal after 3 weeks of dialysis.

Disseminated Intravascular Coagulation and Acute Myoglobinuric Renal Failure

Miller, Frank MD; Friedman, Richard MD; Tanenbaum, Judith MD; Griffin, Anne MD Author Information

A Case of Neuroleptic Malignant Syndrome with Acute Renal Failure after the Discontinuation of Sulpiride and Maprotiline.

A 46-year-old man developed neuroleptic malignant syndrome with acute myoglobinuric renal failure after the discontinuation of sulpiride and maprotiline treatment. He showed the characteristic features of hyperpyrexia, altered consciousness, muscle rigidity, and autonomic dysfunction. Laboratory data showed lysis of skeletal muscle cells and renal impairment. Muscle biopsy revealed necrosis and regenerative changes in muscle fibers. Renal biopsy showed focal tubulitis and interstitial infiltration of small inflammatory cells. The combination of sulpiride and maprotiline has not previously been reported to be the cause of neuroleptic malignant syndrome and acute myoglobinuric renal failure.

Pheochromocytoma presenting as rhabdomyolysis and acute myoglobinuric renal failure

Pheochromocytoma presenting as rhabdomyolysis and acute myoglobinuric renal failure

Pheochromocytoma Presenting as Rhabdomyolysis and Acute Myoglobinuric Renal Failure

We report the case of a previously healthy young woman who presented with the sudden onset of rhabdomyolysis and myoglobinuric renal failure, requiring hemodialysis for 3 weeks. Common causes of rhabdomyolysis were ruled out; as renal function returned, severe hypertension was noted and a pheochromocytoma was diagnosed. We suggest that pheochromocytoma causes rhabdomyolysis and myoglobinuria via catecholamine-mediated vasoconstriction and skeletal muscle ischemia.

Cocaine-associated acute myoglobinuric renal failure : Pogue VA, Nurse HM. Am J Med. 1989;86:183-6

Cocaine-associated acute myoglobinuric renal failure : Pogue VA, Nurse HM. Am J Med. 1989;86:183-6

Cocain-associated acute myoglobinuric renal failure

purpose: Abuse of cocaine is associated with serious medical complications involving the heart, central nervous system, and gastrointestinal tract. Renal complications appear to be uncommon. We describe herein after patients with rhabodmyolysis and acute myoglobinuric renal failure temporally related to cocaine use. case reports: Acue cocaine intoxication was the most common presentation and rhabdomyolysis was an unexpected finding. Renal failure progressed rapidly in all patients, necessitating dialysis in two. The prognosis was good, and all patients survived. The mechanism of cocaine injury is unclear, possibilities include increased muscle activity, muscle compression, hyperthermia, and vasospasm with muscle ischmia. conclusion: Rhabdomyolysis with acute renal failure and should be recognized as a possible complication of cocaine abuse.

CAVH in myorenal syndrome.

Rhabdomyolysis describes the damage of striated muscle cell membranes which leads to fluid and electrolyte imbalances and to liberation of muscle components. The causes leading to rhabdomyolysis are numerous. The renal tubular overload with myoglobin can induce acute renal failure. The acute myoglobinuric renal failure in patients with crush- syndrome has been known since the first description by Bywaters and Beall (1941). This description gave rise to numerous reports on cases of acute renal insufficiency after traumatic or nontraumatic rhabdomyolysis. In about 8-20% of patients with rhabdomyolysis an acute myoglobinuric renal failure is observed. Myoglobinemia, toxic muscle cell membrane components, and alteration of renal perfusion lead to acute tubular necrosis. Circulatory collapse and shock represent additional factors in the pathogenesis of the acute renal failure (Bogaerts et al., 1982; Colombo et al., 1985; Grossmann et al., 1974; Hamilton et al, 1971; Hamilton et al., 1972; Kathrein et al., 1983; Koffler et al., 1976; Rowland and Penn, 1972; Sidorara et al., 1985). The usual therapy consists of adjustment of volume depletion and balancing of acid-base-electrolyte metabolism.KeywordsAcute Renal FailureAcute Tubular NecrosisMalignant HyperthermiaAcute Renal InsufficiencyMyoglobin LevelThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Haloperidol使用者にみられたミオグロビン血症を呈した急性腎不全の2例

向精神薬のhaloperidol使用者にミオグロビン血症を呈した急性腎不全の発生をみた稀な2例を経験したので報告する. 症例1, 55歳, 男性. 1978年8月退行期精神病にて某精神病院へ入院. 同年11月からhaloperidolの投与を受け, 投薬18日頃より, 発熱, 発汗, 嚥下障害, 頻脈, 軽度の意識障害など出現し, 悪性症候群と診断され, 12月はじめhaloperidolの投与は中止された. その後乏尿から無尿となり, 高窒素血症が出現し, 急性腎不全にて12月10日当院へ入院. ただちに血液透析を施行し, 約1ヵ月後には腎不全の回復をみた. 入院時, GOT, LDH, CPK, 血中, 尿中ミオグロビンの高値を示した. 筋生検では神経原性の変化を示し, 腎生検では著変を認めなかった. 症例2, 42歳, 男性. 1980年はじめより, 舞踏病のため抗痙攣剤およびhaloperidolが投与されていたが, 1982年1月haloperidolを, 続いて抗痙攣剤を中止したところ, 不随意運動が激しくなり, 2月17日haloperidol 5mgを筋注した. 18日より乏尿となり, 20日より腹膜灌流を施行. 24日血液透析目的にて当院へ入院. 11回血液透析を施行し, 腎不全の回復をみた. 経過中, GOT, LDH, CPK, 血中ミオグロビンの高値を認めた. 2症例の急性腎不全の原因はrhabdomyolysisによると考えられ, ミオグロビン血症とhaloperidolとの関係について考察を加えた.