Peak value of blood myoglobin predicts acute renal failure induced by rhabdomyolysis

PurposeAcute renal failure (ARF) is the most important complication of rhabdomyolysis. Serial measurements of blood myoglobin might be useful for predicting rhabdomyolysis-induced ARF.MethodsThirty patients with rhabdomyolysis were examined. The causes of rhabdomyolysis were trauma, burns, and ischemia, among others. Serial blood myoglobin levels were measured by immunochromatography, and the peak value was determined. The relationship between blood myoglobin levels and the incidence of ARF was evaluated.ResultsThe median peak blood myoglobin level was 3335 ng/mL. Acute renal failure occurred in 12 patients (40%). Nine patients (30%) underwent renal replacement therapy. Peak creatine kinase and peak blood myoglobin levels in the ARF group were significantly higher than those in the non-ARF group. Three patients in the ARF group were treated with renal replacement therapy before occurrence of uremia because of extremely high levels of blood myoglobin (>10 000 ng/mL). Receiver operating characteristic analysis showed that the area under the curve for blood myoglobin that predicted ARF was 0.88, and the best cutoff value for blood myoglobin was 3865 ng/mL.ConclusionsThe peak value for blood myoglobin might be a good predictor of rhabdomyolysis-induced ARF. Early renal protective therapies should be considered for patients with rhabdomyolysis at high risk of ARF.     

Clinical factors in predicting acute renal failure caused by rhabdomyolysis in the ED

Purpose

This study aimed to determine the clinical factors in predicting acute renal failure (ARF) in rhabdomyolysis and investigate the potential risk of renal replacement therapy (RRT).

Basic Procedures

From 2006 to 2011, we retrospectively analyzed 202 patients 65 years or younger with a definite diagnosis of rhabdomyolysis and serum creatinine phosphokinase levels greater than 1000 IU/L. The related clinical factors were analyzed in the patients with ARF caused by rhabdomyolysis. In addition, receiver operating characteristic curves were used to establish the appropriate cutoff values of serum biomarkers in predicting ARF.

Main Findings

The most common causes of rhabdomyolysis were trauma (n = 54; 26.7%) and infections (n = 37; 18.3%). Of the 202 patients, 29 (14.4%) developed ARF, and RRT was indicated for 5 of these 29 patients. Predictive factors for ARF were dark urine, initial and peak serum myoglobin level, rhabdomyolysis caused by body temperature change, and an elevated serum potassium level. Receiver operating characteristic analysis showed that the best cutoff value of initial serum myoglobin level for predicting ARF was 597.5 ng/mL. Risk factors for RRT in patients with ARF were etiologies of rhabdomyolysis, peak blood urea nitrogen and creatinine levels, and the creatinine phosphokinase level on the third day as rhabdomyolysis developed.

Principal Conclusions

Age, dark urine, etiologies, serum levels of blood urea nitrogen, creatinine and potassium, and initial and peak serum myoglobin levels may serve as important factors in predicting ARF in patients with rhabdomyolysis. We suggest that the appropriate cutoff value of initial serum myoglobin for predicting ARF is 600 ng/mL.     

Etude de la myoglobinemie et de son evolution au cours de l'infarctus du myocardeStudy on myoglobinemia and its development during myocardial infarction

Thirty six patients suffering from myocardial infarction were investigated by assay of their serum myoglobin, total creatine kinase and creatine kinase isoenzyme MB activities. Determination of serum myoglobin presents, with regard to creatine kinase MB, two major advantages: a very early increase after the onset of the pain (about three hours later) and a very quick clearance, allowing the diagnosis of a second episode of necrosis after about one day.     

CRRT联合HP治疗横纹肌溶解综合征伴急性肾损伤的效果及护理

目的探讨连续性肾脏替代治疗（CRRT）联合血液灌流（HP）治疗横纹肌溶解综合征（RM）伴急性肾损伤的临床疗效及护理方法。方法应用CRRT联合HP治疗RM伴急性肾损伤病人12例,给予恰当的护理,观察治疗前、治疗12、24h后病人血肌红蛋白（Mb）、肌酸激酶（CK）、肌酐（Cr）水平变化。结果与治疗前比较,治疗12、24h后病人血Mb、CK、Cr显著下降,差异有显著性（F=4.75~9.68,P〈0.05）。结论应用CRRT联合HP治疗RM伴急性肾损伤,可明显改善肾功能。     

Rhabdomyolysis secondary to lovastatin therapy

We report a case of lovastatin-induced rhabdomyolysis and resulting life-threatening renal failure. Lovastatin, a hypocholesterolemic agent, decreases endogenous cholesterol synthesis by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.88). This agent has been implicated in causing rare serious side effects in various clinical settings; however, the mechanism of these adverse reactions is not understood. The clinical course of our patient was characterized by profound muscle weakness with marked increases in serum creatine kinase and myoglobin. Light- and electron-microscopic studies of skeletal muscle of our patient demonstrated a noninflammatory myopathy suggestive of ongoing rhabdomyolysis with vacuolization and focal degeneration of myocytes. The patient's symptoms and the laboratory values referable to rhabdomyolysis resolved after discontinuation of the drug. We speculate that the rhabdomyolysis was due to mitochondrial damage secondary to inadequate synthesis of coenzyme Q and heme A, members of the electron-transport system of the inner mitochondrial membrane.     

Mechanisms of Toxicity,Clinical Features,and Management of Acute Chlorophenoxy Herbicide Poisoning: A Review

Introduction: Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism. Between January 1962 and January 1999, 66 cases of chlorophenoxy herbicide poisoning following ingestion were reported in the literature. Features following ingestion: Adjuvants in the formulations may have contributed to some of the features observed. Vomiting, abdominal pain, diarrhea, and, occasionally, gastrointestinal hemorrhage were early effects. When present, hypotension was predominantly due to intravascular volume loss, although vasodilation and direct myocardial toxicity may have contributed in some cases. Neurotoxic features included coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation, and paralysis. Hypoventilation occurred not infrequently, usually in association with central nervous system depression, but respiratory muscle weakness was a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, and myotonia were observed and increased creatine kinase activity was noted in some cases. Other clinical features reported included metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia, and hyperventilation. Twenty-two of 66 patients died. Features following dermal and inhalational exposure: Substantial dermal or inhalational 2,4-dichlorophenoxyacetic acid exposure has occasionally led to systemic features but no such reports have been published in the last 20 years and no fatalities have been reported at any time. Substantial dermal exposure has been reported to cause mild gastrointestinal irritation after a latent period followed by progressive mixed sensory-motor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have also occurred after occupational inhalation exposure, with or without dermal exposure. Management: In addition to supportive care, alkaline diuresis to enhance herbicide elimination should be considered in all seriously poisoned patients. Limited clinical data suggest that hemodialysis produces similar herbicide clearance to alkaline diuresis without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient. Conclusions: While chlorophenoxy herbicide poisoning is uncommon, ingestion of a chlorophenoxy herbicide can result in serious and sometimes fatal sequelae. In severe cases of poisoning, alkaline diuresis or hemodialysis to increase herbicide elimination should be considered.     

Acute kidney injury due to rhabdomyolysis and renal replacement therapy: a critical review

Rhabdomyolysis, a clinical syndrome caused by damage to skeletal muscle and release of its breakdown products into the circulation, can be followed by acute kidney injury (AKI) as a severe complication. The belief that the AKI is triggered by myoglobin as the toxin responsible appears to be oversimplified. Better knowledge of the pathophysiology of rhabdomyolysis and following AKI could widen treatment options, leading to preservation of the kidney: the decision to initiate renal replacement therapy in clinical practice should not be made on the basis of the myoglobin or creatine phosphokinase serum concentrations.     

Rapid fall in blood myoglobin in massive rhabdomyolysis and acute renal failure

Objective Myoglobin kinetics of removal from the circulation were studied in patients following massive rhabdomyolysis, to see if myoglobin remains for long in the circulation in the anuric state and if myoglobin elimination was affected by therapeutic manipulation such as haemofiltration or haemodialysis.Design Randomised and controlled study.Setting Intensive care unit of a tertiary care teaching hospital.Patients 26 patients of rhabdomyolysis whose serum myoglobin exceeded more than 500 nmol/l. Thirteen patients developed acute renal failure and underwent treatment with blood purification (Group HD). The remaining 13 patients did not require treatment with blood purification (control subjects, Group non-HD).Interventions In patients of group HD, twelve were treated with haemofiltration and/or haemodialysis. One was treated with peritoneal dialysis. The patient of group non-HD were treated with fluid infusion alone.Measurements and results The serum concentrations of myoglobin were serially determined. The highest levels of myoglobin was 1641±484 nmol/l (mean±SEM) in the group non-HD and were 8957±2300 in the group HD. In the group non-HD, the blood myoglobin fell exponentially once myoglobin release into the circulation ceased. This was also noted in the group HD. The exponential decrease was observed even on the days when the patient passed little urine or treatment with blood purification was not performed.Conclusion In patients with massive myoglobinaemia, the blood myoglobin rapidly fell independent of renal function or any therapeutic manipulation. The results indicate that extrarenal factors played a major role in disposing circulating myoglobin in such patients.     

Prolonged low-dose dopamine infusion induces a transient improvement in renal function in hemodynamically stable, critically ill patients: a single-blind, prospective, controlled study

OBJECTIVE: To evaluate the length of the effects of long-term (48 hrs), low-dose dopamine infusion on both renal function and systemic hemodynamic variables in stable nonoliguric critically ill patients. DESIGN: Prospective, single-blind, controlled clinical study. SETTING: University hospital, 19-bed multidisciplinary intensive care unit. PATIENTS: Eight hemodynamically stable, critically ill patients with a mild nonoliguric renal impairment (creatinine clearance between 30 and 80 mL/min). INTERVENTIONS: Each patient consecutively received 4 hrs of placebo, followed by a 3 microg/kg/min dopamine infusion during 48 hrs, then a new 4-hr placebo period. We measured cardiac output and other hemodynamic variables by using a pulmonary artery catheter. The bladder was emptied to determine urine volume and to collect urine samples. Measurements were performed at six times: after the initial control of 4 hrs of placebo (C1); after 4 hrs (H4), 8 hrs (H8), 24 hrs (H24), and 48 hrs (H48) of dopamine infusion; and after the second control of 4 hrs of placebo (C2). MEASUREMENTS AND MAIN RESULTS: We saw no significant change in systemic hemodynamic variables with dopamine at all times of infusion. Diuresis, creatinine clearance, and the fractional excretion of sodium (FENa) at C1 and C2 were not different. Urine flow, creatinine clearance, and FENa increased significantly 4 hrs after starting dopamine (for all these changes, p < .01 vs. C1 and C2). The maximum changes were obtained at H8, with an increase of 50% for diuresis, 37% for creatinine clearance, and 85% for FENa (for all these changes, p < .01 vs. C1 and C2). But these effects waned progressively from H24, and both creatinine clearance and FENa at H48 did not differ from control values. CONCLUSIONS: In stable critically ill patients, preventive low-dose dopamine increased creatinine clearance, diuresis, and the fractional excretion of sodium without concomitant hemodynamic change. These effects reached a maximum during 8 hrs of dopamine infusion. But despite a slight persistent increase in diuresis, improvement in creatinine clearance and FENa disappeared after 48 hrs. According to these data, it is likely that tolerance develops to dopamine-receptor agonists in critically ill patients at risk of developing acute renal failure.     

运动性横纹肌溶解症37例诊治分析

目的探讨运动性横纹肌溶解症的临床诊治方法,提升治疗效果。 方法回顾性分析武警湖北省总队医院和华中科技大学同济医院2007年10月至2018年11月收治的37例运动性横纹肌溶解症患者的临床资料。37例患者予以抗感染、补充血容量、止吐、退热、碱化尿液等对症治疗。8例急性肾功能不全患者,血肌酐>442 μmol/L或者血钾>6.5 mmol/L,采用血液透析治疗。 结果患者平均住院时间9（4~25）d。37例患者出院时血清肌酸激酶值均降至正常范围或轻度异常升高。8例急性肾功能不全患者经血液透析治疗后,复查肾功能、电解质均恢复正常。 结论运动性横纹肌溶解症首发症状多样,容易误诊、漏诊。早期检查血清肌酸激酶、肌红蛋白有利于及早确定诊断。抗感染治疗、对症治疗、补充血容量、碱化尿液、血液透析等综合治疗有利于患者预后。对运动性横纹肌溶解症所致重度急性肾功能不全患者,行血液透析治疗能有效挽救肾功能,降低患者病死率。     

连续性血液滤过治疗横纹肌溶解症致急性肾损伤患者的效果观察及护理

目的探讨连续性血液滤过治疗横纹肌溶解症致急性肾损伤(akiacutekidneyinjury,AKI)患者的效果及总结护理经验。方法对10例横纹肌溶解症致AKI患者采用连续性血液滤过治疗及相应的护理措施。结果经过治疗,10例患者中有7例肾功能恢复正常,治愈出院;2例病情好转出院;1例需要长期维持性血液透析治疗。治疗后患者血清肌酸磷酸激酶(creatine phosphate kinase,CPK)、肌红蛋白(myoglobin,Mb)、尿素氮(urea nitrogen,BUN)、肌酐(creatinine,Scr)、天门冬氨酸氨基转移酶(aspartate amino transferase,AST)浓度逐渐下降,血K+恢复至正常水平,尿量逐渐增多恢复至正常,治疗前后比较,均P0.05,差异具有统计学意义。结论连续性血液滤过治疗及相应的护理对保证连续性血液滤过治疗的效果,改善横纹肌溶解症预后有着重要意义。     

横纹肌溶解综合征致急性肾衰竭23例诊治分析

目的 :总结横纹肌溶解综合征 (RM)合并急性肾衰竭 (RM ARF)的发生率以及治疗效果和临床转归。方法 :2 3例 RM ARF患者中男 17例 ,女 6例 ;平均年龄 (38.0 0± 17.13)岁。所有患者均检测血清肌酶、血肌红蛋白 (Mb)、白蛋白 (Alb)以及血生化指标检测 ,包括电解质、肝功能、肾功能、血尿酸 (UA)、血红蛋白(Hb)、血气分析等。3例患者行肾活检术 ,并做肾小管 Mb免疫组织化学 En Vision法检测。结果 :RM ARF发生率占同期 ARF的 5 .96 % (2 3/ 386 ) ,占急性小管间质病变的 9.75 % (2 3/ 2 36 )。血肌酸磷酸激酶 (CPK)78.2 6 %升高 (>16 .6 7μmol· s- 1 · L- 1 ) ,血 P3+ 、U A、K+ 分别为 78.2 6 %、95 .6 5 %、86 .96 %升高 ,血 Ca2 +86 .96 %下降 ,代谢性酸中毒 91.30 % ,高分解代谢 82 .6 1%。 3例肾脏病理显示急性肾小管坏死 (ATN) ,肾小管Mb免疫组织化学全部阳性。 8例患者有肌肉损伤 ,但未行肌电图检查和肌肉活检。 18例行血液净化 ,其中 5例血液透析 (HD) ,7例腹膜透析 (CAPD) ,6例连续性静静脉血液滤过 (CVVH)。经综合治疗 ,RM ARF病死率34.78% ,存活率 6 5 .2 2 % ,其中 12例肾功能完全恢复正常。结论 :RM大多为非创伤性 ;血清肌酶和血生化检测可提高 RM ARF诊断率 ;肾脏病理活检有助于确诊 RM AR     

Myoglobin concentration, creatine kinase activity, and creatine kinase B subunit concentrations in serum during thyroid disease

Changes in values for myoglobin, total creatine kinase (EC 2.7.3.2), and creatine kinase B-subunit in the serum of patients with thyroid disease are compared with values for these during the 24-h after myocardial infarction. Concentrations of all three of these muscle-derived proteins were significantly higher than normal in patients with primary hypothyroidism, and declined with treatment. Values for total creatine kinase activity were below-normal in hyperthyroid patients, but increased after treatment. Values for total creatine kinase and, to a lesser extent, myoglobin in hypothyroidism extend into the range of values observed after myocardial infarction. The mechanism of the changes in these analytes in hypothyroidism may be related to increased leakage from skeletal-muscle cells or diminished clearance from the circulation, or both.     

Rhabdomyolysis in the intensive care unit

Rhabdomyolysis is a clinical syndrome defined by muscle breakdown and subsequent release of intracellular contents. There are many etiologies of rhabdomyolysis, classified here as congenital and acquired; compartment syndrome secondary to trauma with reperfusion injury is one common precipitating factor. Regardless of the underlying etiology, the pathophysiology follows a similar pathway via myocyte destruction and release of myoglobin into the systemic circulation. Rhabdomyolysis-induced renal failure is caused by the precipitation of myoglobin in the renal tubules which is enhanced under acidic conditions. A high index of clinical suspicion is required to promptly recognize rhabdomyolysis, especially in the unconscious patient. Presenting symptoms include tea-colored urine and muscle weakness or fatigue. The diagnosis is confirmed most reliably with the finding of elevated serum creatine kinase levels. Early, aggressive resuscitation with either normal saline or lactated Ringer's solution to maintain an adequate urine output is the most important intervention in preventing the development of acute renal failure. There is insufficient clinical evidence supporting the routine administration of diuretics and bicarbonate to protect against the development of acute renal failure.     

Simvastatin-amiodarone interaction resulting in rhabdomyolysis, azotemia, and possible hepatotoxicity

OBJECTIVE: To describe the fifth reported instance, as of February 15, 2006, of a severe interaction between simvastatin and amiodarone and hypothesize inhibition of CYP3A4 as the major mechanism. CASE SUMMARY: A 72-year-old white man (178 cm, 77.2 kg) with diabetes mellitus, hyperlipidemia, hypertension, and mild azotemia was hospitalized on September 21, 2004, with thigh weakness, achiness, and dark urine for 7 days. Coronary artery bypass had been performed on July 7, 2004. Amiodarone 200 mg/day was started on July 10, and simvastatin 80 mg/day was initiated on August 13. Laboratory testing on the present admission included creatine kinase (CK) 19,620 U/L (reference range 60-224), blood urea nitrogen 50 mg/dL, creatinine 2.6 mg/dL, aspartate aminotransferase (AST) 912 U/L (30-60), alanine aminotransferase (ALT) 748 U/L (30-60), urine myoglobin 71,100 microg/L (<50), and serum myoglobin 13,877 microg/L (<110). Simvastatin and amiodarone were discontinued, and the patient was hydrated with forced alkaline diuresis. Thirteen days later, his CK was 323 U/L, creatinine 1.7 mg/dL, ALT 145 U/L, and AST 37 U/L. DISCUSSION: Simvastatin is metabolized primarily by CYP3A4, and amiodarone is a recognized inhibitor of this enzyme. This may, therefore, account for the presumed drug interaction. CONCLUSIONS: An objective causal assessment suggests that rhabdomyolysis, renal failure, and possibly hepatotoxicity were probably related to an amiodarone-simvastatin interaction.     

A Study on the Effects of Severe Repetitive Exercise on Serum Myoglobin, Creatine Kinase, Transaminases and Lactate Dehydrogenase

Two groups of young men taking part in a 24-day training courseinvolving increasingly severe exercise were studied. Serum myoglobin,creatine kinase, creatine kinase-MB, transaminases, lactatedehydrogenase, urea, creatinine, calcium and uric acid wereestimated at intervals. During the first few days, increasesin myoglobin and muscle enzymes correlated with the severityof the preceding exercise. Increases in myoglobin and muscleenzymes after the final most severe exercising were less thanwith the initial exercising, demonstrating the effect of physicaltraining. The changes in myoglobin and the muscle enzymes correlatedclosely. Elevated myoglobin levels persisted for over 24 hours.There was no consistent correlation between changes in myoglobinand uric acid, both of which have been considered responsiblefor the renal failure which may occur with rhabdomyolysis.     

Bench-to-bedside review: Rhabdomyolysis -- an overview for clinicians

Rhabdomyolysis ranges from an asymptomatic illness with elevation in the creatine kinase level to a life-threatening condition associated with extreme elevations in creatine kinase, electrolyte imbalances, acute renal failure and disseminated intravascular coagulation. Muscular trauma is the most common cause of rhabdomyolysis. Less common causes include muscle enzyme deficiencies, electrolyte abnormalities, infectious causes, drugs, toxins and endocrinopathies. Weakness, myalgia and tea-colored urine are the main clinical manifestations. The most sensitive laboratory finding of muscle injury is an elevated plasma creatine kinase level. The management of patients with rhabdomyolysis includes early vigorous hydration.     

Bench-to-bedside review: Rhabdomyolysis – an overview for clinicians

Rhabdomyolysis ranges from an asymptomatic illness with elevation in the creatine kinase level to a life-threatening condition associated with extreme elevations in creatine kinase, electrolyte imbalances, acute renal failure and disseminated intravascular coagulation. Muscular trauma is the most common cause of rhabdomyolysis. Less common causes include muscle enzyme deficiencies, electrolyte abnormalities, infectious causes, drugs, toxins and endocrinopathies. Weakness, myalgia and tea-colored urine are the main clinical manifestations. The most sensitive laboratory finding of muscle injury is an elevated plasma creatine kinase level. The management of patients with rhabdomyolysis includes early vigorous hydration.     

血清心脏型脂肪酸结合蛋白联合糖原磷酸化酶脑型检测在小儿脓毒症心肌损伤诊断中的临床价值

目的研究小儿脓毒症心肌损伤诊断中血清心脏型脂肪酸结合蛋白(FABP3)联合糖原磷酸化酶脑型(GPBB)检测的应用价值。方法采用回顾性分析方法,研究对象为2019年1月至2020年1月葫芦岛市中心医院收治的87例脓毒症患儿,根据是否出现心肌损伤划分为2组,心肌损伤患儿列入A组,共38例,未出现心肌损伤患儿列入B组,共49例;同时,选取同一时期入院就诊的44例的非脓毒症感染性疾病患儿作为研究对象,列入C组。3组患儿均选取用全自动血气分析仪测定肌红蛋白、肌钙蛋白Ⅰ,并选取酶联免疫吸附实验法测定GPBB、FABP3及肌酸激酶同工酶,比较3组患儿肌红蛋白、肌钙蛋白Ⅰ、GPBB、FABP3及肌酸激酶同工酶水平,并分析心肌损伤指标肌红蛋白、肌钙蛋白Ⅰ、肌酸激酶同工酶与血清FABP3、GPBB相关性。结果A组[(396.85±13.07)ng/mL、(3.08±0.06)ng/mL、(22.78±1.02)ng/mL、(34.45±2.41)ng/mL、(44.08±6.53)U/L]、B组[(68.26±12.45)ng/mL、(0.12±0.04)ng/mL、(9.17±1.08)ng/mL、(13.64±2.52)ng/mL、(20.85±7.01)U/L]患儿肌红蛋白、肌钙蛋白Ⅰ、GPBB、FABP3及肌酸激酶同工酶水平明显高于C组[(17.16±10.09)ng/mL、(0.04±0.03)ng/mL、(2.58±1.02)ng/mL、(4.34±3.02)ng/mL、(9.17±6.73)U/L],差异有统计学意义(P<0.05);A组患儿肌红蛋白、肌钙蛋白Ⅰ、GPBB、FABP3及肌酸激酶同工酶水平明显高于B组,差异有统计学意义(P<0.05)。脓毒症患儿血清FABP3、GPBB与肌红蛋白、肌钙蛋白Ⅰ、肌酸激酶同工酶均呈正相关(r=0.602、0.521;r=0.466、0.494;r=0.528、0.489,P<0.05)。结论小儿脓毒症心肌损伤诊断中血清FABP3联合GPBB检测的应用效果显著,可用于评估脓毒症患儿心肌损伤严重程度。     

Mécanismes et prise en charge de la tubulopathie liée à la rhabdomyolyse

Severe damage of skeletal muscle, referred to as rhabdomyolysis, is the cause of 10% of acute kidney injury (AKI) cases and AKI complicates 13–50% of traumatic or nontraumatic rhabdomyolysis. Hypovolemia and the direct nephrotoxic effect of myoglobin are thought to be the main factors involved in rhabdomyolysis-induced AKI. Myoglobin promotes kidney injuries through vasoconstrictive properties, proximal tubular injuries, and distal obstruction. Recently, we demonstrated that macrophages influence the long-term prognosis of this disease by exerting proinflammatory as well as profibrotic properties. Clinical management relies on early diagnosis (creatine kinase > 5,000 UI/l) and fluid resuscitation using isotonic sodium chloride. Despite optimal rehydration, patients can develop AKI and require renal replacement therapy (RRT). Severe hyperkalemia or metabolic acidosis is the main cause of RRT. Thus, intermittent hemodialysis rather than continuous RRT should be used as frontline RRT, if available. To date, alkalinization, as well as prophylactic intermittent hemodialysis with high cut-off membrane, did not demonstrate superiority on long-term renal function compared to conventional approach. While global prognosis is depending upon the cause of rhabdomyolysis, mortality increases from 22% to 59% as soon as patients develop AKI. Long-term prognosis is unknown. Animal models demonstrated that rhabdomyolysis can lead to renal fibrosis after several months of followup. This suggests that patients with rhabdomyolysis should be considered as at high risk to develop chronic kidney disease and therefore referred to nephrologists to minimize long-term consequences of chronic kidney disease.