Severe myoglobinuric acute kidney injury in a kidney recipient: rapid recovery after hemodialysis with the super high-flux membrane Theralite®â€©.

Myoglobinuric acute kidney injury (AKI) is a severe condition requiring early therapeutic strategies. Early recognition and treatment are crucial to reduce morbidity and mortality rate. Here, we report a kidney recipient with severe rhabdomyolysis and AKI secondary to parvovirus B19 infection. Initiation of hemodialysis with the super high-flux filter Theralite® (Gambro, cut-off 45 kDa, 2.1 m2) resulted in the clearance of myoglobin from 61 to 71% after 3 hours. Elimination rates of IL-6 and ß2-microglobulin were ~ 30 - 64% and 55 - 71% after 3 hours, respectively. Renal graft function rapidly recovered. The place of this effective but expensive procedure still needs to be defined and validated in high-risk patients.
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Myoglobin removal using high-volume high-flux hemofiltration in patients with oliguric acute kidney injury.

BACKGROUND: Rhabdomyolysis can cause acute kidney injury (AKI). It remains controversial whether or not myoglobin can be removed from the circulation with extracorporeal therapy and decrease the incidence of AKI. Therefore, we examined myoglobin removal in a series of 11 patients with oliguric AKI treated with high-volume hemofiltration. METHODS: Patients received prefilter hemofiltration using a polysulphone filter with a molecular size cutoff of 65 kDa and a surface area of 1.7 m(2). Sieving coefficients and myoglobin clearances were calculated at 6, 12, and 24 h after the start of hemofiltration. RESULTS: The mean sieving coefficient was 0.158, and the mean myoglobin clearance was 8.7 ml/min. CONCLUSION: Despite the use of high-volume hemofiltration, the removal of myoglobin was negligible. In patients with normal renal function, the anticipated amount of extracorporeal removal would not significantly impact renal exposure to myoglobin.

Border-crossers' nephropathy: the risk of coming to America.

Immigrants attempting to cross the border often wander for days without food or water, subsequently developing acute kidney injury (AKI) secondary to rhabdomyolysis. In this article, we describe our experience with myoglobinuric AKI in these border crossers. Records from all patients in the custody of the border patrol from 1 June 2010 to 30 June 2011, who had AKI defined by the Acute Kidney Injury Network (AKIN) criteria and a CK > 1000 IU/L, were reviewed. The age, gender, temperature, days in the desert, initial serum creatinine, CK on presentation, need for dialysis, length of hospital stay, and serum creatinine at discharge were recorded and analyzed. Forty-two patients developed myoglobinuric AKI with a mean age of 32.5 years. Among them, 38 were males and four females. There was a mean of 4.2 days in the desert. Seven had stage 1 AKI, 10 stage 2, and 25 stage 3. 5 patients required hemodialysis. Only one patient had a temperature >100.6ºF on arrival. CKs ranged between 1101 and 447,966 IU/L. Mean length of stay was 4 days. Two patients were discharged on hemodialysis and eight were discharged with serum creatinine levels of  >1.3 mg/dL. This is the largest series of myoglobinuric AKI reported in border crossers. The kidney injury is presumably due to the excessive heat combined with volume depletion. We have coined the term "border crossers' nephropathy" for this disorder. This is a serious problem that has both political and economic consequences on both sides of the border.

High cut-off renal replacement therapy for removal of myoglobin in severe rhabdomyolysis and acute kidney injury: a case series.

BACKGROUND/AIM: Rhabdomyolysis is associated with the release of myoglobin into the circulation, promoting acute kidney injury (AKI). In severe rhabdomyolysis, dialysis-dependent AKI doubles mortality. Standard blood purification techniques have limited efficacy in removing myoglobin. We describe high cut-off (HCO) renal replacement therapy (RRT) as a novel approach for extracorporeal elimination of myoglobin in rhabdomyolysis-associated AKI. METHODS: With an in vivo molecular cut-off at 45 kDa, HCO filters are effective in removing myoglobin (17.8 kDa). Clearances across standard and HCO filters using continuous or intermittent RRT are reviewed in a case series of 11 patients with severe rhabdomyolysis and dialysis-dependent AKI. RESULTS: Median myoglobin clearance across standard high-flux filters was 3.3 (interquartile range 2.3-3.9) ml/min for sustained low-efficiency daily dialysis (SLEDD) batch hemodialysis (HD) and 3.7 (2.9-6.7) ml/min for conventional HD. Respective clearances using HCO filters (membrane surface area: 1.1 m(2)) were 21.7 (20.3-26.1) ml/min (SLEDD) and 44.2 (41.3-47.0) ml/min (HD). Corrected for filter size, up to 20-fold higher clearances were obtained using HCO filters, resulting in profound and sustained reduction of plasma myoglobin concentration. CONCLUSIONS: As a novel approach, HCO RRT allows for rapid and effective removal of myoglobin from the circulation. In light of the pathogenic role in AKI, reducing exposure of the kidney to myoglobin may improve renal recovery and patient outcome. Our data pave the way for prospective trials, addressing this issue.

Case Report: Red Urine After Day Care Strabismus Surgery.

In the absence of surgery on the urinary tract, the emission of red urine after anesthesia should be considered as a diagnostic emergency because it can be a sign of hematuria, hemoglobinuria, blood transfusion reaction, significant myoglobinuria, or porphyria.This case describes the management of a 12-year-old boy who presented red urine at the day care unit after strabismus surgery.

High body mass index in muscular patients and flank position are risk factors for rhabdomyolysis: case report after laparoscopic live-donor nephrectomy.

BACKGROUND AND PURPOSE: Rhabdomyolysis is well known after traumatic crush injuries or ischemia involving muscles. Postoperatively, it most likely is secondary to surgical positioning and patient muscle mass. We report a case after laparoscopic live-donor nephrectomy. CASE REPORT: A muscular 35-year-old man underwent elective left laparoscopic live-donor nephrectomy in a 70 degrees flank position with four ports. He was in the right-side lying position with hip flexion (flank position) for approximately 4 hours. A kidney bridge had been placed between the iliac crest and the rib cage. Postoperatively, the patient had light-pinkish urine and low urine output. There was marked induration of the buttocks and significant pedal and scrotal edema. With judicious use of alkalinization and diuretics, the patient did not require dialysis, and renal function returned to base level by postoperative day 20. The recipient of the kidney had a normal postoperative course. CONCLUSION: Rhabdomyolysis is a syndrome of muscle necrosis and release of intracellular components into the circulation. Acute renal failure secondary to myoglobinuria is a common complication. We currently use little flexion of the table during donor nephrectomy and bring the table to a neutral position immediately after kidney retrieval. Postoperatively, one needs a high index of suspicion for rhabdomyolysis to avoid or at least promptly recognize this rare but potentially serious condition after any operation lasting >or=4 hours.

Muscle carnitine palmitoyltransferase II deficiency: clinical and molecular genetic features and diagnostic aspects.

Muscle carnitine palmitoyltransferase (CPT) II deficiency is an autosomal recessive disorder of fatty acid oxidation characterized by attacks of myalgia and myoglobinuria. This review summarizes the clinical features of this disease, analyzing data of 28 patients with biochemically and genetically confirmed CPT II deficiency. The review shows that exercise-induced myalgia is the most frequent symptom, whereas myoglobinuria, known as the clinical hallmark, is missing in 21% of the patients. Typically, myalgia starts in childhood, whereas attacks with myoglobinuria mostly emerge in adolescence or early adulthood. However, there are also patients with only myalgia, patients with attacks triggered by factors other than exercise, and patients with late-onset disease. Molecular or biochemical analysis is necessary for diagnosis, since no myopathologic hallmark exists. For screening patients, analysis of not only the common S113L mutation but also the P50H and Q413fs-F448L mutations is recommended. The phenotype of muscle CPT II deficiency might be influenced by the underlying mutation, and patients with a truncating mutation on 1 allele might be affected more severely.

Myoglobin clearance by super high-flux hemofiltration in a case of severe rhabdomyolysis: a case report.

OBJECTIVE: To test the ability of a novel super high-flux (SHF) membrane with a larger pore size to clear myoglobin from serum. SETTING: The intensive care unit of a university teaching hospital. SUBJECT: A patient with serotonin syndrome complicated by severe rhabodomyolysis and oliguric acute renal failure. METHOD: Initially continuous veno-venous hemofiltration was performed at 2 l/hour ultrafiltration (UF) with a standard polysulphone 1.4 m2 membrane (cutoff point, 20 kDa), followed by continuous veno-venous hemofiltration with a SHF membrane (cutoff point, 100 kDa) at 2 l/hour UF, then at 3 l/hour UF and then at 4 l/hour UF, in an attempt to clear myoglobin. RESULTS: The myoglobin concentration in the ultrafiltrate at 2 l/hour exchange was at least five times greater with the SHF membrane than with the conventional membrane (>100,000 microg/l versus 23,003 microg/l). The sieving coefficients with the SHF membrane at 3 l/hour UF and 4 l/hour UF were 72.2% and 68.8%, respectively. The amount of myoglobin removed with the conventional membrane was 1.1 g/day compared with 4.4-5.1 g/day for the SHF membrane. The SHF membrane achieved a clearance of up to 56.4 l/day, and achieved a reduction in serum myoglobin concentration from >100,000 microg/l to 16,542 microg/l in 48 hours. CONCLUSIONS: SHF hemofiltration achieved a much greater clearance of myoglobin than conventional hemofiltration, and it may provide a potential modality for the treatment of myoglobinuric acute renal failure.

Plasma exchange in rhabdomyolysis.

The effect of plasma exchange (PE) was evaluated in 4 patients with rhabdomyolysis. A single 21 PE produced a transient fall of creatinine phosphokinase and did not prevent renal failure. Theoretically PE would need to be performed very frequently to remove toxins in appropriate amounts. Since renal failure in myoglobinuira has a relative good prognosis, we do not recommend intensive PE as therapy.

Severe rhabdomyolysis with good recovery in a patient with head injury: case report.

OBJECTIVE AND IMPORTANCE: We report a case of head injury, in which a hyperosmolar state evolved during the course of treatment, complicated by severe rhabdomyolysis and acute renal failure, which subsequently resulted in a good recovery after intensive supportive treatment. To our knowledge, such high levels of creatine kinase in a patient with head injury and rhabdomyolysis have not been reported. CLINICAL PRESENTATION AND INTERVENTION: A 19-year-old male patient with head injury sustained a compound fracture of the frontal region. He received a hyperosmolar agent to treat brain edema and developed a hyperosmolar state and diabetes insipidus 1 day after the accident. There were no obvious associated injuries at physical examination. After admission to the intensive care unit, the patient developed myoglobinuria and rhabdomyolysis; serum creatine kinase was elevated to a peak of 650,000 IU/L. Four days later, acute renal failure was noted. The patient's myoglobinuria and rhabdomyolysis gradually declined, and he eventually recovered from acute renal failure after supportive treatment and dialysis. CONCLUSION: We postulate that the hyperosmolar state of the patient was the major cause of his severe rhabdomyolysis. Associated hypokalemia and hypophosphatemia are also predisposed to rhabdomyolysis. The most serious complication in rhabdomyolysis is acute renal failure, but most patients who receive supportive treatment and can survive despite the complications can expect to have normal renal function restored.

Myoglobinuria, malignant hyperthermia, neuroleptic malignant syndrome and serotonin syndrome.

This article presents an overview of the causes and manifestations of myoglobinuria and provides criteria for its diagnosis and management. The article also reviews neuroleptic malignant syndrome, malignant hyperthermia, and serotonin syndrome, all of which could cause rhabdomyolysis and myoglobinuria.

Case report: polymyositis-induced myoglobinuric acute renal failure.

Polymyositis rarely leads to myoglobinuric acute renal failure. One such case is reported here, and certain common features in reported cases are discussed. Given therapeutic advances, these patients should do well despite the dismal prognosis reported in the literature, but early diagnosis and prompt treatment are essential.

Myoglobinuria.

Myoglobinuria is still considered to be an uncommon occurrence, however, with the advent of better diagnostic tests it is being increasingly recognized as a potentially life-threatening complication of muscle necrosis. The pathologic consequences of myoglobinuria, including respiratory failure, hyperkalemia, and acute renal failure demand recognition by all who work in areas where this syndrome may develop. This article describes the role of myoglobin in the muscle and how myoglobinuria may develop. It includes the symptoms, differential diagnosis, and treatment of myoglobinuria and possible complications.

Treatment of the multiply injured patient: plans for treatment and problems of major trauma.

Certain principles involved in the treatment of fractures have stood the test of time. The thrust of modern orthopaedics has been to decrease morbidity by combining these principles with developments in physiology, bioengineering, radiology, and antibiotics. The goal remains anatomic bone union without infection and normal joint and muscle function. The surgeon's mission is to achieve this goal. For the multiply injured patient, survival depends on the quality of care. Surgical orientation permits one to stabilize the fractures and restore the patient to activities of daily living. Multiple fractures set the stage for multiple organ failure, and, as we have discussed, stabilization reduces the incidence of these problems. Basically, open fractures must be stabilized with plaster, traction, or surgery. Multiple fractures need rigid stabilization, which can be achieved with various techniques without jeopardizing limb or life. A simple, comprehensive plan should be implemented when the patient arrives in the emergency room. Treatment requires an interdisciplinary approach, with the surgeon heading a team of physicians, nurses, and technicians capable of handling the complications of each organ system. Teamwork and dedication to excellence by all involved will decrease mortality and morbidity. Survival is to be anticipated. If we have restored the anatomy early, before any organ failure, we are then ready to begin rehabilitation and achieve a much finer and enduring end result for the injured patient.

Electric injury, Part II: Specific injuries.

Electric injury can cause disruption of cardiac rhythm and breathing, burns, fractures, dislocations, rhabdomyolysis, eye and ear injury, oral and gastrointestinal injury, vascular damage, disseminated intravascular coagulation, peripheral and spinal cord injury, and Reflex Sympathetic Dystrophy. Secondary trauma from falls, fires, flying debris, and inhalation injury can complicate the clinical picture. Diagnostic and treatment considerations for electric injuries are described in this article, which is the second part of a three-part series on electric injuries.

Rhabdomyolysis as a cause of acute renal failure.

Traumatic rhabdomyolysis with myoglobinuria and renal failure has been recognized for many years. In the past decade, rhabdomyolysis has been found to have various nontraumatic causes as well, including genetic conditions, metabolic disorders, exercise, toxins, infections, and drugs. Characteristic clinical and laboratory features include muscle tenderness, pigmenturia with urine that is orthotoluidine (Hematest) positive, greatly elevated creatine kinase levels, and often, renal failure. Treatment consists of fluid replacement and establishment of adequate urine flow early. If acute renal failure occurs, it should be treated appropriately. Particularly important are reversal of hyperkalemia and withholding of calcium during the hypocalcemic phase to prevent exacerbation of hypercalcemia later.

Emergency treatment and early fluid resuscitation following electrical injuries.

Injuries caused by high-tension electrical current are rare, but pathophysiologically unique with destructive effects. As a form of thermal trauma, electrical injuries represent a connection of skin burns and deep tissue destruction unpredictable in its depth which mostly resembles a crush injury. Emergency treatment measures begin with the separation from the electrical contact if any and prompt transport to the nearest institution with all means for cardiorespiratory resuscitation and complete recovery. Resuscitation of the patient after electric shock continues then with fluid replacement using special formula modified for such cases, correction of acidosis and myoglobinuria and finally with escharotomy and fasciotomy which is most often necessary.