Setting Of Rhabdomyolysis Research Articles

Acute tubular injury and Acute Interstitial Nephritis Secondary to Cocaine Use

Cocaine-associated kidney injury, such as acute kidney injury in the setting of rhabdomyolysis, have well been described in the literature. Acute interstitial nephritis (AIN) is a less frequent complication of cocaine intake. We present the case of a 37-year-old man who snorted cocaine and subsequently developed acute kidney injury in the absence of rhabdomyolysis. He underwent kidney biopsy which showed evidence of both AIN and ATI. He remained non-oliguric and euvolemic during his hospitalization. His renal function improved in two weeks with cessation of cocaine alone. No steroids were administered. In working up acute kidney injury, illicit drug history is important. We highlight the occurrence of cocaine associated ATI without heme pigment-induced AKI, and the presence of concurrent AIN. The clinical, biochemical and urinalysis findings are subtle and often, as in our case, are non-revealing. Renal biopsy is vital to diagnose these pathologies.

Xenobiotic-Induced Rhabdomyolysis and its Relationship with Paraclinical Variables in Poisoned Patients

Background: Rhabdomyolysis is a clinical syndrome that occurs due to the damage to striated muscles after various conditions, one of the most common of which is drug poisoning. This study examined rhabdomyolysis in all types of poisoned hospitalized patients and its relationship with paraclinical variables, such as Creatine Phosphokinase (CPK) and the patients’ level of creatinine, blood urea, and liver enzymes (alanine aminotransferase and aspartate aminotransferase). Methods: A total of 105 patients suffering from rhabdomyolysis caused by poisoning were enrolled. The necessary information of the patients was extracted from their records, recorded in the research questionnaire, and analyzed using SPSS. Descriptive statistics indicators and Pearson’s linear correlation coefficient were used for statistical analysis. Results: The prevalence of rhabdomyolysis was 7.2%. Ninety-seven (92.4%) and 8 (7.6%) poisoned patients suffering from rhabdomyolysis were male and female, respectively. The most prevalent poisoning resulting in rhabdomyolysis was methadone poisoning (31.42%). There was a significantly positive correlation between CPK and urea, Cr, and AST; i.e., by increasing CPK level, urea, Cr, and AST levels also increased, and by decreasing CPK level, urea, Cr, and AST levels also decreased. The incidence of an abnormal aminotransferase in the setting of rhabdomyolysis was high. In addition, the frequency of Acute Kidney Injury (AKI) ranged from 10.9 to over 16.9%. Conclusion: Xenobiotics (e.g., opioids, drugs, alcohol, and poisons), xenobiotic-induced coma, and/or xenobiotic-induced seizure are the causes of rhabdomyolysis in the present study. Briefly, the research findings revealed the highest prevalence of rhabdomyolysis in male youth poisoned by narcotics.

Acute Kidney Injury and Hypothyroidism in a Patient with CKD

Acute kidney injury (AKI) in the setting of hypothyroidism has been documented in the literature. However, hypothyroidism is not generally considered a cause during investigation of an acute kidney injury. Most of the cases described have been reported in setting of rhabdomyolysis, while fewer cases describe AKI occurring in the absence of rhabdomyolysis. Only rarely have case reports been supplemented by renal biopsy findings to ensure other etiologies of acute kidney injury were ruled out, and none of these reports have documented changes in the kidney that could be associated with the hypothyroid state. We report a case of AKI in chronic kidney disease in the absence of rhabdomyolysis, occurring during severe hypothyroidism, that resolved completely after achievement of a euthyroid state. In addition, we provide renal biopsy findings likely associated with the hypothyroid state. We propose that evaluation of the thyroid function should be considered in any patient during evaluation of an acute kidney injury.

Acute Compartment Syndrome in the Setting of Weight Loss Supplements and Exercise-Induced Rhabdomyolysis.

The growing prevalence of obesity in the USA has resulted in increased consumption of weight loss products that promote fat metabolism. Dietary supplements used for weight loss contain a wide variety of ingredients but the amount of scientific information available on these ingredients varies considerably. Such supplements have documented and undocumented adverse effects. Although the FDA frequently issues health advisories, the health consequences of consuming supplements are often overlooked by the general public. A common supplement used for weight loss is Hydroxycut. The ingredients used in the different forms of Hydroxycut products vary but generally include caffeine and green tea extract, which are responsible for a wide range of adverse effects. We present the case of 41-year-old man with a medical history of polysubstance abuse who developed acute compartment syndrome in the setting of rhabdomyolysis from prolonged immobilisation and the use of Hydroxycut. This case demonstrates the possible adverse effects of consuming weight loss herbal supplements like Hydroxycut. Healthcare professionals and consumers are encouraged to report serious adverse events or product quality problems with the use of these supplements to the FDA’s MedWatch adverse event reporting program.LEARNING POINTSThe weight loss supplement Hydroxycut is sold in various formulations whose side effect profiles are not fully known; the latest formulation has a very high concentration of caffeine which increases the risk of rhabdomyolysis.Although uncommon, exercise-induced rhabdomyolysis can cause compartment syndrome, especially in the setting of concurrent use of weight loss supplements.High clinical suspicion, prompt diagnosis and early treatment are key to preventing complications from compartment syndrome.

A Donor With Green Kidneys—To Transplant or Not to Transplant: A Case Report

A Donor With Green Kidneys—To Transplant or Not to Transplant: A Case Report

Imaging Findings in the Setting of Rhabdomyolysis

Imaging Findings in the Setting of Rhabdomyolysis

Patterns of transaminase elevation in rhabdomyolysis versus acetaminophen toxicity.

Transaminase elevations can occur from liver injury or in the setting of rhabdomyolysis. The goal of this study is to evaluate indices that could differentiate acetaminophen toxicity from muscle injury in the setting of transaminase elevations. A retrospective chart review of consecutive cases reported to our regional poison center. Patients with transaminase (AST and ALT) elevation were grouped as those with acetaminophen exposure (AT) and those with elevated creatine phosphokinase (CPK) without evidence of acetaminophen exposure (RHB). Of the 345 patients included in the study, elevated AST/ALT levels were attributed to rhabdomyolysis in 168 patients and attributed to acetaminophen toxicity in 177 patients. The median AST: ALT values also differed between groups, with patients in the RHB group had higher median ratios (p<0.001). Using an AST: ALT value of 2.02 as a diagnostic cutoff produced a specificity of 0.52 (95% CI: 0.37, 0.64) and sensitivity of 0.84 (95% CI: 0.73, 0.94) for acetaminophen detection in the test dataset (N=104). Elevated transaminases due to liver injury from acetaminophen ingestion had a different pattern than elevated transaminases due to rhabdomyolysis. Lower AST:ALT ratios were found in acetaminophen cases, however, the specificity using a ratio threshold of ≤1 would be 83%.

Rhabdomyolysis in an HIV cohort: epidemiology, causes and outcomes

BackgroundThe Literature on rhabdomyolysis in the HIV-positive population is sparse and limited. We aimed to explore the incidence, patient characteristics, etiologies and outcomes of rhabdomyolysis in a cohort of HIV-positive patients identified through the Johns Hopkins HIV clinical registry between June 1992 and April 2014.MethodsA retrospective analysis of 362 HIV-positive patients with non-cardiac CK elevation ≥1000 IU/L was performed. Both inpatients and outpatients were included. Incidence rate and potential etiologies for rhabdomyolysis were ascertained. The development of acute kidney injury (AKI, defined as doubling of serum creatinine), need for dialysis, and death in the setting of rhabdomyolysis were determined. Logistic regression was used to evaluate the association of peak CK level with the development of AKI.ResultsThree hundred sixty two cases of rhabdomyolysis were identified in a cohort of 7079 patients with a 38,382 person years follow-up time. The incidence rate was nine cases per 1000 person-years (95% CI: 8.5–10.5). Infection was the most common etiology followed by compression injury and drug/alcohol use. One-third of cases had multiple potential etiologies. AKI developed in 46% of cases; 20% of which required dialysis. Thirteen percent died during follow-up. After adjustment, AKI was associated with higher CK (OR 2.05 for each 1-log increase in CK [95% CI: 1.40–2.99]), infection (OR 5.48 [95% CI 2.65–11.31]) and higher HIV viral load (OR 1.22 per 1-log increase [95% CI: 1.03–1.45]).ConclusionRhabdomyolysis in the HIV-positive population has many possible causes and is frequently multifactorial. HIV-positive individuals with rhabdomyolysis have a high risk of AKI and mortality.

Diffuse Subcutaneous Upper Extremity Edema in the Setting of Rhabdomyolysis

Diffuse Subcutaneous Upper Extremity Edema in the Setting of Rhabdomyolysis

Liver Aminotransferases Are Elevated with Rhabdomyolysis in the Absence of Significant Liver Injury

Rhabdomyolysis is an uncommon finding in the emergency department. However, the clinical implications of rhabdomyolysis are important, with a significant minority of patients developing acute renal failure and multiorgan failure. When present, the cause of elevated aminotransferases in the setting of rhabdomyolysis is often unclear. We sought to determine the incidence of abnormal aminotransferases (defined as aspartate aminotransferase (AST) or alanine aminotransferase (ALT)>40 U/L) in the setting of rhabdomyolysis and how the aminotransferases decrease relative to the creatine phosphokinase (CPK) concentration as rhabdomyolysis resolves. A retrospective chart review of 215 cases of rhabdomyolysis with CPK of >or=1,000 U/L was performed. The incidence of an abnormal AST in the setting of rhabdomyolysis was 93.1% (95% confidence interval, 88.7% to 95.8%). An abnormal ALT was much less common and found in 75.0% (95% confidence interval, 68.7% to 80.2%) of patients with a CPK of >or=1,000 U/L (p<0.0001). In only one instance was the ALT>40 U/L while the AST was <40 U/L. Furthermore, AST concentrations (and not ALT) fall in parallel with CPK during the first 6 days of hospitalization for patients with rhabdomyolysis. Aminotransferase abnormalities, particularly AST, are common in the setting of rhabdomyolysis. AST concentrations decrease in parallel to CPK, suggesting skeletal muscle may be a significant source of AST elevation in these patients.

A Phase I study using Bortezomib with Weekly Idarubicin for the Treatment of Elderly (>60 YEARS) and Relapsed Patients with Acute Myeloid Leukemia (AML)

In preclinical experiments we have shown that human AML cells overexpress NFkB and suppression of NFkB by proteasome inhibition directly induces apoptosis in primary AML cells, with little effect on normal hematopoietic progenitors. (Guzman, 2001, Blood, 98(8); Guzman, 2002, PNAS, 99(25).) Furthermore, our data has also demonstrated that the combination of the proteasome inhibitor, bortezomib (Bor), with idarubicin (Ida) robustly induced death in primary AML cells, including the relatively quiescent leukemic stem cell. (Howard, 2003, AACR abstr. 1636) From these observations, we hypothesized that Bor in combination with Ida would mediate a tumor-specific, anti-leukemia response in patients (pts) diagnosed with AML. We report the results of a phase I study with a standard up and down design looking at 4 dose levels of Bor in combination with Ida. Eligible were newly diagnosed AML pts age ≥60, with or without myelodysplasia (MDS), or any adult with relapsed AML treated at the Univ of Ky or Univ of Rochester. A minimum of 3 and a maximum of 6 pts were entered at each dose level. Twice weekly bortezomib at 0.8, 1.0, or 1.2mg/m2 was given with weekly Idarubicin 10, or 8mg/m2 for 4 wks. Therapy was administered in the outpatient setting. Bone marrow (BM) analysis was done at entry, day+18 of treatment, and either at time of hematopoietic recovery or day+50, whichever came first. A DSMB was established to review all adverse events (AEs) semiannually. Twenty eligible and consented pts were treated; 13 newly diagnosed (ND) (med age 68 (61–83)) and 7 relapsed (Rel) (med age 58 (40–77)). 10/13 ND and 2/7 Rel pts had prior MDS; of 3 ND pts without prior MDS, 2 were FAB M6 and 1 was FAB M7. Toxicities were evaluated by CTCAE, v3.0 criteria. Two dose limiting toxicities (DLT) occurred at dose level 1(Bor 0.8mg/m2 and Ida 10mg/m2) – gr 4 CPK elevation in setting of rhabdomyolysis (resolved completely) and death due to disseminated aspergillus with aplasia in the BM (gr 5 infection). After unacceptable toxicities at the first dose level, the dose of Ida was reduced to 8mg/m2. No further DLTs were observed. 15/20 patients were admitted for 17 episodes of febrile neutropenia. Only 1 pt died from infection that was treatment related. Common AEs included: infections, constitutional symptoms, pain, and gastrointestinal symptoms (see table). No patient experienced neurotoxicity. The only grade 4 non-hematologic or non-infection toxicity was the CPK elevation. 1 pt died from renal failure unrelated to treatment. All but 2 pts demonstrated a hematologic response to treatment evidenced by decreased circulating blasts. 4 pts achieved CR – 2 at dose level 1 and 2 at dose level 4; 1 pt achieved PR (returned to CMML). The combination of Bor and Ida in this older pt group with mostly poor-risk AML was well tolerated; expected hematologic and infection-related toxicities did not result in a high rate of induction mortality. While this study was not designed to evaluate efficacy, it is noteworthy that there were 4/20 complete remissions. Our results with this combination of drugs in the treatment of poor-risk, older pts with AML are provocative. Future studies should explore alternate dosing of Ida, other potentially synergistic drugs for combination with Bor, or the use of Bor in post-remission therapy.TOXCITIESgr1gr2gr3gr4gr5documented infection including bacteremia151441febrile neutropenia requiring admission17constitutional symptoms - sweats, myalgias, weakness, fatigue, anorexia511Pain54gastrointestinal symptoms4bleeding (any)111Anemia121cardiac114respiratory15metabolic disturbance211renal failure2111rash11

A Case of Occult Compartment Syndrome and Nonresolving Rhabdomyolysis

A 32-year-old African male presented with 10 hours of severe back pain. Initial computed tomography scan of the back showed no abnormality, and initial laboratory investigations were consistent with rhabdomyolysis. Despite stopping potential causative medications, aggressive intravenous hydration, and urine alkalinization, his creatinine kinase continued to steadily climb. Thirty-six hours after admission, a magnetic resonance imaging of his back was done because of new swelling over the right paraspinal muscles and loss of sensation in this region. Marked swelling of the right erector spinae muscles was observed, and right and left compartment pressure measurements were 108 and 21 mm Hg, respectively. He had urgent fasciotomy after which his rhabdomyolysis and pain recovered. Our case highlights the need for early consideration of compartment syndrome as a possible cause of back pain in the setting of rhabdomyolysis. Rhabdomyolysis can present in the absence of late complications such as neurological and vascular compromise.

Bilateral Femoral Neuropathy Complicating Rhabdomyolysis and Acute Renal Failure

Simultaneous bilateral femoral neuropathies are uncommon and are usually seen as a consequence of pelvic surgery or related to pregnancy. This report describes the case of a young man with rhabdomyolysis after a drug-induced coma, which led to intramuscular dystrophic calcification and compression of the femoral nerves. Acute dystrophic calcification has been documented in the setting of rhabdomyolysis with renal failure. This is the first reported case of a compressive neuropathy occurring as a result of such dystrophic calcification.