Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the clinical significance of myoglobin and myoglobin/CA III ratio as a biochemical marker for acute myocardial infarction (AMI) in patients with renal failure; we studied 300 patients admitted to the hospital with a history of symptoms characteristic of AMI, and 33 renal failure patients who were undergoing chronic maintenance dialysis treatment and who did not have clinical or electrocardiographic evidence of AMI. Fifteen of 300 patients admitted to the hospital had AMI based on the WHO criteria, and a concomitant value of serum creatinine concentration (S-Crea) over 140 mumol/l indicating renal failure. Fourteen of these 15 patients (93%) had serum myoglobin concentration over 70 micrograms/l and myoglobin/CA III ratio over 2.20 as measured by time-resolved fluoroimmunoassay (TR-FIA); these values were cutoff values for AMI diagnosis. Twenty-two of 300 patients admitted to the hospital had S-Crea over 140 mumol/l in the absence of myocardial injury. Sixteen of these 22 (73%) patients had increased serum myoglobin concentration, but only four of 22 (18%) had myoglobin/CA III ratio over 2.20. A positive correlation between serum myoglobin and CA III concentrations (rs = 0.933, P < 0.001) was observed in hemodialyzed patients with chronic renal failure. The values for serum myoglobin/CA III ratio observed in this group were similar to those measured in the 22 non-AMI patients with S-Crea over 140 mumol/l admitted to the hospital and differed statistically from that for patients with AMI (P < 0.001). We conclude that serum myoglobin, as well as CA III values, are elevated in patients with renal failure, and therefore S-myoglobin can not be used as a marker for AMI in these patients. Our results suggest that the serum myoglobin/CA III ratio is a reliable AMI marker even in renal failure patients, and therefore provides a tool for AMI diagnosis in this patient group.
 ...
PMID:The use of myoglobin/carbonic anhydrase III ratio as a marker for myocardial damage in patients with renal failure. 935 27

Following isolated limb perfusion (ILP) with TNF alpha and melphalan the damage to muscle tissue and its systemic consequences in terms of myoglobinemia and myoglobinuria as well as the activation of the cytokine cascade were investigated. We measured the compartmental pressure of the limb during and after perfusion and determined the serum changes of myoglobin, creatine kinase (CK), interleukin (IL)-6, IL-1, s-IL-2-receptor, TNF-receptor, and ICAM-1 levels. The compartmental pressure rose significantly during ILP and decreased after reperfusion. Following its course, the decision whether to perform a fasciotomy or not can be more reliably made. Serum myoglobin levels exceeded 200 times normal values and the increase occurred significantly earlier than that of CK, thus enabling judgement of the risk of renal failure (crush kidney syndrome). The elevation of serum IL-1 and IL-6 values correlated with the frequency of cardiopulmonary problems (hyperdynamic shock) and facilitated counter-maneuvers. Our data, although obtained from ILP with TNF alpha, could be used to monitor toxicity also when other drug regimens are administered.
 ...
PMID:[Assessment of regional and systemic toxicity of isolated hyperthermic extremity perfusion with tumor necrosis factor-alpha and melphalan]. 941 Jun 82

Crush syndrome or traumatic rhabdomyolysis constitutes the systemic changes seen after crush injury, i.e. the damages seen after a prolonged period of pressure on a muscle group. The pressure causes necrosis of muscle, and during revascularisation diffusion of calcium, sodium and water into the damaged muscle cells is seen, together with loss of potassium, phosphate, lactic acid, myoglobin and creatinine kinase. Untreated these changes can lead to: hyperkalaemia, acidosis, acute renal failure and hypovolaemic shock. Treatment of the systemic changes should be initiated immediately, aiming at a rapid correction of the extracellular volume and forced mannitol-alkaline diuresis. If renal failure develops, haemodialysis is started. The crush injuries are treated conservatively without fasciotomy, despite high or increasing intracompartmental pressure. The only indications for fasciotomy are lack of a distal pulse or open lesions. If fasciotomy is performed, radical removal of all necrotic muscle is essential.
 ...
PMID:[Traumatic rhabdomyolysis. Physiopathology and treatment]. 947 44

Four patients with end-stage renal failure on intermittent hemodialysis in whom rhabdomyolysis developed after major surgery are described. This possibly underdiagnosed complication was manifested by extreme hyperphosphatemia, hypocalcemia, and elevated creatine phosphokinase levels. Serum myoglobin levels further supported the diagnosis. The metabolic abnormalities reached a peak on the fourth postoperative day. The possible precipitating factors included opiates used for anesthesia and postoperative pain control, anesthetic agents, and surgical position. The preferred treatment option is increasing dialysis to control hyperphosphatemia and hypocalcemia.
 ...
PMID:Postoperative rhabdomyolysis in patients with end-stage renal failure. 950 95

Cardiac troponin T (cTnT) in serum is a highly sensitive and specific marker for myocardial damage. Quantitative immunoassays take 9 min. A rapid test (TropT, CardiacT) using plasma detects cTnT concentrations above 0.10 microg/l within 15 min. Both assays are specific for the cardiac isoform. In a study using the maximal values from serial sampling in 502 infarction-suspected patients, we found a diagnostic sensitivity for non-Q- and Q-wave infarctions of 100%, with a specificity of 99%. cTnT has been shown to be a powerful prognostic marker for risk stratification in acute coronary syndromes. In 30-40% of patients with unstable angina, cTnT > or = 0.10 microg/l detects minor myocardial damage (MMD) with poor prognosis. False positives may be found in certain skeletal muscle diseases, such as polymyositis and Duchenne's muscular dystrophy. Constantly increased values in renal failure may be due to uremic cardiomyositis. Even in uremia, a rapid increase of cTnT will indicate acute myocardial damage. We propose a diagnostic strategy based on timed, parallel determinations of myoglobin + cTnT.
 ...
PMID:Troponin T: a sensitive and specific diagnostic and prognostic marker of myocardial damage. 958 56

Myoglobin, a low molecular-weight heme protein (17800 D) present in both cardiac and skeletal muscle, is an old test with new perspectives. Advantages and disadvantages of myoglobin determination are well known. Myoglobin is the earliest known, commercially available, biochemical marker of acute myocardial infarction (AMI) and its rapid kinetics make it an early, good marker of reperfusion. However, since myoglobin is present in both skeletal and cardiac muscle, any damage to these muscle types results in its release into blood. Serum myoglobin levels are falsely elevated in conditions unrelated to AMI as skeletal muscle and neuromuscular disorders, renal failure, intramuscular injection, strenuous exercise, and after several toxins and drugs intake. New strategies for myoglobin measurement may resolve this limitation. These strategies include both the combined measurement of myoglobin and a skeletal specific marker (carbonic anhydrase III) or a cardiac specific marker (troponin I), as well as the myoglobin evaluation on serial samples. In particular, the diagnostic algorithm based on the combined measurement of myoglobin and troponin I, assuring a satisfactory analytical turnaround time, significantly improves the diagnostic efficiency of laboratory assessment of suspected AMI patients, allowing the successive monitoring of coronary reperfusion.
 ...
PMID:Diagnostic strategies using myoglobin measurement in myocardial infarction. 958 58

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.
 ...
PMID:Myoglobin clearance during continuous veno-venous hemofiltration with or without dialysis. 964 61

Rhabdomyolysis is a condition affecting body homeostasis that results from impaired supply of muscles with energy, nutritional factors and blood. Complex pathophysiological mechanism causes that extended myolysis may complicate different clinical conditions, such as: crush syndrome, excessive physical effort (work, seizures), toxic effect of drugs and toxins, water-electrolyte disturbances, congenital enzymatic deficiencies etc. It seems that on the cellular level, essential role is played by excessively high intracytoplasmatic calcium level, which affects metabolic processes. So high calcium level is a consequence of muscular cell injury irrespective to its reason. It manifests clinically as muscular weakness, pal and oedema and laboratory tests reveal elevated CK, GOT, GPT, aldolase and LDH levels as well as dark brown urine colour. Demonstration of elevated serum myoglobin level or its presence in urine directly confirms development of rhabdomyolysis. In unfavorable conditions, rhabdomyolysis may result in acute renal failure. Appropriately early and adequate water supply and alkalization plays an essential role in prevention of impairment in renal function. In advanced phase of renal failure, hemodialysis is a standard treatment.
 ...
PMID:[Rhabdomyolysis: clinical features, causes, complications and treatment]. 974 Nov 96

Muscle injury (rhabdomyolysis) and subsequent deposition of myoglobin in the kidney causes renal vasoconstriction and renal failure. We tested the hypothesis that myoglobin induces oxidant injury to the kidney and the formation of F2-isoprostanes, potent renal vasoconstrictors formed during lipid peroxidation. In low density lipoprotein (LDL), myoglobin induced a 30-fold increase in the formation of F2-isoprostanes by a mechanism involving redox cycling between ferric and ferryl forms of myoglobin. In an animal model of rhabdomyolysis, urinary excretion of F2-isoprostanes increased by 7.3-fold compared with controls. Administration of alkali, a treatment for rhabdomyolysis, improved renal function and significantly reduced the urinary excretion of F2-isoprostanes by approximately 80%. EPR and UV spectroscopy demonstrated that myoglobin was deposited in the kidneys as the redox competent ferric myoglobin and that it's concentration was not decreased by alkalinization. Kinetic studies demonstrated that the reactivity of ferryl myoglobin, which is responsible for inducing lipid peroxidation, is markedly attenuated at alkaline pH. This was further supported by demonstrating that myoglobin-induced oxidation of LDL was inhibited at alkaline pH. These data strongly support a causative role for oxidative injury in the renal failure of rhabdomyolysis and suggest that the protective effect of alkalinization may be attributed to inhibition of myoglobin-induced lipid peroxidation.
 ...
PMID:A causative role for redox cycling of myoglobin and its inhibition by alkalinization in the pathogenesis and treatment of rhabdomyolysis-induced renal failure. 982 35

We evaluated different diagnostic strategies for the early diagnosis of acute myocardial infarction, combining sensitivity and specificity of different markers evaluated singly and using combination testing in parallel and serial modes. Myoglobin, cardiac troponin I (TnI), creatine kinase (CK), and CK-MB mass were tested in blood samples from 26 patients with acute myocardial infarction collected at admission (T0; mean = 3.3 hours from the onset of chest pain) and 3 and 6 hours later. The comparison group was made up of 70 patients with renal failure, skeletal muscle diseases, stable angina, unstable angina, and chest pain of nonischemic origin. Single tests showed different sensitivities in relation to the different release kinetics; myoglobin was the most sensitive (69% at T0) although less specific (46%), and TnI showed the highest specificity (90%) and a sensitivity of 54%. Combination testing in a parallel mode using myoglobin and TnI or CK-MB had the same sensitivity and specificity as myoglobin tested singly. The best combination in a serial mode is myoglobin and TnI (at T0 sensitivity, 54%; specificity, 98%), as confirmed by the analysis of the positive predictive value, the negative predictive value, and the accuracy evaluated as a function of different disease prevalences.
 ...
PMID:Strategies for the early diagnosis of acute myocardial infarction using biochemical markers. 1076 62


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>