CPK creatine phosphokinase

CPK creatine phosphokinase FRAP fluorescence recovery after photolysis... 

Ca X P calcium phosphorus product serum calcium multiplied by serum phosphorus CKD chronic kidney disease CPK creatine phosphokinase DEO deferoxamine EPO erythropoietin ESKD end-stage kidney disease ESRD end-stage renal disease FEk fractional excretion of potassium FEn fractional excretion of sodium GFR glomerular filtration rate Hct hematocrit HDL high-density fipoprotein Hgb hemoglobin... 

ALT, alanine aminotransferase AST, aspartate aminotransferase CPK, creatine phosphokinase... 

Creatine Phosphokinase (CPK) (rabbit skeletal muscle Calbiochem) Resuspended with deionized RNAse free water to a final concentration of 14 mg/ml and stored at —20°. 

Example In order to measure the activity of an enzyme E, such as creatine phosphokinase (CPK), the concentration of the substrate S, for instance creatine, should be in large excesses so that the products measured shall be in the linear portion of the curve (Part A ) in Figure 2.5. 

Skeletal muscle effects All statins have been associated with myalgia, myopathy (ie, muscle pain, tenderness, or weakness with creatine phosphokinase [CPK] values above 10 times the ULN), and rhabdomyolysis. Factors that may predispose patients... 

Tapering of dose Cases of a symptom complex resembling neuroleptic malignant syndrome characterized by elevated temperature, muscular rigidity, altered consciousness, and elevated creatine phosphokinase (CPK) have been reported in association with the rapid dose reduction or withdrawal of other dopaminergic drugs. 

C), there is a broad range of temperature-induced decreases in enzyme activity. Catalase is seen as the most thermally stable enzyme in this group, while creatine phosphokinase (or CPK) is the most thermally sensitive enzyme. 

In all case reports, the levels of creatine phosphokinase (CPK) were markedly increased to about 70 000mU/ml or more [11], Furthermore, this disorder frequently develops in people who are not accustomed to exercise, and is therefore called white-collar rhabdomyolysis [12], which indicates myoglobin-related acute renal failure. 

Mild rhabdomyolysis (which differs from that in myoglobinuric acute renal failure patients), and serum levels of creatine phosphokinase (CPK) and myoglobin, which are normal or slightly increased (less than 7 times the reference value for serum myoglobin, and less than 9 times the reference value for CPK). 

Serum levels of creatine phosphokinase (CPK) (Fig. 50) were lOOmU/ml or less in 31 patients, and 300mU/ml or more in 36 patients. The mean was 2.0 1.7 times higher than the reference value. No values were more than 9 times higher than the reference value. However, minimal rhabdomyolysis was suggested. 

Type II muscle fibers (white muscle, fast muscle) (Table 6) contribute to rapid muscle contraction by using energy obtained from stored ATP, and ATP production from creatine phosphate and anaerobic glycolysis of glycogen. However, the myoglobin content of these fibers is low [144,145], which may lead to less marked increases in serum myoglobin and creatine phosphokinase (CPK) in patients with ALPE. 

On June 6, this patient developed severe loin pain after he participated in two 150-m sprints at a town athletics meeting. After 5 days, he was referred to the outpatient clinic of our department. His serum creatinine and uric acid levels and FEUA, were 2.9mg/dl, 2.1 mg/dl, and 49.7%, respectively. His creatine phosphokinase (CPK) level was normal. When his serum creatinine level decreased to 1.58 mg/dl, a contrast medium was administered. A delayed computed tomography (CT) scan after 24 and 48 h confirmed patchy wedge-shaped contrast enhancement (Fig. 58). Under a diagnosis of ALPE, his body water balance (hydration) was controlled. In this patient, recovery was achieved 4 weeks after onset, and his serum creatinine and uric acid levels were then 1.0 mg/dl and 0.6 mg/dl, respectively. Furthermore, load tests with a uric acid reabsorption inhibitor (benzbromarone) and a uric acid excretion inhibitor (pyrazinamide) suggested presecretory reabsorption defect-related renal hypouricemia. A kidney biopsy 16 days after onset confirmed the recovery from acute tubular necrosis. 

The following issues, including the etiology, remain to be clarified (a) the pathogenesis of ALPE, (b) the prevention of relapse, and future exercise guidance, (c) why delayed CT shows patchy contrast enhancement even in the recovery phase, (d) whether or not patchy renal vasoconstriction persists for 1-2 weeks, (e) why a contrast medium is present in the kidney for 72 h maximum, (f) the association between ALPE and disorders of type II muscle fibers, (g) the reasons for the less marked increases in serum myoglobin and creatine phosphokinase (CPK), and (h) why ALPE frequently develops in patients with renal hypouricemia. 

The simplest mechanism for generating ATP is phosphagen mobilization. In vertebrate tissues such as muscle containing creatine phosphate (PCr) this mobilization is catalyzed by creatine phosphokinase (CPK), a process which requires no 02 and can be written as follows ... 

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