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.
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http://dx.doi.org/10.1016/s0009-8981(97)00100-9 | DOI Listing |
PLoS One
January 2025
Facultad de Farmacia y Bioquímica, Departamento de Ciencias Biológicas, Cátedra de Biología Celular y Molecular, Universidad de Buenos Aires, Buenos Aires, Argentina.
Chronic kidney disease (CKD) is one of the leading health problems in the world. It is silent in the early stages and gradually progresses, inducing renal physiological and structural alterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and reduced life expectancy.
View Article and Find Full Text PDFBackground: Regionally anticoagulated continuous renal replacement therapy with citrate is the first choice for critically ill patients with acute kidney injury. If citrate that reaches the patient exceeds the metabolic capacity, metabolic alkalosis will follow. Bicarbonate from the treatment fluids will also reach the patient and add to the bicarbonate load.
View Article and Find Full Text PDFRheumatology (Oxford)
January 2025
Division of Nephrology, Nanfang Hospital, Southern Medical University; National Clinical Research Center for Kidney Disease; State Key Laboratory of Organ Failure Research; Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangdong Laboratory, Guangzhou, 510515, China.
Objectives: The relationship between proteomic profiles and incident systemic lupus erythematosus (SLE) remains unclear. We aimed to identify candidate plasma proteins for SLE risk in women, discover potential treatment targets for SLE, and develop and validate a protein-based prediction model for SLE risk.
Methods: 28 220 women from the UK Biobank were randomly split into training (70%) and testing (30%) sets.
J Nephrol
January 2025
Department of Nephrology, Beaumont Hospital, Dublin, Ireland.
Background: Autosomal dominant polycystic kidney disease (ADPKD) is caused primarily by pathogenic variants in the PKD1 and PKD2 genes. Although the type of ADPKD variant can influence disease severity, rare, hypomorphic PKD1 variants have also been reported to modify disease severity or cause biallelic ADPKD. This study examines whether rare, additional, potentially protein-altering, non-pathogenic PKD1 variants contribute to ADPKD phenotypic outcomes.
View Article and Find Full Text PDFAdv Biotechnol (Singap)
June 2024
MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, Guangdong, 510275, China.
Autosomal dominant polycystic kidney disease (ADPKD) is a dominant genetic disorder caused primarily by mutations in the PKD1 gene, resulting in the formation of numerous cysts and eventually kidney failure. However, there are currently no gene therapy studies aimed at correcting PKD1 gene mutations. In this study, we identified two mutation sites associated with ADPKD, c.
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