RESUMO
Cardiovascular disease (CVD) is the major cause of death in chronic kidney disease (CKD). Of the various risk factors, vascular calcification has only recently come into prominence. CKD is associated with an increased risk of vascular calcification. In routine practice, clinicians usually overlook this finding. Screening for vascular calcification is often missed during first contact with nephrologists. With this article, we would like to reiterate the importance of preventing vascular calcification in early stages of CKD and once it starts appearing, its progression needs to be halted early with individualized treatment. The prevalence, sites of involvement, detection, quantification, pathogenesis, risk factors, clinical manifestations and management options have been discussed.
RESUMO
Saccharomyces cerevisiae cells when grown on synthetic medium plates containing 10 mM of 4-aminopyridine (4-AP) undergo cell lysis. Using an ethylmethane sulfonate mutagenesis (EMS) screen, 4-AP resistant mutants (apr) were isolated which could grow on inhibitory concentration of 4-AP. Eighty mutants were obtained that were recessive, monogenic and formed two complementation groups. To identify genes, whose products might be interacting with the apr loci, extragenic suppressors were isolated, which reverted 4-AP resistance phenotype of apr mutants. The suppressors, when genetically characterized, were found to be recessive and represented two loci with overlapping functions. Representative alleles from apr mutants were analyzed for cell wall composition. They were found to have a higher amount of alkali-insoluble glucan signifying the role of alkali-insoluble glucan in cell wall maintenance.