يعرض 31 - 35 نتائج من 35 نتيجة بحث عن '"Elumalai, Ramprasad"', وقت الاستعلام: 1.04s تنقيح النتائج
  1. 31
    دورية أكاديمية

    المصدر: Annals of the Romanian Society for Cell Biology. 2015, Vol. 19 Issue 2, p41-46. 6p. 3 Charts.

    مستخلص: Chronic kidney disease (CKD) is defined as the presence of kidney damage, or a progressive loss of kidney function. Several studies showed that the elevated level of ghrelin in CKD patients is associated with the poor nutritional status. As ghrelin is involved in food intake and meal appreciation the present study is aimed to assess the relationship between total plasma ghrelin levels and CKD in patients on hemodialysis. Forty nine CKD patients undergoing maintenance hemodialysis for more than 6 months at Sri Ramachandra Medical centre and 18 healthy subjects were included in the present study. Serum levels of total ghrelin were measured by Ghrelin human enzyme immunometric assay kit. Serum albumin, haemoglobin and creatinine were measured using standard laboratory methods. Anthropometric variables and dietary intake was measured for assessment of nutritional status. The serum creatinine and ghrelin were higher in CKD group. The ghrelin levels were found to be higher in CKD patients with hypertension and diabetes as main aetiology. Ghrelin levels showed positive correlation with serum creatinine in CKD patients. The present data suggest that the plasma total ghrelin was elevated in CKD patients on hemodialysis. Further studies are warranted to clarify the correlation between ghrelin and CKD. [ABSTRACT FROM AUTHOR]

  2. 32
    دورية

    المصدر: Hong Kong Journal of Nephrology; April 2016, Vol. 18 Issue: 1 p20-25, 6p

    مستخلص: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by numerous epithelium-lined cysts in the kidney and is the leading genetic cause of end-stage renal disease worldwide. Endothelin-1 is a potent vasoactive peptide implicated in the regulation of basal vascular tone. Endothelin (ET)-converting enzyme 1 (ECE1) is well known for its critical role in the process of ET.

  3. 33
    دورية أكاديمية

    المؤلفون: Ramanathan, Gnanasambandan (AUTHOR), Elumalai, Ramprasad (AUTHOR), Periyasamy, Soundararajan (AUTHOR), Lakkakula, Bhaskar (AUTHOR)

    المصدر: Iranian Journal of Kidney Diseases. Jul2014, Vol. 8 Issue 4, p265-277. 13p.

    مستخلص: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited disease of the kidneys and is marked by progressive cyst growth and decline in kidney function, resulting in end-stage renal disease (ESRD). Hypertension is thought to be a significant modifying factor in the progression of renal failure in ADPKD. A number of genetic variations involved in renin-angiotensin-aldosterone system (RAAS) pathway genes have clinical or physiological impacts on pathogenesis of hypertension-induced ESRD in ADPKD. Information on RAAS pathway gene polymorphisms and their association with ESRD and ADPKD, published till March 2013, was collected using MEDLINE search. The present review deals with RAAS gene polymorphisms focused on hypertension-induced ESRD in ADPKD in different populations. The results were inconclusive and limited by heterogeneity in the study designs and the population stratification. In lieu of applying next generation sequencing technologies to study complex diseases, it is also possible to apply the same to unravel the complexity of ESRD in ADPKD. [ABSTRACT FROM AUTHOR]

  4. 34
    دورية أكاديمية

    المصدر: Iranian Journal of Kidney Diseases. Jul2014, Vol. 8 Issue 4, p265-277. 13p.

    مستخلص: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited disease of the kidneys and is marked by progressive cyst growth and decline in kidney function, resulting in end-stage renal disease (ESRD). Hypertension is thought to be a significant modifying factor in the progression of renal failure in ADPKD. A number of genetic variations involved in reninangiotensin- aldosterone system (RAAS) pathway genes have clinical or physiological impacts on pathogenesis of hypertensioninduced ESRD in ADPKD. Information on RAAS pathway gene polymorphisms and their association with ESRD and ADPKD, published till March 2013, was collected using MEDLINE search. The present review deals with RAAS gene polymorphisms focused on hypertension-induced ESRD in ADPKD in different populations. The results were inconclusive and limited by heterogeneity in the study designs and the population stratification. In lieu of applying next generation sequencing technologies to study complex diseases, it is also possible to apply the same to unravel the complexity of ESRD in ADPKD. [ABSTRACT FROM AUTHOR]

  5. 35
    دورية أكاديمية

    المصدر: Indian Journal of Medical Research. Jun2016, Vol. 143 Issue 6, p748-755. 8p.

    مستخلص: Background & objectives: Autosomal dominant polycystic kidney disease (ADPKD) is an inherited systemic disorder, characterized by the fluid filled cysts in the kidneys leading to end stage renal failure in later years of life. Hypertension is one of the major factors independently contributing to the chronic kidney disease (CKD) progression. The renin-angiotensin aldosterone system (RAAS) genes have been extensively studied as hypertension candidate genes. The aim of the present study was to investigate the role of angiotensin converting enzyme tagging - single nucleotide polymorphisms (ACE tag-SNPs) in progression of CKD in patients with ADPKD. Methods: In the present study six ACE tagSNPs (angiotensin converting enzyme tag single nucleotide polymorphisms) and insertion/deletion (I/D) in 102 ADPKD patients and 106 control subjects were investigated. The tagSNPs were genotyped using FRET-based KASPar method and ACE ID by polymerase chain reaction (PCR) and electrophoresis. Genotypes and haplotypes were compared between ADPKD patients and controls. Univariate and multivariate logistic regression analyses were performed to assess the effect of genotypes and hypertension on CKD advancement. Mantel-Haenszel (M-H) stratified analysis was performed to study the relationship between different CKD stages and hypertension and their interaction. Results: All loci were polymorphic and except rs4293 SNP the remaining loci followed Hardy-Weinberg equilibrium. Distribution of ACE genotypes and haplotypes in controls and ADPKD patients was not significant. A significant linkage disequilibrium (LD) was observed between SNPs forming two LD blocks. The univariate analysis revealed that the age, hypertension, family history of diabetes and ACE rs4362 contributed to the advancement of CKD. Interpretation & conclusions: The results suggest that the ACE genotypes are effect modifiers of the relationship between hypertension and CKD advancement among the ADPKD patients. [ABSTRACT FROM AUTHOR]