RESUMEN
Background Chronic kidney disease (CKD) involves a gradual loss of kidney function over months to years. Oxidative stress plays a critical role in the pathogenesis of CKD. Homocysteine (Hcy), an amino acid derivative, is a known risk factor for oxidative stress and endothelial damage. Gamma-glutamyl transferase (GGT), an enzyme abundant on the cell surface of liver and kidney cells, is raised during oxidative stress. The objectives of this study were to estimate the concentrations of serum Hcy and GGT among CKD patients and healthy controls and to determine whether there is an association between serum Hcy and GGT levels in CKD. Methodology A total of 246 participants were needed to meet the calculated sample size. A total of 123 CKD patients meeting the inclusion and exclusion criteria were recruited as cases from the Nephrology outpatient department of our institute. Equal numbers of age- and sex-matched healthy volunteers were recruited as controls. Biophysical profiling of participants was done. Baseline investigations were recorded. A blood sample was collected from each participant and analyzed for GGT and Hcy along with other routine parameters. Results Hcy and GGT concentrations were significantly high in CKD patients compared to healthy controls. There was a significant positive correlation between serum GGT and Hcy levels (r = 0.357). Conclusions Elevated levels of GGT and Hcy in CKD patients compared to healthy controls demonstrated the oxidative stress associated with the disease. GGT and Hcy can be used as prognostic markers of the disease.
RESUMEN
Type 2 Diabetes Mellitus (T2DM) and Major Depressive Disorder (MDD) are highly disabling disorders associated with a multitude of vascular complications. Platelets are known to play a role in the pathogenesis of vascular complications in both T2DM and MDD. These complications could increase in patients with comorbid diabetes and depression. To quantify and compare flow cytometry based platelet activation markers and the inflammatory state between individuals of diabetes with depression, individuals of diabetes without depression and healthy controls. Out of 114 participants, each study group contained 38 participants in diabetic group, diabetics with depression group and matched control group. Diabetes was diagnosed with the American Diabetes Association (ADA) criteria. Screening of MDD was done with Patient Health Questionnaire 2 (PHQ2) and severity of depression assessed with Hamilton Depression Rating (HAM-D) scale. Platelet markers CD41, CD42b, CD62P and CD63 were assayed using flow cytometer. Platelet count, surface expression of platelet activation markers CD62P and CD63, hs-CRP, insulin and HOMA-IR score differed significantly between the groups. Post hoc analysis showed significantly high CD63 expression in patients with comorbid diabetes and depression compared to those having diabetes without depression. Patients with comorbid diabetes and depression have enhanced platelet hyperactivation and a pro inflammatory state which increases susceptibility to vascular complications.