Impact:
This study identifies important metabolic pathways and potential biomarkers for early diagnosis and disease monitoring by revealing diabetes-associated metabolic dysregulation in early-stage chronic kidney disease (CKD). In order to delay the progression of chronic kidney disease (CKD) and lessen complications related to diabetes, these findings promote precision medicine approaches, tailored treatment interventions, and better risk assessment.
Motivation:
Type 2 diabetes mellitus (T2DM) is a primary cause of chronic kidney disease (CKD), accelerating disease development via oxidative stress and complex metabolic disruptions. However, the metabolic mechanism underlying diabetes-associated renal damage in the early stages of CKD are poorly understood.
Aim:
This study used serum ¹H NMR-based metabolomics to assess metabolic changes in early-stage CKD patients with and without type 2 diabetes. It also sought to discover possible biomarkers and disrupted metabolic pathways linked to diabetic CKD.
Method:
¹H NMR spectroscopy was used to assess serum samples from 100 people with early-stage CKD, including patients with and without T2DM. Metabolic pathway analysis was used to discover impacted biochemical pathways after multivariate and univariate statistical approaches were used to find significantly changed metabolites.
Results:
Patients with diabetic and non-diabetic chronic kidney disease (CKD) showed different metabolic profiles; lower levels of citrate, serine, and methionine suggested problems with energy metabolism and one-carbon metabolism; pathway analysis showed notable changes in the tricarboxylic acid (TCA) cycle and amino acid metabolism, indicating the metabolic impact of diabetes in early CKD.
Conclusion:
The three metabolites that were identified—methionine, citrate, and serine—may be useful biomarkers for the early identification and description of diabetic chronic kidney disease (CKD), assisting with better risk assessment and individualized treatment plans.