Metabolic syndrome and renal injury

Abstract

Both metabolic syndrome (MetS) and chronic kidney disease (CKD) are major global health issues. Current clinical markers used to reflect renal injury include albuminuria and estimated glomerular filtration rate (eGFR). Given the same eGFR level, urine albumin might be a better risk marker to predict progression of CKD and future development of cardiovascular diseases (CVDs). Serum Cystatin C is emerging as a new biomarker for early detection of renal injury associated with MetS and cardiovascular risk. In addition to each component, MetS per se influences the incidence and prognosis of renal injury and the odds ratios increased with the increase in the number of metabolic abnormalities. Hyperinsulinemia, activation of rennin-angiotensin-aldosterone system, increase of oxidative stress, and inflammatory cytokines are proposed to be the plausible biological link between MetS and CKD. Weight control, stick control of blood pressure, glucose, and lipids disorders may lead to lessening renal injury and even the subsequent CVD.

Figure 1

Mechanisms of insulin resistance with the consequent development of renal injury and the target of treatments. SNS: sympathetic nervous system, RAS: renin-angiotensin system, PPAR: peroxisome proliferator-activated receptors, ACEI: angiotensin-converting enzyme inhibitor, ARB: angiotensin II receptor blocker, TZD: thiazolidinediones.