Role and Treatment of Insulin Resistance in Patients with Chronic Kidney Disease: A Review

Abstract

Patients with chronic kidney disease (CKD) and dialysis have higher mortality than those without, and cardiovascular disease (CVD) is the main cause of death. As CVD is caused by several mechanisms, insulin resistance plays an important role in CVD. This review summarizes the importance and mechanism of insulin resistance in CKD and discusses the current evidence regarding insulin resistance in patients with CKD and dialysis. Insulin resistance has been reported to influence endothelial dysfunction, plaque formation, hypertension, and dyslipidemia. A recent study also reported an association between insulin resistance and cognitive dysfunction, non-alcoholic fatty liver disease, polycystic ovary syndrome, and malignancy. Insulin resistance increases as renal function decrease in patients with CKD and dialysis. Several mechanisms increase insulin resistance in patients with CKD, such as chronic inflammation, oxidative stress, obesity, and mineral bone disorder. There is the possibility that insulin resistance is the potential future target of treatment in patients with CKD.

Association Between the Surrogate Markers of Insulin Resistance and Chronic Kidney Disease in Chinese Hypertensive Patients

“…IR is a pathological state in which tissues have a decreased sensitivity to insulin, leading to a compensatory rise in circulating insulin to maintain normal blood glucose levels ( 18 , 19 ). The gold standard for evaluating IR is the hyperinsulinemic-normoglycemic clamp test ( 20 ).…”

Association between triglyceride-glucose index and risk of end-stage renal disease in patients with type 2 diabetes mellitus and chronic kidney disease

“…IR appears in a very early stage of CKD in patients with or without diabetes and worsens as renal functions decline ( 36 ). The etiology of IR in CKD is complex and multifactorial, including unhealthy lifestyles, chronic inflammation, oxidative stress, uremic toxins, metabolic acidosis, anemia, vitamin D deficiency, and disturbed gut microbiome ( 36 – 38 ). IR accelerates the development and progression of CKD via various mechanisms, including worsening renal hemodynamics, affecting podocyte viability, promoting glomerular mesangial expansion and renal tubular interstitial fibrosis ( 12 , 13 ).…”

A zsírszövet mint a 2-es típusú diabetest kísérő inzulinrezisztencia egyik célszerve.

“…Az inzulinrezisztencia az egész szervezetet érinti. Kitüntetett célszövetei -a máj-, vese-, izom-és zsírszövet − patogenetikai és az ennek hátterében álló molekuláris biológiai folyamatai részben eltérőek [6,7]. Bár számos próbálkozás történt az egyes meghatározó szövetek biokémiai folyamatainak célzott befolyásolására -az antidiabetikumok közül például metformin (máj-, izomszövet), tiazolidindionok (zsírszövet), illetve GLP1-receptor-agonisták (máj) alkalmazásával, a vese esetében D-vitaminnal −, a kérdés megnyugtató megoldása még várat magára.…”