Atherogenic dyslipidemia and diabetic nephropathy
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REVIEW
Atherogenic dyslipidemia and diabetic nephropathy Giuseppina Russo1 · Pamela Piscitelli2 · Annalisa Giandalia1 · Francesca Viazzi3 · Roberto Pontremoli3 · Paola Fioretto4 · Salvatore De Cosmo2 Received: 23 December 2019 / Accepted: 11 April 2020 © Italian Society of Nephrology 2020
Abstract Chronic kidney disease is associated with altered lipid metabolism and lipid accumulation. Although it is though that hyperlipemia is a consequence of kidney dysfunction, several lines of evidence support that hyperlipidemia may contribute to the onset and progression of kidney disease, also in diabetes. This review describes the results of recent observational studies supporting the concept that glucose is only partly responsible for kidney damage onset, while a cluster of factors, including hypertriglyceridemia and low HDL-cholesterol, could play a relevant role in inducing onset and progression of DKD. We also report the results of randomized clinical trials investigating in type 2 diabetic patients the role of drug improvement of hypertriglyceridemia on renal outcomes. Finally, we discuss putative mechanisms linking hyperlipidemia (i.e. hypertriglyceridemia or low HDL cholesterol) with kidney disease. Keywords Atherogenic dyslipidemia · HDL-C · Triglycerides · Diabetic kidney disease
Introduction Diabetic kidney disease (DKD) develops in up 30–40% of all individuals with diabetes and is the leading cause of ESRD worldwide, accounting for almost half of patients on renal replacement treatment [1]. The loss of kidney function corresponds with histopathological changes, including progressive thickening of the glomerular and tubular basement membranes, mesangial expansion, podocyte effacement and loss, tubule-interstitial fibrosis and arteriolar hyalinosis [2]. DKD is also strongly associated with high cardiovascular risk. In fact patients with DKD frequently die for cardiovascular disease (CVD) and most of the augmented risk of cardiovascular mortality for subjects with diabetes is related to the presence of DKD [3]. * Salvatore De Cosmo [email protected] 1
Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy
2
Unit of Internal Medicine, Department of Medical Sciences, IRCCS Casa Sollievo Della Sofferenza, Viale Cappuccini 1, 71013 San Giovanni Rotondo, FG, Italy
3
University of Genova and Ospedale Policlinico San Martino-IST, Genoa, Italy
4
Department of Medicine, University of Padova, Padova, Italy
The role of intensive glycemic control in reducing the onset and progression of DKD has been shown in DCCT study in patients with type 1 diabetes [4] and in the UKPDS [5], ACCORD [6], ADVANCE [7], VADT [8] studies in patients with T2DM. Overall, the results of these intervention trials suggest that glucose is only partly responsible for kidney damage onset, rather a cluster of factors, including hypertension and dyslipidemia, could play a relevant role in inducing onset and progression of DKD. Hyperlipemia is a well recognized risk factor for CVD, also in patie
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