Insulin resistance in diabetic nephropathy — cause or consequence?

Svensson, Maria; Eriksson, Jan W.

doi:10.1002/dmrr.648

Cited by 39 publications

(24 citation statements)

References 142 publications

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“…So, PTX-3 was the only parameter related to the disease stage and proteinuria in our study by mechanisms that we could not be able to explain. Our study also supports the studies showing increased insulin resistance in CKD patients since serum insulin, C-peptide and HOMA-IR were significantly increased in lower GFR groups 31 ( Table 1).…”

Section: Discussionsupporting

confidence: 92%

Changes in the inflammatory markers with advancing stages of diabetic nephropathy and the role of pentraxin-3

et al. 2016

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Background: Immunological and inflammatory mechanisms have been shown to have role in both the development and progression of diabetic nephropathy (DNP). There is need for more specific markers for inflammation as the ones commonly used are influenced by many factors. Pentraxin-3 (PTX-3) seems to be a potential candidate. We aimed in our study to evaluate the changes of PTX-3 levels in different stages of DNP and its relationship with other inflammatory markers.Methods: This is a cross sectional study in which patients with DNP at different stages were involved. Patient were divided into three groups according to estimated glomerular filtration rate (eGFR), microalbuminuria and proteinuria levels: Group-1: eGFR >60 mL/min and microalbuminuria, Group-2: eGFR >60 mL/min and macroalbuminuria, Group-3: eGFR <60 mL/min and macroalbuminuria. Besides the routine biochemical parameters, levels of PTX-3, high sensitivity C-reactive protein (hsCRP), interleukin (IL)-1 and tumor necrosis factor (TNF)-a was measured. Groups were compared with each other regarding the study parameters and correlation of PTX-3 with other markers was evaluated. Results: The mean PTX-3 level in Group-2 (0.94 ± 0.26 ng/mL) and -3 (1.35 ± 1.55 ng/mL) were higher than in Group-1 (0.81 ± 0.25 ng/mL) (p ¼ 0.009 and p ¼ 0.012). There was a significant correlation of PTX-3 with proteinuria (r ¼ 0.266, p ¼ 0.016), microalbuminuria (r ¼ 0.304, p ¼ 0.014) and hypoalbuminemia (r ¼ 0.197, p ¼ 0.043). PTX-3 was not correlated with other markers of inflammation (IL-1, TNF-a and hsCRP) and diabetic metabolic parameters (hbA1c, C-peptide, insulin and HOMA-IR). PTX-3, IL-1 and TNF-a levels increased with the advancing stage of DNP while hsCRP level did not change. Conclusion: PTX-3 that increases similar to other markers of inflammation (IL-1, TNF-a) is a better inflammatory marker than hsCRP. Furthermore, there is a relationship between PTX-3 and proteinuria independent from eGFR.

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Section: Discussionsupporting

confidence: 92%

Changes in the inflammatory markers with advancing stages of diabetic nephropathy and the role of pentraxin-3

et al. 2016

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“…Insulin resistance and compensatory hyperinsulinemia are common in both diabetic and nondiabetic CKD patients and increase as the GFR decreases over the course of the disease [133,134]. Evidence exists that insulin resistance and elevated circulating plasma insulin levels cause sympathetic activation, impaired BRS, and hypertension or potentiate the hypertensive effects of other pressor agents, including Ang II [135,136].…”

Section: Insulinmentioning

confidence: 98%

Cardiovascular Autonomic Dysfunction in Chronic Kidney Disease: a Comprehensive Review

Salman

2015

Curr Hypertens Rep

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Cardiovascular autonomic dysfunction is a major complication of chronic kidney disease (CKD), likely contributing to the high incidence of cardiovascular mortality in this patient population. In addition to adrenergic overdrive in affected individuals, clinical and experimental evidence now strongly indicates the presence of impaired reflex control of both sympathetic and parasympathetic outflow to the heart and vasculature. Although the principal underlying mechanisms are not completely understood, potential involvements of altered baroreceptor, cardiopulmonary, and chemoreceptor reflex function, along with factors including but not limited to increased renin-angiotensin-aldosterone system activity, activation of the renal afferents and cardiovascular structural remodeling have been suggested. This review therefore analyzes potential mechanisms underpinning autonomic imbalance in CKD, covers results accumulated thus far on cardiovascular autonomic function studies in clinical and experimental renal failure, discusses the role of current interventional and therapeutic strategies in ameliorating autonomic deficits associated with chronic renal dysfunction, and identifies gaps in our knowledge of neural mechanisms driving cardiovascular disease in CKD.

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“…Apolipoprotein (apo) B48, a major component of chylomicron, is also increased in diabetes, suggesting an accumulation of chylomicron remnants [11]. It has been demonstrated that insulin resistance is aggravated along with the progression of DN, even in the early stage of microalbuminuria [12]. An elevation in the serum levels of apoC-III, an inhibitor of LPL, is also observed in subjects with DN [3].…”

Section: Etiology and Epidemiology Of Diabetic Dyslipidemiamentioning

confidence: 99%

Dyslipidemia in diabetic nephropathy

2016

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Diabetic nephropathy (DN) not only is a major cause of end-stage renal disease (ESRD) in developing and developed countries but also plays a critical role as a risk factor for cardiovascular disease. The pathogenesis of DN is multifactorial and remains to be elucidated. It is well known that dyslipidemia is frequently complicated with diabetes. Recently, dyslipidemia has been recognized to be involved in the progression of DN. In general, diabetic dyslipidemia is caused by impaired action of lipoprotein lipase (LPL) that is localized to the endothelial cells, resulting in increased serum levels of increased triglyceride (TG) and decreased high-density lipoprotein cholesterol (HDL-C). Smaller size and modified low-density lipoprotein (LDL), such as glycated and oxidized LDL, play important roles to induce vascular and renal cellular dysfunction. Previous studies demonstrated that dyslipidemia enhances macrophage infiltration and excessive extracellular matrix (ECM) production in the glomeruli under diabetic conditions, leading to the development of DN. Clinical studies have demonstrated that lipid-lowering therapy shows a protective effect on the renal function. It is well known that statins reduce albuminuria in patients with DN. A series of our studies indicated that this effect is mediated by Rho-kinase inhibition. Rho-kinase plays a key role in the pathogenesis of DN by activating the inflammatory pathway, including oxidative stress, NF-κB, and hypoxia inducible factor (HIF)-1. Intriguingly, Rho-kinase inhibitors have been shown to attenuate glomerulosclerosis as well as atherosclerosis. Therefore, Rho-kinase could be a promising therapeutic target for both DN and cardiovascular disease.

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Insulin resistance in diabetic nephropathy — cause or consequence?

Cited by 39 publications

References 142 publications

Changes in the inflammatory markers with advancing stages of diabetic nephropathy and the role of pentraxin-3

Changes in the inflammatory markers with advancing stages of diabetic nephropathy and the role of pentraxin-3

Cardiovascular Autonomic Dysfunction in Chronic Kidney Disease: a Comprehensive Review

Dyslipidemia in diabetic nephropathy

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