Nephropathy in Patients with Type 2 Diabetes Mellitus

Ritz, Eberhard; Orth, Stephan R.

doi:10.1056/nejm199910073411506

Cited by 663 publications

(460 citation statements)

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“…Diabetic nephropathy is a common complication of diabetes and the leading cause of end-stage renal disease in developed countries (1,2). Several studies have reported that diabetic nephropathy is related to the onset of cardiovascular disease, which worsens the overall prognosis (3,4).…”

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confidence: 99%

Serum High-Sensitivity C-Reactive Protein Levels Are Associated With High Risk of Development, Not Progression, of Diabetic Nephropathy Among Japanese Type 2 Diabetic Patients: A Prospective Cohort Study (Diabetes Distress and Care Registry at Tenri [DDCRT7])

et al. 2014

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OBJECTIVETo assess the prospective association between baseline serum hs-CRP concentration and the subsequent risk of development or progression of diabetic nephropathy. RESEARCH DESIGN AND METHODSLongitudinal data were obtained from 2,518 patients with type 2 diabetes registered in a Japanese diabetes registry. To assess the independent correlations between serum baseline hs-CRP and either the development or progression of diabetic nephropathy 1 year later, the Cox proportional hazards model was used and adjusted for potential confounders. RESULTSThe mean patient age, BMI, and HbA 1c level were 66.1 years, 24.6 kg/m 2 , and 7.5% (57.6 mmol/mol), respectively. Baseline serum hs-CRP levels were significantly associated with the urinary albumin-to-creatinine ratio at baseline (P < 0.001). Multivariable adjusted hazard ratio for the development from normoalbuminuria to microalbuminuria was 1.31 (95% CI 0.80-2.17; P = 0.286), 1.55 (1.16-2.08; P = 0.003), and 1.57 (1.22-2.03; P = 0.001), respectively, for the second, third, and fourth quartiles of serum hs-CRP levels, showing a statistically significant linear trend across categories (P < 0.001). We did not observe a significant association between hs-CRP levels and the subsequent risk of diabetic nephropathy progression (P for trend = 0.575). CONCLUSIONSSerum hs-CRP levels, independent of possible confounders, were associated with a subsequent risk of developing, not progressing, diabetic nephropathy in type 2 diabetic patients. Serum hs-CRP may be useful for predicting the future risk of developing diabetic nephropathy.

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Serum High-Sensitivity C-Reactive Protein Levels Are Associated With High Risk of Development, Not Progression, of Diabetic Nephropathy Among Japanese Type 2 Diabetic Patients: A Prospective Cohort Study (Diabetes Distress and Care Registry at Tenri [DDCRT7])

et al. 2014

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“…3, 4,5,6,7]. It has been suggested that these effects are, at least in part, independent from the reduction of the systemic blood pressure [8,9,10].…”

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Angiotensin II induces human TGF-β1 promoter activation: similarity to hyperglycaemia

et al. 2002

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Aims/hypothesis. Activation of the renal renin-angiotensin system has been implicated in the pathogenesis of diabetic nephropathy. Because previous in vitro studies demonstrated the angiotensin II (ang II)-mediated up-regulation of the prosclerotic transforming growth factor β1 (TGF) we studied the molecular mechanism of ang II-induced TGF-β1 gene activation. Methods. Mesangial cells were stimulated with 100 nmol/l ang II with or without inhibitors of protein kinase C (PKC) and p38 MAPK and the TGF-β1 promoter activity was determined by promoter-reporter assays. The effect of ang II on the binding of nuclear proteins to the regulatory AP-1 site B, previously shown to mediate the high glucose-response of the TGF-β1 promoter, was studied by electrophoretic mobility shift assays. Results. Ang II enhanced the activity of the TGF-β1 promoter fragment -453/+11 approximately 1.6-fold.Mutation of each of two AP-1 binding sites or inhibition of the PKC-and p38 MAPK-dependent pathways blocked the ang II-stimulated activity completely. Furthermore, ang II activated the binding of nuclear proteins to the AP-1 box B of the TGF-β1 promoter. These effects were similar to those previously observed with high glucose. Co-incubation with ang II and high glucose had no additive effect on TGF-β1 promoter activity, protein binding to the AP-1 box B or activation of p38 MAPK. Conclusion/interpretation. The findings indicate that ang II and hyperglycaemia stimulate the TGF-β1 gene activation through the same PKC-and p38 MAPK-dependent pathways by the same regulatory elements of the TGF-β1 promoter. Our data could also be relevant for e.g. hypertension-induced glomerulosclerosis. [Diabetologia (2002) 45:890-898]

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“…ACEIs and ARBs have been shown to slow down the progression of kidney disease [7][8][9][10][11]. However, there is no effective therapy to halt the progression to the end-stage renal disease (ESRD) after the nephropathy has been established [12].…”

Section: Diabetic Kidney Diseasementioning

confidence: 99%

microRNAs in Diabetic Kidney Disease

Chung

2015

Advances in Experimental Medicine and Biology

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Nephropathy in Patients with Type 2 Diabetes Mellitus

Cited by 663 publications

References 67 publications

Serum High-Sensitivity C-Reactive Protein Levels Are Associated With High Risk of Development, Not Progression, of Diabetic Nephropathy Among Japanese Type 2 Diabetic Patients: A Prospective Cohort Study (Diabetes Distress and Care Registry at Tenri [DDCRT7])

Serum High-Sensitivity C-Reactive Protein Levels Are Associated With High Risk of Development, Not Progression, of Diabetic Nephropathy Among Japanese Type 2 Diabetic Patients: A Prospective Cohort Study (Diabetes Distress and Care Registry at Tenri [DDCRT7])

Angiotensin II induces human TGF-β1 promoter activation: similarity to hyperglycaemia

microRNAs in Diabetic Kidney Disease

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