Diabetic Nephropathy in Type 2 Diabetes Prevention and Patient Management

Wolf, Günter; Ritz, Eberhard

doi:10.1097/01.asn.0000065639.19190.cf

Cited by 101 publications

(75 citation statements)

References 104 publications

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“…Systemic hypertension, particularly increased systolic BP, not only predisposes to the development of diabetic renal disease but also accelerates its progression (18,19). In addition, in animal studies, increased glomerular capillary hydraulic pressure (i.e., intraglomerular capillary hypertension) as a result of Ang II-mediated efferent arteriolar vasoconstriction has been identified as a potential therapeutic target for prevention of progressive diabetic renal damage, and the use of RAS inhibitors attenuated the course of renal disease in diabetic animals independent of their effect on BP (20).…”

Section: Discussionmentioning

confidence: 99%

Chronic Angiotensin II Receptor Blockade Reduces (Intra)Renal Vascular Resistance in Patients with Type 2 Diabetes

Fliser¹,

Wagner²,

Loos³

et al. 2005

Journal of the American Society of Nephrology

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Increased (intra)renal activity of the renin-angiotensin system may cause a persistent increase in renovascular resistance and intraglomerular pressure in patients with diabetes, thus contributing to the development of diabetic renal damage. The effect of chronic angiotensin II subtype 1 receptor blockade on (intra)renal hemodynamics in patients with type 2 diabetes was examined in a double-blind parallel group study. Patients were treated with 40 mg of olmesartan (n ‫؍‬ 19) or placebo (n ‫؍‬ 16), and renal hemodynamics were assessed before and after 12 wk of treatment using inulin and para-aminohippurate clearance techniques. Olmesartan significantly reduced 24-h ambulatory systolic and diastolic BP (both P < 0.05). In parallel, effective renal plasma flow increased significantly from 602 ؎ 76 to 628 ؎ 87 ml/min per 1.73 m 2 , whereas filtration fraction and renovascular resistance decreased significantly (all P < 0.05). With placebo treatment, effective renal plasma flow decreased and filtration fraction increased significantly (both P < 0.05). GFR was not affected by both treatments. Active plasma renin concentration increased considerably (P < 0.05) with olmesartan therapy but remained unchanged with placebo treatment. Nitric oxide metabolism (plasma nitrate and nitrite) and asymmetric dimethylarginine blood levels were not affected by olmesartan and placebo therapy. In contrast, plasma 8-isoprostane 15(S)-8-iso-prostaglandin F 2a concentration, a biochemical marker of oxidative stress, decreased significantly (P < 0.05) with olmesartan treatment. Chronic angiotensin II subtype 1 receptor blockade decreases (intra)renal vascular resistance and increases renal perfusion despite significant BP reduction. In addition, it significantly reduces oxidative stress. These effects of angiotensin II receptor antagonists may contribute to their beneficial long-term renal effects in patients with type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Chronic Angiotensin II Receptor Blockade Reduces (Intra)Renal Vascular Resistance in Patients with Type 2 Diabetes

Fliser¹,

Wagner²,

Loos³

et al. 2005

Journal of the American Society of Nephrology

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“…renin-angiotensin system being more effective than calcium channel blockers (18,19). In contrast, little information is available regarding the ability of anti-hyperglycemia agents to prevent or lower albuminuria.…”

Section: ͻ0001mentioning

confidence: 99%

Renal Function in Type 2 Diabetes with Rosiglitazone, Metformin, and Glyburide Monotherapy

Lachin

Viberti

Zinman

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives In ADOPT (A Diabetes Outcomes Prevention Trial), initial monotherapy with rosiglitazone provided more durable glycemic control than metformin or glyburide in patients with recently diagnosed type 2 diabetes. Herein, we examine differences in albumin excretion, renal function (estimated GFR), and BP over 5 years between treatment groups.Design, setting, participants, & measurements A total of 4351 recently diagnosed, drug-naïve patients with type 2 diabetes were treated and followed for up to 5 years with rosiglitazone, metformin, or glyburide and were examined with periodic assessments of albumin/creatinine ratio (ACR), modification of diet in renal disease (MDRD)-estimated GFR, and BP. ResultsThe ACR rose slowly with metformin. It fell with rosiglitazone and less so with glyburide over the first 2 years, and then rose slowly over time. Estimated GFR (eGFR) with all therapies rose into the high normal range over the first 3 to 4 years, more so with rosiglitazone, and then declined, more so with glyburide. Systolic BP was stable over time, values with rosiglitazone being lower, and diastolic BP declined over time, more so with rosiglitazone than with metformin or glyburide. There was no difference among groups in the incidence of emergent albuminuria (ACR Ն30 mg/g), hypertension, or impaired eGFR (Ͻ60 ml/min per 1.73 m 2 ).Conclusions Over a 5-year period, initial monotherapy with rosiglitazone retards the rise of ACR compared with metformin, preserves eGFR compared with glyburide, and lowers BP relative to both comparators.

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“…In addition, type 2 diabetic patients fare poorly on dialysis and have an excess mortality. While the pathogenesis of DN in type 1 diabetic patients has been better characterised, its pathogenesis in type 2 diabetic patients is less well understood [1]. Type 2 diabetes is characterised by insulin resistance and accumulation of fat in parenchymal organs.…”

Section: Introductionmentioning

confidence: 99%

Systemic and renal growth hormone–IGF1 axis involvement in a mouse model of type 2 diabetes

et al. 2007

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Aims/hypothesis In previous studies we have shown a significant involvement of the growth hormone (GH)-IGF axis in animal models of type 1 diabetes mellitus, but the role of this endocrine system in type 2 diabetes mellitus is less well characterised. We therefore examined the endocrine and renal GH-IGF axis changes in db/db mice, a model of type 2 diabetes mellitus and nephropathy. Materials and methods Obese and lean animals were followed, beginning at hyperglycaemia onset, for 4 weeks. Albuminuria and creatinine clearance, as well as kidney and glomerular morphology were assessed. Tissue protein levels were determined by western blotting and mRNA levels by RT-PCR.Results Serum GH and IGF1 levels immediately prior to killing were decreased and liver mRNA levels of insulinlike growth factor binding protein 1 (Igfbp1) were increased in obese animals. Kidney weight was increased in obese animals, associated with hyperfiltration, albuminuria and glomerular hypertrophy. Administration of a somatostatin analogue (PTR-313) did not improve any of these parameters of diabetic renal involvement. Renal Igf1 mRNA was decreased and renal Igfbp1 mRNA and protein were significantly increased in obese animals. Renal insulindriven levels of phosphorylated forkhead box O1 (FOXO1) were decreased in obese animals. Conclusions/interpretation Diabetic db/db mice show significant renal changes (and IGFBP1 renal accumulation), similar to the findings in models of type 1 diabetes mellitus. A decreased signalling through the insulin receptor and decreased FOXO1 phosphorylation may allow Igfbp1 gene transcription. These renal changes are associated with low circulating IGF1 and GH levels and unchanged hepatic growth hormone receptor expression, unlike the condition in type 1 diabetes mellitus. This suggests that further GH inhibition to modulate renal complications in type 2 diabetes mellitus is not indicated.

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Diabetic Nephropathy in Type 2 Diabetes Prevention and Patient Management

Cited by 101 publications

References 104 publications

Chronic Angiotensin II Receptor Blockade Reduces (Intra)Renal Vascular Resistance in Patients with Type 2 Diabetes

Chronic Angiotensin II Receptor Blockade Reduces (Intra)Renal Vascular Resistance in Patients with Type 2 Diabetes

Renal Function in Type 2 Diabetes with Rosiglitazone, Metformin, and Glyburide Monotherapy

Systemic and renal growth hormone–IGF1 axis involvement in a mouse model of type 2 diabetes

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