Dataset Information

High risk of renal dysfunction in patients with fulminant type 1 diabetes.

ABSTRACT:

Aims/introduction

To compare the incidence rate of renal dysfunction between patients with fulminant type 1 diabetes and those with acute-onset type 1 diabetes.

Materials and methods

The present retrospective cohort study included patients with fulminant type 1 diabetes and acute-onset type 1 diabetes diagnosed during April 1993 to March 2016 at a national center in Japan. Glycated hemoglobin levels, incidence rates of renal dysfunction defined as an estimated glomerular filtration rate of <60 mL/min/1.73 m² and microalbuminuria were examined.

Results

In total, 115 patients with type 1 diabetes (10 with fulminant type 1 diabetes and 105 with acute-onset type 1 diabetes) were included. The median glycated hemoglobin levels were significantly lower in patients with fulminant type 1 diabetes than in those with acute-onset type 1 diabetes 0, 3, 6 and 9 years after diabetes onset (6.5 vs 12.7%, 6.5 vs 7.9%, 6.7 vs 8.2%, 7.5 vs 8.5%, respectively). Kaplan-Meier analysis showed a significantly higher incidence rate of renal dysfunction in patients with fulminant type 1 diabetes than in those with acute-onset type 1 diabetes (hazard ratio 1.72, 95% confidence interval 1.01-2.97, P = 0.037). The incidence rate of microalbuminuria did not significantly differ between the groups (hazard ratio 0.97, 95% confidence interval 0.34-2.77, P = 0.95). Sensitivity analysis using age- and sex-matched patients with fulminant type 1 diabetes and acute-onset type 1 diabetes yielded similar results.

Conclusions

The risk of developing renal dysfunction is higher in patients with fulminant type 1 diabetes than in those with acute-onset type 1 diabetes, despite better glycemic control.

SUBMITTER: Takahashi N

PROVIDER: S-EPMC5754524 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Publications

High risk of renal dysfunction in patients with fulminant type 1 diabetes.

Takahashi Nobuyuki N Tsujimoto Tetsuro T Chujo Daisuke D Kajio Hiroshi H

Journal of diabetes investigation 20170413 1

<h4>Aims/introduction</h4>To compare the incidence rate of renal dysfunction between patients with fulminant type 1 diabetes and those with acute-onset type 1 diabetes.<h4>Materials and methods</h4>The present retrospective cohort study included patients with fulminant type 1 diabetes and acute-onset type 1 diabetes diagnosed during April 1993 to March 2016 at a national center in Japan. Glycated hemoglobin levels, incidence rates of renal dysfunction defined as an estimated glomerular filtratio ...[more]

PMID: 28267278

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Project description:Diabetic nephropathy is characterized by excessive accumulation of extracellular matrix (ECM) leading to renal fibrosis, progressive deterioration of renal function, and eventually to end stage renal disease. Matrix metalloproteinases (MMPs) are known to regulate synthesis and degradation of the ECM. Earlier, we demonstrated that imbalanced MMPs promote adverse ECM remodeling leading to renal fibrosis in type-1 diabetes. Moreover, elevated macrophage infiltration, pro-inflammatory cytokines and epithelial‒mesenchymal transition (EMT) are known to contribute to the renal fibrosis. Various bioactive compounds derived from the medicinal plant, Azadirachta indica (neem) are shown to regulate inflammation and ECM proteins in different diseases. Nimbidiol is a neem-derived diterpenoid that is considered as a potential anti-diabetic compound due to its glucosidase inhibitory properties. We investigated whether Nimbidiol mitigates adverse ECM accumulation and renal fibrosis to improve kidney function in type-1 diabetes and the underlying mechanism. Wild-type (C57BL/6J) and type-1 diabetic (C57BL/6-Ins2Akita/J) mice were treated either with saline or with Nimbidiol (0.40 mg kg-1 d-1) for eight weeks. Diabetic kidney showed increased accumulation of M1 macrophages, elevated pro-inflammatory cytokines and EMT. In addition, upregulated MMP-9 and MMP-13, excessive collagen deposition in the glomerular and tubulointerstitial regions, and degradation of vascular elastin resulted to renal fibrosis in the Akita mice. These pathological changes in the diabetic mice were associated with functional impairments that include elevated resistive index and reduced blood flow in the renal cortex, and decreased glomerular filtration rate. Furthermore, TGF-β1, p-Smad2/3, p-P38, p-ERK1/2 and p-JNK were upregulated in diabetic kidney compared to WT mice. Treatment with Nimbidiol reversed the changes to alleviate inflammation, ECM accumulation and fibrosis and thus, improved renal function in Akita mice. Together, our results suggest that Nimbidiol attenuates inflammation and ECM accumulation and thereby, protects kidney from fibrosis and dysfunction possibly by inhibiting TGF-β/Smad and MAPK signaling pathways in type-1 diabetes.

Dataset Information

High risk of renal dysfunction in patients with fulminant type 1 diabetes.

Aims/introduction

Materials and methods

Results

Conclusions

Publications

High risk of renal dysfunction in patients with fulminant type 1 diabetes.

Similar Datasets

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