The Japanese Registries of Diabetic Nephropathy/Diabetic Kidney Disease

2020 ◽  
pp. 15-29
Author(s):  
Miho Shimizu ◽  
Takashi Wada
2003 ◽  
Vol 284 (6) ◽  
pp. F1138-F1144 ◽  
Author(s):  
Kumar Sharma ◽  
Peter McCue ◽  
Stephen R. Dunn

Diabetic nephropathy is increasing in incidence and is now the number one cause of end-stage renal disease in the industrialized world. To gain insight into the genetic susceptibility and pathophysiology of diabetic nephropathy, an appropriate mouse model of diabetic nephropathy would be critical. A large number of mouse models of diabetes have been identified and their kidney disease characterized to various degrees. Perhaps the best characterized and most intensively investigated model is the db/ db mouse. Because this model appears to exhibit the most consistent and robust increase in albuminuria and mesangial matrix expansion, it has been used as a model of progressive diabetic renal disease. In this review, we present the findings from various studies on the renal pathology of the db/ db mouse model of diabetes in the context of human diabetic nephropathy. Furthermore, we discuss shortfalls of assessing functional renal disease in mouse models of diabetic kidney disease.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Abraham Cohen-Bucay ◽  
Gautham Viswanathan

Diabetic nephropathy, the leading cause of renal failure worldwide, affects approximately one-third of all people with diabetes. Microalbuminuria is considered the first sign and the best predictor of progression to renal failure and cardiovascular events. However, albuminuria has several limitations. Therefore, earlier, more sensitive and specific biomarkers with greater predictability are needed. The aim of this paper is to discuss the current literature on biomarkers of glomerular injury that have been implicated in diabetic kidney disease.


Molecules ◽  
2019 ◽  
Vol 24 (15) ◽  
pp. 2857 ◽  
Author(s):  
Sun ◽  
Wu ◽  
Cao ◽  
Zhu ◽  
Liu ◽  
...  

Diabetic kidney disease develops in approximately 40% of diabetic patients and is a major cause of chronic kidney diseases (CKD) and end stage kidney disease (ESKD) worldwide. Hydrogen sulfide (H2S), the third gasotransmitter after nitric oxide (NO) and carbon monoxide (CO), is synthesized in nearly all organs, including the kidney. Though studies on H2S regulation of renal physiology and pathophysiology are still in its infancy, emerging evidence shows that H2S production by renal cells is reduced under disease states and H2S donors ameliorate kidney injury. Specifically, aberrant H2S level is implicated in various renal pathological conditions including diabetic nephropathy. This review presents the roles of H2S in diabetic renal disease and the underlying mechanisms for the protective effects of H2S against diabetic renal damage. H2S may serve as fundamental strategies to treat diabetic kidney disease. These H2S treatment modalities include precursors for H2S synthesis, H2S donors, and natural plant-derived compounds. Despite accumulating evidence from experimental studies suggests the potential role of the H2S signaling pathway in the treatment of diabetic nephropathy, these results need further clinical translation. Expanding understanding of H2S in the kidney may be vital to translate H2S to be a novel therapy for diabetic renal disease.


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Lian-ji Zhou ◽  
Da-wei Yang ◽  
Li-Na Ou ◽  
Xing-Rong Guo ◽  
Biao-liang Wu

Background. Long noncoding RNA MALAT1 is closely related to diabetes and kidney diseases and is expected to be a new target for the diagnosis and treatment of diabetic nephropathy. Objective. This study aimed to explore the circulating expression level and significance of lncRNA Malat1 in patients with type 2 diabetes mellitus (T2DM) and diabetic kidney disease (DKD). Methods. Quantitative real-time PCR (qPCR) was conducted to assess the expression of lncRNA Malat1 in 20 T2DM patients, 27 DKD patients, and 14 healthy controls, and then, the clinical significance was analyzed. Results. LncRNA MALAT1 expression in peripheral blood mononuclear cells (PBMC) was significantly upregulated in T2DM and DKD groups when compared to control. Pearson’s correlation analysis showed correlation of lncRNA MALAT1 levels with ACR, urine β2-microglobulin (β2-MG), urine α1-microglobulin (α1-MG), creatinine (Cr), and glycosylated hemoglobin (HbA1c), while negative with superoxide dismutase (SOD) (r=−0.388, P<0.05). Binary regression analysis showed that ACR, creatinine, α1-MG, and LncRNA Malat1 were the risk factors for diabetic nephropathy with OR value of 1.166, 1.031, 1.031, and 2.019 (P<0.05). The area under ROC curve (AUC) of DKD identified by the above indicators was 0.914, 0.643, 0.807, and 0.797, respectively. The AUC of Joint prediction probability of DKD recognition was 0.914, and the sensitivity and specificity of DKD diagnosis were 1.0 and 0.806, respectively. (Take ≥0.251 as the diagnostic cutoff point). Conclusion. LncRNA Malat1 is highly expressed in DKD patients, and the combined detection of ACR, creatinine, α1-MG, and LncRNA Malat1 with diabetes mellitus may be the best way to diagnose diabetic nephropathy.


2019 ◽  
Vol 20 (20) ◽  
pp. 5101 ◽  
Author(s):  
Angelo Di Vincenzo ◽  
Claudio Tana ◽  
Hamza El Hadi ◽  
Claudio Pagano ◽  
Roberto Vettor ◽  
...  

Diabetes mellitus is a metabolic disorder characterized by the development of vascular complications associated with high morbidity and mortality and the consequent relevant costs for the public health systems. Diabetic kidney disease is one of these complications that represent the main cause of end-stage renal disease in Western countries. Hyperglycemia, inflammation, and oxidative stress contribute to its physiopathology, and several investigations have been performed to evaluate the role of antioxidant supplementation as a complementary approach for the prevention and control of diabetes and associated disturbances. Vitamin E compounds, including different types of tocopherols and tocotrienols, have been considered as a treatment to tackle major cardiovascular outcomes in diabetic subjects, but often with conflicting or even negative results. However, their effects on diabetic nephropathy are even less clear, despite several intervention studies that showed the improvement of renal parameters after supplementation in patients with diabetic kidney disease. Then we performed a review of the literature about the role of vitamin E supplementation on diabetic nephropathy, also describing the underlying antioxidant, anti-inflammatory, and metabolic mechanisms to evaluate the possible use of tocopherols and tocotrienols in clinical practice.


2018 ◽  
Vol 06 (02) ◽  
pp. 106-108
Author(s):  
Sanjay Kalra ◽  
Manisha Sahay ◽  
Rakesh Sahay

AbstractDiabetic nephropathy, including diabetic kidney disease (DKD), is a major complication of diabetes. Appropriate management of DKD requires multispecialty intervention under the guidance of endocrinology and nephrology. However, delayed referral to specialized nephrology services usually occurs, and this leads to suboptimal outcomes. This multispecialty consensus suggests simple clinical and biochemical parameters that should prompt referral of DKD patients to nephrology. A checklist for physicians who manage DKD is also provided.


2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i360-i360
Author(s):  
Bo Zhang ◽  
Suyan Duan ◽  
Chengning Zhang ◽  
Yanggang Yuan ◽  
Zhiming Huang ◽  
...  

Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Denisha Spires ◽  
Daria Ilatovskaya ◽  
Vladislav Levchenko ◽  
Oleg Palygin ◽  
Alexander Staruschenko

2015 ◽  
Vol 41 (3) ◽  
pp. 220-230 ◽  
Author(s):  
Punithavathi Ranganathan ◽  
Riyaz Mohamed ◽  
Calpurnia Jayakumar ◽  
Michael W. Brands ◽  
Ganesan Ramesh

Background: Guidance cue netrin-1 was shown to have protective effects in diabetic nephropathy. However, the role of its receptor UNC5B in diabetic kidney disease is unknown. Moreover, whether netrin-1 is protective against diabetic kidney disease in a genetic model of nephropathy and in the nephropathy prone DBA background is also unknown. The aim of this study was to determine the significance of UNC5B in tubular epithelial cells in chronic kidney disease due to diabetes and evaluate whether netrin-1 is also protective in the case of a nephropathy-prone mouse. Methods: Proximal tubular epithelium-specific UNC5B knockout mice as well as heterozygous UNC5B knockout mice were used to determine the roles of UNC5B in nephropathy. Diabetes was induced in these tissue-specific knockout, heterozygous and WT mice, and albuminuria was then monitored. Results: WT and heterozygous diabetic mice developed significant albuminuria at 8 weeks after induction of diabetes as compared to buffer-treated control mice. However, albuminuria was significantly more pronounced in mice with proximal tubule specific deletion of UNC5B. Transgenic overexpression of netrin-1 in proximal tubules in the DBA background and administration of recombinant netrin-1 to Ins2Akita mice also significantly reduced diabetes-induced albuminuria and suppressed glomerular and interstitial lesions. Conclusion: Our data suggested that netrin-1 signaling in proximal tubular epithelium may play a critical role in the protection of kidney against diabetic kidney disease.


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