Diabetic kidney disease in thedb/dbmouse

2003 ◽  
Vol 284 (6) ◽  
pp. F1138-F1144 ◽  
Author(s):  
Kumar Sharma ◽  
Peter McCue ◽  
Stephen R. Dunn
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Mouse Model ◽  
Renal Disease ◽  
Mouse Models ◽  
Diabetic Kidney Disease ◽  
Diabetic Kidney ◽  
Matrix Expansion ◽  
Stage Renal Disease ◽  
End Stage

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.

scholarly journals Immunity and inflammation in diabetic kidney disease: translating mechanisms to biomarkers and treatment targets

2017 ◽  
Vol 312 (4) ◽  
pp. F716-F731 ◽  
Author(s):  
Raimund Pichler ◽  
Maryam Afkarian ◽  
Brad P. Dieter ◽  
Katherine R. Tuttle
Keyword(s):  
Kidney Disease ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Diabetic Kidney Disease ◽  
The United States ◽  
Diabetic Kidney ◽  
Amyloid A ◽  
Obesity And Diabetes ◽  
Stage Renal Disease ◽  
End Stage

Increasing incidences of obesity and diabetes have made diabetic kidney disease (DKD) the leading cause of chronic kidney disease and end-stage renal disease worldwide. Despite current pharmacological treatments, including strategies for optimizing glycemic control and inhibitors of the renin-angiotensin system, DKD still makes up almost one-half of all cases of end-stage renal disease in the United States. Compelling and mounting evidence has clearly demonstrated that immunity and inflammation play a paramount role in the pathogenesis of DKD. This article reviews the involvement of the immune system in DKD and identifies important roles of key immune and inflammatory mediators. One of the most recently identified biomarkers is serum amyloid A, which appears to be relatively specific for DKD. Novel and evolving treatment approaches target protein kinases, transcription factors, chemokines, adhesion molecules, growth factors, advanced glycation end-products, and other inflammatory molecules. This is the beginning of a new era in the understanding and treatment of DKD, and we may have finally reached a tipping point in our fight against the growing burden of DKD.

scholarly journals Synopsis of Sweet! Mouse Models of Diabetic Kidney Disease

2018 ◽  
Vol 46 (8) ◽  
pp. 970-975 ◽  
Author(s):  
Kathleen M. Heinz-Taheny ◽  
Shannon M. Harlan ◽  
Zhonghua Qi ◽  
Josef G. Heuer
Keyword(s):  
Kidney Disease ◽  
Mouse Models ◽  
Diabetic Kidney Disease ◽  
Standard Of Care ◽  
Developed Countries ◽  
Current Standard ◽  
Diabetic Kidney ◽  
Progression Of Kidney Disease ◽  
Stage Renal Disease ◽  
End Stage

Diabetes mellitus (types 1 and 2) is the leading cause of glomerular disease and end-stage renal disease in most developed countries, with estimates that one-third of people living with diabetes will develop diabetic kidney disease (DKD). The current standard of care medications slow but do not arrest progression of kidney disease, and therefore, therapy for DKD is a highly unmet medical need for patients. To discover and test novel and durable new therapies, it is necessary to develop animal models of human DKD, which authentically recapitulate the human disease state and provide translatable efficacy to human patients. Here, we review selected mouse models of human DKD, which demonstrate many of the features of type 2 human DKD.

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