scholarly journals Mechanistic Insight and Management of Diabetic Nephropathy: Recent Progress and Future Perspective

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Rui Xue ◽  
Dingkun Gui ◽  
Liyang Zheng ◽  
Ruonan Zhai ◽  
Feng Wang ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Recent Progress ◽  
Developed Countries ◽  
Future Perspective ◽  
Therapeutic Approaches ◽  
Mechanistic Insight ◽  
Novel Drugs ◽  
Genetic And Environmental Factors ◽  
Stage Renal Disease ◽  
End Stage

Diabetic nephropathy (DN) is the most serious microvascular complication of diabetes and the largest single cause of end-stage renal disease (ESRD) in many developed countries. DN is also associated with an increased cardiovascular mortality. It occurs as a result of interaction between both genetic and environmental factors. Hyperglycemia, hypertension, and genetic predisposition are the major risk factors. However, the exact mechanisms of DN are unclear. Despite the benefits derived from strict control of glucose and blood pressure, as well as inhibition of renin-angiotensin-aldosterone system, many patients continue to enter into ESRD. Thus, there is urgent need for improving mechanistic understanding of DN and then developing new and effective therapeutic approaches to delay the progression of DN. This review focuses on recent progress and future perspective about mechanistic insight and management of DN. Some preclinical relevant studies are highlighted and new perspectives of traditional Chinese medicine (TCM) for delaying DN progression are discussed in detail. These findings strengthen the therapeutic rationale for TCM in the treatment of DN and also provide new insights into the development of novel drugs for the prevention of DN. However, feasibility and safety of these therapeutic approaches and the clinical applicability of TCM in human DN need to be further investigated.

scholarly journals Recent advances in managing and understanding diabetic nephropathy

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 1044 ◽  
Author(s):  
Sydney C.W. Tang ◽  
Gary C.W. Chan ◽  
Kar Neng Lai
Keyword(s):  
Diabetic Nephropathy ◽  
Management Strategies ◽  
Standard Of Care ◽  
Pressure Control ◽  
Review Article ◽  
Therapeutic Approaches ◽  
Current Standard ◽  
Developed Economies ◽  
Stage Renal Disease ◽  
End Stage

Diabetic nephropathy is the commonest cause of end-stage renal disease in most developed economies. Current standard of care for diabetic nephropathy embraces stringent blood pressure control via blockade of the renin-angiotensin-aldosterone system and glycemia control. Recent understanding of the pathophysiology of diabetic nephropathy has led to the development of novel therapeutic options. This review article focuses on available data from landmark studies on the main therapeutic approaches and highlights some novel management strategies.

scholarly journals Recent advances in the understanding and management of IgA nephropathy

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 161 ◽  
Author(s):  
Kar Neng Lai ◽  
Joseph C.K. Leung ◽  
Sydney C.W. Tang
Keyword(s):  
Iga Nephropathy ◽  
Specific Treatment ◽  
Developed Countries ◽  
Current Data ◽  
Therapeutic Approaches ◽  
Clinical Progression ◽  
Primary Glomerulonephritis ◽  
New Therapeutic Approaches ◽  
Stage Renal Disease ◽  
End Stage

Since its first description in 1968, IgA nephropathy has remained the most common form of primary glomerulonephritis leading to chronic kidney disease in developed countries. The clinical progression varies, and consequent end-stage renal disease occurs in 30% to 40% of patients 20 to 30 years after the first clinical presentation. Current data implicate overproduction of aberrantly glycosylated IgA1 as being pivotal in the induction of renal injury. Effective and specific treatment is still lacking, and new therapeutic approaches will be developed after better understanding the disease pathogenesis.

scholarly journals Special Issue “Diabetic Nephropathy: Diagnosis, Prevention and Treatment”

2020 ◽  
Vol 9 (3) ◽  
pp. 813 ◽  
Author(s):  
Marta Ruiz-Ortega ◽  
Raul R. Rodrigues-Diez ◽  
Carolina Lavoz ◽  
Sandra Rayego-Mateos
Keyword(s):  
Diabetic Nephropathy ◽  
Renal Damage ◽  
Molecular Mechanisms ◽  
Complex Disease ◽  
Clinical Medicine ◽  
Histopathological Changes ◽  
Special Issue ◽  
Genetic And Environmental Factors ◽  
Stage Renal Disease ◽  
End Stage

Diabetic nephropathy (DN) is the main cause of end-stage renal disease. DN is a complex disease mediated by genetic and environmental factors, and many cellular and molecular mechanisms are involved in renal damage in diabetes. There are no biomarkers that reflect the severity of the underlying renal histopathological changes and can effectively predict the progression of renal damage and stratify the risk of DN among individuals with diabetes mellitus. Current therapeutic strategies are based on the strict control of glucose and blood pressure levels and, although there are new anti-diabetic drugs, these treatments only retard renal damage progression, being necessary novel therapies. In this Special Issue, there are several comprehensive reviews and interesting original papers covering all these topics, which would be of interest to the growing number of readers of the Journal of Clinical Medicine.

scholarly journals Inflammatory Cytokines in Diabetic Nephropathy

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Javier Donate-Correa ◽  
Ernesto Martín-Núñez ◽  
Mercedes Muros-de-Fuentes ◽  
Carmen Mora-Fernández ◽  
Juan F. Navarro-González
Keyword(s):  
Diabetic Nephropathy ◽  
Renal Disease ◽  
Diabetic Complication ◽  
Therapeutic Approaches ◽  
New Therapeutic Approaches ◽  
Molecular Events ◽  
Patients With Diabetes ◽  
Inflammatory Processes ◽  
Stage Renal Disease ◽  
End Stage

Probably, the most paradigmatic example of diabetic complication is diabetic nephropathy, which is the largest single cause of end-stage renal disease and a medical catastrophe of worldwide dimensions. Metabolic and hemodynamic alterations have been considered as the classical factors involved in the development of renal injury in patients with diabetes mellitus. However, the exact pathogenic mechanisms and the molecular events of diabetic nephropathy remain incompletely understood. Nowadays, there are convincing data that relate the diabetes inflammatory component with the development of renal disease. This review is focused on the inflammatory processes that develop diabetic nephropathy and on the new therapeutic approaches with anti-inflammatory effects for the treatment of chronic kidney disease in the setting of diabetic nephropathy.

scholarly journals Long non-coding RNA TUG1 alleviates high glucose induced podocyte inflammation, fibrosis and apoptosis in diabetic nephropathy via targeting the miR-27a-3p/E2F3 axis

RSC Advances ◽  
2019 ◽  
Vol 9 (64) ◽  
pp. 37620-37629
Author(s):  
Yang Li ◽  
Denggao Huang ◽  
Linlin Zheng ◽  
Hui Cao ◽  
Yuanhui Gao ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Renal Disease ◽  
High Glucose ◽  
End Stage Renal Disease ◽  
Developed Countries ◽  
Common Cause ◽  
Non Coding Rna ◽  
Stage Renal Disease ◽  
End Stage ◽  
Long Non Coding Rna

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD) in developed countries.

scholarly journals Recent Progress in Stem Cell Therapy for Diabetic Nephropathy

2015 ◽  
Vol 2 (1) ◽  
pp. 20-27 ◽  
Author(s):  
Yang Liu ◽  
Sydney C.W. Tang
Keyword(s):  
Stem Cells ◽  
Diabetic Nephropathy ◽  
Stem Cell ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Recent Progress ◽  
Patient Specific ◽  
Cell Based Therapy ◽  
Stage Renal Disease ◽  
End Stage

Background: Diabetic nephropathy (DN) represents the leading cause of end-stage renal disease. Current therapeutic strategies for DN are very limited, and none of them can stop end-stage renal disease progression. Stem cell-based therapy showed encouraging outcomes in kidney disease, including experimental DN. Summary: Both podocytes and proximal tubular epithelial cells play key roles in the pathogenesis of DN and, accordingly, could be regarded as treatment targets. Multiple kinds of stem cells contribute to the regeneration of the injured kidney, including embryonic stem cells (ESCs), mesenchymal stem cells, and induced pluripotent stem cells (iPSCs). Stem cells exert reparatory effects mainly by homing to injured sites, directing differentiation, paracrine action, and immunoregulation. However, poor survival after transplantation under diabetic conditions and unsatisfactory animal models of advanced DN are major obstacles for achieving an efficacious therapeutic effect from stem cell transplantation. Recently, remarkable progress has been made both in the direct differentiation of human ESCs and iPSCs into renal cells and in the generation of tissue- and patient-specific iPSCs, offering a powerful tool to investigate DN mechanisms and to identify the ideal candidate cell for future clinical application. Key Message: This review provides updated information on recent progress and limitations of stem cell-based therapy for DN.

scholarly journals TGF-Beta as a Master Regulator of Diabetic Nephropathy

2021 ◽  
Vol 22 (15) ◽  
pp. 7881
Author(s):  
Li Wang ◽  
Hong-Lian Wang ◽  
Tong-Tong Liu ◽  
Hui-Yao Lan
Keyword(s):  
Diabetic Nephropathy ◽  
Initial Step ◽  
Therapeutic Approaches ◽  
Smad Signaling ◽  
Signaling Mechanisms ◽  
Non Coding Rnas ◽  
Stage Renal Disease ◽  
End Stage ◽  
Tgf Β1

Diabetic nephropathy (DN) is one of the most common complications in diabetes mellitus and the leading cause of end-stage renal disease. TGF-β is a pleiotropic cytokine and has been recognized as a key mediator of DN. However, anti-TGF-β treatment for DN remains controversial due to the diverse role of TGF-β1 in DN. Thus, understanding the regulatory role and mechanisms of TGF-β in the pathogenesis of DN is the initial step towards the development of anti-TGF-β treatment for DN. In this review, we first discuss the diverse roles and signaling mechanisms of TGF-β in DN by focusing on the latent versus active TGF-β1, the TGF-β receptors, and the downstream individual Smad signaling molecules including Smad2, Smad3, Smad4, and Smad7. Then, we dissect the regulatory mechanisms of TGF-β/Smad signaling in the development of DN by emphasizing Smad-dependent non-coding RNAs including microRNAs and long-non-coding RNAs. Finally, the potential therapeutic strategies for DN by targeting TGF-β signaling with various therapeutic approaches are discussed.

L-carnosine and its Derivatives as New Therapeutic Agents for the Prevention and Treatment of Vascular Complications of Diabetes

2020 ◽  
Vol 27 (11) ◽  
pp. 1744-1763 ◽  
Author(s):  
Stefano Menini ◽  
Carla Iacobini ◽  
Claudia Blasetti Fantauzzi ◽  
Giuseppe Pugliese
Keyword(s):  
Diabetic Nephropathy ◽  
Life Quality ◽  
Vascular Complications ◽  
Carbonyl Stress ◽  
Complications Of Diabetes ◽  
Diabetic Vascular Complications ◽  
Reactive Carbonyl Species ◽  
Stage Renal Disease ◽  
Stress Dependent ◽  
End Stage

Vascular complications are among the most serious manifestations of diabetes. Atherosclerosis is the main cause of reduced life quality and expectancy in diabetics, whereas diabetic nephropathy and retinopathy are the most common causes of end-stage renal disease and blindness. An effective therapeutic approach to prevent vascular complications should counteract the mechanisms of injury. Among them, the toxic effects of Advanced Glycation (AGEs) and Lipoxidation (ALEs) end-products are well-recognized contributors to these sequelae. L-carnosine (β-alanyl-Lhistidine) acts as a quencher of the AGE/ALE precursors Reactive Carbonyl Species (RCS), which are highly reactive aldehydes derived from oxidative and non-oxidative modifications of sugars and lipids. Consistently, L-carnosine was found to be effective in several disease models in which glyco/lipoxidation plays a central pathogenic role. Unfortunately, in humans, L-carnosine is rapidly inactivated by serum carnosinase. Therefore, the search for carnosinase-resistant derivatives of Lcarnosine represents a suitable strategy against carbonyl stress-dependent disorders, particularly diabetic vascular complications. In this review, we present and discuss available data on the efficacy of L-carnosine and its derivatives in preventing vascular complications in rodent models of diabetes and metabolic syndrome. We also discuss genetic findings providing evidence for the involvement of the carnosinase/L-carnosine system in the risk of developing diabetic nephropathy and for preferring the use of carnosinase-resistant compounds in human disease. The availability of therapeutic strategies capable to prevent both long-term glucose toxicity, resulting from insufficient glucoselowering therapy, and lipotoxicity may help reduce the clinical and economic burden of vascular complications of diabetes and related metabolic disorders.

scholarly journals Herba Artemisiae Capillaris Extract Prevents the Development of Streptozotocin-Induced Diabetic Nephropathy of Rat

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Jianan Geng ◽  
Xiaoyan Yu ◽  
Chunyu Liu ◽  
Chengbo Sun ◽  
Menghuan Guo ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Tissue Transglutaminase ◽  
Blood Lipid ◽  
High Dose ◽  
Oxygen Species ◽  
Promising Candidate ◽  
Ecm Degradation ◽  
Stage Renal Disease ◽  
End Stage ◽  
Excessive Accumulation

Diabetic nephropathy (DN) is a major cause of end-stage renal disease throughout the world; until now there is no specific drug available. In this work, we use herba artemisiae capillaris extract (HACE) to alleviate renal fibrosis characterized by the excessive accumulation of extracellular matrix (ECM) in rats, aiming to investigate the protective effect of the HACE on DN. We found that the intragastric treatment of high-dose HACE could reverse the effect of streptozotocin not only to decrease the level of blood glucose and blood lipid in different degree but also further to improve renal functions. It is worth mentioning that the effect of HACE treatment was comparable to the positive drug benazepril. Moreover, we found that HACE treatment could on one hand inhibit oxidative stress in DN rats through regulating enzymatic activity for scavenging reactive oxygen species and on the other hand increase the ECM degradation through regulating the activity of metalloproteinase-2 (MMP-2) and the expression of tissue transglutaminase (tTG), which explained why HACE treatment inhibited ECM accumulation. On the basis of above experimental results, we conclude that HACE prevents DN development in a streptozotocin-induced DN rat model, and HACE is a promising candidate to cure DN in clinic.

scholarly journals Identification of Novel Biomarker for Early Detection of Diabetic Nephropathy

Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 457
Author(s):  
Kyeong-Seok Kim ◽  
Jin-Sol Lee ◽  
Jae-Hyeon Park ◽  
Eun-Young Lee ◽  
Jong-Seok Moon ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Early Stage ◽  
Kidney Injury ◽  
Diabetic Patients ◽  
High Morbidity ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Zucker Diabetic Fatty Rats ◽  
Kidney Injury Molecule 1 ◽  
Stage Renal Disease ◽  
End Stage

Diabetic nephropathy (DN) is one of the most common complications of diabetes mellitus. After development of DN, patients will progress to end-stage renal disease, which is associated with high morbidity and mortality. Here, we developed early-stage diagnostic biomarkers to detect DN as a strategy for DN intervention. For the DN model, Zucker diabetic fatty rats were used for DN phenotyping. The results revealed that DN rats showed significantly increased blood glucose, blood urea nitrogen (BUN), and serum creatinine levels, accompanied by severe kidney injury, fibrosis and microstructural changes. In addition, DN rats showed significantly increased urinary excretion of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL). Transcriptome analysis revealed that new DN biomarkers, such as complementary component 4b (C4b), complementary factor D (CFD), C-X-C motif chemokine receptor 6 (CXCR6), and leukemia inhibitory factor (LIF) were identified. Furthermore, they were found in the urine of patients with DN. Since these biomarkers were detected in the urine and kidney of DN rats and urine of diabetic patients, the selected markers could be used as early diagnosis biomarkers for chronic diabetic nephropathy.

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