scholarly journals Dietary Phosphorus as a Marker of Mineral Metabolism and Progression of Diabetic Kidney Disease

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 789
Author(s):  
Agata Winiarska ◽  
Iwona Filipska ◽  
Monika Knysak ◽  
Tomasz Stompór
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Mineral Metabolism ◽  
Careful Analysis ◽  
Diabetic Kidney ◽  
Dietary Phosphorus ◽  
Patients With Diabetes ◽  
Cv Disease ◽  
End Stage ◽  
Phosphorus Intake

Phosphorus is an essential nutrient that is critically important in the control of cell and tissue function and body homeostasis. Phosphorus excess may result in severe adverse medical consequences. The most apparent is an impact on cardiovascular (CV) disease, mainly through the ability of phosphate to change the phenotype of vascular smooth muscle cells and its contribution to pathologic vascular, valvular and other soft tissue calcification. Chronic kidney disease (CKD) is the most prevalent chronic disease manifesting with the persistent derangement of phosphate homeostasis. Diabetes and resulting diabetic kidney disease (DKD) remain the leading causes of CKD and end-stage kidney disease (ESRD) worldwide. Mineral and bone disorders of CKD (CKD-MBD), profound derangement of mineral metabolism, develop in the course of the disease and adversely impact on bone health and the CV system. In this review we aimed to discuss the data concerning CKD-MBD in patients with diabetes and to analyze the possible link between hyperphosphatemia, certain biomarkers of CKD-MBD and high dietary phosphate intake on prognosis in patients with diabetes and DKD. We also attempted to clarify if hyperphosphatemia and high phosphorus intake may impact the onset and progression of DKD. Careful analysis of the available literature brings us to the conclusion that, as for today, no clear recommendations based on the firm clinical data can be provided in terms of phosphorus intake aiming to prevent the incidence or progression of diabetic kidney disease.

scholarly journals GLP-1 receptor agonists in diabetic kidney disease: from the patient-side to the bench-side

2018 ◽  
Vol 315 (6) ◽  
pp. F1519-F1525 ◽  
Author(s):  
Brad P. Dieter ◽  
Radica Z. Alicic ◽  
Katherine R. Tuttle
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Microvascular Complications ◽  
Renin Angiotensin System ◽  
Diabetic Kidney ◽  
Receptor Agonists ◽  
Patients With Diabetes ◽  
Glucagon Like Peptide 1 ◽  
Patient Side ◽  
End Stage

Diabetic kidney disease (DKD), one of the most common and severe microvascular complications of diabetes, is the leading cause of chronic kidney disease and end-stage kidney disease worldwide. Since the development of renin-angiotensin system inhibition nearly three decades ago, no new therapeutic agents have received regulatory approval for treatment of DKD. Glucagon-like peptide-1 (GLP-1) receptor agonists, a class of newer antihyperglycemic agents, have shown promise for prevention of DKD onset and progression. This perspective summarizes clinical and experimental observations to give insight into biological mechanisms beyond glycemic control, such as natriuresis and anti-inflammatory actions, for preservation of kidney function in patients with diabetes.

scholarly journals Inflammatory Cytokines in Diabetic Kidney Disease: Pathophysiologic and Therapeutic Implications

2021 ◽  
Vol 7 ◽  
Author(s):  
Javier Donate-Correa ◽  
Carla M. Ferri ◽  
Fátima Sánchez-Quintana ◽  
Atteneri Pérez-Castro ◽  
Ainhoa González-Luis ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Diabetic Kidney ◽  
Therapeutic Implications ◽  
Cardiovascular Morbidity And Mortality ◽  
Patients With Diabetes ◽  
Traditional Risk Factors ◽  
Stage Renal Disease ◽  
End Stage ◽  
Underlying Processes

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease and a main contributing factor for cardiovascular morbidity and mortality in patients with diabetes mellitus. Strategies employed to delay the progression of this pathology focus on the control of traditional risk factors, such as hyperglycemia, and elevated blood pressure. Although the intimate mechanisms involved in the onset and progression of DKD remain incompletely understood, inflammation is currently recognized as one of the main underlying processes. Untangling the mechanisms involved in the appearing of a harmful inflammatory response in the diabetic patient is crucial for the development of new therapeutic strategies. In this review, we focus on the inflammation-related pathogenic mechanisms involved in DKD and in the therapeutic utility of new anti-inflammatory strategies.

scholarly journals Association of British Clinical Diabetologists (ABCD) and Renal Association clinical guidelines: Hypertension management and renin-angiotensin-aldosterone system blockade in patients with diabetes, nephropathy and/or chronic kidney disease

2017 ◽  
Vol 17 (4) ◽  
pp. 160-164 ◽  
Author(s):  
Indranil Dasgupta ◽  
Debasish Banerjee ◽  
Tahseen A Chowdhury ◽  
Parijat De ◽  
Mona Wahba ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Cardiovascular Complications ◽  
Diabetic Kidney ◽  
Cardiovascular Morbidity And Mortality ◽  
Patients With Diabetes ◽  
The Uk ◽  
Stage Renal Disease ◽  
End Stage ◽  
Audit Standards

Diabetes is the commonest cause of end-stage renal disease; over a quarter of patients who are on dialysis in the UK have diabetes. Diabetic kidney disease is associated with high cardiovascular morbidity and mortality. Hypertension is a modifiable risk factor for cardiovascular complications and progression of diabetic kidney disease.The Association of British Clinical Diabetologists and the Renal Association have jointly developed guidelines for management of hypertension through different stages of diabetic kidney disease. Here we present a summary of clinical practice recommendations, audit standards, and areas that require further research.

scholarly journals Association of UBE3C Variants with Reduced Kidney Function in Patients with Diabetic Kidney Disease

2020 ◽  
Vol 10 (4) ◽  
pp. 210
Author(s):  
Ying-Chun Chen ◽  
Mei-Yi Wu ◽  
Zhi-Lei Yu ◽  
Wan-Hsuan Chou ◽  
Yi-Ting Lai ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Kidney Function ◽  
Diabetic Kidney Disease ◽  
Clinical Role ◽  
Diabetic Kidney ◽  
Factors Affecting ◽  
Patients With Diabetes ◽  
Stage Renal Disease ◽  
End Stage ◽  
Reduced Kidney Function

Diabetic kidney disease (DKD) is the leading cause of morbidity and mortality in patients with diabetes mellitus (DM) and the most common variant of end-stage renal disease (ESRD) globally. The economic burden of ESRD treatment with dialysis is substantial. The incidence and prevalence of ESRD in Taiwan remain the highest worldwide. Therefore, identifying genetic factors affecting kidney function would have valuable clinical implications. We performed microarray experiments and identified that ubiquitin protein ligase E3C (UBE3C) is differentially expressed in two DKD patient groups with extreme (low and high) urine protein-to-creatinine ratios. A follow-up genotyping study was performed in a larger group to investigate any specific variants of UBE3C associated with DKD. A total of 263 patients were included in the study, comprising 172 patients with DKD and 91 control subjects (patients with DM without chronic kidney disease (CKD)). Two UBE3C variants (rs3802129(AA) and rs7807(CC)) were determined to be associated with reduced kidney function. The haplotype analysis revealed that rs3802129/rs3815217 (block 1) with A/G haplotype and rs8101/rs7807 (block 2) with T/C haplotype were associated with higher risks of CKD phenotypes. These findings suggest a clinical role of UBE3C variants in DKD risk.

scholarly journals Metabolic Changes and Oxidative Stress in Diabetic Kidney Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1143
Author(s):  
Midori Sakashita ◽  
Tetsuhiro Tanaka ◽  
Reiko Inagi
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Stress Responses ◽  
Diabetic Kidney Disease ◽  
Renin Angiotensin System ◽  
Therapeutic Agents ◽  
Metabolic Changes ◽  
Diabetic Kidney ◽  
Glucose Levels ◽  
Patients With Diabetes

Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease, and it is crucial to understand the pathophysiology of DKD. The control of blood glucose levels by various glucose-lowering drugs, the common use of inhibitors of the renin–angiotensin system, and the aging of patients with diabetes can alter the disease course of DKD. Moreover, metabolic changes and associated atherosclerosis play a major role in the etiology of DKD. The pathophysiology of DKD is largely attributed to the disruption of various cellular stress responses due to metabolic changes, especially an increase in oxidative stress. Therefore, many antioxidants have been studied as therapeutic agents. Recently, it has been found that NRF2, a master regulator of oxidative stress, plays a major role in the pathogenesis of DKD and bardoxolone methyl, an activator of NRF2, has attracted attention as a drug that increases the estimated glomerular filtration rate in patients with DKD. This review outlines the altered stress responses of cellular organelles in DKD, their involvement in the pathogenesis of DKD, and discusses strategies for developing therapeutic agents, especially bardoxolone methyl.

scholarly journals Therapeutic Strategies for Diabetic Kidney Disease

Diabetology ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 31-35
Author(s):  
Keiichiro Matoba
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Intensive Therapy ◽  
Therapeutic Strategies ◽  
Therapeutic Interventions ◽  
Hemodynamic Changes ◽  
Diabetic Kidney ◽  
Global Epidemic ◽  
Stage Renal Disease ◽  
End Stage

Diabetic kidney disease (DKD) is a global epidemic leading to end-stage renal disease (ESRD) and susceptibility to cardiovascular disease, with few therapeutic interventions. A hallmark of DKD is the activation of the renin-angiotensin-aldosterone system and hemodynamic changes in glomerulus. Although intensive therapy with agents that targets those abnormalities lowers the risk of DKD progression, it does not completely abolish the risk of ESRD and cardiovascular events. Recent studies have illustrated the importance of renal inflammation, oxidative stress, and activated Rho-associated protein kinase (ROCK) signaling as essential pathogenesis for the development of DKD. In this commentary, these topics will be discussed.

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 Diabetic Kidney Disease in Childhood and Adolescence: Conventional and Novel Renoprotective Strategies

2020 ◽  
pp. 68-77
Author(s):  
Samuel N Uwaezuoke ◽  
Adaeze C Ayuk
Keyword(s):  
Diabetes Mellitus ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Microvascular Complications ◽  
Clinical Syndrome ◽  
Clinical Staging ◽  
Childhood And Adolescence ◽  
Diabetic Kidney ◽  
Haemodynamic Changes ◽  
End Stage

Diabetic kidney disease (DKD) is defined as a clinical syndrome consisting of persistent macroalbuminuria, progressive decline in glomerular filtration rate (GFR), hypertension, increased cardiovascular disease events, and the associated mortality of these conditions. The disease evolves from the microvascular complications of poorly controlled Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM). The pathogenic pathways comprise renal haemodynamic changes, ischaemia and inflammation, and overactive renin–angiotensin–aldosterone system (RAAS), through which several events cascade down from hyperglycaemia to renal fibrosis. Conventional and novel renoprotective strategies target modifiable DKD risk factors and specific stages of the pathogenic pathways, respectively. Although these strategies may slow DKD progression to end-stage kidney disease (ESKD), novel drugs are still undergoing trials for validation in human participants. This narrative review appraises these renoprotective strategies and highlights the current clinical staging and pathogenesis of the disease.

scholarly journals Glycaemic Monitoring in Diabetic Kidney Disease – Is HbA1c Reliable?

2021 ◽  
Author(s):  
Salbiah Binti Isa ◽  
Rohayu Hami ◽  
Alma’ Norliana JA ◽  
Siti Salmah Noordin ◽  
Tuan Salwani Tuan Ismail
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Glycated Albumin ◽  
Glucose Monitoring ◽  
Diabetic Control ◽  
Haemoglobin A1c ◽  
Diabetic Kidney ◽  
Serum Fructosamine ◽  
Potential Factors ◽  
End Stage

Diabetic kidney disease (DKD) is a known complication of diabetes mellitus that increases patients’ risks of developing end-stage renal failure requiring dialysis treatment and vulnerability of fatal outcomes resulted from cardiovascular events. Therefore, a good diabetic control among patients with DKD is essential. Nevertheless, monitoring glycaemia in DKD is very challenging. The use of the gold standard glycaemic marker, haemoglobin A1c (HbA1c), is complicated by many hindrances associated with both biochemical and physiological derangements of DKD. Despite the constraints, the Kidney Disease Improving Global Outcome has recommended the use of HbA1c as a reliable glycaemic marker in DKD patients, whose estimated glomerular filtration rate is down to 30 millilitres/minute per 1.73 meter2 . In this article, we discuss the reliability and limitations of HbA1c as an advocated glycaemic marker in DKD. Considering that the reliability of HbA1c is highly dependent on the interpretation of the results, we also highlighted the common potential factors that can affect HbA1c interpretation in patients with DKD. The article also discusses the issues related to the utility of glycated albumin and serum fructosamine as alternative glycaemic biomarkers, and continuous glucose monitoring as a complementary marker to HbA1c in clinical practice. Understanding the HbA1c values and their limitations is important to ensure accurate interpretation of glycaemic status and to achieve optimal diabetic control in patients with DKD.

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