scholarly journals Compromised calcium and phosphorus metabolism in patients with diabetes mellitus and chronic kidney disease

2012 ◽  
Vol 15 (4) ◽  
pp. 74-80 ◽  
Author(s):  
Margarita Stanislavovna Biragova ◽  
Svetlana Alexandrovna Gracheva ◽  
Sergey Andreevich Martynov
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mineral Metabolism ◽  
Hormone Secretion ◽  
Therapeutic Agents ◽  
Phosphorus Metabolism ◽  
Novel Approach ◽  
Patients With Diabetes ◽  
Per Se ◽  
Calcium And Phosphorus

Disturbance of bone and mineral metabolism (BMM) is one of manifestations of chronic kidney disease (CKD), but its significance goes beyond bone disorders per se. Current discourse is as broad as to include vascular calcification, anemia and arterial hypertension, - conditions increasing mortality in patients with CKD. In this regard the active search for and development of novel approach to correction of BMM is under way. Apart from capacity to normalize calcium and phosphorus metabolism, parathyroid hormone secretion and to reduce morphologic alterations of bone tissue, modern therapeutic agents feature cardio- and renoprotective capabilities, which make them a treatment of choice for compromised BMM in CKD.

scholarly journals Low Magnesium Exacerbates Osteoporosis in Chronic Kidney Disease Patients with Diabetes

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Jui-Hua Huang ◽  
Fu-Chou Cheng ◽  
Hsu-Chen Wu
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Mineral ◽  
Mineral Metabolism ◽  
Inverse Correlation ◽  
Mineral Density ◽  
Lower Serum ◽  
Patients With Diabetes ◽  
The Impact ◽  
Low Serum

The aim of this study is to investigate the impact of serum Mg on bone mineral metabolism in chronic kidney disease (CKD) patients with or without diabetes. A total of 56 CKD patients not receiving dialysis were recruited and divided into two groups, one group of 27 CKD patients with diabetes and another group of 29 CKD patients without diabetes. Biochemical determinations were made, and the estimated glomerular filtration rate (eGFR) was measured. Bone mineral density was measured by dual-energy X-ray absorptiometry. Serum Mg was inversely correlated with serum CaP=0.023and positively correlated with serum parathyroid hormone (PTH)P=0.020, alkaline phosphataseP=0.044, and phosphateP=0.040in the CKD patients with diabetes. The CKD patients with diabetes had lower serum albumin and a higher proportion of hypomagnesemia and osteoporosis than the nondiabetic patients didP<0.05. Serum Mg was inversely correlated with eGFR in the CKD patients with or without diabetesP<0.05. Serum Mg showed an inverse correlation with 25-hydroxyvitamin D in CKD patients without diabetesP=0.006. Furthermore, the diabetic CKD patients with low serum Mg had a lower iPTHP=0.007and a higher serum Ca/Mg ratioP<0.001than the other CKD patients. The lower serum Mg subgroup showed a higher incidence of osteoporosis than the moderate and higher serum Mg subgroups did (66.7%, 39.4%, and 29.4%, resp.). In conclusion, low serum Mg may impact iPTH and exacerbates osteoporosis in CKD patients, particularly with diabetes.

scholarly journals Current and Emerging Drugs in the Treatment of Anemia in Patients with Chronic Kidney Disease

2020 ◽  
Vol 23 ◽  
pp. 278-288
Author(s):  
Hongzhen Zhong ◽  
Wenshan Lin ◽  
Tianbiao Zhou
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Hypoxia Inducible Factor ◽  
Phosphorus Metabolism ◽  
Common Complication ◽  
Public Attention ◽  
Common Causes ◽  
Incident Heart Failure ◽  
Calcium And Phosphorus ◽  
Erythropoietin Stimulating Agents

Anemia is a common complication of chronic kidney disease (CKD), and its prevalence has shown a tendency to increase in many countries. Anemia is associated with incident heart failure and increases mortality in CKD patients, garnering public attention. Here, we reviewed recent studies about CKD with anemia, and tried to summarize the risks and causes and new progress in the treatment of renal anemia. Among the risks and causes, calcium and phosphorus metabolism disorders should be pointed out along with common causes such as iron and erythropoietin deficiencies, hypoxia, inflammation and uremic toxins, and so on. The new anti-anemia treatments mainly include hematopoietic materials supplementation, erythropoietin-stimulating agents, calcium and phosphorus regulators and hypoxia-inducible factor prolyl hydroxylase inhibitors.

Inferring Disease Mechanisms from Epidemiological Data in Chronic Kidney Disease: Calcium and Phosphorus Metabolism

2009 ◽  
Vol 112 (3) ◽  
pp. c137-c147 ◽  
Author(s):  
Ana Pires ◽  
Teresa Adrag&atilde;o ◽  
Maria Jo&atilde;o Pais ◽  
Jos&eacute; Vinhas ◽  
Hugo Gil Ferreira
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Epidemiological Data ◽  
Phosphorus Metabolism ◽  
Disease Mechanisms ◽  
Calcium And Phosphorus

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 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.

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