Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease

2015 ◽  
Vol 28 (6) ◽  
pp. 564-577 ◽  
Author(s):  
Arnold J. Felsenfeld ◽  
Barton S. Levine ◽  
Mariano Rodriguez
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Calcium Phosphorus

scholarly journals Parathyroid Hormone Fragments: New Targets for the Diagnosis and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Huimin Chen ◽  
Xiaxia Han ◽  
Ying Cui ◽  
Yangfan Ye ◽  
Yogendranath Purrunsing ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Vital Role ◽  
Diagnosis And Treatment ◽  
Mineral And Bone Disorder ◽  
Bone Disorder ◽  
Calcium Phosphorus ◽  
Further Development ◽  
Made In

As a common disorder, chronic kidney disease (CKD) poses a great threat to human health. Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a complication of CKD characterized by disturbances in the levels of calcium, phosphorus, parathyroid hormone (PTH), and vitamin D; abnormal bone formation affecting the mineralization and linear growth of bone; and vascular and soft tissue calcification. PTH reflects the function of the parathyroid gland and also takes part in the metabolism of minerals. The accurate measurement of PTH plays a vital role in the clinical diagnosis, treatment, and prognosis of patients with secondary hyperparathyroidism (SHPT). Previous studies have shown that there are different fragments of PTH in the body’s circulation, causing antagonistic effects on bone and the kidney. Here we review the metabolism of PTH fragments; the progress being made in PTH measurement assays; the effects of PTH fragments on bone, kidney, and the cardiovascular system in CKD; and the predictive value of PTH measurement in assessing the effectiveness of parathyroidectomy (PTX). We hope that this review will help to clarify the value of accurate PTH measurements in CKD-MBD and promote the further development of multidisciplinary diagnosis and treatment.

Independent association of osteoprotegerin with cardio-vascular damage while chronic kidney disease III–V stages

2014 ◽  
Vol 20 (29) ◽  
pp. 83-89
Author(s):  
Сопоев ◽  
Mikhail Sopoev ◽  
Бестаева ◽  
Tamara Bestaeva ◽  
Дзгоева ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Calcium Phosphorus ◽  
Blood Pressures ◽  
Independent Association ◽  
Cardio Vascular ◽  
High Level

To detect the pathophysiologic link between osteoprotegerin with myocardial failare in chronic kidney disease (СКD) stages III–V was the aim of his research. Osteoprotegerin was measured using commercially kits in 72 CKD stages III–V patients (40 females and 35 males aged 34–67 years). The patients were examined clinically with estimation of the levels of calcium, phosphorus parathormone. Echocardiography on Aloka-4000 unit was made. Left ventricular geometry was assessed by J.Gottdiener classification. Therapy included the correction of anemia, arterial hypertension and phosphorus-calcium metabolism. Mean age of patients was 48±6 years, mean systolic and diastolic blood pressures were 161±22/81±11 mm Hg. Osteoprotegerin high level correlated with renal function and severity of left ventricular hypertrophy. We have shown that the changes of mediator of mineral-bone metabolism osteoprotegerin induced by CKD are independently associated with cardiovascular disfunction.

Pathophysiology of chronic kidney disease-mineral and bone disorder

2015 ◽  
Author(s):  
Alexandra Voinescu ◽  
Nadia Wasi Iqbal ◽  
Kevin J. Martin
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Serum Levels ◽  
Mineral And Bone Disorder ◽  
Vitamin D Metabolism ◽  
Bone Disorder ◽  
Calcium Phosphorus

Chronic kidney disease is associated with the inability to control normal mineral homeostasis, resulting in abnormalities in serum levels of calcium, phosphorus, parathyroid hormone, fibroblast growth factor 23 (FGF23) and vitamin D metabolism. These disturbances lead to the development of secondary hyperparathyroidism, skeletal abnormalities, vascular calcifications, and other systemic manifestations. Traditionally, mineral and bone abnormalities seen in chronic kidney disease were included in the term ‘renal osteodystrophy’. More recently, the term chronic kidney disease-mineral and bone disorder was introduced to define the biochemical abnormalities of phosphorus, parathyroid hormone, FGF23, calcium, or vitamin D metabolism, abnormalities in bone remodelling and mineralization, and vascular or other soft tissue calcifications.

scholarly journals The Calcium/Phosphorus Homeostasis in Chronic Kidney Disease: From Clinical Epidemiology to Pathophysiology

2017 ◽  
Vol 30 (6) ◽  
pp. 485 ◽  
Author(s):  
Ana Pires ◽  
Luis Sobrinho ◽  
Hugo Gil Ferreira
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Data ◽  
Serum Concentrations ◽  
Set Point ◽  
Pathophysiological Mechanisms ◽  
Dihydroxyvitamin D ◽  
Metabolism Regulation ◽  
1,25 Dihydroxyvitamin D ◽  
Calcium Phosphorus

Introduction: A simple data filtering process together with some basic concepts of control theory applied to electronically stored clinical data were used to identify some of the pathophysiological mechanisms underlying the perturbations of the calcium/phosphorus homeostasis in chronic kidney disease.Material and Methods: Retrospective data (a set per patient of serum single value concentrations of creatinine, calcium, phosphorus, parathormone, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D) from 2507 patients with stable chronic kidney disease not on renal replacement therapy were studied. The variables were paired and subjected sequentially to a moving average and partioned into frequency classes. The plots were interpreted using the concept of a feedback loop comprising two branches of opposite sign and of set point of the loop. The set point for each pair of variables is displaced in the course of the disease and this displacement indicates which of the two factors involved (the serum concentrations of calcium or parathormone, for example) is primarily affected.Results: This analysis showed that in the course of the development of chronic kidney disease the relationships between the observed variables progressed following a monotonous, a biphasic or a triphasic pattern.Discussion: As chronic kidney disease progresses, calcium/phosphorus metabolism regulation evolves through different phases. Later, there is a progressive loss of the parathyroid gland sensitivity to the control by the serum concentrations of calcium and phosphorus. The sensitivity to the inhibitory action of 1,25-dihydroxyvitamin D decreases monotonously but never releases the gland.Conclusion: The clinical data analysis used permits to illustrate the underlying pathophysiological mechanisms.

scholarly journals Cardiovascular Biomarkers in Chronic Kidney Disease

2010 ◽  
Vol 29 (4) ◽  
pp. 298-303 ◽  
Author(s):  
Mirjana Đerić ◽  
Velibor Čabarkapa
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Disease ◽  
Left Ventricular ◽  
Calcium Phosphorus ◽  
Traditional Risk Factors ◽  
Cardiovascular Biomarkers

Cardiovascular Biomarkers in Chronic Kidney DiseaseCardiovascular morbidity and mortality are markedly increased in chronic renal failure patients. Although it cannot be regarded as a cardiovascular disease risk equivalent, kidney dysfunction is considered an independent predictor of increased cardiovascular risk that increases with deteriorating kidney function. The association is a very complex one, and the term cardiorenal syndrome is now widely used. Cardiovascular disease in chronic kidney disease patients usually manifests as ischemic heart disease (in the form of angina, acute coronary syndrome or sudden cardiac death), cerebrovascular disease, peripheral vascular disease, and congestive heart failure. Vascular disease includes atherosclerosis and vascular calcifications, and cardiomyopathy comprises left ventricular hypertrophy, cardiac fibrosis and left ventricular systolic and diastolic dysfunction. In addition to the well-established traditional risk factors such as hypertension, hyperlipidemia, insulin resistance and diabetes mellitus, the association is supported by synergistic action of non-traditional risk factors such as excessive calcium-phosphorus load, hyperparathyroidism, anemia, hemodynamic overload, malnutrition, inflammation, hyperhomocysteinemia, altered nitric oxide synthase and increased oxidative stress. This paper summarizes the current understanding of the significance of specific uremic retention solutes, natriuretic peptides, biochemical markers of disorders in calcium-phosphorus homeostasis, systemic inflammation, oxidative stress, and dyslipidemia.

scholarly journals Calcium, Phosphorus and PTH in Patients with End Stage of Chronic Kidney Disease, Undergoing Hemodialysis

2020 ◽  
Vol 3 (2) ◽  
pp. 21
Author(s):  
Serfa Faja ◽  
Amir Shoshi
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Estimated Glomerular Filtration Rate ◽  
Treatment Options ◽  
Chronic Kidney Disease Stage ◽  
Disease Stage ◽  
Phosphate Binders ◽  
Calcium Phosphorus ◽  
End Stage

Renal hyperparathyroidism (rHPT) is a common complication of chronic kidney disease characterized by elevated parathyroid hormone levels secondary to derangements in the homeostasis of calcium, phosphate, and vitamin D. Patients with rHPT experience increased rates of cardiovascular problems and bone disease. The Kidney Disease: Improving Global Outcomes guidelines recommend that screening and management of rHPT be initiated for all patients with chronic kidney disease stage 3 (estimated glomerular filtration rate, - 60 mL/min/1.73 m2). Since the 1990s, improving medical management with vitamin D analogs, phosphate binders, and calcimimetic drugs has expanded the treatment options for patients with rHPT, but some patients still require a parathyroidectomy to mitigate the sequelae of this challenging disease.

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