<p>Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD): Current Perspectives</p>

Abstract

Despite the availability of global and regional guidelines to curtail the adverse clinical outcomes associated with chronic kidney disease-mineral and bone disorder (CKD-MBD), most CKD patients are still affected by the consequences of abnormalities of CKD-MBD. This important clinical complication of CKD continues to be studied, in order to improve the understanding and management of CKD-MBD. Some notable discoveries include the role of fibroblast growth factor 23 (FGF23) in the pathogenesis of CKD-MBD, leading to a shift from the previous well-established classic trade-off hypothesis to the updated trade-off hypothesis. More recently, there has been a shift from the treatment of CKD-MBD based on a single level of biomarkers to serial measurements of calcium, phosphate and parathyroid hormone (PTH). Furthermore, some clinical trials have emerged after the 2009 Kidney Disease-Improving Global Outcomes (KDIGO) Guidelines, leading to the 2017 KDIGO updated recommendations. Hence, this review gives an overview of the rapidly evolving trends in CKD-MBD, linking the past and current concepts of CKD-MBD.

Fucoidan Ameliorates Renal Injury-Related Calcium-Phosphorus Metabolic Disorder and Bone Abnormality in the CKD–MBD Model Rats by Targeting FGF23-Klotho Signaling Axis

“…Bone abnormalities in the patients and animal models with CKD–MBD are characterized by renal osteodystrophy, disorder of mineral metabolism and volume and increased propensity to fracture ( Tamagaki et al, 2006 ; Aleksova et al, 2018 ; Watanabe et al, 2018 ; Waziri et al, 2019 ). In which, calcium-phosphorus metabolic disorder and osteoporosis-like pathological lesions are the early hallmarks in these CKD–MBD patients with advanced renal dysfunction ( Aleksova et al, 2018 ; Waziri et al, 2019 ). Recently, FGF23 as a phosphate-regulating hormone has been discovered by the studies on rare hypophosphatemic disorder, whereas Klotho, which subsequently turns out to be a co-receptor for FGF23, is identified in a mouse model showing hyperphosphatemia and multiple aging-like traits.…”

Evaluation of bone densitometry by dual-energy x-ray absorptiometry as a fracture prediction tool in women with chronic kidney disease

“…Supporting our findings, a meta-analysis by Bucur et al found that BMD predicts fracture risk in CKD patients regardless of the measuring site ( Bucur et al, 2014 ). This suggests that the pathophysiology of CKD bone disorders is complex and does not depend solely on PTH levels ( Salam et al, 2014 ; Waziri et al, 2019 ). Despite this, hip BMD is recognized as the best fracture predictor among CKD patients ( Jamal et al, 2012 ; Iimori et al, 2012 ; Yenchek et al, 2012 ) due to the PTH predominantly exercising its effect on cortical bone, which is the main form in the hip whereas the lumbar spine is formed mostly by trabecular bone ( Yenchek et al, 2012 ; Duan et al, 1999 ; Denburg et al, 2013 ; Clarke, 2008 ).…”

When CKD-MBD is not just CKD-MBD, a case of humoral hypercalcemia of malignancy in a dialysis patient

“…Fibroblast growth factor 23, a phosphotonin, concentrations begin to rise as early as stage 2 chronic kidney disease. 9 In stage 3 chronic kidney disease, activated vitamin D begins to decrease with a compensatory increase in parathyroid hormone. 9 As vitamin D is hydroxylated in the kidney, this is felt to be one of the primary mechanisms for this cascade.…”

“…9 In stage 3 chronic kidney disease, activated vitamin D begins to decrease with a compensatory increase in parathyroid hormone. 9 As vitamin D is hydroxylated in the kidney, this is felt to be one of the primary mechanisms for this cascade. 10 Hypocalcemia is common among CKD patients and contributes to increased PTH secretion and abnormal bone remodeling.…”