Mineral Bone Disorder in Chronic Kidney Disease, Mechanics and Management

Abstract

Citation: Mahmood A Mineral Bone Disorder in Chronic Kidney Dis- ease, Mechanics and Management. J Nephrol Renal Ther 4: 016. rise in plasma phosphate resulting into hypocalcaemia and inhibition of calcitriol [9-11]. These changes result into secondary hyperparathyroidism [12-14] which contribute further to phosphate load due to mobilization of phosphate and calcium from the bone as a corrective attempt. Additionally proximal tubular phosphate reab-sorption continues to rise due to its reduced excretion with progression of renal failure. Initial rise of PTH is beneficial in order to maintain phosphate balance, correction of hypocalcaemia and calcitriol but hyperphosphatemia over prolong period results into autonomous parathyroid gland with rising secretions as a consequence of skeletal resistance with advanced renal failure [11]. Hyperphosphatemia has direct stimulatory effect on PTH independent of calcium and calcitriol levels [15-18]. Another effect of hyperparathyroidism is high fibroblast growth factor 23 (FGF 23), decrease vitamin D, Calcium Sensing Receptors (CaSR), fibroblast receptors and klotho in PTH. FGF 23 is the main factor causing low calcitriol, not reduce neph-ron mass [10] as a result of inhibition of enzyme 1 alpha hydroxy-lase which converts 25 hydroxy vitamin D to calcitriol. FGF 23 is produced from osteocytes in response to high phosphate, calcitriol and renal injury and establish its phosphaturic effect with the help of coenzyme klotho [19] to maintain phosphate homeostasis. It`s clearance is decrease in CKD. Reduced calcitriol levels stimulate PTH [20-22] by mechanism which decrease absorption from the gut and reduce mobilization from the bones resulting into hypocalcemic state triggering PTH activation resulting in release of hormone. Abstract Bone health is seriously affected in Chronic Kidney Disease (CKD). Subtle changes begin from the initial stages. Skeletal ill ef- fects are related to imbalance homeostasis of four main players, calcium, phosphate, Parathyroid Hormone (PTH) and vitamin D. Their regulated action is important and interdependent for normal skeletal development, architectural integrity and strength. Dysregu- lation in these regulators result in progressive skeletal dystrophy if mechanism goes unnoticed which imparts extra skeletal deleterious effects with grave long term consequences in terms of bone pain, fractures, vascular, valvular and soft tissue calcification. Term renal osteodystrophy has been replaced by Mineral Bone Disorder (MBD) which include spectrum of diseases like adynamic bone disease, osteomalacia, osteitis fibrosa cystica, osteopenia and osteoporo -sis. Close surveillance with CKD stage appropriate investigations and timely action is crucial to detect and prevent skeletal and extra skeletal complications in order to minimize morbidity and mortality in CKD population with the outcome of improved quality adjusted life years. This article will help improve our understanding about the highly complex group of bone disorders in a practical and simplistic way with clinic-pathological correlation, diagnostic approach and ev- idence based management of MBD in a candid way.