لخّصلي

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a recently acknowledged metabolic abnormality, proposed in 2006 by the Kidney Disease: Improving Global Outcomes (KDIGO) working group.The latter includes regular dialysis to remove blood phosphorus, which is considered to be of limited value in removal of phosphates, highlighting the importance of dietary restriction.The clinical features of CKD-MBD are primarily due to the compromised renal excretion of minerals, leading to abnormality in circulating calcium, phosphorous, parathyroid hormone (PTH), and vitamin D. The secondary effects of this renal insufficiency include abnormalities in bone turnover, mineralization, volume, linear growth, strength, and ectopic calcification (vascular and soft tissues).This distinct naming of varied clinical syndromes (CKD-MBD) that develop due to impaired mineral regulation in chronic kidney disease (CKD) was to differentiate it from the histologically well-defined renal osteodystrophy1.Hyperphosphatemia in patients with CKD, apart from inducing secondary hyperparathyroidism and renal osteodystrophy, CV calcification is also an important prognostic factor for morbidity and mortality in patients with end-stage renal disease (ESRD) undergoing dialysis.CKD-MBD is considered to be a progressive disorder, affecting the homeostasis among the renal, skeletal, and cardiovascular (CV) systems, thereby leading to a kidney-bone-vascular axis pathophysiological hypothesis.The prognostic role of serum phosphorous as a modifiable risk factor has also been reported in multiple observational studies, highlighting the potential effect of lowering blood phosphorous (Pi and phosphates) in CKD-MBD.

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a recently acknowledged metabolic abnormality, proposed in 2006 by the Kidney Disease: Improving Global Outcomes (KDIGO) working group. This distinct naming of varied clinical syndromes (CKD-MBD) that develop due to impaired mineral regulation in chronic kidney disease (CKD) was to differentiate it from the histologically well-defined renal osteodystrophy1. CKD-MBD is considered to be a progressive disorder, affecting the homeostasis among the renal, skeletal, and cardiovascular (CV) systems, thereby leading to a kidney–bone–vascular axis pathophysiological hypothesis.
The classical clinical manifestations of CKD-MBD defined by the KDIGO clinical practice guidelines also re-affirms the kidney–bone–vascular axis hypothesis. The clinical features of CKD-MBD are primarily due to the compromised renal excretion of minerals, leading to abnormality in circulating calcium, phosphorous, parathyroid hormone (PTH), and vitamin D. The secondary effects of this renal insufficiency include abnormalities in bone turnover, mineralization, volume, linear growth, strength, and ectopic calcification (vascular and soft tissues).
Among the different pathogenic factors, phosphate homeostasis is one of the initiating factors for the onset of CKD-MBD, which is initiated during early stages of CKD. This anomaly in phosphate homeostasis was evidently shown by elevated fibroblast growth factor 23 (FGF23) levels (hormone-regulating phosphate excretion) in early stages of CKD. The two main homeostatic mechanisms that regulate circulating phosphates are intestinal absorption and renal excretion. While intestinal absorption depends on the dietary pattern, renal excretion promotes removal of excess phosphates even in case of phosphate-rich diet through regulation of FGF23 and PTH.
Hyperphosphatemia in patients with CKD, apart from inducing secondary hyperparathyroidism and renal osteodystrophy, CV calcification is also an important prognostic factor for morbidity and mortality in patients with end-stage renal disease (ESRD) undergoing dialysis. The prognostic role of serum phosphorous as a modifiable risk factor has also been reported in multiple observational studies, highlighting the potential effect of lowering blood phosphorous (Pi and phosphates) in CKD-MBD. This was also substantiated in a meta-analysis including a total of 4651 patients with non-dialysis CKD, in whom a 35% increase in mortality was observed per mg increase in phosphate.
The therapeutic management of hyperphosphatemia includes decreasing intestinal absorption of phosphorus and increasing its renal removal. The former includes dietary restriction to reduce phosphorus intake and a phosphorus binder to reduce oral phosphorus absorption. The latter includes regular dialysis to remove blood phosphorus, which is considered to be of limited value in removal of phosphates, highlighting the importance of dietary restriction.
Therefore, it is evident that excessive PTH levels are harmful, but low PTH levels have also been linked to vascular calcifications and growth impairment due to the underlying adynamic bone. Therefore, in order to improve the care of these patients, it became necessary to develop an understanding of how low phosphorus containing formula affects the level of parathyroid hormone in children on dialysis.