Abstract

Chronic kidney disease (CKD) is becoming a public-health problem, at a global level. In CKD, patients progressively lose the ability to excrete phosphorus. Several observational studies have determined hyperphosphatemia emerging as an independent cardiovascular risk factor in CKD-Mineral and Bone Disorder (CKD-MBD). In early CKD, serum Klotho declines and fibroblast growth factor-23 (FGF‐23) starts increasing which coincides with its effects on augmenting urinary phosphate excretion with reduced serum phosphate reabsorption and decreased levels of calcitriol. The Klotho/FGF23 axis should be a novel target for renal clinicians being pathogenic contributors to CKD progression and cardiovascular disease (CVD) development. The high phosphorous load has been found to increase serum FGF-23 levels in the early stages of CKD which further leads to CVD and increased mortality. To control hyperphosphatemia, a potentially simple and effective approach of dietary phosphate control should be incorporated to reduce the early clinical consequences of CKD-MBD. Along with the amount of dietary phosphorus intake, its type (organic vs. inorganic), its source (animal vs. plant derived), phosphorus-to-protein ratio and preparation of food by boiling should also be made aware to patients which is likely a neglected aspect of dietary counselling in CKD. A kidney-friendly diet plan is needed to protect kidneys from further damage which is rather an arduous period for making patients follow a phosphate-restricted diet. Here, the role of the renal dietitian appears mandatory in counselling and educating the patients to effectively integrate dietary interventions into the therapeutic approach of CKD-MBD.

Full Text
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