FGF-23 and Hyperphosphatemia in Dialysis Dependent Chronic Kidney Disease Patients

Dialysis dependent chronic kidney disease (CKD) has become a worldwide public health problem. It is known to increase patient morbidity and mortality risks which can cause major economic strain on the health-care systems. A population based study has shown that the incidence of this end stage renal disease (ESRD) in India was 160 per million population (p.m.p.) in the year 2008 [1]. One of the most commonly encountered challenges in the management of dialysis dependent CKD patients is increasing levels of serum phosphorus secondary to a decrease in the glomerular filtration rate (GFR) less than 15%. Hyperphosphatemia develops as a consequence of diminished phosphorus filtration and excretion with the progression of CKD. Decreased phosphorus excretion can initially be overcome by increased secretion of parathyroid hormone (PTH), which decreases reabsorption of phosphate in the proximal tubules by regulating NaPi-2a and NaPi2c activities and thus induces an increase of urinary phosphate excretion [2] According to the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF–K/DOQI) classification, phosphorus levels are usually within normal range until the GFR falls below approximately 30 ml/min, or CKD stage 4 [3]. In more advanced stages of CKD, the blunted urinary excretion of phosphorus can no longer keep pace with the obligatory intestinal phosphate absorption, resulting in hyperphosphatemia [4]. Therefore, majority of dialytic CKD patients have significant hyperphosphatemia which further leads to several clinical conditions including cardiovascular diseases, bone diseases and secondary hyperparathyroidism (SHPT) [5].