DIETARY PROTEIN INTAKE IS INDEPENDENTLY ASSOCIATED WITH THE URINARY EXCRETION OF PHOSPHATE

Abstract

Decrease of urinary phosphate (P) excretion and P retention triggers activation of phosphotonins and subsequent development of secondary hyperparathyroidism in progressing of chronic kidney disease (CKD). The main source of P is dietary protein. No large studies are presented to-date to evaluate the relationship between dietary protein intake and parameters of P metabolism in CKD patients. This was a goal of the cross-sectional cohort study .11315 CKD patients were entered (males 43%). Median (10th-90th percentile) of age and estimated glomerular filtration rate (GFR) were 46 (24-69) and 64 (24-104). The analyzed data were: age, gender, body mass index (BMI) serum albumin, creatinine, calcium and phosphate; 24-h urine creatinine, phosphate (P),proteinuria (DP). Estimated parameters includes: eGFR, fractional P excretion (FEP), 24-h P excretion (24-h UP), and P clearance (CP). Dietary protein intake (DPI) was based on 24-h urinary urea excretion. No significant differences in serum phosphate were found in groups with various DPI. FEP, 24-h UP and CP were significantly higher in higher DPI range. DPI was positively associated with 24-h UP ( β =0,287, p <0.000001) in multivariate model adjusted for age, gender, DP, eGFR, serum P, FEP, BMI, and Ca. Thus, DPI is considered to be the independent factor influencing urinary P excretion and hence contributing to progression of mineral and bone disease in renal dysfunction.