[Investigation of tubular reabsorption of phosphates in patients with chronic kidney disease].

Introduction: Moderate to medium decrease in glomerular filtration (GFR) in individuals with chronic kidney disease (CKD) does not need to be associated with hyperphosphatemia due to an adaptive decrease in tubular reabsorption of phosphates (TRPi) in residual nephrons. The clinical assessment of this function is performed based on the measurement of fractional phosphate excretion (FEPi), which is a quantity specifying the proportion of the filtered amount of phosphates which is excreted in the urine. This quantity may provide useful information about the involvement of kidneys in phosphate homeostasis of the internal environment. This study focuses on the comparison of a kr(FEPi) value examined based on a ratio of a phosphate clearance (CPi) and a creatinine clearance (CKr) marked kr(FEPi), and a value calculated based on a ratio of CPi and an exactly measured GFR as an inulin clearance (Cin), marked as in(FEPi).The goal of comparing the two methods of examining FEPi was to establish to what extent it is possible to evaluate the degree of inhibition of tubular phosphate transport in residual nephrons based on a simple examination of kr(FEPi) .
Methodology: The examination of in(FEPi) and kr(FEPi) was carried out for 53 patients with CKD. The values of the examined quantities were as follows: SKr 199±45 µmol/l; SPi 1.41±0.29 mmol/l; CKr 0,95±0.36 ml/s/1.73 m2; Cin 0.71±0.25 ml/s/1.73 m2. For the purpose of comparison a cohort of 18 healthy volunteers was examined.
Results: For individuals with CKD an average value of kr(FEPi) equalled 29.1±10.9% and in(FEPi) 52.4±4.3%. The values of in(FEPi) were higher than kr(FEPi) (p<0.001) for all patients, although an average CPi value for patients with CKD did not significantly differ from the control cohort (0.22 vs 0.21 ml/s/1.73 m2). The values of in(FEPi) increased proportionally to SKr values and at higher values SKr (>300 µmol/l) they gradually approached 100% (indicating the complete inhibition of tubular reabsorption of phosphates in residual nephrons). The values of in(FEPi) were higher in all patients with CKD than kr(FEPi) as expected, likely because the value CKr decreases at a slower rate than Cin (GFR) in individuals with CKD as a result of increased tubular secretion of creatinine in residual nephrons.
Conclusion: The results of this study support the assumption that, provided the values of kr(FEPi) which are easily measurable in clinical practice have reached 50-60%, almost complete inhibition of tubular reabsorption of phosphates in residual nephrons must be assumed and no favourable effect of phosphatonins on renal phosphate excretion can be expected. When looking for new possibilities of inhibition of tubular phosphate reabsorption, potential adverse effects of phosphatonins on organs must be considered.