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      New Method for Phosphate Kinetics Estimation during Hemodialysis and On-Line Hemodiafiltration with Endogenous Reinfusion

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          Aim: The purpose of this study was to optimize the operative and analytical methodologies to a more exact determination of intradialytic kinetics of the phosphates (P) tested in hemodialysis (HD) and in on-line hemodiafiltration with endogenous reinfusion (HFR – Hemo Filtrate Reinfusion). Methods: The mass balance measurements of urea and P were carried out in 18 clinically stable HD patients. The effective blood flow (Qb) was measured with a Transonic<sup>®</sup> monitor. The plasma was deproteinized with 10% trichloroacetic acid to prevent breakdown of the proteins and the consequent pseudohyperphosphatemia. Subsequently the supernatant containing the ultrafiltrable phosphates was made to react with a solution of ammonium molybdate for a spectrophotometric reading. Results: The mean urea mass transfer in HD was 16.9 g/session and in HFR 15.4 g/session. The mean P mass transfer in HD was 726 mg/session and in HFR 679 mg/session. Nevertheless, in HFR a significant difference was verified between the clearances of P, between the plasma water side (122.4 ± 30.8 ml/min) and the dialysate side (105.9 ± 19.4 ml/min). Conclusion: As far as the P mass transfer is concerned, the data obtained is able to be superimposed with that described in the literature during HD, while in HFR it is possible to hypothesize a high efficiency, thanks to an increased output of P in relation to the phenomenon of adsorption which, although is limited, contributes to the transfer of the total mass. Based on this study and re-examining the literature on P kinetics, there is space for methodological improvement both on the operating front with careful determination of the effective Qb, and on the chemical front overcoming the inaccuracy of automatic analyzers in determining the plasma P owing to possible overestimation of phosphatemia and poor sensitivity in measuring the lower levels of P present in the dialysate and/or ultrafiltrate.

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          Most cited references 18

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          Phosphate kinetics during hemodialysis: Evidence for biphasic regulation.

          Hyperphosphatemia in the hemodialysis population is ubiquitous, but phosphate kinetics during hemodialysis is poorly understood. Twenty-nine hemodialysis patients each received one long and one short dialysis, equivalent in terms of urea clearance. Phosphate concentrations were measured during each treatment and for one hour thereafter. A new model of phosphate kinetics was developed and implemented in VisSim. This model characterized additional processes involved in phosphate kinetics explaining the departure of the measured data from a standard two-pool model. Pre-dialysis phosphate concentrations were similar in long and short dialysis groups. Post-dialysis phosphate concentrations in long dialysis were higher than in short dialysis (P < 0.02) despite removal of a greater mass of phosphate (P < 0.001). In both long and short dialysis serum phosphate concentrations initially fell in accordance with two-pool kinetics, but thereafter plateaued or increased despite continuing phosphate removal. Implementation of an additional regulatory mechanism such that a third pool liberates phosphate to maintain an intrinsic target concentration (1.18 +/- 0.06 mmol/L; 95% confidence intervals, CI) explained the data in 24% of treatments. The further addition of a fourth pool hysteresis element triggered by critically low phosphate levels (0.80 +/- 0.07 mmol/L, CI) yielded an excellent correlation with the observed data in the remaining 76% of treatments (cumulative standard deviation 0.027 +/- 0.004 mmol/L, CI). The critically low concentration correlated with pre-dialysis phosphate levels (r=0.67, P < 0.0001). Modeling of phosphate kinetics during hemodialysis implies regulation involving up to four phosphate pools. The accuracy of this model suggests that the proposed mechanisms have physiological validity.
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            Are we mismanaging calcium and phosphate metabolism in renal failure?

             Fang-Chi Hsu (1997)
            Secondary hyperparathyroidism and renal osteodystrophy are the consequences of abnormal calcium, phosphate, and calcitriol metabolism ensuing from renal failure. Evidence suggests that calcium balance tends to become negative as we grow older than 35 years of age; however, the current dialysis modalities provide patients regardless of age with excessive calcium during dialysis. Administration of calcitriol in the management of hyperparathyroidism further increases the calcium and phosphate absorption. Furthermore, the current thrice-weekly renal replacement therapies fail to remove the daily absorbed phosphate, and we have to use calcium carbonate as a primary phosphate-binding agent to reduce intestinal phosphate absorption. The large calcium mass transfer and phosphate retention could lead to soft tissue calcification, especially in older end-stage renal disease (ESRD) patients. Consequently, only by maintaining a negative calcium balance during renal replacement therapy can we safely use calcitriol and calcium carbonate for the management of secondary hyperparathyroidism. Recent studies have indicated that phosphate restriction alone independent of plasma calcitriol or calcium can lower plasma parathyroid hormone (PTH) in renal failure and prevent hyperplasia of parathyroid glands. Therefore, phosphate control perhaps is the most important means to prevent secondary hyperparathyroidism. Previous studies have shown that ferric compounds are potent phosphate-binding agents; hence, these compounds warrant further trial in the management of phosphate metabolism in renal failure.
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              Estimating phosphate removal in haemodialysis: an additional tool to quantify dialysis dose.

              Half of the dialysis population suffers from hyperphosphataemia, which is now recognized as a major factor of haemodialysis (HD) morbidity and mortality. Current control is focussed on reducing dietary phosphate intake and diminishing absorption using phosphate binders, whereas control and quantification of phosphate removal by HD is undervalued. The aim of this prospective study was to develop a simple, bedside formula to estimate dialytic phosphate removal in stable HD patients.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                April 2006
                27 April 2006
                : 24
                : 3
                : 301-308
                aUnità Operativa Territoriale di Nefrologia e Dialisi, Azienda USL n. 8, Cagliari, bFormer Director of the Unità Operativa di Nefrologia e Dialisi, A. O. ‘S. Croce e Carle’, Cuneo, cServizio Nefrologia e Dialisi, Ospedale SS. Trinità, Azienda USL n. 8, Cagliari, dServizio Nefrologia e Dialisi, Ospedale S. Martino, Azienda USL n. 5, Oristano, eDivisione Nefrologia e Dialisi, Ospedale S. Francesco, Azienda USL n. 3, Nuoro, fServizio Nefrologia e Dialisi, Ospedale Civile di Alghero, Azienda USL n. 1, Sassari, Italy
                91451 Blood Purif 2006;24:301–308
                © 2006 S. Karger AG, Basel

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                Figures: 3, Tables: 3, References: 38, Pages: 8
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