Effects of Efficiency and Length of Acetate-Free Biofiltration Session
on Postdialysis Solute Rebound
Paolo Giannattasio, MD, Roberto Minutolo, MD, PhD, Vincenzo Bellizzi, MD, PhD,
Biagio R. Di Iorio, MD, Raffaele Scigliano, MD, Pasquale Zamboli, MD, Guglielmo Venditti, MD,
Rocco Manganelli, MD, Walter De Simone, MD, Filippo Aucella, MD, Carmine Stallone, MD,
Stefano Spiezia, MD, Giuseppe Conte, MD, and Luca De Nicola, MD, PhD
● Background: Postdialytic rebound (PDR) of plasma solutes is a relevant drawback of intermittent hemodialysis,
but its pathophysiological process remains undefined. We assessed the independent effects of efficiency and
length of dialytic session on PDR of urea, phosphate, and potassium. Methods: Uremic patients were evaluated at
the beginning and end of dialysis and after 180 minutes in 2 randomized crossover studies. In study 1, we compared
the effect of standard versus higher efficiency acetate-free biofiltration (AFB) while maintaining the same duration
of 4 hours. In study 2, we compared the effect of 3- versus 5-hour AFB sessions while maintaining similar efficiency.
Results: In study 1, greater Kt/V (1.49 0.20 versus 1.22 0.15; P < 0.0001) was coupled with significant
increases in both absolute removal and PDR of urea and phosphate (PDR of urea, 45% versus 29%; PDR of
phosphate, 79% versus 52%), but not of potassium. Similarly, in study 2, shortening the AFB session while
maintaining similar absolute removal and Kt/V (1.28 0.09 versus 1.31 0.09) significantly increased PDR of urea
and phosphate (PDR of urea, 32% versus 19%; PDR of phosphate, 63% versus 36%), but not of potassium. In
both studies, greater PDRs of urea and phosphate were associated with estimated greater removal of these solutes
per hour. Conclusion: The rate of removal of phosphate and urea is a critical determinant of their PDR; conversely,
potassium is not influenced by removal rate, likely because of its marked cell compartmentalization. Am J Kidney
Dis 47:1045-1054.
© 2006 by the National Kidney Foundation, Inc.
INDEX WORDS: Urea; potassium; phosphate; dialysis efficiency.
D
URING HEMODIALYSIS (HD), removal
of a solute occurs exclusively from the
portion of its volume of distribution that perfuses
the dialyzer (central compartment), whereas se-
questration of a solute occurs in the remaining
volume (peripheral compartment). This gener-
ates a concentration gradient between the 2 com-
partments that becomes clinically evident through
the increase in plasma level of solutes after the
end of dialysis, the so-called postdialysis re-
bound (PDR).
1-6
PDR of the main solutes re-
tained in uremia, such as urea, phosphate, and
potassium, is a relevant drawback of intermittent
HD because it does not allow adequate control of
their plasma levels from the end of the dialytic
session up to the subsequent treatment.
7,8
Specifi-
cally, PDR of urea interferes with the assessment
of dialysis adequacy indices based on urea ki-
netic models.
9,10
Moreover, PDR of phosphate is
so marked to allow achievement of the predialysis
level within 4 to 6 hours after the end of the dialytic
session, even in the presence of normal levels at the
end of the treatment, with a consequent immediate
increase in parathyroid hormone levels.
6,7,11
Fi-
nally, the extent of potassium rebound can be so
large to cause death, as described in patients with
tumor lysis syndrome.
12
Despite the major clinical relevance, the patho-
physiological process of this phenomenon is still
unclear. Mathematic models have even been
proposed to theoretically predict dialytic and
postdialytic kinetics of urea and phosphate in
the presence of different dialysis regimens.
9,13,14
However, how changes in the 2 main parameters
of dialysis prescription, such as session length
and efficiency, may affect the magnitude of PDR
remains unknown in patients. Some studies
showed a significant relationship between PDR
From the Nephrology and Dialysis Unit, School of Medicine,
Second University of Naples, Country Hospital in Solofra;
Nephrology and Dialysis Unit, School of Medicine, Second
University of Naples, Country Hospital in Avellino; IRCCS
Casa Sollievo della Sofferenza, S Giovanni Rotondo; and
Department of Surgery, S M d P I-ASL NA1, Naples, Italy.
Received January 11, 2006; accepted in revised form
March 13, 2006.
Originally published online as doi:10.1053/j.ajkd.2006.03.035
on May 3, 2006.
Support: None. Potential conflicts of interest: None.
Address reprint requests to Luca De Nicola, MD, PhD,
Via S A Capodimonte, 46, Pco Villa Teresa-Ed 30, 80131
Naples, Italy. E-mail: luca.denicola@unina2.it
© 2006 by the National Kidney Foundation, Inc.
0272-6386/06/4706-0013$32.00/0
doi:10.1053/j.ajkd.2006.03.035
American Journal of Kidney Diseases, Vol 47, No 6 (June), 2006: pp 1045-1054 1045