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Hemodialysis urea rebound: The effect of increasing dialysis efficiency
Hemodialysis Urea Rebound: The Effect of Increasing Dialysis Efficiency David M. Spiegel, MD, Penny L. Baker, DO, Susan Babcock, Robert Contiguglia, MD, and Melvyn Klein, MD
MD,
0 Urea rebound has been documented to occur after hemodialysis, but the magnitude and causes are not clearly defined. In this study we evaluated the effect of high-flux hemodialysis on urea rebound and KW. Blood urea nitrogen samples were obtained before, immediately after, and 30 minutes after hemodialysis in 49 patiints. Rebound was evaluated with respect to dialysis efficiency, dialysis treatment time, the occurrence of hypotension, and hematocrit. Urea rebound was significant and resulted in an overall decrease in KW from 1.2 ? 0.3 to 1.0 T 0.2 (P < 0.001). Df the 43 patients with a measured KW of greater than 1.0,40% had an actual delivered KW of less than 1.0 once rebound was taken into account. Urea rebound correlated strongly with dialysis efficiency but not with hypotension, suggesting that rebound resulted primarily from delayed urea mass transfer across cell membranes. We conclude that increasing dialysis efficiency increases urea rebound and increases the error in KW determinations from single pool urea kinetics. 0 1995 by the National Kidney Foundation, inc. INDEK WORDS: Urea rebound;
high-flux
hemodialysis;
T
HE DOSE OF delivered dialysis considered to be optimal therapy remains controversial, despite widespread use of single pool urea kinetic modeling to measure dialysis adequacy. While urea rebound has been described following hemodialysis,‘32 the significance of urea rebound on delivered dialysis dose and the factors that govem rebound are not well established. Urea rebound is in part caused by delayed urea transfer from intracellular to extracellular fluid as urea is removed from the extracellular space during hemodialysis.’ There is also evidence that regional blood flow is altered during hemodialysis, resulting in relatively underperfused tissue beds. Restoration of adequate blood flow following dialysis results in washout of accumulated urea nitrogen, contributing to urea rebound.*,” If urea rebound occurs due to delayed urea transfer across cell membranes, then increasing dialysis efficiency, the rate of removal of urea from the extracellular space, should increase rebound. If urea rebound results from restoration of blood flow to underperfused tissue beds, then it should
From the Division of Nephrology and Hypertension, The University of Colorado Health Sciences Center and The Rocky Mountain Kidney Center, Denver, CO. Received May 19, 1994; accepted in revised form August HP 1994. Address reprint requests to David M. Spiegel, MD, Division of Nephrology and Hypertension, The University of Colorado Health Sciences Center, Box C-281,4200 E Ninth Ave, Denver, CO 80262. 0 1995 by the National Kidney Foundation, Inc. 0272-6386/95RSOl-0005$3.00/O 26
American
Journal
KW, dialysis efficiency.
be worsened by intradialytic hypotension and other factors that influence tissue perfusion, such as shortened time for ultrafiltration. Therefore, if urea rebound results from restoration of blood flow to underperfused tissue beds, it should be more effected by intradialytic hypotension and dialysis treatment time rather than by dialysis efficiency. Therefore, the purpose of this study was to document the degree of urea rebound following high-flux hemodialysis. We also sought to determine the factors that govern urea rebound. We reasoned that if urea rebound was due to delayed transcellular urea shifts, then it would increase as dialysis efficiency increased. However, if postdialysis urea rebound was caused by return of blood flow to underperfused tissue beds, then dialysis treatment time and hemodynamic changes might effect rebound more than dialysis efficiency. MATERIALS AND METHODS Forty-nine chronic hemodialysis patients, all dialyzed with high-flux polysulfone F-80 dialyzers, were randomly recruited from our outpatient hemodialysis facility. Following acquisition of informed consent, blood was sampled for urea nitrogen at the start, immediately after hemodialysis (following disconnection of the dialysis tubing), and at 30 minutes posthemodialysis. Thirty minutes was chosen because previous work had shown that most urea rebound occurred by this time, yet urea production was not significant.’ The blood urea nitrogen (BUN) samples were measured in a routine clinical laboratory (MetWest, Inc. Denver, CO). A spun hematocrit was performed at the beginning of each treatment. Weight was recorded at the beginning and end of each treatment, and automated blood pressures were recorded every 30 minutes. Hypotension was defined as symptoms of warmth, nausea, of Kidney
Diseases,
Vol 25, No 1 (January), 1995: pp 26-29
UREA REBOUND AND DIALYSIS EFFICIENCY
0.6
0.8
1
1.2
1.4
1.6
1.8
2
27
2.2
2.4
1.5
KW From 30’ Post-HD BUN Fig 1. KW determined from BUN values immediately postdialysis versus KW determined from BUN values 30 minutes posthemodialysis. Each point represents one patient. The diagonal line is the line of identity. Vertical line delineates a deliired KW of 1 .O allowing for urea rebound. Patients to the left have actual KWs of less than 1.0. Note that most of these patients have KW greater than 1.0 when calculated from the BUN immediately posthemodialysis.
or cramping requiring treatment with normal or hypertonic saline, or as a decrease in mean arterial pressure of more than 20 mm Hg in any 30-minute period. Documented hypotension was defined as a decrease in mean blood pressure of more than 20 mm Hg in any 30-minute period. The blood flow rate was maintained between 250 and 450 mUmin and the dialysate flow was set at 600 mL/min. Percent urea rebound was calculated by the following equation: BUNr, - BUNJBUN,
x 100.
where BUNJO represents the BUN value at 30 minutes posthemodialysis and BUN, represents the BUN value obtained immediately at the end of the hemodialysis treatment. Kt/V values were calculated by the second-generation formula of Daugirdas4 using both the end of hemodialysis and the 30minute posthemodialysis BUN values, the prehemodialysis BUN, and the intradialytic weight loss.
2
2.5
4.5
Dialysis Tredent
Ti$
(HrsJ4
Fig 2. Percent urea rebound versus hemodialysis treatment time. f = -0.38, P = 0.007.
tients had Kt/V values of 2 1.Ousing the immediate posthemodialysis BUN. Of these 45 patients, 18 (40%) had a Kt/V value lower than 1.0 using the 30-minute posthemodialysis BUN. In an attempt to determine the factors responsible for urea rebound, the percent rebound was correlated with dialysis treatment time, dialysis efficiency (Kt/V per hour), and the predialysis hematocrit. Urea rebound was also compared between patients who were hemodynamically stable and those who had symptomatic or asymptomatic hypotension. As shown in Fig 2, urea rebound was inversely correlated with dialysis treatment time (r = -0.38, P < 0.01). However, the r value was low, suggesting that treatment time explained approximately 16% of the observed variability. More importantly, urea rebound strongly correlated with the efficiency of urea removal (Kt/V per hour) (Fig 3) (r = 0.66,
Statistics
50
Differences between groups were evaluated using nonpaired r-tests for single comparisons and ANOVA followed by Tuke-Kramer multiple comparison test for multiple groups (Instat Statistical Software, San Diego, CA). Linear regression analysis was performed with Instat. P < 0.05 was considered significant. RESULTS
Urea rebound was documented in all but two patients. For the entire population, Kt/V decreased from 1.2 ? 0.3 (mean + 1 SD) using the immediate postdialysis BUN to 1.0 + 0.2 USing the 30 minutes posthemodialysis BUN (P < 0.001). Figure 1 shows that 45 of the 49 pa-
40 z a a 30 B I20 5 s
10
0.2
0.3
0.4
0.5
0.6
0.7
0.8
KW per Hour Fig 3. Percent urea rebound versus hemodialysis efficiency (KW per hour). r = 0.66, P < 0.0001.
SPIEGEL
28 Table
Treatment Time (hr)
<2.5 2.5-2.9 3.0-3.4 23.5
1. Observed Hemodialysis
Decrease in KtN Based Treatment Time
Mean Time (21 SD)
2.19 2.58 3.08 3.70
+ r 2 -c
l f < 0.05 vtreatment
No. of Patients
0.20 0.12 0.15 0.21
6 12 19 12 time
on
Observed Decrease in KW (Mean 2 1 SD)
0.21 0.20 0.21 0.11
+ 2 2 c
0.08 0.11 0.08 0.08
of 3.0 to 3.4 hours.
P < O.OOOl), suggesting that dialysis efficiency accounts for a major portion (40%) of the variability observed in the urea rebound. There was no correlation between urea rebound and predialysis hematocrit. Patients who developed any form of hypotension (n = 22) had urea rebound values that were slightly higher than those in patients without hypotension (20.6 + 11.3 v 16.2 + 9.1; P = 0.14), although the difference was not statistically significant. Patients with documented hypotension (n = 19) had urea rebound that was not different from that in patients without hypotension (19.1 + 10.6 v 17.5 + 10.2; P = 0.60). Tables 1 and 2 show the decrease in delivered Kt/V based on dialysis treatment time and dialysis efficiency (Kt/V per hour), respectively. As treatment time decreased below 3.5 hours, the delivered Kt/V fell by 0.2. More importantly, as dialysis efficiency progressively increased (Table 2), the actual delivered Kt/V decreased by as much as 0.3 for the most efficient hemodialysis treatments. DISCUSSION
This study demonstrates that urea rebound has a significant impact on delivered Kt/V in highflux hemodialysis. Urea rebound correlated strongly with dialysis efficiency and only weakly with dialysis treatment time, suggesting that rebound is due to the relatively slow urea mass transfer out of cells seen with highly efficient dialysis. The finding that hypotension did not result in increased urea rebound further supports the idea that decreased tissue perfusion during dialysis is not the primary cause of urea rebound. While dialysis adequacy remains controversial, the American Association of Kidney Pa-
ET AL
tients and the National Institutes of Health Consensus Development Conference on Morbidity and Mortality of Dialysis have recommended a delivered Kt/V of 1.2.5.6 These groups did not distinguish between standard or high-flux/highefficiency hemodialysis. Our study clearly demonstrates that both the urea rebound and the error in single pool urea kinetics increase as dialysis efficiency increases. With short, highly efficient dialysis treatments, the target Kt/V, using single pool urea kinetics, must be increased to ensure adequate therapy. If the desired delivered single pool Kt/V is 1.2, our data suggest that the target Kt/V should be increased by 0.1 to 0.3. Although treatment time was not as strong a determinant as dialysis efficiency in predicting rebound, our data suggest that the target Kt/V be increased by 0.2 for treatment times less than 3.5 hours. While we did not measure or correct for urea generation in this study, previous work has shown that it contributes minimally to urea rebound.’ Furthermore, urea generation would be greater in large patients who were dialyzed for longer periods of time. As a group, these patients tended to have less urea rebound. The use of polysulfone membranes suggests that the increased catabolism reported following cuprophan dialysis7 was not a factor in this study. We did not measure residual renal function in our patients, a factor shown to effect urea rebound.* However, the differences in urea rebound reported were small (4% to 6%)* and could not explain the significant influence that dialysis efficiency had on urea rebound. While dialysis efficiency accounted for much of the variability in urea rebound, a significant percentage remains unexplained by our study. We suspect that much of Table
2. Observed Decrease in KM/ Dialysis Efficiency
Dialysis Efficiency (KW per hr)
Mean KVV per Hr
<0.35 0.35-0.44 0.45-0.54 20.55
0.31 0.41 0.50 0.69
‘P < 0.05, tP ciency of ~0.35.
? 2 2 +
0.03 0.03 0.03 0.06
c 0.01,
No. of Patients
16 18 10 5
and SP < 0.001
Based
on
Observed Decrease in KtiV (Mean + 1 SD)
0.11 0.18 0.24 0.31
+ 2 -c t
Y dialysis
0.06 0.08* 0.07t O.ll$ effi-
UREA
REBOUND
AND
DIALYSIS
EFFICIENCY
this variability is due to large differences in urea mass transfer coefficients between patients.’ In summary, urea rebound is clinically important in high-flux hemodialysis. Nephrologists should recognize that Kt/V determined from single pool urea kinetics increasingly overestimates delivered Kt/V as dialysis efficiency is increased. Target Kt/V goals may need to be adjusted upward as dialysis efficiency increases. ACKNOWLEDGMENT The authors thank the dedicated nurses and staff at the Rocky Mountain Kidney Center for their help with this study and their excellent patient care. The authors also thank the patients at the kidney center for their participation in this study. REFERENCES I. Pedrini LA, Zereik S, Rasmy S: Causes, kinetics and clinical implications of post-hemodialysis urea rebound. Kidney Int 34:817-824, 1988
29
2. Daugirdas JT, Schneditz D: Postdialysis urea rebound: Measurement, prediction and effects of regional blood flow. Dial Transplant 23: I66- 173, 1994 3. Schneditz D, Pflederer BR, von Albertini B, Lau AH, Daugirdas JT: The muscle/bone/skin blood flow fraction from post-dialysis urea rebound using a regional blood flow kinetic model. J Am Sot Nephrol 4:384A, 1993 (abstr) 4. Daugirdas JT: Second generation logarithmic estimates of single-pool variable volume Kt/V: An analysis of error. J Am Sot Nephrol 4:1205-1213, 1993 5. Patient issues in ESRD: AAKP adopts guidelines on adequacy. Nephrol News & Issues December 21-23, 1993 6. Morbidity and mortality of dialysis. NIH Consensus Statement I I : l-33, 1993 7. Gutierrez A, Alvestrand A, Wahren I, Bergstrom J: Effect of in vivo contact between blood and dialysis membranes on protein catabolism in humans. Kidney Int 38:487494, 1990 8. Albouze G, Yanai M, Calamai M, Testou D, Jungers P, Man NK, Robinet M: Urea rebound and residual function in the calculation of Kt/V and protein catabolic rate. Kidney Int 43:S278-281, 1993 9. Star RA, Hootkins R, Thompson JR, Poole T, Toto RD: Variability and stability of two pool urea mass transfer coefficient. J Am Sot Nephrol 3:395A, 1992 (abstr)
MD,
0 Urea rebound has been documented to occur after hemodialysis, but the magnitude and causes are not clearly defined. In this study we evaluated the effect of high-flux hemodialysis on urea rebound and KW. Blood urea nitrogen samples were obtained before, immediately after, and 30 minutes after hemodialysis in 49 patiints. Rebound was evaluated with respect to dialysis efficiency, dialysis treatment time, the occurrence of hypotension, and hematocrit. Urea rebound was significant and resulted in an overall decrease in KW from 1.2 ? 0.3 to 1.0 T 0.2 (P < 0.001). Df the 43 patients with a measured KW of greater than 1.0,40% had an actual delivered KW of less than 1.0 once rebound was taken into account. Urea rebound correlated strongly with dialysis efficiency but not with hypotension, suggesting that rebound resulted primarily from delayed urea mass transfer across cell membranes. We conclude that increasing dialysis efficiency increases urea rebound and increases the error in KW determinations from single pool urea kinetics. 0 1995 by the National Kidney Foundation, inc. INDEK WORDS: Urea rebound;
high-flux
hemodialysis;
T
HE DOSE OF delivered dialysis considered to be optimal therapy remains controversial, despite widespread use of single pool urea kinetic modeling to measure dialysis adequacy. While urea rebound has been described following hemodialysis,‘32 the significance of urea rebound on delivered dialysis dose and the factors that govem rebound are not well established. Urea rebound is in part caused by delayed urea transfer from intracellular to extracellular fluid as urea is removed from the extracellular space during hemodialysis.’ There is also evidence that regional blood flow is altered during hemodialysis, resulting in relatively underperfused tissue beds. Restoration of adequate blood flow following dialysis results in washout of accumulated urea nitrogen, contributing to urea rebound.*,” If urea rebound occurs due to delayed urea transfer across cell membranes, then increasing dialysis efficiency, the rate of removal of urea from the extracellular space, should increase rebound. If urea rebound results from restoration of blood flow to underperfused tissue beds, then it should
From the Division of Nephrology and Hypertension, The University of Colorado Health Sciences Center and The Rocky Mountain Kidney Center, Denver, CO. Received May 19, 1994; accepted in revised form August HP 1994. Address reprint requests to David M. Spiegel, MD, Division of Nephrology and Hypertension, The University of Colorado Health Sciences Center, Box C-281,4200 E Ninth Ave, Denver, CO 80262. 0 1995 by the National Kidney Foundation, Inc. 0272-6386/95RSOl-0005$3.00/O 26
American
Journal
KW, dialysis efficiency.
be worsened by intradialytic hypotension and other factors that influence tissue perfusion, such as shortened time for ultrafiltration. Therefore, if urea rebound results from restoration of blood flow to underperfused tissue beds, it should be more effected by intradialytic hypotension and dialysis treatment time rather than by dialysis efficiency. Therefore, the purpose of this study was to document the degree of urea rebound following high-flux hemodialysis. We also sought to determine the factors that govern urea rebound. We reasoned that if urea rebound was due to delayed transcellular urea shifts, then it would increase as dialysis efficiency increased. However, if postdialysis urea rebound was caused by return of blood flow to underperfused tissue beds, then dialysis treatment time and hemodynamic changes might effect rebound more than dialysis efficiency. MATERIALS AND METHODS Forty-nine chronic hemodialysis patients, all dialyzed with high-flux polysulfone F-80 dialyzers, were randomly recruited from our outpatient hemodialysis facility. Following acquisition of informed consent, blood was sampled for urea nitrogen at the start, immediately after hemodialysis (following disconnection of the dialysis tubing), and at 30 minutes posthemodialysis. Thirty minutes was chosen because previous work had shown that most urea rebound occurred by this time, yet urea production was not significant.’ The blood urea nitrogen (BUN) samples were measured in a routine clinical laboratory (MetWest, Inc. Denver, CO). A spun hematocrit was performed at the beginning of each treatment. Weight was recorded at the beginning and end of each treatment, and automated blood pressures were recorded every 30 minutes. Hypotension was defined as symptoms of warmth, nausea, of Kidney
Diseases,
Vol 25, No 1 (January), 1995: pp 26-29
UREA REBOUND AND DIALYSIS EFFICIENCY
0.6
0.8
1
1.2
1.4
1.6
1.8
2
27
2.2
2.4
1.5
KW From 30’ Post-HD BUN Fig 1. KW determined from BUN values immediately postdialysis versus KW determined from BUN values 30 minutes posthemodialysis. Each point represents one patient. The diagonal line is the line of identity. Vertical line delineates a deliired KW of 1 .O allowing for urea rebound. Patients to the left have actual KWs of less than 1.0. Note that most of these patients have KW greater than 1.0 when calculated from the BUN immediately posthemodialysis.
or cramping requiring treatment with normal or hypertonic saline, or as a decrease in mean arterial pressure of more than 20 mm Hg in any 30-minute period. Documented hypotension was defined as a decrease in mean blood pressure of more than 20 mm Hg in any 30-minute period. The blood flow rate was maintained between 250 and 450 mUmin and the dialysate flow was set at 600 mL/min. Percent urea rebound was calculated by the following equation: BUNr, - BUNJBUN,
x 100.
where BUNJO represents the BUN value at 30 minutes posthemodialysis and BUN, represents the BUN value obtained immediately at the end of the hemodialysis treatment. Kt/V values were calculated by the second-generation formula of Daugirdas4 using both the end of hemodialysis and the 30minute posthemodialysis BUN values, the prehemodialysis BUN, and the intradialytic weight loss.
2
2.5
4.5
Dialysis Tredent
Ti$
(HrsJ4
Fig 2. Percent urea rebound versus hemodialysis treatment time. f = -0.38, P = 0.007.
tients had Kt/V values of 2 1.Ousing the immediate posthemodialysis BUN. Of these 45 patients, 18 (40%) had a Kt/V value lower than 1.0 using the 30-minute posthemodialysis BUN. In an attempt to determine the factors responsible for urea rebound, the percent rebound was correlated with dialysis treatment time, dialysis efficiency (Kt/V per hour), and the predialysis hematocrit. Urea rebound was also compared between patients who were hemodynamically stable and those who had symptomatic or asymptomatic hypotension. As shown in Fig 2, urea rebound was inversely correlated with dialysis treatment time (r = -0.38, P < 0.01). However, the r value was low, suggesting that treatment time explained approximately 16% of the observed variability. More importantly, urea rebound strongly correlated with the efficiency of urea removal (Kt/V per hour) (Fig 3) (r = 0.66,
Statistics
50
Differences between groups were evaluated using nonpaired r-tests for single comparisons and ANOVA followed by Tuke-Kramer multiple comparison test for multiple groups (Instat Statistical Software, San Diego, CA). Linear regression analysis was performed with Instat. P < 0.05 was considered significant. RESULTS
Urea rebound was documented in all but two patients. For the entire population, Kt/V decreased from 1.2 ? 0.3 (mean + 1 SD) using the immediate postdialysis BUN to 1.0 + 0.2 USing the 30 minutes posthemodialysis BUN (P < 0.001). Figure 1 shows that 45 of the 49 pa-
40 z a a 30 B I20 5 s
10
0.2
0.3
0.4
0.5
0.6
0.7
0.8
KW per Hour Fig 3. Percent urea rebound versus hemodialysis efficiency (KW per hour). r = 0.66, P < 0.0001.
SPIEGEL
28 Table
Treatment Time (hr)
<2.5 2.5-2.9 3.0-3.4 23.5
1. Observed Hemodialysis
Decrease in KtN Based Treatment Time
Mean Time (21 SD)
2.19 2.58 3.08 3.70
+ r 2 -c
l f < 0.05 vtreatment
No. of Patients
0.20 0.12 0.15 0.21
6 12 19 12 time
on
Observed Decrease in KW (Mean 2 1 SD)
0.21 0.20 0.21 0.11
+ 2 2 c
0.08 0.11 0.08 0.08
of 3.0 to 3.4 hours.
P < O.OOOl), suggesting that dialysis efficiency accounts for a major portion (40%) of the variability observed in the urea rebound. There was no correlation between urea rebound and predialysis hematocrit. Patients who developed any form of hypotension (n = 22) had urea rebound values that were slightly higher than those in patients without hypotension (20.6 + 11.3 v 16.2 + 9.1; P = 0.14), although the difference was not statistically significant. Patients with documented hypotension (n = 19) had urea rebound that was not different from that in patients without hypotension (19.1 + 10.6 v 17.5 + 10.2; P = 0.60). Tables 1 and 2 show the decrease in delivered Kt/V based on dialysis treatment time and dialysis efficiency (Kt/V per hour), respectively. As treatment time decreased below 3.5 hours, the delivered Kt/V fell by 0.2. More importantly, as dialysis efficiency progressively increased (Table 2), the actual delivered Kt/V decreased by as much as 0.3 for the most efficient hemodialysis treatments. DISCUSSION
This study demonstrates that urea rebound has a significant impact on delivered Kt/V in highflux hemodialysis. Urea rebound correlated strongly with dialysis efficiency and only weakly with dialysis treatment time, suggesting that rebound is due to the relatively slow urea mass transfer out of cells seen with highly efficient dialysis. The finding that hypotension did not result in increased urea rebound further supports the idea that decreased tissue perfusion during dialysis is not the primary cause of urea rebound. While dialysis adequacy remains controversial, the American Association of Kidney Pa-
ET AL
tients and the National Institutes of Health Consensus Development Conference on Morbidity and Mortality of Dialysis have recommended a delivered Kt/V of 1.2.5.6 These groups did not distinguish between standard or high-flux/highefficiency hemodialysis. Our study clearly demonstrates that both the urea rebound and the error in single pool urea kinetics increase as dialysis efficiency increases. With short, highly efficient dialysis treatments, the target Kt/V, using single pool urea kinetics, must be increased to ensure adequate therapy. If the desired delivered single pool Kt/V is 1.2, our data suggest that the target Kt/V should be increased by 0.1 to 0.3. Although treatment time was not as strong a determinant as dialysis efficiency in predicting rebound, our data suggest that the target Kt/V be increased by 0.2 for treatment times less than 3.5 hours. While we did not measure or correct for urea generation in this study, previous work has shown that it contributes minimally to urea rebound.’ Furthermore, urea generation would be greater in large patients who were dialyzed for longer periods of time. As a group, these patients tended to have less urea rebound. The use of polysulfone membranes suggests that the increased catabolism reported following cuprophan dialysis7 was not a factor in this study. We did not measure residual renal function in our patients, a factor shown to effect urea rebound.* However, the differences in urea rebound reported were small (4% to 6%)* and could not explain the significant influence that dialysis efficiency had on urea rebound. While dialysis efficiency accounted for much of the variability in urea rebound, a significant percentage remains unexplained by our study. We suspect that much of Table
2. Observed Decrease in KM/ Dialysis Efficiency
Dialysis Efficiency (KW per hr)
Mean KVV per Hr
<0.35 0.35-0.44 0.45-0.54 20.55
0.31 0.41 0.50 0.69
‘P < 0.05, tP ciency of ~0.35.
? 2 2 +
0.03 0.03 0.03 0.06
c 0.01,
No. of Patients
16 18 10 5
and SP < 0.001
Based
on
Observed Decrease in KtiV (Mean + 1 SD)
0.11 0.18 0.24 0.31
+ 2 -c t
Y dialysis
0.06 0.08* 0.07t O.ll$ effi-
UREA
REBOUND
AND
DIALYSIS
EFFICIENCY
this variability is due to large differences in urea mass transfer coefficients between patients.’ In summary, urea rebound is clinically important in high-flux hemodialysis. Nephrologists should recognize that Kt/V determined from single pool urea kinetics increasingly overestimates delivered Kt/V as dialysis efficiency is increased. Target Kt/V goals may need to be adjusted upward as dialysis efficiency increases. ACKNOWLEDGMENT The authors thank the dedicated nurses and staff at the Rocky Mountain Kidney Center for their help with this study and their excellent patient care. The authors also thank the patients at the kidney center for their participation in this study. REFERENCES I. Pedrini LA, Zereik S, Rasmy S: Causes, kinetics and clinical implications of post-hemodialysis urea rebound. Kidney Int 34:817-824, 1988
29
2. Daugirdas JT, Schneditz D: Postdialysis urea rebound: Measurement, prediction and effects of regional blood flow. Dial Transplant 23: I66- 173, 1994 3. Schneditz D, Pflederer BR, von Albertini B, Lau AH, Daugirdas JT: The muscle/bone/skin blood flow fraction from post-dialysis urea rebound using a regional blood flow kinetic model. J Am Sot Nephrol 4:384A, 1993 (abstr) 4. Daugirdas JT: Second generation logarithmic estimates of single-pool variable volume Kt/V: An analysis of error. J Am Sot Nephrol 4:1205-1213, 1993 5. Patient issues in ESRD: AAKP adopts guidelines on adequacy. Nephrol News & Issues December 21-23, 1993 6. Morbidity and mortality of dialysis. NIH Consensus Statement I I : l-33, 1993 7. Gutierrez A, Alvestrand A, Wahren I, Bergstrom J: Effect of in vivo contact between blood and dialysis membranes on protein catabolism in humans. Kidney Int 38:487494, 1990 8. Albouze G, Yanai M, Calamai M, Testou D, Jungers P, Man NK, Robinet M: Urea rebound and residual function in the calculation of Kt/V and protein catabolic rate. Kidney Int 43:S278-281, 1993 9. Star RA, Hootkins R, Thompson JR, Poole T, Toto RD: Variability and stability of two pool urea mass transfer coefficient. J Am Sot Nephrol 3:395A, 1992 (abstr)