Nephrol Dial Transplant (1998) 13 [Suppl 6 ]: 25–30
Nephrology
Dialysis
Transplantation
Urea rebound and effectively delivered dialysis dose
S. Alloatti, A. Molino, M. Manes and G. M. Bosticardo1
Dialysis Unit, Aosta and 1Dialysis Unit, Ivrea, Italy
Introduction
Although the non-single-pool behaviour of urea kinetics has been pointed out [1–5], and shown to be
relevant particularly in high-efficiency dialysis [6 ], the
need to take urea disequilibrium into account even for
practical purposes has become evident in recent years,
in that it has improved knowledge of urea rebound
( UR), which is a direct consequence of disequilibrium.
At least five causes may contribute to UR genesis
(Figure 1), and their respective roles are analysed here.
Access recirculation (AR)
The sharp increase in urea concentration in the first
seconds after the blood pump stops depends on the
AR, if present, the degree of which is influenced by
schedule parameters and patient vascular dynamics
( Table 1). The AR reversal lasts a few seconds after
the interruption of the cycling of some venous blood
flow to the dialyser. Its recognition is one of the most
important goals of urea kinetics, in order to detect the
cause of a decrease in efficiency of dialysis or to predict
Table 1. Main causes of access recirculation
$ Stenosis post-venous needle
—anatomical
—functional (vasoconstriction)
$ Excessive proximity of the needles
$ Large vessel diameter, especially if protesic, with consequently
reduced blood flow
$ Needle reversal
$ Fistula/blood pump flow ratio near 1
—in baseline condition due to insufficient flow
—during dialysis session due to reduction of cardiac output or
blood pressure
—high blood pump flow
Fig. 1. Different phenomena involved in the genesis of urea rebound ( UR).
Correspondence and offprint requests to: S. Alloatti, Servizio di
Nefrologia e Dialisi, Ospedale Regionale di Aosta, Viale Ginevra,
3, 11100 Aosta, Italy.
© 1998 European Renal Association–European Dialysis and Transplant Association
26
a vascular access stenosis [7,8] treatable surgically or
by angioplasty. The reduction in efficiency depends on
the concentration of toxic substances at the dialyser
inlet artefactually lowered by AR, proportionally
decreasing the ‘effective’ body clearance, while the
dialyser clearance remains unchanged.
The factor ( f ) to correct the dialyser clearance for
ar
AR is expressed by the following formula [9]:
f =(1−R)/[1−R(1−K /Q )]
ar
d b
where R is the recirculation fraction, K is the dialyser
d
clearance and Q is the blood flow. Therefore, K
b
ar
(dialyser clearance reduced by AR)=K ×f . It is
d ar
evident that AR affects the dialysis efficiency mainly
for low molecular weight toxins with fractional extraction ( K /Q ) near unity [10].
d b
Cardiopulmonary recirculation (CPR)
The dialytic relevance of this phenomenon, well known
in physiology (Figure 2), has been recognized only
recently [9,11,12]: the dialysed blood coming from the
filter is mixed with venous systemic blood, lowering its
urea concentration, and is pumped by the right ventricle to pulmonary tissue (where the change in solute
concentration is negligible), and then reaches, via the
left ventricle, the peripheral arterial circulation as far
as the A–V fistula. As a result of CPR, blood at the
dialyser inlet has a urea concentration lower than that
of systemic venous blood (i.e. at the opposite arm
vein), again reducing the effective body clearance.
CPR is also the cause of the surprising reduction in
urea concentration that occurs in the first minutes at
the start of dialysis.
The arterial–venous gradient is maintained during
the whole dialytic phase, and its reversal begins about
20 s after stopping the blood pump at the end of
dialysis (or after switching to isolated ultrafiltration);
this delay corresponds to the time needed for cardiopulmonary transit, while the complete reversal takes
~2 min [9].
The relevance of CPR to reduction in dialysis efficiency has been estimated in high-efficiency dialysis to
S. Alloatti et al.
be ~11% (range 7–22%) [9]. The factor to correct the
dialyser clearance, or to predict urea concentration at
the filter inlet, may be obtained by the following
formula:
f =1/[1+K /(CO–Q )]
cpr
d
ac
where K is the dialyser clearance, CO is the cardiac
d
output and Q is the fistula flow. Therefore, K
ac
cpr
(dialyser clearance reduced by CPR)=K ×f .
d cpr
As these parameters may change during dialysis
(mainly CO), consequently CPR will also vary, as will
dialysis efficiency.
Another point regards the obvious absence of CPR
when venous blood is employed instead of an A–V
fistula: this can make up for the presence of AR, often
affecting double lumen central venous catheters.
Besides the reduction in efficiency, another important
consequence of CPR is the interference with AR measurement: the traditional procedure using the systemic
sample ( Table 2a) is wrong and invariably overestimates AR. In many studies, a blood urea nitrogen
(BUN ) concentration difference between systemic and
arterial samples was constantly found and was erroneously attributed to AR. The correct procedure
( Table 2b) is based on a sampling technique that avoids
only AR, as do ‘low flow’ or ‘stop flow’ methods [10].
It is critical to obtain a reliable A2 sample. We have
to ensure: (i) a time delay before sampling which is
long enough to allow AR reversal; (ii) an interval no
longer than 20 s that artefactually should increase the
BUN concentration as a consequence of partial CPR
reversal; and (iii) a complete wash-out of blood affected by AR (the sampling port in the arterial line should
be placed as near as possible to the arterial needle).
However, due to the slight concentration difference
between A1 and A2, the AR measurement could be
affected by routine laboratory inaccuracy [13]; besides
the urea method, several recent technical devices allow
detection and quantification of AR, as a saline bolus
measured by ultrasound doppler [14], optical [15] or
conductivity methods [16 ], or by duplex colour flow
doppler [17]. Alternatively, the thermal bolus method
[18] implemented in some dialysis machines is simpler
and automated, although it produces overlapping of
AR and CPR due to the duration of dialysate cooling
(2 min). Finger occlusion of the vein between the two
needles [19] with evaluation of arterial pre-pump and
venous pressure change is less reliable and does not
allow any quantification.
Table 2. Formulae for measuring AR
(a) Classic formula
AR=
Fig. 2. Cardiopulmonary recirculation (CPR). Values are expressed
in BUN (mg/dl ). As a consequence of CPR, an arterio-venous urea
gradient of 5 mg/dl between the arterial blood to the dialyser and
the systemic venous blood is set up.
S–A
×100
S–V
(b) Correct formula
AR=
A2–A1
×100
A2–V
In (a) S, systemic urea concentration; A, arterial urea, blood pump
running; V, venous urea concentration. In (b) A2, arterial urea with
low flow or stop flow; A1, arterial urea, blood pump running; V,
venous urea concentration.
Urea rebound and dialysis dose
27
Intercompartmental membrane-dependent
disequilibrium
According to this well-recognized theory, the human
body is composed of two or more compartments
(Figure 3), disposed ‘in series’ and separated by cell
membranes; equilibration between compartments
should follow first order kinetics, with a mass transfer
coefficient dependent on membrane resistance.
However, in the literature, a large variability of this
coefficient has been found in dialysis patients, ranging
from 0.3 to 1.8 l/min [20], difficult to explain as a
physiologic cell membrane phenomenon, while a value
of 0.9 l/min has been measured by 15N-labelled urea
infusion between dialysis sessions [21].
Intercompartmental flow-dependent disequilibrium
This concept revisits a theory already described by
Dedrick [22] based on different blood flows in various
body tissues. Skin, muscle and bone containing up to
80% of the urea pool are perfused by 15–20% of the
cardiac output, at a markedly lower flow rate compared
with better perfused organs [23]. During dialysis, a
concentration gradient among body compartments
with different blood flow in capillary beds leads to
accumulation of urea in those organs which are less
well perfused. The compartment disposition is thus ‘in
parallel’ and no longer ‘in series’ ( Figure 4).
New mathematical two- or multi-pool models have
been proposed, the ‘regional blood flow model’ [24]
and the ‘heterogeneous blood flow model’ [25], that
may predict the UR without the need for further
explanation, even assuming an infinite transcellular
membrane permeability.
The blood flow models are more compatible with
the large variation in UR found in the literature for
different patients and even within the same session,
because blood flow may be influenced by several physiologic factors, such as vasoconstriction which may
functionally exclude some tissue beds from active circulation. This phenomenon is also known as peripheral
Fig. 4. Regional blood flow model. Two or more body compartments
(in parallel ) with different blood flows can explain ‘per se’ urea
disequilibrium.
sequestration, body district hypoperfusion and compartmentalization.
The concentration gradient induces a diffusion of
stored urea to blood, causing UR after the session,
and sometimes possibly during dialysis, as evidenced
by irregular BUN profiles obtained with frequent
sequential samples. Several factors can influence this
phenomenon: (i) ultrafiltration, as demonstrated by a
14% increase of UR in dialysis with marked ultrafiltration compared with the results obtained in sessions
without water removal [26 ]; (ii) cardiac output,
inversely related to UR, as observed when comparing
patients with low cardiac index with others with high
values [23]; (iii) duration of dialysis, as vasoconstriction, and consequently UR, can increase during the
dialysis treatment [27]; (iv) physical activity during
dialysis has been proven to reduce UR [28]; and
(v) temperature, that may play an important role, as
shown by experimental reduction of the concentration
gradient between the peripheral vein and vascular
access after immersion of the contralateral arm in hot
water at 39°C [29]. Somewhat surprisingly, in another
experiment, cold dialysate did not increase the compartmentalization effect: this has been explained as a
vascular effect limited mainly to the skin, that represents only 10–15% of body water volume without
affecting the muscle mass perfusion [30].
All this evidence supports the regional flow model
that explains UR better than the membrane-dependent
model. Nevertheless, the exact relative role of both
phenomena in urea compartmentalization has not yet
been quantified.
Dialysis-induced hypercatabolism
Fig. 3. Two-compartment model (in series). The dialyser draws out
urea from the extracellular compartment. Urea shift from the intrato the extracellular compartment is regulated by transcellular clearance (~900 ml/min).
This phenomenon was suggested in the past as a
possible cause of UR [5,31,32]: although recirculation
and disequilibrium may now be recognized as the
fundamental explanation, a possible role for hypercatabolism has not been disproven. After the end of
dialysis, the urea generation contributes to UR, and
equilibrated samples obtained at 30–60 min should be
corrected by subtracting the urea generated to obtain
the ‘net rebound’. It must, however, be pointed out
that the urea generation rate is not constant, being
28
lower during the long interdialytic interval of classical
schedules, as reported by Lopot [33]. In our opinion,
this phenomenon merits further clarification.
Theoretical and practical consequences of UR
An important field of urea kinetics has been the
comparison between the classical single-pool urea kinetic model ( UKM ) and direct dialysis quantification
(DDQ). Several authors have pointed out the significant differences of results [34–36 ]: our group recently
has demonstrated that by taking account of the UR
phenomenon by equilibrated samples (30 min postdialysis) and by using the correct formulae, UKM and
DDQ models may be reconciled, giving quite similar
kinetic outputs [37].
Classical UKM [38] and analysis of the National
Cooperative Dialysis Study results [39] were based on
the assumption of a single-pool urea behaviour, while
it is well recognized that UR significantly affects the
post-dialysis BUN, and therefore we must clearly distinguish between single-pool Kt/V ( Kt/V ) and the
sp
equilibrated one ( Kt/V ) that expresses the true diaeq
lysis dose more reliably. From a practical viewpoint,
other important consequences cannot be neglected:
urea generation rate and protein catabolic rate are also
artefactually influenced by UR, resulting in overestimation by single-pool kinetics.
Therefore, it must be emphasized that the degree of
UR may be measured as the simple ratio:
UR1=(C –C )/C ×100
eq post post
or by the alternative expression:
UR2=(C -C )/(C −C )×100
eq post
pre
post
Although UR2 expresses better the meaning of
rebound as the ratio to the pre-post concentration
drop, and usually gives lower results than UR1, in our
opinion the latter is preferable because its percentage
value better approximates to the percentage difference
between Kt/V and Kt/V .
sp
eq
The relevance of UR, and consequently the difference between Kt/V and Kt/V , is proportional to
sp
eq
the efficiency of dialysis, that may be expressed by the
K/V ratio, or Kt/V per h: Spiegel observed a Kt/V
difference of 11% with Kt/V per h <0.35, that rose to
31% with Kt/V per h >0.55 [40].
S. Alloatti et al.
(ii) Long dialysis time, as the French experience has
demonstrated [41], either because very high Kt/V
values >1.8 may be easily achieved, or due to the
reduced difference between Kt/V and Kt/V consp
eq
sequent to low Kt/V per h values. (iii) Daily dialysis
schedules [42], mainly with long sessions [43],
which obviously offset the UR phenomenon and
the consequent disequilibrium. (iv) Bi- or multicompartmental kinetic models, according to membrane-dependent or flow-dependent models, may more
rationally predict toxin removal than one-compartment
models; however, these approaches are not simple
enough for clinical practice. (v) Equilibrated singlepool kinetics: this simple and reliable approach is not
well accepted by the patients due to the practical
difficulty of obtaining an equilibrated sample at 30 min
post-dialysis. (vi) Standard single-pool kinetics corrected in the single patient for the percentage overestimation by periodical Kt/V checks. (vii) Estimation
eq
of UR from ‘inbound’. The equilibrated post-dialysis
BUN may be estimated by the Smye algorithm
( Table 3) [43], based on an intradialytic sample drawn
at about one-third of the way through the dialysis
session: from the difference beween the measured value
and that predicted according to an exponential decline
of urea concentration, the post-dialysis BUN is corrected to estimate the equilibrated one. Experimental
tests have confirmed the reliability of this procedure
[20,45]: it must be emphasized that exactly identical
sampling modalities have to be employed intra- and
post-dialysis (both with the blood pump running or
both with the low flow technique) [45] and it must be
ensured that AR and CPR do not change. In seven
cases, we have also found a sufficient approximation
Table 3. Correction formulae to obtain Kt/V
Smye
Daugirdas
Tattersall
eq
from Kt/V
sp
C =C e−ltl=1/(t–s) In (C /C
eq
o
s t
Kt/V =Kt/V ×
eq
sp
[1–0.6/(t/60)]+0.03
Kt/V =Kt/V ×t/(t+35)
eq
sp
C =concentration at the equilibrium; C =urea concentration at
eq
o,s,t
the start, at time s and at the end of dialysis; t=dialysis time, s=
time s (about one-third of the way through the session).
How may UR be overcome by the nephrologist’s
choices?
There are many possible strategies which may be
undertaken. (i) Large dialysis doses is one obvious
solution: a target Kt/V higher than the usual values
may offer a safety margin for the Kt/V difference
attributable to UR, therefore making up for occasional
pitfalls that may compromise dialysis efficiency further
(such as dialyser clotting, recirculation, inadequate
blood pump effective flow, co-current flows, etc.).
Fig. 5. Percentage differences between Kt/V and Kt/V obtained
sp
eq
with the Daugirdas and Tattersall correction formulae. Mathematical
simulation with a Kt/V =1.0 hypothesis.
sp
Urea rebound and dialysis dose
29
Fig. 6. Percentage differences between measured Kt/V and Kt/V
eq
eq
obtained with the Daugirdas and Tattersall correction formulae, in
13 cases. Average %D using the Daugirdas formula: −1.229, SD
6.1. Average %D using the Tattersall formula: −0.885, SD 6.2.
of the predicted to measured values: (C equilibrated,
measured=0.364 mg/dl, C Smye=0.359 mg/dl, D%=
–1.4%, SD=8.7). A similar concept of predicting UR
by comparison of the single-pool profile with that
measured in plasma water or dialysate has been implemented in automated urea monitors [46,47], where the
multiple-point curve may theoretically guarantee a
better reliability. (viii) Simple mathematical correction
of Kt/V to Kt/V has been suggested recently [48,49]
sp
eq
derived by the K/V ratio (Table 3), as an index of
dialysis efficiency that is well correlated to UR.
In Figure 5, a mathematical simulation with the
above formulae is shown for a Kt/V target of 1.0 over
a wide range of dialysis times. The differences between
the two Kt/Vs are very slight with long dialysis time,
while they are substantial with very short treatments.
We have compared in 13 cases (Figure 6) the Kt/V
eq
estimated by Daugirdas and Tattersall formulae with
a reference Kt/V obtained by dialysate collection
eq
[37]: the average values seem quite satisfactory, however, with data dispersion, also expressed by the large
standard deviation of the percentage difference. In our
opinion, however, besides published data, larger scale
studies are advisable to evaluate these very interesting
approaches more thoroughly.
In conclusion, UR results from several physiological
and dialytic phenomena, particularly relevant during
high-efficiency dialysis: the simple increase in dialyser
performance to compensate for time reduction invariably leads to underdelivery of dialysis dose, for the
reasons summarized in Figure 7. Raised blood flow
may increase the degree of AR, and high clearance
values per se will change the CPR and disequilibrium,
without producing a proportional amelioration of
‘effective’ body clearance; also increased hourly ultrafiltration to compensate for reduced dialysis time may
affect disequilibrium and compartmentalization by
inducing hypotension, requiring the blood pump to be
lowered further.
The risk of prescribing an insufficient dialysis dose
is prevented by the adequate knowledge of such complex phenomena which the nephrologist must recognize readily.
Fig. 7. Risk of delivering an insufficient dialysis dose by compensating dialysis time reduction with dialyser clearance increase. K,
dialyser clearance; t, dialysis time; V, urea distribution volume; Q ,
b
blood pump flow; AR, access recirculation; CPR, cardiopulmonary
recirculation; Q , ultrafiltration rate; C , urea concentration at
uf
in
dialyser inlet.
Acknowledgements. The authors thank Mrs M. Bernardi and
C. Alerci for technical assistance and for typing the manuscript.
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