Clinical Science (1970) 39, 51-60.
CHANGES I N ACID-BASE BALANCE D U R I N G
PERITONEAL DIALYSIS WITH F L U I D CONTAINING
LACTATE IONS
S . R. D I X O N * , W . I . M c K E A N , J . E. P R Y O R
AND
R. 0. H. I R V I N E
Department of Medicine, University of Otago Medical School, Dunedin, New Zealand
(Received 14 February 1970)
SUMMARY
1. Twenty-three peritoneal dialyses with fluid containing 45 mEq lactate per litre
were carried out on six patients with acute or chronic renal failure. During dialysis
arterial blood pH and base excess rose.
2. The lactate ions were rapidly and almost completely absorbed from the fluid
in the peritoneal cavity. Blood lactate concentration rose, but in patients with adequate
liver function it did not exceed the normal range. One patient with poor hepatic function and renal failure showed abnormally high blood lactate levels after peritoneal
dialysis, but metabolic acidosis was still corrected.
3. The concentration of bicarbonate ions in the fluid drained from the peritoneal
cavity rose as the dialysis progressed. A significant positive correlation was found
between the arterial blood bicarbonate concentration and the bicarbonate concentration in the fluid drained from the peritoneal cavity.
4. If the lactate ions absorbed from the peritoneal cavity had not been metabolized
the loss of bicarbonate ions in the fluid drained from the peritoneal cavity would
have increased the metabolic acidosis.
Peritoneal dialysis has been used extensively in the treatment of patients with renal failure.
Dialysis solutions contain a buffer or a potential buffer to help correct the metabolic acidosis
which accompanies renal failure. Bicarbonate was used initially (Boen, 1961),but was replaced
with lactate when it was found that calcium carbonate precipitated and the solution became
alkaline during autoclaving. The lactate ion absorbed from the peritoneal cavity acts as a
buffer only after it has been metabolized by the patient. The use of lactate has been questioned
on the grounds that some patients with uraemia may metabolize lactate incompletely (Burns,
Henderson, Hager & Merrill, 1962; Lee, Hill, Hewitt, Ralston & Berlyne, 1967).
The present investigation was carried out to study the acid-base changes during peritoneal
* Present address: Royal Children’s Hospital, Parkville, Victoria 3052, Australia.
Correspondence: Professor R. 0. H. Irvine, University of Otago Medical School, P.O. Box 913, Dunedin,
New Zealand.
51
S. R. Dixon et al.
52
dialysis with dialysis fluid containing 45 mEq of lactate per litre. The rate of lactate absorption
from the peritoneal cavity and the blood lactate and pyruvate levels before and after peritoneal
dialysis were studied. The loss of bicarbonate ions into the dialysis fluid was also measured.
METHODS
Twenty-three peritoneal dialyses were carried out on six patients with acute or chronic renal
failure. The average duration of dialysis was 43.0 h (range 18.4 to 64.8 h). The average number
of exchanges in each dialysis was 29 (range 13-46).
Technique of dialysis
Peritoneal dialysis was performed by the midline abdominal approach (Maxwell, Rockney,
Kleeman & Twiss, 1959). Two litres of dialysis fluid were run into the peritoneal cavity and
allowed to remain there for 1 h, before being drained back into the same bottles. This cycle
was then repeated a number of times until the desired therapeutic effect was achieved. The
average duration of an exchange, that is, the total time taken for inflow, equilibration in the
peritoneal cavity and outflow, was approximately 80-90 min.
1000 i.u. of heparin was added to each 2 litres of dialysis fluid to prevent blockage of the
catheter; no antibiotic was added. A side-tube on the dialysis infusion set, located close to the
catheter, was used to obtain samples of dialysis fluid.
Composition of dialysis fluid
Four varieties of dialysis fluid were used (Table 1). The pH of the solutions was measured
with an EIL capillary pH electrode at 37". The choice of solution used for dialysis was determined by the degree of hydration of the patient and the serum potassium level.
TABLE
1. Composition of peritoneal dialysis fluid
Na
Solution (mEq/l)
A
B
140
140
C
140
D
140
c1
(mEq/l)
Ca
(mEq/l)
Mg
(mEq/l)
K
(mEq/l)
Lactate
(mEq/l)
D-glucose
(mmol/l)
105.5
110.5
105.5
110.5
4
4
4
4
1.5
1.5
0
5
0
5
45
45
45
45
83.3
83.3
416.7
416.7
1 3
I3
PH
(kSD)
5.53k0.24
5.53k0.17
5.29k0.06
5.15k0.02
The distilled water used in the preparation of the fluid had a pH of 6-0;after the chemicals
had been added pH fell to 5.7. Sodium metabisulphite (60-100 mg/l) was added to prevent
discolouration and degradation of the D-glucose. After sterilization the pH was approximately
5.5. Solutions C and D, which contained larger amounts of glucose, had lower pH values than
A and B. It would appear that some degradation of glucose occurred during the sterilization
procedure, but the lactate concentration remained unaltered.
Arterial blood samples
Arterial blood samples were obtained from the brachial artery by intermittent percutaneous
puncture with 1% lignocaine for local anaesthesia. Care was taken to prevent changes in
Acid-base balance during peritoneal dialysis
53
respiration which might have altered the arterial P c o , value. Samples were taken before,
during and after dialysis. Blood pH and Pcoz were measured with an EIL capillary pH electrode, and Severinghaus electrode system respectively. The bicarbonate concentration was
calculated from the Henderson-Hasselbalch equation and the base excess from the SigaardAndersen alignment nomogram which makes allowance for the patient's haemoglobin value
(Sigaard-Andersen, 1963).
Venous blood samples
Venous blood was taken from the antecubital veins without stasis for measurement of
lactate and pyruvate concentrations. The blood was added immediately to an equal volume of
6% perchloric acid at 0" C and mixed well before being centrifuged at 3000 r.p.m. for 10
min at 5" C . The supernatant was separated and stored at 4" C . The blood lactate and pyruvate
levels were measured in the supernatant using enzymatic kits supplied by C . F. Boehringer and
Soehne, GMBH, Mannheim, Germany.
Peritoneal fluid samples
Samples of fluid were obtained from the side-tube under anaerobic conditions during
drainage of the dialysis fluid. Five ml of the fluid were used for lactate estimation and the
remainder, which was maintained under anaerobic conditions, was used in the determination
of the pH and Pco, by the method used for arterial blood samples. The bicarbonate concentration was calculated from the Henderson-Hasselbalch equation.
To estimate the lactate concentration of the dialysis fluid, protein was precipitated by
perchloric acid as described for the blood samples in a 1 in 50 dilution made of the supernatant. Lactate and pyruvate levels were measured in 0.1 ml of the dilute solution using the enzymatic kits (Varley, 1962). A blank solution was prepared using 5 ml of water instead of the
dialysis fluid, and 5 ml of 6% perchloric acid was added. 92-95% recovery was obtained with
standard lactate solutions, fresh dialysis solution and solutions with 500 i.u. units of heparin
added per litre. Heparin was observed to interfere with the estimation if used in higher concentrations than 500 units/l.
Collection periods
Where possible, samples of peritoneal fluid were obtained at the end of three or four consecutive exchanges at the beginning, in the middle and at the end of each dialysis. Bicarbonate and lactate levels were measured and the total amount of bicarbonate removed and lactate
absorbed were calculated for each exchange.
RESULTS
Arterial acid-base changes
Table 2 shows the mean acid-base values before and after twenty-threeperitoneal dialyses in
six patients. In eleven of the twenty-three dialyses the arterial pH was less than 7.36 before
dialysis commenced. Mean values for these dialyses are shown in Table 3. In both tables the
difference between means before and after dialysis is significant ( P <0*001)for all values.
Although the arterial pH was above 7-44 after fourteen of the twenty-three dialyses, base
S. R. Dixon et al.
54
excess reached a positive value on two occasions only. Arterial Pcoz rose in all dialyses, but
reached the normal range in only four of the twenty-three dialyses.
Changes in venous lactate and pyruvate concentrations
Venous lactate and pyruvate concentrations and lactate to pyruvate ratios (L/P) before and
after seventeen dialyses in four patients with normal hepatic function are shown in Table 4.
There was a significant rise in blood lactate (P<O.Ol) and L/P ratio (P<0.05),
but the change
TABLE2. Arterial pH, Pco2, bicarbonate and base
excess values before and after twenty-three peritoneal
dialyses in six patients
PH
Pcoz mmHg
HC03 mEq/l
Base excess mEq/l
Before dialysis
After dialysis
7.345 k0.115
25.9+ 6.7
14.3k4.9
-10.7k8.2
7.4502 0.042
29.7k5.3
19.92 3.2
-4.1 k 3.4
k indicate SD
TABLE3. Arterial pH, Pcoz, bicarbonate and base
excess values before and after eleven peritoneal dialyses
in five patients whose arterial pH was less than 7.36
before dialysis
~
Before dialysis
After dialysis
7.309k0.049
28.3 2 7.1
14.1k4.3
-11.6k5.2
7.42220.028
31.9k6.1
20.0k3.3
-3.4k3.0
~
PH
PCOZm H g
HC03mEq/l
BaseexcessmEq/l
~
k indicate SD
TABLE
4. Blood lactate and pyruvate concentrations and lactate
to pyruvate ratios (L/P) before and after seventeen peritoneal
dialyses in four patients with normal hepatic function
Blood lactate (mg/lOO ml)
Blood pyruvate (mg/lOO ml)
L/P values
Before dialysis
After dialysis
6.8k2.7
0.54rt0.21
14.0k6.3
10-4?;3-6
0.56k0.15
19.6k7.6
It indicate SD
in blood pyruvate was not significant ( P > 0-3). In only one dialysis was the second blood lactate (16.9 mg/100 ml) outside the normal range (6-16 mg/100 ml).
In one patient with hepatic insufficiency in addition to renal failure there was a marked
elevation in blood lactate concentrations and L/P values (Table 5). In spite of this change in
blood lactate concentration, the arterial pH rose in all but one dialysis. In the dialysis in which
pH did not rise, the increase in lactate concentration was very small.
after
7.471
7.539
7.478
7.465
7.438
before
7354
7.438
7.488
7.450
7.292
Arterial pH
29.6
12.6
8.8
7.5
3.5
before
33.4
15.9
10.0
20.0
15.9
after
Lactate concentration
(md100 ml)
0.57
0.96
0.62
0.72
0.48
before
0-36
1.20
0.69
0-52
0.96
after
Pyruvate concentration
(mgI100ml)
51.9
13.1
14.2
10.4
7.3
92.8
13.3
14.5
32.3
16.6
before after
L/P values
8
50
40
(%I
75
30
25
BSP
Transaminase
retention
Liver function tests
TABLE
5. Arterial pH, venous lactate and pyruvate concentrations and lactate to pyruvate ratios (L/P) before and after five
peritoneal dialyses in one patient with impairment of liver function
56
S. R. Dixon et al.
One patient received 345 mEq sodium lactate by intravenous infusion before and during the
peritoneal dialysis. The blood lactate concentration rose from 4-7 to 11.8 mg/100 ml and the
arterial pH rose from 6.930 to 7.472.
Changes in dialysis j h i d composition during a single exchange
An example of the absorption curve for lactate and the changes in acid-base values during
one exchange are shown in Fig. I . The dialysis fluid remained in the peritoneal cavity for 60
50
-
45 -
- 7.5
40 -
- 35-
- 7.0
gp
* E
-6.5 5
Q E 30? = 25o\
tw"
4 2
20-
i'
- 6.0
AI
- 5.5
15-
a
10-
0 -
c -
o\
e:
e
m
50Slay in abdomen (rnin)
FIG.1. An example of the absorption curve for lactate and the changes in the acid-base values in
dialysis fluid during one exchange.The dialysis fluid remained in the peritoneal cavity for 60 min.
0 = Lactate, A = pH, 0 = Bicarbonate and A = Pco2.
min. There was a marked fall in the lactate concentration during the first 15 min and then a
more gradual fall to a final concentration of 2 mEq/l. There was a rapid rise in the pH and
Pco, and a gradual rise in the bicarbonate concentration to a final level of 14.2 mEq/l.
Rates of lactate absorption and bicarbonate loss during dialysis
Table 6 shows the absorption rates for lactate ions calculated at the beginning, middle and
end of a number of dialyses and expressed both as mEq of lactate per exchange and mEq
lactate 1-' h-'. T h s latter value corrects for variations in the volume of dialysis fluid run into
the peritoneal cavity and for the variable duration of dialysis. There was no significant change
in the rates of lactate absorption throughout the dialyses.
Acid-base balance during peritoneal dialysis
57
The rates of loss of bicarbonate ions during the early and late stages of a number of dialyses
are shown in Table 7. There was a significant rise in the loss when measured per exchange
(P<O.O5), but the difference was not significant when calculated per litre per hour (P>O.l).
There was a significant correlation (r = +0.69; P<O.Ool) between the bicarbonate concenTABLE
6. Absorption rates for lactate ions during the early
(I), intermediate (11) and late (111) stages of peritoneal dialysis
Stage
Lactate absorbed
mEq/exchange
Lactate absorbed
mEq 1-' h-'
I
I1
I11
72.0k 11.9
72.4k8.6
73.3k8.1
25.5k5.3
( n = 20)
23.9k3.5
( n = 11)
25.3k2.7
(n = 7)
indicate SD; n = number of collection periods in which
measurements were made
TABLE
7. Rate of loss of bicarbonate ions during the early
(I) and late stages (111) of peritoneal dialysis
Stage
Bicarbonate mEqlexchange
Bicarbonate
mEq I-' h-'
I
I11
23.6k 7.7
7.9k2.3
(n = 17)
2 9 4 k 5.3
9.0k1.4
(n = 18)
f indicate SD; n = number of collection periods in
which measurements were made
tration in arterial blood and in peritoneal dialysis fluid at the end of the thirty-six exchanges in
which both values were measured.
The changes in the arterial blood acid-base values at the beginning and end of two collection
periods in one patient is shown in Table 8, together with the total amount of lactate absorbed
and bicarbonate lost during the collection period. It is assumed that the blood bicarbonate
concentration reflects the concentration throughout the total body water and the total body
bicarbonate in mEq is calculated from the initial blood concentration and the total body
water. The bicarbonate ions lost during the collection period are subtracted from this total. If
it is assumed that none of the lactate ions absorbed are metabolized, the calculated blood
bicarbonate concentration is less than the measured value in both collection periods, whereas
if it is assumed that all lactate ions are converted to bicarbonate, the calculated bicarbonate
concentration is very close to the measured value in both collection periods. These calculations support the suggestion that most of the lactate ions absorbed are completely metabolized,
producing a rise in bicarbonate ion concentration in the blood.
DISCUSSION
Peritoneal dialysis corrects the biochemical disturbances that occur in uraemia (Boen, 1961;
Doolan, Murphy, Wiggins, Carter, Cooper, Watten & Alpen, 1959; Wertheimer, Nielsen &
Stevens, 1967), and recently has been shown to be slightly more effective than haemodialysis
S. R. Dixon et al.
TABLE
8. Alterations in the composition of blood and dialysis fluid during two
collection periods in a patient of body weight 65 kg and estimated total body
water 39 litres (65 x 0.6)
Collection
period (1)
ARTERIAL
BLOOD
PH
HC03 (mEs/l)
PCOZ( m H d
DIALYSIS
FLUID
Volume (1.)
Duration of collection period (h)
Total lactate absorbed (mEq)
Total HCO, lost (mEq)
CALCULATIONS
If none of the lactate ions were
metabolized, blood HCO,
would be (mEq)
If all lactate ions were converted
to HCO, ions blood HCO,
would be (mEq)
Collection
period (2)
Beginning
End
Beginning
End
7.375
21.2
37.4
7.349
24.3
45.5
7.362
18.2
33.0
7.388
19.7
33.8
6.1
4.3
189.1
73.2
6.1
4.3
234.5
47.0
19.3
144
24.1
204
in the treatment of the acid-base disturbances that accompany renal failure (Morrell & Parsons, 1967, 1968). This is probably related to the longer duration of peritoneal dialysis which
allows time for gradual improvement in acid-base status and respiratory compensation.
Dialysis solutions contain a buffer or a potential buffer to help correct the metabolic acidosis
and over the last 10 years sodium lactate has been the compound of choice. Recently, the
effectiveness of sodium lactate has been questioned on the grounds that some patients may not
metabolize lactate completely and it has been suggested that some other buffer should be
used (Burns et al., 1962; Lee et al., 1967).
The results of the present study support the clinical impression that adequate correction of
the metabolic acidosis can be achieved with dialysis fluid containing lactate ions. Significant
rises to normal values or even above occurred in arterial blood pH ,bicarbonate and base-excess
in twenty-three peritoneal dialyses carried out on six patients with renal failure. The compensatory respiratory alkalosis that occurs in renal acidosis persisted after dialysis and accounted
for the alkalaemia that was seen on a number of occasions. A similar finding has been reported
by Cowie, Lambie & Robson (1962), who suggest that an abnormal hydrogen ion gradient
persists between cells of the respiratory centre and the cerebrospinal fluid and is responsible
for maintaining hyperventilation.
Eighty to 85% of the lactate ions in the peritoneal fluid was absorbed and appeared to be
adequately metabolized, because, although the blood lactate concentration rose during dialysis, the levels were still within the normal range when dialysis was finished. In one patient with
Acid-base balance during peritoneal dialysis
59
poor hepatic function, abnormally high blood lactate levels occurred after dialysis, but metabolic acidosis was still corrected.
These results differ from those of Lee et al. (1967) who found blood lactate concentrations
above the normal range in thirteen out of twenty-three patients after peritoneal dialysis. Their
patients did not have a hyperlacticacidaemia as suggested, but a hyperlactataemia as lactic acid
is fully ionized at the pH of arterial blood. Three out of the nineteen patients of Lee et al.
(1967) had elevated lactate levels before dialysis and all had normal hepatic function on biochemical evidence. Campanacci, Guarnieri, Siliprandi & Fiaschi, (1968) found normal blood
lactate and pyruvate concentrations in thirty-five patients with chronic renql failure.
The lactate ions absorbed from the peritoneal cavity must be converted to pyruvate before
being further metabolized to glucose or to carbon dioxide via the tricarboxylic acid cycle. If
there were a block in the conversion to pyruvate, the blood lactate concentration would rise. A
block further down the metabolic pathway might lead to an elevation of pyruvate and lactate
concentrations. The lactate to pyruvate ratio (L/P) has been used to demonstrate the balance
between lactate and pyruvate. If both lactate and pyruvate concentrations rose the L/P value
would remain constant suggesting some limit in the metabolic steps beyond pyruvate. A rise
of the L/P value would suggest that incomplete conversion of lactate to pyruvate had occurred
in the patients studied. The L/P values rose during peritoneal dialysis but the majority remained
within the normal range of 5-25. However, the results do suggest that the conversion of
lactate to pyruvate may be a rate limited step. A rise in blood lactate and pyruvate has been
shown to occur in man following the intravenous infusion of sodium lactate (Altschule, Perrin
& Holliday, 1956). The rise of blood lactate was in excess of pyruvate during the infusion, but
the blood pyruvate fell more slowly than the lactate following the infusion.
There are a number of factors that influence the utilization of lactate but their role in man is
not known with certainty. Although the liver is the major site for lactate metabolism, the
kidney is known to utilize lactate (Levy, 1965) and lactate is excreted in the urine. It is possible
that a failure to excrete lactate ions might affect the blood levels to a small extent. Hyperventilation has been shown to produce a rise in the blood lactate concentration and this may be
reduced by the inhalation of 5% carbon dioxide (Dossetor, Zborowski, Dixon & Par6, 1965).
However, other studies on acute hyperventilation in man have shown only small increases in
blood lactate concentration (Arbus, Herbert, Levesque, Etstein & Schwartz, 1969). Although
the rise in blood lactate concentration in hyperventilation may be due to increased production
it has been shown that the hepatic arterial supply may be markedly reduced when Pa,CO,
is low (Cohn & Kountz, 1963); in this situation the uptake of lactate by the liver may be reduced. Hepatic congestion, which may be seen in the over-hydrated patient with renal failure,
might also impair lactate metabolism. An inadequate supply of thiamine is known to produce
elevations of blood pyruvate and lactate concentrations and this might occur in patients on
restricted protein diets and intermittent peritoneal dialysis.
The lactate clearance rate has been estimated from the results of intravenous lactate tolerance tests to be approximately240 g/24 h (Soffer, Dantes & Sobdtka, 1938) or 2500 mEq/24 h
(Berry, 1967). The mean intraperitoneal lactate load in the dialyses reported in the
study was 1410 mEq/24 h, which is below the estimated clearance rate. In this study a lactate
tolerance test was performed via the intraperitoneal route and was found to be normal in
patients with adequate hepatic function. In patients with decreased hepatic function lactate may
not be metabolized completely, although the liver which is the major site for lactate metabolism
S. R. Dixon et al.
has an enormous metabolic capacity. In the present study one patient with poor hepatic
function showed abnormally high blood lactate levels after dialysis, but metabolic acidosis was
corrected.
Bicarbonate ions are lost during peritoneal dialysis at the same time as lactate ions are
absorbed. If the lactate ions are metabolized normally, the bicarbonate ions lost in the peritoneal fluid would not exert a significant effect on the total body buffer. However, if none of the
lactate ions were metabolised the continued loss of bicarbonate ions could lead to a dete-rioration in the metabolic acidosis.
ACKNOWLEDGMENTS
This study was supported by a Project Grant from the New Zealand Medical Research Council.
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