Peritoneal Fluid and Solute Transport: Influence of Treatment Time, Peritoneal Dialysis Modality, and Peritonitis Incidence
Andreas Fußhöller,
Sandra zur Nieden,
Bernd Grabensee and
Jörg Plum
Department of Nephrology and Rheumatology, Heinrich Heine-University, Düsseldorf, Germany.
Correspondence to: Dr. Andreas Fußhöller, Department of Nephrology and Rheumatology, Heinrich Heine-University, Moorenstrasse 5, Düsseldorf 40225, Germany. Phone: 0211-811-7726; Fax: 0211-811-7722; E-mail: plum{at}uni-duesseldorf.de
ABSTRACT. The integrity of the peritoneal membrane in peritonealdialysis (PD) is of major importance for adequate dialysis andfluid balance. However, alterations in peritoneal fluid transport,such as ultrafiltration failure, often develop during long-termPD. To investigate peritoneal solute and fluid transport andto analyze the influence of treatment time, peritonitis incidence,and PD modality (continuous ambulatory PD [CAPD] or automatedPD [APD]), a cross-sectional study with an extended peritonealtransport test that used dextran 70 in 2 L of glucose was performedin 23 nonselected chronic PD patients. Compared were long-term(>40 mo) with short-term PD patients (<40 mo), CAPD withAPD patients, and those with a peritonitis incidence of >0.25/yrto those with an incidence of <0.25/yr. Dialysate/plasma(D/P) ratio and mass transfer area coefficient of creatinine,lymphatic absorption rate (LAR), transcapillary ultrafiltration,and effective ultrafiltration were measured. Long-term PD patientshad higher D/P ratio of creatinine (73.5 ± 2.3% versus65.9 ± 2.2%; P < 0.01) and higher LAR (243 ±69 ml/4 h versus 96 ± 31 ml/4 h; P < 0.03), both resultingin lower effective ultrafiltration (242 ± 35 ml/4 h versus324 ± 30 ml/4 h; P < 0.05). D/P ratio (r = 0.66) andLAR (r = 0.67) were positively correlated to PD duration. Patientson APD compared with those on CAPD and patients with a historyof peritonitis compared with those without did not differ interms of D/P ratio, mass transfer area coefficient, LAR, transcapillaryultrafiltration, and effective ultrafiltration. Lower ultrafiltrationafter long-term PD is both the result of increased small solutetransport and increased lymphatic absorption. APD or CAPD modalityand peritonitis incidence do not have a significant influenceon small solute transport or fluid kinetics.
In peritoneal dialysis (PD), adequate peritoneal transport characteristicsand fluid kinetics are of major importance for establishingthe optimal treatment modality (1,2), and they play a pivotalrole for patient’s clinical outcome (3). Data by Davieset al. (3) showed that patients with increased small solutetransport (dialysate/plasma ratio of creatinine [D/Pcrea]) hada worse clinical outcome. D/Pcrea turned out to be an independentpredictor of death. On the basis of the individual peritonealmembrane properties, the optimal PD regimen must be found tooptimize the fluid balance and to ensure adequate clearancetargets. Both are even more important and challenging in anuricPD patients, as numerous studies have stressed (2,4,5). Datafrom the Canada-USA study (5) demonstrated that adequate totalcreatinine and urea clearance are strong predictors for thesurvival of chronic PD patients and are the basis for the clearancetargets recommended by the Dialysis Outcome Quality Initiativeguidelines (6). Optimal fluid balance is also an important factorfor patient’s clinical outcome because the incidence ofultrafiltration failure in PD, especially in anuric long-termPD patients, determines not only the system survival of PD,but also the patient’s mortality (3,7,8). Long-term PDpatients often develop an increase in small solute transportand therefore experience decreased ultrafiltration capacity.
Macromolecule transport is reported to be stable (9–12).It is hypothesized that the incidence of ultrafiltration failureand altered transport characteristics with time on PD may reflectthe chronic damage of the peritoneal membrane by the long-terminfluence of the "unphysiologic" solution (13). It is speculatedthat low pH, glucose (14), and the formation of advanced glycosylationend products (14–16) influence transcapillary and transcellular(aquaporins) water transport in PD patients (17). The importanceof glucose in this regard is underlined by the histologic findingsof diabetes-like alterations in the peritoneal capillaries ofPD patients (18–20). Although the influence of PD treatmenttime and peritonitis episodes on transport characteristics isunder debate (9,21), little is known about the influence ofthe PD modality (continuous ambulatory PD [CAPD] or automatedPD [APD]) on peritoneal transport. If the effect of pH, glucose,and advanced glycosylation end products on the peritoneal membraneand transport properties is as negative as it is speculatedto be, then it can be hypothesized that APD, with larger volumesof solution and more frequent contact times with fresh and unphysiologicdialysate, may enhance the negative effect of the solution.Because the usage of automated PD has steadily increased asa result of higher dialysis efficiency, lower rates of infections,and higher quality of life, this hypothesis is of clinical relevance(22–24).
Intraperitoneally applied dextran as a volume marker allowsthe exact calculation of peritoneal fluid kinetics (25–27).Dextran 70 is a macromolecule, and its disappearance rate correlatesto the lymphatic absorption rate (LAR). Transcapillary ultrafiltration(TCUF) is calculated from the dilution of dextran correctedfor the amount disappeared by lymphatic absorption. The finaleffective ultrafiltration is the difference of TCUF and LAR.
In this study, we calculated detailed fluid kinetics and transportproperties in chronic PD patients via an extended transportanalysis with intraperitoneal dextran 70. We subsequently investigatedperitoneal fluid kinetics in chronic PD patients and analyzedthe influence of treatment time, PD modality, and peritonitisincidence.
Patients
After providing informed consent, 23 PD patients in our unitwere subjected to an extended peritoneal transport analysis.Excluding any special selection criteria, the transport analysiswas performed within 6 mo in patients who otherwise would havehad a routine peritoneal equilibration test. The patients werestable on PD, had not changed from CAPD to APD or vice versaduring the last year, and had been free of peritonitis for atleast 3 mo before the transport analysis.
Baseline sociodemographic data and clinical characteristicsof the patients assessed in this study are listed in Table 1.Average treatment time was 43.4 ± 9 mo, and peritonitisincidence was low, at 0.25/yr. Treatment time did not differbetween APD and CAPD patients (40.3 ± 9.2 mo versus 48.2± 8.3 mo; NS) as a condition for a valid interpretationof the data. Only 2 of the 14 APD patients started PD treatmentwith CAPD for a shorter period of time (50 and 36 mo) comparedwith the final APD treatment (73 and 50 mo). At the day of transportanalysis, both of these patients were on APD for more than 4yr. The design of the study was prospective, nonrandomized,and cross sectional.
Table 1. Anthropometrical and clinical data of 23 patients investigated with an extended transport analysis for fluid kineticsa
For treatment time, the patient group was divided into 2 groupsof equal number by using the statistical median of 40 mo PDtreatment time. For peritonitis, we first compared those patientswith one or more peritonitis episodes in their history to thosewithout peritonitis episodes. Because treatment time was significantlyhigher in patients with an episode of peritonitis, we also lookedfor the peritonitis incidence, and we compared patients witha peritonitis incidence higher than the average of >0.25/yrwith those with a lower incidence (<0.25/yr) and adjustedfor equal treatment time (n = 14) by excluding patients withvery short (<20 mo) and very long treatment times (>90mo).
Methods
Patients provided written consent before the test procedurewas initiated. The permeability analysis was performed with2 L of 1.36% glucose solution (Dianeal; Baxter, Deerfield, IL)according to Krediet et al. (25) and Ho-dac-Pannekeet et al.(26). In brief, 6% dextran 70 (Longasteril; Fresenius, Bad Hamburg,Germany) in 0.9% NaCl was added to the test bag (final concentrationof 8.4 g/L) and mixed thoroughly. During the first rinsing procedure,a blood sample was taken, and 20 ml of low-molecular-weightdextran 1 (Promit; Pharmalink AB) was intravenously administeredto prevent possible anaphylactic reaction to dextran. The standardized4-h dwell with the test bag was preceded and followed by a shortrinsing bag (2 L of 1.36% glucose solution). Repetitive dialysatesampling of the test bag (at 0, 15, 60, 120, and 240 min) andfrom the effluent rinsing bag was performed; blood samples weredrawn twice (at 0 and 240 min).
Glucose was determined by the glucose oxidase-peroxidase methodand creatinine by the modified Jaffe method. Dextran was measuredvia high-performance gel-permeation liquid chromatography (28).An LC-250 isocratic pump system (Perkin-Elmer, Rodgau-Jügesheim,Germany), a Bio-Gel TSK 30 XL column (Bio-Rad, Munich, Germany),and a LC-30 refractive index detector (Perkin-Elmer) were used.Dialysate creatinine concentration was corrected for the glucoseconcentration (27). D/Pcrea and mass transfer area coefficientof creatinine (MTACcrea) were calculated (29). Fluid parameterswith TCUF, lymphatic absorption (LAR), effective ultrafiltration,and residual peritoneal volume were calculated according toKrediet et al. (25) and Imholz et al. (27). The disappearancerate of dextran as a macromolecule correlates to the lymphaticabsorption. LAR was determined from the difference between theinstilled and the recovered amount of dextran (in the test bagand in the second rinsing bag) divided by the product of meandialysate concentration and dwell time. TCUF was calculatedfrom the relative dilution of dextran corrected for the amountreabsorbed by LAR. Effective ultrafiltration was the differencebetween TCUF and LAR. Residual peritoneal volume was calculatedfrom the recovery of dextran in the second rinsing bag.
Statistical Analyses
Results are expressed as mean ± SEM. Distribution wastested to be normal. Paired and unpaired t tests were used forstatistical analysis. An alpha error at P < 0.05 was judgedto be significant. Correlations were calculated by the least-squaresmethod.
The LAR of all patients was 0.72 ± 0.24 ml/min, resultingin an average lymphatic absorption of 172 ± 59 ml duringthe 4-h dwell. TCUF was 453 ± 61 ml, and average ultrafiltrationafter 4 h was 281 ± 35 ml. D/Pcrea was 69.9 ±2.5%; average MTACcrea was 11.6 ± 0.8 ml/min (Table 2).
Table 2. Small solute transport and fluid kinetics in 23 patients investigated with an extended transport analysis using intraperitoneally administered dextrana
Treatment Time
Long-term (>40 mo) PD patients showed a significant increasein D/Pcrea (73.5 ± 2.3% versus 65.9 ± 2.2%, P= 0.01) and a trend to increased MTACcrea (12.4 ± 0.8ml/min versus 10.8 ± 0.6 ml/min, P = 0.06). They hada lower effective ultrafiltration after 4 h (242 ± 35ml/4 h versus 324 ± 30 ml/4 h, P = 0.04). Lymphatic absorptionwas significantly higher in long-term PD patients than in short-termpatients (243 ± 69 ml versus 96 ± 31 ml, P = 0.03)(Figure 1). Lymphatic absorption was well correlated to treatmenttime on PD (r = 0.67), as was D/Pcrea (r = 0.66) (both P <0.05). According to regression analysis, the D/Pcrea increasedby 2.3% and lymphatic absorption by 52.9 ml/4 h per patienttreatment year.
Figure 1. Graph illustrating fluid kinetics after treatment time on PD. Fluid kinetics of transcapillary ultrafiltration, lymphatic absorption, and effective ultrafiltration during the 4-h dwell with a 1.36% glucose solution (n = 23) are shown. Kinetics are compared for patients on peritoneal dialysis (PD) for <40 mo (dashed lines) and for >40 mo (solid lines). Significance was reached at a level of P < 0.05 for lymphatic absorption and effective ultrafiltration for PD >40 mo versus PD <40 mo. IPV, change in intraperitoneal volume.
PD Modality
APD and CAPD patients showed no significant difference concerningsmall solute transport data (D/Pcrea 69.7 ± 1.7% versus70.1 ± 1.8%; MTACcrea 11.8 ± 0.8 ml/min versus11.3 ± 0.7 ml/min). Lymphatic absorption with 149 ±58 ml/4 h versus 208 ± 58 ml/4 h and effective ultrafiltrationwith 291 ± 31 ml/4 h versus 265 ± 40 ml/4 h didnot statistically differ between APD and CAPD patients (Figure 2).
Figure 2. Graph illustrating fluid kinetics dependent on the mode of dialysis. Fluid kinetics of transcapillary ultrafiltration, lymphatic absorption, and effective ultrafiltration during the 4-h dwell with a 1.36% glucose solution (n = 23) are shown. Kinetics are compared for automated peritoneal dialysis patients (dashed lines) and continuous ambulatory peritoneal dialysis patients (solid lines); differences NS. IPV, change in intraperitoneal volume.
Peritonitis
Small solute transport was increased in patients with a historyof peritonitis. D/Pcrea was significantly increased (73.5 ±2.2% versus 67.0 ± 2.4%, P < 0.03). MTACcrea did notreach statistical significance (12.2 ± 0.8 ml/min versus11.2 ± 0.7 ml/min). Lymphatic absorption was also increasedin patients with a history of peritonitis (239 ± 69 ml/4h versus 122 ± 42 ml/4 h, P = 0.05). TCUF and effectiveultrafiltration did not differ. However, because these datawere not adjusted with regard to a longer treatment time inpatients with an episode of peritonitis (62.0 ± 9.1 moversus 29.1 ± 5.6 mo, P = 0.005), we corrected for treatmenttime on the basis of a peritonitis incidence higher or lowerthan 0.25/yr. Under these conditions, there was no differencein terms of small solute transport, lymphatic absorption, TCUF,and effective ultrafiltration (D/Pcrea 71.7 ± 1.4% versus68.8 ± 2.4%; MTACcrea 11.5 ± 0.5 ml/min versus11.3 ± 0.9 ml/min; LAR 142 ± 30 ml/4 h versus162 ± 44 ml/4 h; TCUF 411 ± 57 versus 423 ±34 ml/4 h; effective ultrafiltration 269 ± 44 versusml/4 h 261 ± 33 ml/4 h).
The risk of developing a clinically relevant ultrafiltrationfailure increases with time on PD and is assumed to be approximately35% after 6 yr (30). Four known mechanisms for ultrafiltrationfailure (10) are known. The most common reason is an increasein peritoneal transport for small solutes (type 1), resultingin a rapid loss of the osmotic gradient (9,10). More recently,the importance of the small pore, transcellular water transportby aquaporine channels (type 2) has been emphasized (14). Datademonstrate impaired aquaporine-mediated water transport inlong-term PD patients (14–16). It is speculated that thisobservation is due to the negative influence of glucose, glucosedegradation products, and especially advanced glycosylationend products on the peritoneal membrane. Findings of diabetes-likealterations in the peritoneal vessels with increasing numbersof capillaries (20) emphasize the correlation of long-term exposureto PD solution, histologically proven signs of neoangiogenesis,and increased small solute transport due to a higher effectiveperitoneal surface area. A hypopermeable peritoneum (type 3)with a loss of peritoneal surface area, typically after severeperitonitis with adhesions, or in the case of sclerosing peritonitis,is probably a rare mechanism of effective ultrafiltration failure.A poor effective ultrafiltration due to high lymphatic absorption(type 4) is also considered to be rare.
In this study, however, we were able to show that the ultrafiltrationcapacity of long-term PD patients is impaired not only as aresult of an increase in permeability for small solutes, butalso as a result of a higher LAR. Lymphatic absorption was wellcorrelated to treatment time on PD (r = 0.67). Because exactintraperitoneal fluid kinetics in chronic PD patients have hardlybeen investigated in this regard, this is a new result thatemphasizes the importance of the lymphatic absorption for thechanges of ultrafiltration capacity in general. Although thedata presented here are the result of a cross-sectional study,which may weaken the its strength to a certain extent, we believethat the data actually represent the alterations of peritonealtransport over time, rather than being the result of patientselection. The study was performed in a cross-sectional modewithin a narrow time interval, and patients were introducedto the study in a nonselected way. It is also unlikely thatthe patients with increased solute transport and lymphatic absorptionhad a positive bias concerning treatment time because they arethe patients with a higher chance of ultrafiltration failureand increased mortality on PD (3). This circumstance may thereforestrengthen our findings.
In terms of lymphatic absorption, no comparable data are availableto date on alterations during long-term PD treatment. In general,LAR was considered to be a stable parameter (10), dependingonly on the individual morphologic conditions of the lymphaticgaps of a PD patient. Acute changes in LAR have been attributedto other factors, such as the amount of intraperitoneal fillingand pressure (31,32). In this regard, the position during PDtreatment is also known to play a role: in the upright position,lymphatic absorption is slightly higher as a result of higherintra-abdominal pressure, compared with PD treatment in therecumbent position (33). On the basis of our data, one mightspeculate that a mechanical effect of long-term PD may be importantfor the increase of the lymphatic absorption in the long run.A continuously increased intraperitoneal pressure may have adilating effect on the lymphatic gaps, finally resulting inhigher lymphatic absorption after long-term treatment. Whetherlower fill volumes or the use of APD with reduced intraperitonealpressure as a result of the recumbent position during PD havea positive effect on fluid kinetics with regard to lower lymphaticabsorption is an open question. The LAR in our study—1.01± 0.23 ml/min for long-term and 0.4 ± 0.13 ml/minfor short-term PD patients—falls into the lower rangeof data provided in the literature, in which rates of 0.46 to1.37 ml/min (14,26,34) are reported. This is most likely dueto the high individual variability and the nondefined influenceof treatment time reported in the literature.
This study found that APD and CAPD patients with comparabletreatment time did not show significant differences concerningsmall solute transport, lymphatic absorption, TCUF, and effectiveultrafiltration. However, although statistical significancewas not reached, it was interesting to find that APD patientstended to have a lower lymphatic absorption compared with CAPDpatients (149 ± 58 ml/4 h versus 208 ± 58 ml/4h). When our findings are extended to a larger database, itmay turn out that statistical significance is reached. On thebasis of the data already discussed, this could support thehypothesis of a potential dilating effect of the higher intraperitonealpressure in CAPD versus APD on the peritoneal lymphatic gaps.
Concerning the influence of peritonitis (Table 2) on peritonealfluid kinetics, the data show enhanced solute transport andlymphatic absorption in patients with one or more episodes ofperitonitis in the past. However, after correction for the longertreatment time of those patients, no significant differencein terms of small solute transport and fluid kinetics were found.These data need to be interpreted with caution because therestill might be an effect of peritonitis on transport data thatcould not be detected as a result of the low overall peritonitisincidence of only 0.25/yr and the low number of events. Otherstudies reported that recurrences of peritonitis were relatedto an increase of solute transport (21).
We conclude that ultrafiltration capacity of chronic PD patientsdecreases with time on PD as a result of an increased permeabilityto small solutes as well as an increase in lymphatic absorption.PD modality (CAPD versus APD) had no statistically significantinfluence on fluid kinetics, as was found for the peritonitisincidence when corrected for treatment time.
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Received for publication April 5, 2001.
Accepted for publication October 3, 2001.
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Top
Abstract
Introduction
IPV, change in intraperitoneal volume.