Key Points
Question
Is peritonitis, a major complication of peritoneal dialysis, associated with adverse outcomes after kidney transplant?
Findings
In this large cohort study including 4957 patients with a median (IQR) follow-up duration of 6.0 (2.6-9.3) years, history of peritonitis pretransplant was significantly associated with increased risks of graft failure and death. Recent peritonitis (within 6 months before transplantation) was associated with higher risks of acute rejection and graft failure, whereas peritonitis requiring hemodialysis transfer was associated with increased risk of graft failure.
Meaning
These findings highlight the importance of comprehensive pretransplant assessment and longitudinal risk stratification among patients undergoing peritoneal dialysis followed by kidney transplant.
This cohort study examines the association between history of peritonitis and posttransplant outcomes among patients undergoing peritoneal dialysis followed by kidney transplant.
Abstract
Importance
Peritoneal dialysis (PD) is a common dialysis modality before kidney transplant. Peritonitis, a major complication of PD, may be associated with adverse posttransplant outcomes.
Objective
To examine the association between history of peritonitis and outcomes among patients undergoing PD followed by kidney transplant.
Design, Setting, and Participants
This is a retrospective cohort study of the Australia and New Zealand Dialysis and Transplant Registry. Patients who initiated PD as first kidney replacement therapy and underwent kidney transplant during 2006 to 2024 were included and followed-up from transplant until death, loss to follow-up, or December 31, 2024.
Exposures
History of peritonitis.
Main Outcomes and Measures
The primary outcomes were biopsy-proven acute rejection, death-censored graft failure, and all-cause mortality. Time-to-event outcomes were evaluated using multivariable Cox proportional hazard regression models.
Results
A total of 4957 patients (median [IQR] age, 52 [42-61] years; 2912 male [59%]) were included, with a median (IQR) follow-up duration of 6.0 (2.6-9.3) years. Patients with peritonitis (1483 patients [30%]) were more likely to have obesity, have a higher comorbidity burden with a history of smoking, longer dialysis duration, and prior treatment with continuous ambulatory PD. Multivariable Cox regression analyses showed that peritonitis history was associated with shorter time to graft failure (adjusted hazard ratio [aHR], 1.55; 95% CI, 1.26-1.90) and death (aHR, 1.25; 95% CI, 1.06-1.48), but not with acute rejection (aHR, 1.09; 95% CI, 0.94-1.25). These findings were consistent across inverse probability–weighted Cox regression analyses and Fine-Gray competing risk models. Patients with recent peritonitis (≤6 months before transplant) had significantly higher risks of acute rejection (aHR, 1.52; 95% CI, 1.22-1.88), graft failure (aHR, 2.28; 95% CI, 1.73-3.00), and death (aHR, 1.37; 95% CI, 1.04-1.80), compared with those without peritonitis history. These associations were not consistently observed among patients with more remote peritonitis. Furthermore, peritonitis resulting in transfer to hemodialysis was associated with increased risk of graft failure (aHR, 1.99; 95% CI, 1.49-2.67; reference, no peritonitis), whereas a more modest increase was observed in cases not requiring hemodialysis transfer (aHR, 1.40; 95% CI, 1.11-1.76; reference, no peritonitis).
Conclusions and Relevance
These findings suggest that a history of peritonitis is associated with increased risks of graft failure and death after kidney transplant and highlight the importance of comprehensive pretransplant assessment and longitudinal risk stratification.
Introduction
Peritoneal dialysis (PD) is a commonly used kidney replacement therapy (KRT) prior to transplant and offers several advantages, including improved quality of life, better residual kidney function preservation, and avoidance of central venous catheter–related complications.1 As a home-based dialysis modality, PD demands substantial patient engagement and adherence, traits that may also support successful posttransplant management.2,3 Consistent with this, patients undergoing PD are approximately 40% more likely to undergo kidney transplant than those undergoing hemodialysis.4 Moreover, pretransplant PD has been associated with lower risks of graft failure and delayed graft function (DGF) compared with hemodialysis.5
Peritonitis is a major complication of PD and is associated with substantial morbidity, mortality, and hemodialysis transfer.6,7 Although most episodes resolve with standard therapy and do not preclude transplant, their implications for posttransplant outcomes remain uncertain. Peritonitis induces systemic inflammation, with cytokine activation persisting beyond clinical resolution.8 These effects may extend into the peritransplant period, contributing to heightened immune activation and vulnerability. Recipients undergoing pretransplant PD have been shown to experience higher rates of posttransplant infectious complications, including peritonitis and urinary tract infection,9 which may adversely affect graft function and survival. Peritonitis is also associated with adverse nutritional and metabolic effects, including protein loss and inflammation-driven catabolism,10,11 which may further impair physiologic resilience. In addition, long-term PD and peritonitis induce structural changes in the peritoneum,12 potentially increasing susceptibility to perioperative intra-abdominal complications.13 Importantly, peritonitis may reflect adherence and/or vulnerability, encompassing not only technique-related factors but also broader influences, such as socioeconomic context, training adequacy, and vulnerability.14 These factors may persist after transplant through ongoing health behaviors, including follow-up adherence and infection prevention practices.
Despite these potential mechanisms, limited data exist regarding posttransplant outcomes among patients with a history of peritonitis. To address this knowledge gap, we aimed to investigate the association between peritonitis and graft and patient outcomes in a binational cohort of kidney transplant recipients who received PD as a first KRT treatment, using data from the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry. We hypothesized that a history of peritonitis would be associated with adverse posttransplant outcomes. Clarifying this association will provide important insights into risk stratification, patient selection, and posttransplant management strategies.
Methods
This was a retrospective cohort study using data from the ANZDATA Registry, a clinical quality registry that collects data for patients receiving KRT from every unit in Australia and New Zealand. The study protocol was reviewed and approved by the Metro South Health Human Research Ethics Committee of Queensland, Australia (HREC/2025/QMS/123747). Consent was waived because the study used deidentified data from the ANZDATA Registry, which collects data under an opt-out consent model. The study adhered to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guidelines in reporting results.15
Study Participants
Adult (aged ≥18 years) patients with kidney failure, who commenced PD as their initial KRT and subsequently underwent kidney transplant between January 1, 2006, and December 31, 2024, were included. All patients were followed-up from transplant until death, loss to follow-up, or December 31, 2024, whichever occurred first.
Patient-Level Covariates
Demographic characteristics and clinical parameters were obtained at the time of kidney transplant, including age, sex, race (via self-report), body mass index, primary kidney disease, and comorbid conditions. Data on race are included in this study as a confounder given its potential association with peritonitis and transplant outcomes. For each patient, pretransplant dialysis duration, initial PD modality, donor characteristics (age and living or deceased), induction therapy, initial maintenance immunosuppressants, and DGF occurrence immediately after transplant were retrieved.
Exposures
The primary exposure was history of PD-related peritonitis (presence or absence). PD-related peritonitis was diagnosed at each center according to International Society for Peritoneal Dialysis guidelines,16,17,18,19 with all episodes and relevant clinical data reported to the ANZDATA Registry. For clarity, the term peritonitis in this article to refers specifically to PD-related peritonitis.
Patients with a history of peritonitis were further categorized by (1) timing (>6 vs ≤6 months before transplant), (2) number of episodes (1 vs multiple), and (3) severity, defined by whether peritonitis led to hemodialysis transfer. A 6-month cut point was selected on the basis of prior evidence indicating that the elevated mortality risk associated with peritonitis in patients undergoing PD resolves by this time point.6
Outcomes
Outcomes included biopsy-proven acute rejection, death-censored graft failure, and all-cause mortality after transplant. All acute rejection episodes were included, with analyses repeated after excluding events occurring within the first 7 days after transplant. Graft failure was defined as decline in allograft function necessitating resumption of dialysis or retransplant.
Statistical Analysis
Continuous variables were summarized as mean (SD) for normally distributed data and as median (IQR) for nonnormally distributed data. The normality of the continuous variables was assessed using the Shapiro-Wilk test. Categorical variables were reported as frequencies and percentages. Baseline characteristics between 2 patient groups were compared using Mann-Whitney U test for nonnormally distributed continuous variables and χ2 tests for categorical variables.
Kaplan-Meier curves were used to estimate probabilities of acute rejection-free survival, graft survival, and patient survival across groups. Time-to-event outcomes were evaluated using multivariable Cox proportional hazard regression models. Proportional hazards assumptions were assessed using Schoenfeld residuals. DGF violated the assumption and was, therefore, included as a stratification variable. Acute rejection was defined as a time-dependent variable in Cox models for graft failure and death to mitigate immortal time bias related to first acute rejection occurrence.20 Fine-Gray subdistribution hazard regression was applied to account for the competing risk of death with a functioning graft. Inverse probability of treatment weighting based on propensity scores was applied to adjust for baseline differences between patients with and without peritonitis history. Covariate balance was assessed using standardized mean differences, with all postweighting standardized mean differences less than 0.1 (eFigure in Supplement 1). Weighted Cox models were fitted to estimate associations between peritonitis and outcomes.
These models adjusted for all plausible confounders according to clinical rationale, with history of peritonitis or peritonitis categories as exposure variables. Missing rates for covariates were less than 1% except for DGF (124 patients [3%]), and 4735 patients (96%) had complete data for all covariates. Therefore, complete-case analysis was applied for all models. Multicollinearity among covariates was evaluated using variance inflation factors, with all values less than 2. To evaluate the robustness of the associations to unmeasured confounding, E-values were calculated for point estimates and lower bounds of the 95% CIs.21
All statistical analyses were conducted using R statistical software version 4.5.1 (R Project for Statistical Computing). P < .05 was considered statistically significant.
Results
Patient Characteristics
During the study period, 4957 patients (median [IQR] age, 52 [42-61] years; 2912 [59%] male) who received PD as initial KRT underwent kidney transplant. Median (IQR) follow-up duration was 6.0 (2.6-9.3) years, with 39 patients (1%) lost to follow-up. A total of 1672 patients (34%) underwent transplant between 2006 and 2015 (median [IQR] follow-up, 11.0 years [9.3-13.4] years), 1841 (37%) did so between 2016 and 2020 (median [IQR] follow-up, 6.2 [5.0-7.5] years), and 1444 (29%) did so between 2021 and 2024 (median [IQR] follow-up, 1.7 [0.9-2.7] years).
There were 1483 patients (30%) with a history of peritonitis. Median (IQR) follow-up was 6.3 (2.7-10.0) years for patients with peritonitis and 5.9 (2.6-9.1) years for those without. Among patients with peritonitis, 326 (22%) had recent peritonitis (≤6 months before transplant), 553 (37%) had multiple episodes, and 414 (28%) experienced peritonitis resulting in hemodialysis transfer (Figure 1).
Figure 1. Flowchart of Patient Enrollment.
KRT indicates kidney replacement therapy; and PD, peritoneal dialysis.
Compared with patients without peritonitis, those with peritonitis were more likely to have obesity (416 patients [28%] vs 748 patients [22%]), have a higher comorbidity burden (diabetes, coronary artery disease, and peripheral vascular disease), more likely to have a smoking history and a longer dialysis duration (median [IQR], 3.1 [1.8-4.6] vs 1.6 [0.8-2.9] years), had greater use of continuous ambulatory PD (1094 patients [74%] vs 2252 patients [65%]), and were less likely to receive a living donor graft (249 patients [17%] vs 814 patients [23%]) (Table 1).
Table 1. Baseline Characteristics of Kidney Transplant Recipients Who Initiated PD as First Kidney Replacement Therapy, by Peritonitis History.
| Characteristic | Overall (N = 4957) | No peritonitis (n = 3474) | Peritonitis (n = 1483) | P value |
|---|---|---|---|---|
| Age group, y | ||||
| ≤40 | 1139 (23) | 815 (23) | 324 (22) | .50 |
| >40 to ≤50 | 1098 (22) | 773 (22) | 325 (22) | |
| >50 to ≤60 | 1380 (28) | 949 (27) | 431 (29) | |
| >60 | 1340 (27) | 937 (27) | 403 (27) | |
| Sex | ||||
| Male | 2912 (59) | 2057 (59) | 855 (58) | .31 |
| Female | 2045 (41) | 1417 (41) | 628 (42) | |
| Body mass indexa | ||||
| <18.5 | 143 (3) | 115 (3) | 28 (2) | <.001 |
| 18.5 to <25.0 | 1825 (37) | 1292 (38) | 533 (36) | |
| 25.0 to 30.0 | 1780 (36) | 1279 (37) | 501 (34) | |
| 30.0 to <35.0 | 854 (17) | 560 (16) | 294 (20) | |
| ≥35.0 | 310 (6) | 188 (6) | 122 (8) | |
| Race | ||||
| Asian | 979 (20) | 701 (20) | 278 (19) | <.001 |
| Aboriginal and Torres Strait Islander | 139 (3) | 71 (2) | 68 (5) | |
| Māori | 159 (3) | 73 (2) | 86 (6) | |
| Pacific Islander | 171 (4) | 102 (3) | 69 (5) | |
| White | 3280 (66) | 2362 (68) | 918 (62) | |
| Otherb | 212 (4) | 151 (4) | 61 (4) | |
| Primary kidney disease | ||||
| Diabetic nephropathy | 1015 (21) | 683 (20) | 332 (22) | .24 |
| Glomerular disease | 1871 (38) | 1318 (38) | 553 (37) | |
| Hereditary kidney disease | 742 (15) | 536 (15) | 206 (14) | |
| Hypertension and/or kidney vascular disease | 415 (8) | 297 (9) | 118 (8) | |
| Tubulointerstitial disease | 552 (11) | 380 (11) | 172 (12) | |
| Others or uncertain | 343 (7) | 246 (7) | 97 (7) | |
| Comorbidities | ||||
| Diabetes | 1336 (27) | 897 (26) | 439 (30) | .006 |
| Coronary artery diseasec | 770 (16) | 484 (14) | 286 (19) | <.001 |
| Chronic lung diseasec | 407 (8) | 269 (8) | 138 (9) | .07 |
| Cerebrovascular accidentc | 280 (6) | 192 (6) | 88 (6) | .57 |
| Peripheral vascular diseasec | 460 (9) | 295 (9) | 165 (11) | .003 |
| Smoking | ||||
| Current | 404 (8) | 243 (7) | 161 (11) | <.001 |
| Former | 1646 (34) | 1131 (33) | 515 (35) | |
| Never | 2863 (58) | 2064 (60) | 799 (54) | |
| Dialysis duration, median (IQR), y | 2.0 (1.0-3.4) | 1.6 (0.8-2.9) | 3.1 (1.8-4.6) | <.001 |
| Initial PD modality | ||||
| Automatic PD and/or intermittent PD | 1611 (32) | 1222 (35) | 389 (26) | <.001 |
| Continuous ambulatory PD | 3346 (68) | 2252 (65) | 1094 (74) | |
| Living donor transplant | 1063 (21) | 814 (23) | 249 (17) | <.001 |
| Donor age, median (IQR), y | 49 (35-59) | 49 (34-59) | 49 (36-59) | .28 |
| Delayed graft function | 918 (19) | 578 (17) | 340 (23) | <.001 |
| Immunosuppressants | ||||
| Basiliximab and/or daclizumab | 4260 (93) | 2988 (93) | 1272 (92) | .52 |
| Prednisolone | 4771 (99) | 3341 (99) | 1430 (99) | .25 |
| Mycophenolate (mycophenolate mofetil or mycophenolate sodium) | 4760 (99) | 3332 (99) | 1428 (99) | .54 |
| Calcineurin inhibitor (tacrolimus or cyclosporin A) | 4746 (99) | 3323 (99) | 1423 (98) | .45 |
Abbreviation: PD, peritoneal dialysis.
Body mass index is calculated as weight in kilograms divided by height in meters squared.
Other includes South American, sub-Saharan African, not stated, and unknown.
Refers to confirmed or suspected disease.
Acute Rejection
Overall, 1357 episodes of biopsy-proven acute rejection occurred in 1030 patients (21%), with a median (IQR) time to first rejection of 0.20 (0.02-0.83) years. The incidence of acute rejection was higher among patients with peritonitis history (5.1 vs 4.3 episodes per 100 patient-years; absolute risk difference, 0.8 episodes per 100 patient-year) (Figure 1), accompanied by shorter acute rejection-free survival (Figure 2A). In multivariable Cox regression analysis, history of peritonitis was not associated with acute rejection (adjusted hazard ratio [aHR] 1.09; 95% CI, 0.94-1.25) (Table 2) with similar results from weighted Cox regression analysis (aHR, 1.14; 95% CI, 1.00-1.30).
Figure 2. Kaplan-Meier Curves of Transplant Outcomes in Kidney Transplant Recipients Who Initiated Peritoneal Dialysis as First Kidney Replacement Therapy, Stratified by Peritonitis History.
Kaplan-Meier curves are shown for acute rejection-free probability (A), graft survival probability (B), and patient survival probability (C).
Table 2. Multivariable Cox Regression Models Assessing the Association of Peritonitis History With Transplant Outcomes.
| Variable | Acute rejection | Graft failure | Death | |||
|---|---|---|---|---|---|---|
| aHR (95% CI) | P value | aHR (95% CI) | P value | aHR (95% CI) | P value | |
| Peritonitis (reference, no peritonitis) | 1.09 (0.94-1.25) | .24 | 1.55 (1.26-1.90) | <.001 | 1.25 (1.06-1.48) | .008 |
| Age group, y (reference, >50 to ≤60) | NA | <.001 | NA | <.001 | NA | <.001 |
| ≤40 | 1.58 (1.32-1.89) | <.001 | 2.17 (1.64-2.89) | <.001 | 0.33 (0.24-0.45) | <.001 |
| >40 to ≤50 | 1.12 (0.93-1.35) | .22 | 1.54 (1.15-2.07) | .004 | 0.57 (0.44-0.73) | <.001 |
| >60 | 0.91 (0.76-1.09) | .32 | 1.16 (0.86-1.57) | .33 | 2.10 (1.76-2.51) | <.001 |
| Female sex (reference, male) | 0.94 (0.82-1.07) | .33 | 1.10 (0.90-1.35) | .33 | 0.82 (0.70-0.97) | .02 |
| Body mass index (reference, 18.5 to <25.0)a | NA | .41 | NA | .68 | NA | .16 |
| <18.5 | 0.92 (0.62-1.36) | .67 | 0.91 (0.49-1.69) | .76 | 1.74 (1.09-2.77) | .02 |
| 25.0 to 30.0 | 1.02 (0.88-1.19) | .75 | 1.07 (0.85-1.34) | .58 | 0.98 (0.82-1.17) | .79 |
| 30.0 to <35.0 | 1.13 (0.94-1.36) | .19 | 1.03 (0.77-1.37) | .85 | 1.04 (0.83-1.30) | .73 |
| ≥35.0 | 1.04 (0.80-1.36) | .76 | 1.03 (0.68-1.53) | .90 | 0.97 (0.70-1.36) | .88 |
| Race (reference, White) | NA | .62 | NA | .009 | NA | .04 |
| Asian | 0.89 (0.74-1.06) | .17 | 1.01 (0.77-1.33) | .95 | 0.72 (0.58-0.91) | .005 |
| Aboriginal and Torres Strait Islander | 0.95 (0.66-1.36) | .77 | 0.76 (0.42-1.38) | .37 | 0.85 (0.53-1.38) | .52 |
| Māori | 0.95 (0.68-1.33) | .78 | 1.11 (0.66-1.86) | .70 | 1.17 (0.80-1.71) | .41 |
| Pacific Islander | 0.94 (0.66-1.35) | .74 | 1.92 (1.23-3.01) | .004 | 0.85 (0.54-1.34) | .49 |
| Otherb | 0.82 (0.59-1.14) | .24 | 0.47 (0.25-0.89) | .02 | 0.74 (0.47-1.16) | .18 |
| Primary kidney disease (reference, glomerular disease) | NA | .009 | NA | .06 | NA | <.001 |
| Diabetic nephropathy | 1.30 (1.09-1.55) | .004 | 1.00 (0.76-1.33) | .99 | 2.31 (1.87-2.84) | <.001 |
| Hereditary kidney disease | 0.82 (0.66-1.01) | .07 | 0.64 (0.46-0.89) | .009 | 0.98 (0.77-1.26) | .89 |
| Hypertension and/or kidney vascular disease | 1.06 (0.83-1.36) | .61 | 0.79 (0.52-1.19) | .26 | 1.19 (0.90-1.57) | .23 |
| Tubulointerstitial disease | 1.15 (0.94-1.41) | .17 | 0.88 (0.65-1.19) | .41 | 0.76 (0.55-1.05) | .09 |
| Others or uncertain | 0.91 (0.69-1.20) | .52 | 0.88 (0.58-1.34) | .54 | 1.50 (1.11-2.03) | .009 |
| Comorbidities (confirmed or suspected vs none) | ||||||
| Coronary artery disease | 0.95 (0.78-1.14) | .56 | 1.22 (0.91-1.65) | .19 | 1.30 (1.08-1.56) | .006 |
| Chronic lung disease | 0.98 (0.78-1.24) | .89 | 1.12 (0.78-1.60) | .54 | 1.17 (0.92-1.49) | .19 |
| Cerebrovascular disease | 0.78 (0.57-1.06) | .12 | 0.94 (0.58-1.53) | .81 | 0.92 (0.69-1.22) | .55 |
| Peripheral vascular disease | 0.94 (0.74-1.20) | .64 | 0.83 (0.55-1.25) | .36 | 1.30 (1.04-1.63) | .02 |
| Smoking (reference, never) | NA | .03 | NA | .01 | NA | <.001 |
| Current | 1.34 (1.08-1.66) | .007 | 1.59 (1.17-2.18) | .004 | 2.13 (1.65-2.74) | <.001 |
| Former | 1.07 (0.93-1.23) | .36 | 1.18 (0.95-1.47) | .13 | 1.27 (1.08-1.50) | .004 |
| Dialysis duration, y | 1.02 (0.98-1.05) | .36 | 0.98 (0.92-1.03) | .42 | 1.06 (1.02-1.11) | .008 |
| Initial PD modality (automatic or intermittent PD vs continuous ambulatory PD) | 0.96 (0.84-1.10) | .55 | 0.91 (0.73-1.13) | .40 | 0.94 (0.79-1.12) | .48 |
| Donor age, y | 1.00 (1.00-1.01) | .08 | 1.02 (1.01-1.02) | <.001 | 1.01 (1.01-1.02) | <.001 |
| Living donor transplant (reference, no) | 1.22 (1.04-1.43) | .02 | 0.97 (0.76-1.23) | .79 | 0.87 (0.71-1.06) | .18 |
| Acute rejectionc | NA | NA | 3.72 (3.05-4.54) | <.001 | 1.47 (1.24-1.74) | <.001 |
Abbreviations: aHR, adjusted hazard ratio; NA, not applicable; PD, peritoneal dialysis.
Body mass index is calculated as weight in kilograms divided by height in meters squared.
Other includes South American, sub-Saharan African, not stated, and unknown.
Acute rejection was examined as a time-dependent variable in Cox regression models for graft failure and death. Graft failure refers to death-censored graft failure. All models were stratified by delayed graft function (yes or no).
When patients were categorized by peritonitis timing (>6 or ≤6 months pretransplant; reference, no peritonitis), there was a significant difference in risk of acute rejection (Figure 3 and eTable 1 in Supplement 1), with the highest risk among patients with recent peritonitis (aHR, 1.52; 95% CI, 1.22-1.88). The number of peritonitis episodes or peritonitis severity (requiring hemodialysis transfer) was not associated with acute rejection risk (Figure 3 and eTable 2 and eTable 3 in Supplement 1).
Figure 3. Dot Plots of Associations of Peritonitis Categories With Transplant Outcomes.
Multivariable Cox proportional hazard regression models were conducted adjusting for age, sex, body mass index, race, primary kidney disease, comorbidities, smoking, dialysis duration, initial peritoneal dialysis modality, donor age, living donor, and acute rejection (time-dependent variable, for graft failure and death). All models were stratified by delayed graft function (yes or no). aHR indicates adjusted hazard ratio.
Death-Censored Graft Failure
During follow-up, 456 death-censored graft failures (9%) occurred (median [IQR] graft survival duration, 4.0 [1.1-7.1] years), with a higher incidence (2.1 vs 1.3 episodes per 100 patient-year; absolute risk difference, 0.8 episodes per 100 patient-year) (Figure 1) and shorter graft survival (Figure 2B) in patients with peritonitis. Causes of graft failure mainly included chronic allograft nephropathy (69 patients [15%]), acute rejection (47 patients [10%]), gradual graft failure (43 patients [9%]), and chronic antibody-mediated rejection (38 patients [8%]). Multivariable Cox regression analysis showed that peritonitis history was associated with a shorter time to graft failure (aHR, 1.55; 95% CI, 1.26-1.90; E-value, 2.47; lower-bound E-value, 1.83) (Table 2). Peritonitis was associated with a higher risk of graft failure when death was considered as a competing event (subdistribution HR, 1.53; 95% CI, 1.25-1.88; E-value, 2.43; lower-bound E-value, 1.81) (eTable 4 in Supplement 1). Weighted Cox regression analysis showed similar results (aHR, 1.52; 95% CI, 1.25-1.83; E-value, 2.41; lower-bound E-value, 1.81).
Peritonitis timing was significantly associated with graft failure, with the highest risks observed in patients with recent peritonitis (aHR, 2.28; 95% CI, 1.73-3.00) (Figure 3 and eTable 1 in Supplement 1). Furthermore, peritonitis resulting in hemodialysis transfer was associated with increased risk of graft failure (aHR, 1.99; 95% CI, 1.49-2.67), whereas a more modest increase was observed in cases not requiring hemodialysis transfer (aHR, 1.40; 95% CI, 1.11-1.76) (Figure 3 and eTable 3 in Supplement 1). Increased risk was also observed across subgroups of peritonitis episode number (Figure 3 and eTable 2 in Supplement 1), with similar effect size for 1 (aHR, 1.49; 95% CI, 1.18-1.88) and multiple (aHR, 1.66; 95% CI, 1.26-2.21) episodes.
Death
Overall, 730 patients (15%) died during follow-up, with a median (IQR) patient survival duration of 5.5 (2.6-8.6) years. Cardiovascular disease was the leading cause of death (194 patients [27%]), followed by infection (162 patients [22%]) and cancer (136 patients [19%]). Mortality was higher in patients with a peritonitis history (3.0 vs 2.0 episodes per patient-year; absolute risk difference, 1.0 episodes per 100 patient-year) (Figure 1 and Figure 2C). Peritonitis history was associated with increased mortality risk in both multivariable (aHR, 1.25; 95% CI, 1.06-1.48; E-value, 1.81; lower-bound E-value, 1.31) (Table 2) and weighted Cox (aHR, 1.48; 95% CI, 1.28-1.71; E-value, 2.32; lower-bound E-value, 1.88) models.
Peritonitis categories were significantly associated with mortality (Figure 3), with consistently increased risks observed across timing (≤6 months pretransplant, aHR, 1.37; 95% CI, 1.04-1.80; >6 months pretransplant, aHR, 1.22; 95% CI, 1.01-1.46) (eTable 1 in Supplement 1), number of episodes (1 episode, aHR 1.22; 95% CI, 1.01-1.48; multiple episodes, aHR 1.31; 95% CI, 1.05-1.64) (eTable 2 in Supplement 1), and severity (requiring hemodialysis transfer, aHR 1.26; 95% CI, 0.99-1.62; without hemodialysis transfer, aHR 1.25; 95% CI, 1.04-1.50) (eTable 3 in Supplement 1). In particular, mortality was higher among patients with peritonitis requiring hemodialysis transfer compared with those without a history of peritonitis (92 patients [22%] vs 431 patients [12%]).
Sensitivity Analyses
In a sensitivity analysis excluding patients with any hemodialysis transfer, peritonitis remained significantly associated with graft failure (aHR, 1.69; 95% CI, 1.28-2.23) (eTable 5 in Supplement 1). Sensitivity analysis excluding early acute rejection events (≤7 days posttransplant) showed no significant association between peritonitis and acute rejection (eTable 6 in Supplement 1), consistent with the primary models.
Discussion
In this binational registry cohort study of 4957 kidney transplant recipients who commenced PD as their initial KRT, nearly one-third experienced peritonitis before transplant. A history of peritonitis was associated with higher risks of graft failure and mortality. Patients with recent peritonitis (≤6 months pretransplant) experienced higher risks of acute rejection and graft failure. Peritonitis necessitating hemodialysis transfer was associated with an increased risk of graft failure. Collectively, these findings suggest that both the occurrence and clinical profile of peritonitis may be associated with adverse posttransplant outcomes.
A history of peritonitis was significantly associated with increased graft failure risk after adjustment for comorbidities and dialysis-related and transplant-related confounders and remained consistent across multivariable Cox, inverse probability of treatment weighting–weighted Cox, and Fine-Gray models. In contrast, a prior study22 of 1090 pediatric transplant recipients with prior PD failed to find an association between peritonitis and graft survival. However, their results were limited by substantial missing peritonitis data (>30%).22 Moreover, the clinical implications of peritonitis in adults with higher comorbidity burdens differ from those in the pediatric population. In another study13 of 158 simultaneous pancreas-kidney transplant recipients (pretransplant dialysis modality, PD, 39 patients vs hemodialysis, 139 patients), patients receiving PD showed a higher incidence of pancreas loss due to intra-abdominal infection. Among patients receiving PD, however, the incidence of intra-abdominal infection did not differ between those with (10 patients) and without (29 patients) peritonitis history, although the interpretation of the comparison was limited by small sample size. Acute peritonitis triggers systemic inflammation, potentially heightening alloimmune responsiveness and increasing susceptibility to allograft injury.8 It may also impair nutritional and metabolic reserve, reducing physiologic resilience at the time of transplant,10,11 and induce peritoneal injury and intra-abdominal changes that may predispose to postoperative complications.12,13 These mechanisms provide biologically plausible explanations for the observed associations with poorer graft outcomes. Importantly, peritonitis may reflect adherence and/or vulnerability, including factors such as socioeconomic circumstances, housing conditions, training adequacy, and underlying immune function,23,24 all of which may influence posttransplant outcomes alongside established risks such as inadequate adherence to immunosuppressive therapy.2,3
We also found that peritonitis history was associated with shorter time to posttransplant death. However, it is important to recognize that patients with peritonitis in this cohort had a higher comorbidity burden, including diabetes, coronary artery disease, and peripheral vascular disease, and a more frequent smoking history, which have been identified as risk factors for both peritonitis and posttransplant mortality.25,26,27,28,29,30 These observations raise the possibility that highly comorbid patients may be more susceptible both to developing peritonitis and to experiencing adverse posttransplant outcomes, with additional posttransplant risk arising from peritonitis occurrence during PD.
Peritonitis within 6 months before transplant was also associated with higher risks of acute rejection and graft failure, consistent with evidence that its adverse impact on mortality is most pronounced in the early postinfection period.6 This temporal association is biologically plausible, as peritonitis induces systemic inflammatory responses that may persist beyond clinical resolution, potentially priming alloimmune activity and increasing rejection risk.8 Prior studies have reported an elevated risk of mortality following peritonitis even after apparent recovery.6 In addition, peritonitis-related catabolic stress and malnutrition may impair physiologic resilience and immune regulation.10 Recent peritonitis may also necessitate hemodialysis transfer, a transition associated with increased short-term mortality risk.31
Patients with multiple episodes of peritonitis had higher risks of graft failure and mortality, although a dose-response association between the number of episodes and transplant outcomes was not observed. Multiple episodes may reflect a more complex clinical phenotype, including increased susceptibility to infection, challenges in maintaining technique, or underlying comorbidity. Prior studies32,33 have demonstrated an episode-dependent increase in mortality and PD discontinuation, with effects persisting long term, including associations with cardiovascular mortality. Collectively, this suggests that cumulative peritonitis burden may serve as a marker of broader clinical instability, rather than an isolated complication. Peritonitis necessitating hemodialysis transfer was also associated with an increased risk of graft failure. Transition to hemodialysis often reflects more severe or treatment-refractory episodes, including recurrent or fungal peritonitis, which may disrupt peritransplant stability and contribute to poorer graft outcomes.31,34 Although mortality was higher among patients with peritonitis requiring hemodialysis transfer compared with those without a history of peritonitis (22% vs 12%), the association with death was modest, possibly reflecting the relatively small size of this subgroup.
Although age at kidney transplant did not differ between groups, age exhibited divergent associations with posttransplant outcomes. Although older patients were at an increased risk of death, young recipients had higher risks of acute rejection and graft failure. The increase in death with older age mirrors prior reports of heightened mortality risk in older transplant recipients, which may be explained by greater comorbidity and susceptibility to infectious complications.35,36,37 The inverse association between recipient age and graft outcomes observed in our study was supported by a prior study of 145 470 transplant recipients, showing that the fully adjusted risk of death-censored graft failure decreased with increasing age.38 These findings may reflect the higher competing risk of death in older recipients, and also the lower incidence of acute rejection in this age group, since immunologic aging is associated with diminished alloimmune responsiveness.39,40 Consistent with our results, previous studies have demonstrated that increasing recipient age is associated with lower risks of both T cell–mediated and antibody-mediated rejection.41,42 Living-donor transplant was associated with an increased risk of acute rejection in this study, consistent with a prior Australian study demonstrating higher rejection rates in living-donor recipients (44% vs 28%) and lower risk with deceased donation.43 Several factors may contribute to this observation. Living-donor recipients in our cohort were younger, and younger age is a well-established risk factor for acute rejection owing to a more robust alloimmune response.40,41,42 In addition, lower competing mortality in younger recipients may increase the likelihood of detecting and recording rejection episodes.
Limitations
This study is strengthened by its large, well-characterized cohort, extended follow-up, and use of robust analytical approaches, including multivariable Cox regression analyses, Fine-Gray competing risk models, and inverse probability weighting. However, several limitations merit consideration. As an observational study, residual confounding and indication bias cannot be excluded. Given the evaluation of multiple outcomes, findings should be interpreted on the basis of the overall pattern and consistency of associations rather than individual P values. Key immunological variables, including panel reactive antibody and human leukocyte antigen mismatch, were unavailable, limiting interpretation of graft-related outcomes. In addition, organism-specific effects of peritonitis could not be assessed because of missing data and heterogeneity across episodes within the same patient. The cohort was restricted to patients who underwent transplant, potentially introducing survivor bias and underestimating the impact of severe peritonitis. In addition, although peritonitis may reflect inflammation, malnutrition, and vulnerability, these mechanisms could not be directly examined because of a lack of corresponding clinical and adherence data.
Conclusions
In this large registry-based study, we demonstrated that a history of peritonitis was associated with adverse posttransplant outcomes. These findings highlight the importance of comprehensive pretransplant assessment and longitudinal risk stratification. A deeper understanding of the biological and behavioral pathways linking peritonitis to posttransplant risk will require further studies incorporating detailed clinical characteristics and objective adherence metrics. The learnings from these studies will be essential to determine whether targeted peritransplant and posttransplant interventions can mitigate these risks and ultimately improve long-term graft and patient survival.
eFigure. Standardized Mean Differences for Covariates Before and After Propensity Score Weighting for Peritonitis History
eTable 1. Multivariable Cox Regression Models Assessing the Association of Time-Stratified Peritonitis with Transplant Outcomes
eTable 2. Multivariable Cox Regression Models Assessing the Dose–Response Relationship Between Peritonitis Episodes and Transplant Outcomes
eTable 3. Multivariable Cox Regression Models Assessing the Association of Peritonitis Severity with Transplant Outcomes
eTable 4. Fine–Gray Competing Risks Regression Assessing the Association of Peritonitis History with Graft Failure (Death as a Competing Event)
eTable 5. Multivariable Cox Regression Models Assessing the Association of Peritonitis History with Transplant Outcomes After Excluding Patients with a History of HD Transfer
eTable 6. Multivariable Cox Regression Models Assessing the Association of Peritonitis History with Acute Rejection After Excluding Rejection Events Within 7 Days Post-Transplant
Data Sharing Statement
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
eFigure. Standardized Mean Differences for Covariates Before and After Propensity Score Weighting for Peritonitis History
eTable 1. Multivariable Cox Regression Models Assessing the Association of Time-Stratified Peritonitis with Transplant Outcomes
eTable 2. Multivariable Cox Regression Models Assessing the Dose–Response Relationship Between Peritonitis Episodes and Transplant Outcomes
eTable 3. Multivariable Cox Regression Models Assessing the Association of Peritonitis Severity with Transplant Outcomes
eTable 4. Fine–Gray Competing Risks Regression Assessing the Association of Peritonitis History with Graft Failure (Death as a Competing Event)
eTable 5. Multivariable Cox Regression Models Assessing the Association of Peritonitis History with Transplant Outcomes After Excluding Patients with a History of HD Transfer
eTable 6. Multivariable Cox Regression Models Assessing the Association of Peritonitis History with Acute Rejection After Excluding Rejection Events Within 7 Days Post-Transplant
Data Sharing Statement
