Applied Nephrology
Clinically reviewed Master EditionReviewed and approved by Tariq Zayan on 6 September 2026.

Applied Peritoneal Dialysis · Master Edition

Chapter 14

Long-Term Peritoneal Membrane Failure and Encapsulating Peritoneal Sclerosis

Source integrity
377c286f6dd0
Clinical review
Tariq Zayan · 6 September 2026
Publication state
Published Master Edition

Applied Nephrology Master Series

Chapter 14

Long-Term Peritoneal Membrane Failure and Encapsulating Peritoneal Sclerosis

Membrane Trajectory | Acquired Ultrafiltration Failure | Long-Term Risk | EPS | CT Diagnosis | Nutrition | Medical Therapy | Surgery

CHAPTER MISSION Track the peritoneal membrane as a changing organ: recognise acquired transport and ultrafiltration failure before volume control collapses; separate long-term membrane dysfunction from encapsulating peritoneal sclerosis; discuss EPS risk without imposing an arbitrary PD “time limit”; recognise the post-PD risk window; diagnose EPS from the clinical–radiologic syndrome; and organise nutrition, medical therapy and expert surgery around the dominant disease phenotype.
Figure 14.1 — Long-term membrane dysfunction and EPS are related but not synonymous.
Figure 14.1 — Long-term membrane dysfunction and EPS are related but not synonymous. Acquired transport failure should trigger risk discussion and shared decision-making, but most patients with long PD exposure or membrane dysfunction do not develop EPS.
MASTER PRINCIPLE Follow the TRAJECTORY, not the CLOCK. Long PD duration raises EPS risk, but there is no evidence-based duration at which every patient should stop PD. The decisive questions are whether membrane function is deteriorating, whether clinical goals remain achievable, whether new gastrointestinal symptoms suggest EPS, and what alternative kidney-replacement options fit the person.

0. One-page chapter map

Table 14.1 — The eight decisions that govern long-term membrane and EPS care.

Decision Core question Bedside output
1. Trajectory Is membrane function stable, adapting, or progressively deteriorating? Named functional trajectory
2. Mechanism Is the problem fast PSTR, low osmotic conductance, non-membrane fluid loss, or mixed? Mechanism of low UF
3. Risk Does long PD exposure plus membrane/inflammatory history meaningfully raise EPS concern? Individualized risk discussion
4. Symptoms Are there recurrent obstructive, inflammatory or nutritional gastrointestinal signals? EPS suspicion level
5. Imaging Does CT show bowel encapsulation/tethering and characteristic peritoneal abnormalities? Clinical–radiologic synthesis
6. Support Is there intestinal failure, malnutrition, sepsis or another immediate threat? Nutrition + acute-care plan
7. Treat Is the phenotype inflammatory, fibrotic/obstructive, or mixed? Medical / surgical strategy
8. Transition Can PD remain safe, or is planned modality change required? Shared modality plan + follow-up

Learning outcomes

EVIDENCE POSTURE The current ISPD guideline repository still lists the 2017 position paper on length of time on PD and EPS as the dedicated EPS guidance. It concludes that EPS is rare, risk increases with longer PD exposure, discussion is reasonable around years 3–4, and there is insufficient evidence for a single maximum PD duration. The 2021 ISPD membrane-dysfunction recommendations provide current functional thresholds and explicitly state that acquired intrinsic membrane injury during prolonged PD should trigger discussion of EPS risk and modality transition. Diagnostic, pharmacologic and surgical EPS evidence remains dominated by observational cohorts, registries and expert-centre experience; no randomized trial establishes corticosteroid, tamoxifen or surgical timing as a universal standard. [1–8]

1. Core concept: membrane failure and EPS are related—but not the same disease

Long-term PD changes the peritoneal membrane. Some patients develop faster small-solute transport, reduced glucose-driven ultrafiltration, diminished free-water transport or a progressively less efficient membrane. These functional changes matter because they can threaten sodium-volume control and increase glucose exposure. They are not, by themselves, encapsulating peritoneal sclerosis. EPS is a distinct clinical syndrome in which a fibrotic/neo-membranous process encapsulates bowel and produces recurrent or progressive intestinal obstruction, inflammation and nutritional failure. [1–4]

Table 14.2 — Do not collapse these three entities into one.

Entity What it means What it does NOT mean
Long-term membrane remodeling Structural and functional change with prolonged PD exposure Inevitable technique failure or EPS
Acquired membrane dysfunction Measured transport/UF abnormality developing over time A diagnosis of EPS
EPS Clinical syndrome of bowel encapsulation/obstruction with characteristic imaging/context Any long PD vintage, calcification or fast transporter status
BEDSIDE TRANSLATION A declining sodium dip or worsening UF can identify an injured membrane that deserves a modality-risk discussion. It cannot diagnose the fibrous bowel-cocoon syndrome of EPS.

2. Long-term membrane remodeling: repeated injury changes both vessels and interstitium

Figure 14.2 — Repeated inflammatory and dialysate-related exposures can increase effective vascular surface area, angiogenesis and vasculopathy while fibrosis thickens the interstitial barrier.
Figure 14.2 — Repeated inflammatory and dialysate-related exposures can increase effective vascular surface area, angiogenesis and vasculopathy while fibrosis thickens the interstitial barrier. The functional result may be rapid dissipation of glucose osmotic force, poor ultrafiltration and reduced free-water transport. [2,4,9]

The pathobiology is not a simple linear “mesothelium becomes scar” story. Long-term exposure to glucose and glucose-degradation products, episodes of peritoneal inflammation, uremic biology, angiogenesis and vasculopathy all interact. Contemporary Japanese pathologic work also emphasizes that established EPS may involve formation of a fibrin-rich neo-membrane over an injured peritoneal surface rather than merely an extreme degree of ordinary peritoneal sclerosis. [4,9]

Table 14.3 — Mechanism → functional consequence → clinical signal.

Mechanism Functional consequence Bedside signal
Inflammation / increased vascular surface area Faster PSTR; rapid glucose absorption Long glucose dwells lose osmotic force early
Angiogenesis / vasculopathy Altered effective capillary exchange Transport phenotype changes over time
Interstitial fibrosis Lower osmotic conductance to glucose Low UF despite strong glucose gradient
Reduced effective free-water transport Blunted early sodium dilution Small/absent 1-h sodium dip
Persistent fibrin/inflammatory response in susceptible patient Neo-membrane, adhesions, encapsulation Obstructive EPS phenotype
MECHANISM DISCIPLINE Peritoneal fibrosis is biologically important, but neither fibrosis nor calcification alone is synonymous with EPS. EPS is defined clinically by the bowel-encapsulating syndrome.

3. Functional surveillance: measure change when the clinical trajectory changes

Figure 14.3 — Membrane surveillance begins with a clinical signal, then separates delivery/mechanical causes from transport biology.
Figure 14.3 — Membrane surveillance begins with a clinical signal, then separates delivery/mechanical causes from transport biology. A single PET label should never substitute for longitudinal clinical interpretation.

ISPD recommends characterizing PSTR with a 4-hour PET early in PD and subsequently when clinically indicated. Long-term surveillance becomes particularly important when a previously stable prescription no longer controls volume, when glucose exposure rises, when daily UF falls, or when membrane behavior appears to have changed. [2]

Table 14.4 — Long-term membrane surveillance signals.

Signal What to measure/check Interpretive caution
Falling net UF Delivered prescription, drain completeness, leaks, daily UF, PET UF capacity Low UF is not automatically membrane failure
Increasing hypertonic glucose use Sodium intake, RKF trend, PSTR, long-dwell strategy Prescription escalation can mask the mechanism
New fast PSTR Inflammation/peritonitis history, PET trend Fast PSTR can be acquired or transient
Blunted sodium dip High-glucose PET with 1-h sodium measurement Reduced FWT can reflect fibrosis but is not EPS-specific
Congestion despite adherence Total sodium/water balance + membrane testing Chapter 8 differential still applies
SERIAL RULE A change from the patient’s own previous membrane behavior is often more clinically informative than a one-time transporter label.

4. Acquired intrinsic ultrafiltration insufficiency: when the membrane itself is failing

The 2021 ISPD membrane recommendations define low UF capacity as a valuable screening phenotype. Insufficient UF should be suspected when net UF from a 4-hour PET is <400 mL using 3.86% glucose/4.25% dextrose or <100 mL using 2.27% glucose/2.5% dextrose, and/or when daily UF cannot maintain adequate fluid status. These thresholds identify low UF capacity; they do not by themselves specify the mechanism. [2]

When intrinsic membrane dysfunction is suspected, ISPD recommends supplementing the 4-hour high-glucose PET with a 1-hour sodium dip. A sodium dip ≤5 mmol/L and/or sodium sieving ratio ≤0.03 at 1 hour indicates UF insufficiency due to impaired free-water/osmotic conductance physiology. Acquired intrinsic dysfunction developing after years on PD—particularly when residual kidney function is absent—should prompt discussion of the risks of continuing PD, including EPS, versus transition to another modality. [2]

Table 14.5 — ISPD functional anchors that belong in long-term PD review.

Measure Current ISPD anchor Clinical meaning
4-h UF, 3.86% glucose/4.25% dextrose <400 mL Low UF capacity; search mechanism
4-h UF, 2.27% glucose/2.5% dextrose <100 mL Low UF capacity; search mechanism
1-h sodium dip, high-glucose PET ≤5 mmol/L Supports intrinsic UF insufficiency
1-h sodium sieving ratio ≤0.03 Supports intrinsic UF insufficiency
Daily UF unable to maintain fluid status Clinical practice point Low UF capacity may be clinically important even beyond test thresholds
DO NOT SHORT-CIRCUIT Before calling a membrane intrinsically failed, exclude catheter dysfunction, leak, incomplete drainage, excessive sodium/fluid intake, prescription mismatch and increased fluid absorption. Chapter 8 remains the UF-failure diagnostic pathway.

5. EPS risk: duration matters—but there is no stopwatch rule

EPS is strongly associated with prolonged PD exposure, and incidence rises with PD vintage. The 2017 ISPD position paper emphasizes that EPS remains uncommon and that the majority of long-term PD patients do not develop it. The paper found insufficient evidence to support a single maximum safe duration of PD. It specifically argues against withholding or stopping PD solely because a clock threshold has been reached. [1]

A 2022 meta-analysis of 10 studies (12,595 participants) found associations with longer PD duration, higher transporter status, longer peritonitis duration, younger age at PD onset and glomerulonephritis history; the evidence is observational and does not create a validated individual prediction score. [5]

Table 14.6 — EPS risk factors: use for context, not deterministic prediction.

Factor Evidence signal How to use it
Longer PD duration Most consistent epidemiologic association Raises vigilance; does not set an automatic stop date
Acquired fast PSTR / low FWT Associated with long-term membrane injury and EPS risk in observational studies Prompts functional review and shared decision
Prolonged/severe peritonitis burden Associated in observational data Strengthens concern when membrane function also deteriorates
PD discontinuation / post-transplant period Many cases present after PD stops Continue symptom vigilance after modality change
Younger age at PD onset / GN history Meta-analysis associations Context only; not actionable thresholds
RISK LANGUAGE Say “risk is higher” rather than “EPS is developing” unless the patient has the clinical–radiologic syndrome.

6. When to discuss EPS and modality transition

The ISPD 2017 position paper recommends that EPS should be discussed with patients on long-term PD—not necessarily when PD starts, but reasonably around years 3–4—so that future choices are anticipated rather than presented during a crisis. The discussion should integrate prognosis, PD duration, dialysis quality, UF/volume control, peritonitis frequency, transplant access, HD risks and the patient’s quality-of-life priorities. [1]

Table 14.7 — The long-term PD shared-decision conversation.

Domain Question Why it changes the decision
Membrane Is function stable or progressively deteriorating? Progressive intrinsic dysfunction may make continued PD less safe/effective
Clinical goals Can sodium-volume and biochemical goals still be achieved? Technique viability is clinical, not just historical
Peritonitis history Is there repeated/prolonged inflammatory injury? Adds membrane and EPS concern
Transplant Is transplantation likely soon? Competing pathway may dominate timing
HD feasibility Vascular access, haemodynamic tolerance, home-HD options? Alternative modality risk matters
Patient goals What burden/trade-off is acceptable? No evidence justifies a one-size-fits-all stop rule
SHARED DECISION RULE Do not use EPS fear to force an otherwise well patient off PD. Do not use patient preference to ignore progressive inability to achieve safe volume control. Both risk and benefit belong in the same conversation.

7. After PD stops: the risk conversation is not over

EPS commonly becomes clinically apparent after PD has been discontinued, either after transfer to haemodialysis or following kidney transplantation. In a European multicentre study, post-transplant EPS and classical EPS were histologically similar; diagnosis occurred earlier after PD cessation in the post-transplant group. This reinforces an important practical rule: stopping PD does not instantly remove EPS risk. [6,10]

Table 14.8 — Post-PD vigilance.

Situation What to remember Clinical response
Transferred to HD after long PD EPS may present months or later after stopping Educate about GI symptoms; investigate promptly
Kidney transplant after long PD Post-transplant EPS is recognized Do not attribute vomiting/weight loss automatically to drugs/infection
Acquired UF failure before stopping Higher-risk membrane phenotype Document trajectory in handover
Asymptomatic former PD patient No validated routine CT/biomarker screening standard Clinical vigilance rather than indiscriminate imaging
HANDOVER PEARL When a long-vintage PD patient transfers to transplant or HD, include “prior PD duration + membrane trajectory + EPS vigilance” in the receiving-team handover.

8. The EPS clinical syndrome: think bowel obstruction, inflammation and nutritional decline

EPS most often presents as a gastrointestinal syndrome rather than as a dialysis-number abnormality. Common features include recurrent or progressive abdominal pain, anorexia, nausea, vomiting, early satiety, weight loss and episodes of partial or complete bowel obstruction. Hemoperitoneum, ascites or sterile inflammatory episodes may occur. Malnutrition is not merely a consequence; it is a major determinant of outcome. [3,4,7]

Table 14.9 — EPS bedside phenotypes.

Phenotype Typical clues Urgency
Prodromal/inflammatory Anorexia, weight loss, abdominal pain, inflammatory markers, ascites Early specialist assessment
Intermittent obstruction Recurrent vomiting/distension, episodic constipation/obstruction CT + surgical/nutrition MDT
Fixed obstruction Persistent vomiting, dilated bowel, inability to tolerate intake Urgent intestinal-failure/surgical pathway
Complicated disease Sepsis, ischemia, perforation, fistula, severe cachexia Emergency surgical/critical-care pathway
CLINICAL TRIGGER In a current or former long-term PD patient, recurrent “subacute bowel obstruction” is EPS until the diagnosis has been seriously considered.

9. Diagnosis: symptoms create the question; CT tests it

Figure 14.4 — EPS is diagnosed by synthesizing the obstructive/inflammatory clinical syndrome with characteristic abdominal CT findings and the PD context.
Figure 14.4 — EPS is diagnosed by synthesizing the obstructive/inflammatory clinical syndrome with characteristic abdominal CT findings and the PD context. Histology may support difficult cases but routine diagnostic surgery/biopsy is not required.

No blood test diagnoses EPS. Biomarkers such as CA-125, IL-6, PAI-1 and free-water transport have shown research signals in small case-control cohorts, but no validated screening strategy is recommended for routine asymptomatic surveillance. CT is the principal imaging modality when EPS is clinically suspected. [3,8,11]

Table 14.10 — Diagnostic sequence for suspected EPS.

Step Data required Interpretation
1. Clinical syndrome Obstructive symptoms, weight loss, inflammatory features, prior PD history Defines pre-test probability
2. Safety screen Sepsis, perforation, ischemia, severe dehydration/malnutrition Determines urgent pathway
3. CT abdomen/pelvis Peritoneal + bowel + fluid findings Confirms characteristic pattern / alternative diagnosis
4. Multidisciplinary synthesis Nephrology + radiology + surgery + nutrition Determines treatment phenotype
5. Histology/laparotomy Only when obtained for clinical/surgical reasons or diagnosis remains uncertain Supportive—not a routine screening test
SCREENING BOUNDARY A CT scan can support diagnosis in symptomatic patients. Routine serial CT of every long-term asymptomatic PD patient is not an established prevention strategy.

10. CT pattern: diagnose the constellation, not one calcified line

Experienced radiologists identify EPS from a combination of findings. In the classic case-control study, peritoneal enhancement, thickening and calcification; adhesions/tethering of bowel loops; signs of obstruction; and loculated/septated fluid were more frequent in EPS than in long-term PD controls. Contemporary radiology reviews continue to regard CT as the imaging modality of choice. [8,12]

Table 14.11 — CT findings that support EPS.

CT feature What it represents Important caution
Bowel tethering/clustering/encapsulation Fibrous cocoon/adhesive process Most meaningful when symptoms fit
Peritoneal thickening/enhancement Inflammatory/fibrotic membrane change Not specific alone
Peritoneal calcification Chronic peritoneal injury Can exist without clinical EPS
Loculated/septated ascites Adhesive compartmentalization Also occurs in infection/other disease
Bowel wall thickening/dilatation Obstruction/inflammatory consequence Assess ischemia/perforation when severe
Transition points / obstruction Mechanical consequence of encasement Drives surgical urgency
RADIOLOGY PEARL The highest-value CT question is not “Is there calcification?” It is “Is there a bowel-encapsulating adhesive pattern that explains this patient’s obstructive syndrome?”

11. Differential diagnosis: not every long-vintage PD obstruction is EPS

Table 14.12 — Major EPS mimics.

Alternative Clues How to separate
Adhesive small-bowel obstruction after surgery Prior abdominal surgery; focal transition point CT pattern lacks diffuse encapsulating process
Peritoneal carcinomatosis Cancer history, nodularity, masses, ascites Imaging/biopsy where indicated
Tuberculous peritonitis Exposure/risk, fever, lymphadenopathy, ascites Microbiology/histology; can itself cause sclerosing peritonitis
Active bacterial/fungal peritonitis Cloudy effluent, PMN/culture pattern, systemic infection Chapter 10 pathway
Mesenteric ischemia Pain severity, lactate/vascular clues, acute deterioration Emergency vascular/surgical assessment
Medication / transplant GI toxicity Temporal drug relation, diarrhea rather than obstruction Medication/infectious work-up
Malignancy-related obstruction Mass/transition point/weight loss CT + oncologic evaluation
DIAGNOSTIC HUMILITY EPS is uncommon. In a patient with acute focal peritonism, severe sepsis or a clear focal transition point, pursue the dangerous alternative diagnosis in parallel rather than forcing the EPS label.

12. Immediate management when EPS is strongly suspected or diagnosed

Management begins with stabilization and removal of continuing peritoneal injury, not with a reflex drug prescription. Patients with established EPS generally require transition away from PD, correction of fluid/electrolyte abnormalities, early nutrition support and multidisciplinary assessment. Infection, ischemia and perforation must be excluded or treated. Exact catheter timing and replacement KRT planning depend on whether peritonitis, transplantation or other access issues coexist. [3,7]

Table 14.13 — First management bundle.

Domain Immediate task Why
Kidney replacement Plan non-PD KRT if PD is still ongoing Avoid continued peritoneal exposure in established syndrome
Bowel Assess degree of obstruction and decompression needs Determines medical vs surgical urgency
Nutrition Dietitian/intestinal-failure assessment early Malnutrition strongly affects outcome
Fluid/electrolytes Correct dehydration, K/Mg/P and acid–base abnormalities Vomiting/poor intake create rapid deficits
Infection Culture/image when indicated; treat sepsis Infection can mimic/complicate EPS
Specialist referral Experienced EPS surgical + nephrology centre Outcome depends on multidisciplinary expertise
FIRST-DAY RULE Treat EPS as an intestinal-failure disease occurring in a kidney-replacement patient—not merely as “another PD complication.”

13. Nutrition is core treatment—not supportive decoration

Reduced oral intake, vomiting, chronic inflammation and recurrent obstruction can produce severe protein-energy wasting and intestinal failure. Contemporary EPS reviews consistently identify malnutrition as a major driver of mortality. Enteral nutrition is preferred when the gut can be used safely; parenteral nutrition may be required when obstruction prevents adequate enteral intake and is particularly important for preoperative optimization in advanced disease. [3,7,13]

Table 14.14 — Nutrition reasoning in EPS.

Problem Clinical consequence Management direction
Early satiety / intermittent obstruction Falling intake before obvious cachexia Early dietitian + energy/protein plan
Persistent vomiting / fixed obstruction Inability to meet needs enterally Intestinal-failure team; parenteral nutrition when appropriate
Severe weight loss / sarcopenia Higher operative/infectious risk Optimize before elective surgery when feasible
Refeeding after prolonged undernutrition P/K/Mg shifts and fluid complications Controlled refeeding + biochemical monitoring
Postoperative bowel recovery Prolonged nutritional vulnerability Continue enteral/parenteral support until intake adequate
CROSS-REFERENCE Chapter 15 develops protein-energy wasting, dietary assessment and metabolic health in PD. In EPS, the extra priority is intestinal-failure physiology and preoperative nutrition.

14. Medical therapy: plausible biology, low-certainty evidence

No randomized controlled trial establishes a universal pharmacologic regimen for EPS. Corticosteroids have been used most often when inflammatory activity is prominent, based on case series and expert practice. Tamoxifen is used for its antifibrotic effects; a Dutch multicentre retrospective study associated tamoxifen exposure with lower mortality, but confounding and treatment-selection bias remain substantial. Other immunosuppressive or antifibrotic therapies lack sufficient evidence for routine use. [3,7,14]

Table 14.15 — Medical therapy evidence calibration.

Therapy Where it may fit Evidence boundary / safety
Corticosteroids Inflammatory phenotype after infection excluded Observational evidence; infection, diabetes and catabolic risks
Tamoxifen Fibrotic/mixed phenotype in selected patients Observational evidence; thromboembolic/endometrial and other risks require individualized assessment
Combination therapy Sometimes used when phenotype overlaps No trial proves superiority
Other immunosuppression Only selected specialist contexts / another indication Not routine EPS standard
Routine prophylactic drug therapy in asymptomatic high-risk PD Not established No validated preventive pharmacologic standard
EVIDENCE CALIBRATION “Commonly used” does not mean “proven.” In EPS, pharmacologic treatment should be framed as specialist, phenotype-guided therapy supported mainly by observational evidence.

15. Surgery: fixed obstruction is an anatomical problem

Advanced EPS with persistent or recurrent mechanical bowel obstruction often requires surgical enterolysis, with removal/dissection of the encapsulating fibrotic membrane and peritonectomy as appropriate. This is complex high-risk surgery: inadvertent enterotomy, fistula, sepsis, recurrent obstruction and reoperation are recognized complications. Outcomes are best reported from specialist centres with large accumulated experience. [7,15]

In the 24-year Japanese single-centre series, 243 patients underwent surgery and long-term survival improved compared with older historical expectations, supporting the modern principle that surgery should not be dismissed as futile. These results reflect exceptional expertise and should not be generalized to low-volume centres. [15]

Table 14.16 — When surgical referral becomes central.

Clinical problem Why surgery enters the pathway Operational principle
Persistent complete or recurrent obstruction Fixed mechanical encasement is unlikely to resolve with medication alone Refer early to experienced EPS surgeon
Progressive nutritional failure from obstruction Anatomy prevents adequate intake Optimize nutrition before surgery when feasible
Recurrent admissions despite conservative therapy Disease burden remains uncontrolled Expert enterolysis assessment
Ischemia/perforation/acute abdomen Life-threatening bowel complication Emergency surgery; EPS expertise if possible
Mild inflammatory symptoms without fixed obstruction Potential medical/nutritional window Avoid premature high-risk surgery
SURGICAL PEARL The mistake is not only operating too early. It is also referring too late, after repeated obstruction has produced profound malnutrition and sepsis risk.

16. Prevention and risk reduction: protect the membrane without promising prevention

No intervention has been proven in randomized trials to prevent EPS. The ISPD position paper nevertheless supports risk-reduction logic that aligns with high-quality PD practice: minimize unnecessary glucose exposure without compromising volume control; prevent and promptly treat peritonitis; monitor membrane function; use icodextrin and optimized dwell architecture when appropriate; and avoid continuing PD simply to preserve modality identity when the membrane can no longer achieve safe goals. [1,2]

Table 14.17 — Practical risk-reduction strategy.

Strategy Rationale Do not overclaim
Minimize unnecessary hypertonic glucose Reduces chronic metabolic/membrane exposure Not proven to prevent EPS
Optimize long dwell with icodextrin when indicated May reduce glucose burden and improve UF Not an EPS prophylactic drug
Prevent peritonitis Reduces repeated inflammatory hits Not all peritonitis has equal EPS risk
Serial membrane review when clinically indicated Detects acquired dysfunction No validated EPS screening schedule
Shared modality transition when PD goals fail Avoids unsafe prolonged exposure No universal year-based stop rule
Use more biocompatible solutions where available Observational/biological rationale; Japanese experience suggests lower severity/incidence Not definitive causal trial evidence
PREVENTION LANGUAGE The correct promise is “reduce avoidable membrane stress and detect deterioration early,” not “this prevents EPS.”

17. Long-term follow-up after diagnosis: measure recovery in patient-important terms

Treatment response should be assessed through symptom burden, obstructive events, oral/enteral tolerance, weight and muscle trajectory, inflammatory/infectious complications, need for parenteral nutrition, imaging when clinically useful and the ability to sustain the chosen kidney-replacement modality. CT appearance alone is not the therapeutic endpoint.

Table 14.18 — EPS follow-up dashboard.

Domain What to track Escalation trigger
Obstruction Vomiting, distension, admissions, bowel movements Persistent/recurrent obstruction
Nutrition Weight trajectory, intake, sarcopenia, micronutrients/electrolytes Progressive nutritional failure
Inflammation/infection Clinical sepsis/inflammation, catheter history if present New infection or persistent inflammatory state
Treatment toxicity Steroid/tamoxifen adverse effects where used Risk exceeds likely benefit
Imaging CT when symptoms/management require it Progressive obstruction/complication
KRT HD/transplant function, vascular access, volume control Modality instability
OUTCOME RULE A patient who eats, gains strength and remains free of obstruction is improving even if the CT is not “normal.”

18. Major clinical algorithms

Flowchart 14.1 — Long-term membrane dysfunction.
Flowchart 14.1 — Long-term membrane dysfunction. First exclude non-membrane causes of low UF, then use PET/UF capacity and sodium-dip physiology to identify fast PSTR versus acquired intrinsic dysfunction. [2]
Flowchart 14.2 — Suspected EPS.
Flowchart 14.2 — Suspected EPS. Compatible gastrointestinal symptoms in a current or former long-term PD patient trigger safety assessment and CT; characteristic imaging plus the syndrome activates the multidisciplinary EPS pathway.
Flowchart 14.3 — EPS management architecture.
Flowchart 14.3 — EPS management architecture. Nutrition, medical treatment and surgery are complementary streams selected according to obstruction, inflammation, fibrosis and patient fitness; evidence for drug therapy is low certainty.
Flowchart 14.4 — After PD discontinuation.
Flowchart 14.4 — After PD discontinuation. EPS can present after transfer to HD or kidney transplantation; asymptomatic former PD patients do not have an established routine CT/biomarker screening standard, but new GI symptoms require prompt evaluation.

19. Retention tables: pattern recognition

Table 14.19 — If you see this, think this first.

Finding First hypothesis Immediate action
Rising glucose requirement + falling UF Acquired membrane dysfunction or non-membrane fluid problem Chapter 8 differential + PET when indicated
4-h high-glucose PET UF <400 mL Low UF capacity Identify fast PSTR vs intrinsic dysfunction vs non-membrane cause
1-h sodium dip ≤5 mmol/L Impaired free-water/osmotic conductance physiology Discuss acquired intrinsic dysfunction if new/progressive
Long PD vintage but clinically well Higher EPS risk, not EPS Shared discussion; no automatic stop date
Recurrent vomiting + weight loss after PD stopped Possible EPS CT + urgent multidisciplinary assessment
Calcification on CT without symptoms Chronic peritoneal injury; not diagnostic alone Interpret in clinical context
Fixed recurrent bowel obstruction + cocooning CT Advanced EPS phenotype Nutrition + expert surgical referral
Asymptomatic high-risk patient asks for “screening CT” No validated routine strategy Explain limits; monitor clinically/functionally

Table 14.20 — What not to confuse.

Do not confuse With Correction
Long PD duration A diagnosis of EPS Duration is risk context only
Fast PSTR EPS Fast transport has many causes
Low UF capacity Intrinsic membrane failure Exclude leak/catheter/prescription/fluid absorption
Low sodium dip Bowel encapsulation It measures FWT physiology, not EPS anatomy
Peritoneal calcification EPS by itself Diagnosis requires syndrome + imaging constellation
Stopping PD Eliminating EPS risk Post-PD EPS is well recognized
Tamoxifen/corticosteroid use Evidence-based cure Evidence is observational
Parenteral nutrition Failure of treatment Often essential intestinal-failure support

20. Clinical pearls

21. Common pitfalls — and the correction

Table 14.21 — High-frequency errors in long-term membrane/EPS care.

Pitfall Why it fails Correction
Stopping PD automatically at year 5 No evidence supports a universal clock rule Use individualized function, risk and alternatives
Calling fast transport “pre-EPS” Poor specificity Separate transport phenotype from EPS syndrome
Diagnosing EPS from calcification alone Calcification is not specific Require compatible symptoms + imaging pattern
Escalating dextrose indefinitely for falling UF May worsen exposure while hiding membrane failure Re-diagnose mechanism; discuss modality transition
Forgetting post-transplant EPS Symptoms misattributed to drugs/infection Keep EPS in differential after PD cessation
Routine biomarkers as screening tests Not validated for clinical screening Use research tests only in appropriate settings
Waiting for complete obstruction before referral Allows malnutrition and frailty to progress Refer early when recurrent obstruction develops
Treating with steroids before excluding infection Can worsen occult infection Exclude/treat infection first
Presenting tamoxifen as proven therapy Observational evidence only Shared specialist decision with adverse-effect review
Viewing parenteral nutrition as “support only” Underestimates intestinal failure Treat nutrition as core management

22. Mini-cases: decisions, not trivia

Case 1 — The long-vintage patient who is still doing well

A 58-year-old has completed 6 years of PD. Volume control is good, PET pattern is stable, peritonitis burden is low and the patient strongly prefers PD.

BEST NEXT STEP Do not transfer solely because of duration. Discuss EPS as a long-term risk, document shared decision-making, continue clinically indicated membrane surveillance and preserve alternative modality planning.

Case 2 — Rising glucose requirement

A patient on PD for 7 years needs progressively stronger glucose to maintain the same UF. Mechanical causes and sodium intake have been addressed.

BEST NEXT STEP Perform structured membrane reassessment. If acquired intrinsic UF insufficiency is confirmed, discuss the risks/benefits of continued PD versus transition rather than simply escalating glucose indefinitely.

Case 3 — Blunted sodium dip

A high-glucose PET shows UF <400 mL at 4 h and a 1-h sodium dip of 3 mmol/L.

BEST NEXT STEP This supports low UF capacity with intrinsic membrane dysfunction physiology. It does not diagnose EPS. Integrate the longitudinal trajectory, volume control, RKF and modality options, and discuss EPS risk in context.

Case 4 — Vomiting after transplantation

Six months after kidney transplantation, a former long-term PD patient develops recurrent vomiting, early satiety and 8-kg weight loss.

BEST NEXT STEP Post-PD/post-transplant EPS must be considered. Obtain urgent clinical and CT assessment rather than attributing the syndrome solely to mycophenolate or infection.

Case 5 — Calcification without symptoms

CT performed for another reason shows peritoneal calcification in an asymptomatic former PD patient.

BEST NEXT STEP Calcification alone is not EPS. Review PD history and symptoms, but do not diagnose the syndrome without compatible clinical/radiologic features.

Case 6 — Inflammatory EPS phenotype

A patient with characteristic CT findings has abdominal pain, inflammatory features and progressive anorexia but no fixed complete obstruction. Infection has been excluded.

BEST NEXT STEP Activate the multidisciplinary EPS pathway: stop ongoing PD exposure if still present, optimize nutrition and consider specialist phenotype-guided medical therapy; evidence for corticosteroids/tamoxifen is observational.

Case 7 — Recurrent fixed obstruction

Despite nutritional and medical management, the patient has repeated admissions with obstructive symptoms and cannot sustain enteral intake.

BEST NEXT STEP Refer to an experienced EPS surgical centre for enterolysis/peritonectomy assessment while optimizing nutrition and correcting electrolyte deficits.

Case 8 — “Can you screen me every year?”

An asymptomatic patient with 8 years of PD asks for annual CT and effluent biomarkers to make sure EPS is not developing.

BEST NEXT STEP Explain that no routine CT/biomarker screening strategy is validated. Use clinical vigilance, membrane trajectory and shared decision-making; investigate promptly if symptoms or function change.

23. Active recall

MUST MEMORIZE

Table 14.22 — Core facts.

Prompt Answer
Long-term membrane dysfunction = EPS? No. They are related but distinct.
ISPD maximum safe PD duration? None established.
When is EPS discussion reasonable? Around years 3–4 of long-term PD, then individualized thereafter.
4-h high-glucose PET low-UF threshold? <400 mL using 3.86% glucose/4.25% dextrose.
4-h 2.27% glucose/2.5% dextrose low-UF threshold? <100 mL.
1-h sodium dip indicating intrinsic UF insufficiency? ≤5 mmol/L.
1-h sodium sieving ratio anchor? ≤0.03.
Does low sodium dip diagnose EPS? No.
Core EPS clinical phenotype? Recurrent/progressive bowel obstruction with pain, vomiting, anorexia/weight loss ± inflammation.
Principal imaging test? CT abdomen/pelvis.
Classic CT constellation? Peritoneal thickening/enhancement/calcification + bowel tethering/encapsulation + loculation/obstruction.
Routine asymptomatic CT/biomarker screening? Not established.
Can EPS present after PD stops? Yes—after HD transfer or transplantation.
Most important supportive treatment? Early nutrition/intestinal-failure support.
Corticosteroids/tamoxifen evidence level? Observational/low certainty.
When is surgery central? Persistent/recurrent fixed obstruction or advanced fibrotic disease in an expert centre.

USE AS REFERENCE

24. Flashcards: spaced repetition

1. Q: What is the key difference between membrane dysfunction and EPS? A: Membrane dysfunction is a transport/UF phenotype; EPS is a bowel-encapsulating obstructive clinical syndrome.

2. Q: Does ISPD recommend stopping PD after a fixed number of years? A: No.

3. Q: When should long-term EPS risk be discussed? A: Reasonably around 3–4 years of PD and revisited as circumstances change.

4. Q: Low UF on 4-h 3.86%/4.25% PET? A: <400 mL.

5. Q: Low UF on 4-h 2.27%/2.5% PET? A: <100 mL.

6. Q: Intrinsic UF dysfunction: sodium dip? A: ≤5 mmol/L at 1 h on high-glucose PET.

7. Q: Intrinsic UF dysfunction: sodium sieving ratio? A: ≤0.03 at 1 h.

8. Q: What does a blunted sodium dip measure? A: Reduced free-water/osmotic conductance physiology—not EPS anatomy.

9. Q: Core EPS symptom cluster? A: Pain, anorexia, nausea/vomiting, weight loss and recurrent/complete bowel obstruction.

10. Q: Best imaging test? A: CT abdomen/pelvis.

11. Q: Is peritoneal calcification diagnostic? A: No.

12. Q: Can EPS appear after kidney transplantation? A: Yes.

13. Q: Routine annual CT in asymptomatic long-term PD? A: Not established.

14. Q: Routine effluent biomarkers for screening? A: Not established.

15. Q: Why is nutrition central? A: Obstruction and inflammation cause intestinal failure and malnutrition, which drive morbidity/mortality.

16. Q: Corticosteroid evidence? A: Low-certainty observational; considered mainly for inflammatory phenotype after infection excluded.

17. Q: Tamoxifen evidence? A: Observational and conflicting; specialist selective use.

18. Q: When to refer for surgery? A: Persistent/recurrent obstruction, progressive nutritional failure or advanced fibrotic disease.

19. Q: Why expert surgery? A: Enterolysis/peritonectomy is complex with risks of enterotomy, fistula, sepsis and recurrence.

20. Q: Final mental model? A: Trajectory → membrane phenotype → individualized risk → GI symptoms → CT → nutrition/medical/surgery → reassess.

25. Rapid differential / troubleshooting

Table 14.23 — Long-term membrane/EPS troubleshooting from problem to action.

Problem Differential First actions
Falling UF Fast PSTR; low OCG; leak; catheter; increased absorption; sodium excess Verify delivery/mechanics + PET/UF capacity when indicated
High glucose dependence RKF loss; sodium excess; fast PSTR; intrinsic dysfunction Do not just increase glucose; localize mechanism
Fast PSTR after peritonitis Inflammatory change vs chronic remodeling Repeat when clinically appropriate; optimize dwell architecture
Long PD duration, no symptoms Risk context only Shared discussion; no automatic modality transfer
Anorexia/weight loss after PD stopped EPS; malignancy; drug toxicity; infection CT + broad differential
Recurrent partial SBO EPS; adhesions; malignancy CT pattern + surgical review
Peritoneal calcification Chronic injury vs EPS Look for symptoms + encapsulation/tethering
Elevated inflammatory markers EPS inflammation vs infection Exclude infection and other inflammatory causes
Severe malnutrition EPS intestinal failure; PEW; malignancy/infection Dietitian + intestinal-failure team; consider parenteral support
No response to medical therapy Fixed fibrosis/obstruction or wrong diagnosis Reassess imaging/diagnosis; expert surgical referral

26. Final revision sheet

CORE CONCEPT Long-term PD should be managed as a changing membrane trajectory. Acquired intrinsic UF dysfunction raises concern and may justify modality transition, but EPS is a separate clinical–radiologic bowel-encapsulation syndrome. No fixed PD duration prevents EPS; diagnosis depends on symptoms + CT; treatment depends on nutrition, disease phenotype and expert surgery when obstruction is fixed.

Table 14.24 — One-minute revision.

Domain Must remember
Long-term PD Risk rises with time; no universal stop year
Low UF capacity <400 mL on 4-h 3.86%/4.25% PET or <100 mL on 2.27%/2.5% PET
Intrinsic dysfunction 1-h sodium dip ≤5 mmol/L and/or sodium sieving ratio ≤0.03
EPS discussion Reasonable around PD years 3–4; individualize thereafter
EPS syndrome Bowel encapsulation/obstruction + pain/vomiting/anorexia/weight loss ± inflammation
Post-PD risk EPS may present after HD transfer or kidney transplantation
Diagnosis Clinical syndrome + characteristic CT; biomarkers not routine screening
CT pattern Encapsulation/tethering + peritoneal change + loculation/obstruction
Nutrition Core treatment; parenteral support when intestinal failure prevents adequate intake
Medical therapy Corticosteroids/tamoxifen may be considered selectively; evidence observational
Surgery Expert enterolysis/peritonectomy for persistent/recurrent obstruction
Prevention Reduce avoidable membrane stress; prevent inflammation; monitor function; no guarantee of EPS prevention
TEN TAKE-HOME RULES 1) Membrane failure is not EPS. 2) Follow trajectory, not clock. 3) No fixed maximum PD duration is evidence based. 4) Acquired low OCG/falling FWT should trigger risk and modality discussion. 5) EPS can present after PD stops. 6) Recurrent bowel obstruction + weight loss is the key clinical signal. 7) CT diagnoses the pattern; calcification alone does not. 8) No validated routine CT/biomarker screening strategy exists. 9) Nutrition is central treatment. 10) Fixed obstruction belongs in an experienced EPS surgical pathway.

Table 14.25 — One-minute bedside synthesis.

If you see… Think… Do now…
Long PD + stable function Higher risk but clinically viable PD Discuss EPS risk; continue individualized PD
Falling UF + blunted sodium dip Acquired intrinsic membrane dysfunction Discuss continuation vs modality transition
Vomiting + weight loss after transplant Post-PD EPS possible CT + multidisciplinary assessment
Calcification only Chronic injury, not necessarily EPS Correlate clinically
Cocooning + obstruction Established EPS phenotype Nutrition + specialist medical/surgical plan
Severe malnutrition Intestinal failure Urgent nutrition support
Persistent obstruction despite conservative care Fixed fibrotic disease Expert enterolysis referral
FINAL MENTAL MODEL Long-term exposure → membrane trajectory → functional testing when indicated → acquired dysfunction? → individualized EPS-risk discussion → GI symptoms? → CT syndrome → nutrition + phenotype-guided medical therapy + expert surgery when needed → patient-important recovery.

Rapid oral viva

SAFETY BOUNDARY This chapter teaches longitudinal membrane reasoning and EPS diagnostic/management architecture. Exact drug doses, duration of corticosteroid/tamoxifen therapy, anticoagulation implications, parenteral-nutrition formulation, refeeding protocols, operative timing/technique and catheter-removal timing require specialist protocols and individualized multidisciplinary assessment. Acute obstruction, perforation, ischemia and sepsis override routine outpatient PD logic.

27. Selected authoritative references

1. Brown EA, Bargman J, van Biesen W, et al. Length of Time on Peritoneal Dialysis and Encapsulating Peritoneal Sclerosis—Position Paper for ISPD: 2017 Update. Perit Dial Int. 2017;37(4):362–374. https://doi.org/10.3747/pdi.2017.00018. PMID: 28676507.

2. Morelle J, Stachowska-Pietka J, Öberg C, et al. ISPD recommendations for the evaluation of peritoneal membrane dysfunction in adults: classification, measurement, interpretation and rationale for intervention. Perit Dial Int. 2021;41(4):352–372. https://doi.org/10.1177/0896860820982218. PMID: 33563110.

3. Pepereke S, Shah AD, Brown EA. Encapsulating peritoneal sclerosis: Your questions answered. Perit Dial Int. 2023;43(2):119–127. https://doi.org/10.1177/08968608221125606. PMID: 36189954.

4. Nakayama M, Miyazaki M, Hamada C, Ito Y, Honda K; Peritoneal Biopsy Study Group of the Japanese Society for Peritoneal Dialysis. Pathophysiology of encapsulating peritoneal sclerosis: lessons from findings of the past three decades in Japan. Clin Exp Nephrol. 2023;27(9):717–727. https://doi.org/10.1007/s10157-023-02360-y. PMID: 37278945.

5. Li D, Li Y, Zeng H, Wu Y. Risk factors for Encapsulating Peritoneal Sclerosis in patients undergoing peritoneal dialysis: A meta-analysis. PLoS One. 2022;17(3):e0265584. https://doi.org/10.1371/journal.pone.0265584. PMID: 35312717.

6. Latus J, Habib SM, Kitterer D, et al. Histological and clinical findings in patients with post-transplantation and classical encapsulating peritoneal sclerosis: a European multicenter study. PLoS One. 2014;9(8):e106511. https://doi.org/10.1371/journal.pone.0106511. PMID: 25171219.

7. Jagirdar RM, Bozikas A, Zarogiannis SG, Bartosova M, Schmitt CP, Liakopoulos V. Encapsulating Peritoneal Sclerosis: Pathophysiology and Current Treatment Options. Int J Mol Sci. 2019;20(22):5765. https://doi.org/10.3390/ijms20225765. PMID: 31744097.

8. Srisajjakul S, Prapaisilp P, Bangchokdee S. Imaging pearls and differential diagnosis of encapsulating peritoneal sclerosis: Emphasis on computed tomography. Clin Imaging. 2023;94:116–124. https://doi.org/10.1016/j.clinimag.2022.12.001. PMID: 36527797.

9. Wang Y, Zhang J, Ma X, et al. Mechanisms underlying the involvement of peritoneal macrophages in the pathogenesis and novel therapeutic strategies for dialysis-induced peritoneal fibrosis. Front Immunol. 2024. PMID: 39749340.

10. Davenport A. Late presentation of encapsulating peritoneal sclerosis following renal transplantation and the potential under-reporting of the incidence and prevalence of encapsulating peritoneal sclerosis. Nephrology (Carlton). 2015;20(7):499–501. https://doi.org/10.1111/nep.12477. PMID: 26063486.

11. Lopes Barreto D, Sampimon DE, Struijk DG, Krediet RT. Early Detection of Imminent Encapsulating Peritoneal Sclerosis: Free Water Transport, Selected Effluent Proteins, or Both? Perit Dial Int. 2019;39(1):83–89. https://doi.org/10.3747/pdi.2017.00194. PMID: 30478138.

12. Vlijm A, Stoker J, Bipat S, et al. Computed tomographic findings characteristic for encapsulating peritoneal sclerosis: a case-control study. Perit Dial Int. 2009;29(5):517–522. https://doi.org/10.1177/089686080902900508. PMID: 19776044.

13. Danford CJ, Lin SC, Smith MP, Wolf JL. Encapsulating peritoneal sclerosis. World J Gastroenterol. 2018;24(28):3101–3111. https://doi.org/10.3748/wjg.v24.i28.3101. PMID: 30065556.

14. Korte MR, Fieren MWJA, Sampimon DE, Lingsma HF, Weimar W, Betjes MGH; Dutch Multicentre EPS Study. Tamoxifen is associated with lower mortality of encapsulating peritoneal sclerosis: results of the Dutch Multicentre EPS Study. Nephrol Dial Transplant. 2011;26(2):691–697. https://doi.org/10.1093/ndt/gfq362. PMID: 20584735.

15. Kawanishi H, Banshodani M, Yamashita M, Shintaku S, Dohi K. Surgical Treatment for Encapsulating Peritoneal Sclerosis: 24 Years’ Experience. Perit Dial Int. 2019;39(2):169–174. https://doi.org/10.3747/pdi.2018.00042. PMID: 29991561.

16. Brown EA, Van Biesen W, Finkelstein FO, et al. Length of time on peritoneal dialysis and encapsulating peritoneal sclerosis: position paper for ISPD. Perit Dial Int. 2009;29(6):595–600. PMID: 19910558.

17. Vlijm A, van Schuppen J, Lamers AB, Struijk DG, Krediet RT. Imaging in encapsulating peritoneal sclerosis. NDT Plus. 2011;4(4):281–284. https://doi.org/10.1093/ndtplus/sfr068.

18. Blake PG, Bargman JM. Peritoneal dialysis: long-term membrane complications and encapsulating peritoneal sclerosis. In: Brenner & Rector’s The Kidney. 12th ed. Elsevier; 2024.

SOURCE NOTE ISPD guideline status and contemporary EPS/membrane evidence were checked 3 September 2026. The 2017 ISPD EPS position paper remains the dedicated EPS guidance listed by ISPD; the 2021 membrane-dysfunction recommendations provide the current functional testing framework. Because EPS treatment evidence remains largely observational, this chapter deliberately avoids presenting drug doses, treatment durations, CT-screening schedules or operative timing as universal standards.