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Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis

Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis
Literature review current through: Jan 2024.
This topic last updated: Apr 19, 2022.

INTRODUCTION — Peritonitis is a common complication of peritoneal dialysis. Peritonitis is associated with significant morbidity, catheter loss, transfer to hemodialysis, transient loss of ultrafiltration, possible permanent membrane damage, and occasionally death [1-6].

This topic reviews the clinical presentation and diagnosis of peritonitis in patients undergoing peritoneal dialysis. Most of the discussion relates to the presentation and diagnosis of bacterial peritonitis, although a few specific issues unique to fungal and tuberculosis peritonitis are also addressed. Prevention and treatment are discussed separately. (See "Risk factors and prevention of peritonitis in peritoneal dialysis" and "Microbiology and therapy of peritonitis in peritoneal dialysis" and "Fungal peritonitis in peritoneal dialysis".)

CAUSES — Among peritoneal dialysis patients, peritonitis may be directly related to peritoneal dialysis or secondary to a nondialysis-related intra-abdominal or systemic process. Most cases are peritoneal dialysis-related. In one review, nondialysis-related causes were responsible for less than 6 percent of cases of peritonitis in chronic ambulatory peritoneal dialysis (CAPD) patients [7].

Peritoneal dialysis-related — Peritoneal dialysis-related peritonitis is either due to contamination with pathogenic skin bacteria during exchanges (ie, touch contamination), or to an exit-site or tunnel infection. (See "Peritoneal catheter exit-site and tunnel infections in peritoneal dialysis in adults", section on 'Prognosis'.)

Secondary peritonitis — Secondary peritonitis is caused by underlying pathology of the gastrointestinal tract and occasionally (albeit rarely) due to hematogenous spread (ie, following dental procedures).

Causes of secondary peritonitis include cholecystitis, appendicitis, ruptured diverticulum, treatment of severe constipation, bowel perforation, bowel ischemia, and incarcerated hernia. Secondary peritonitis may also be caused by seeding from the blood or vagina, but this is less common compared with the intra-abdominal causes listed above.

Secondary peritonitis may occur after endoscopic or other invasive procedures [8-11].

Secondary peritonitis is often associated with a worse prognosis than dialysis-related peritonitis [12-14]. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Prognosis'.)

CLINICAL PRESENTATION — The most common symptoms of peritonitis among peritoneal dialysis patients are abdominal pain and cloudy peritoneal effluent [15,16]. Other symptoms include fever, nausea, and diarrhea.

Historical reviews of peritonitis among peritoneal dialysis patients reported the following frequency of symptoms and signs [15,16]:

Abdominal pain – 79 to 88 percent

Fever (greater than 37.5ºC) – 29 to 53 percent

Nausea or vomiting – 31 to 51 percent

Cloudy effluent – 84 percent

Hypotension – 18 percent

The onset of pain and the appearance of cloudy fluid may not occur at the same time. In some cases, pain is the presenting symptom and the dialysate fluid is initially clear, becoming cloudy after the next exchange or on the next day [17].

In contrast to chronic ambulatory peritoneal dialysis (CAPD), patients undergoing automated peritoneal dialysis (APD) commonly present without a history of cloudy fluid. APD uses a cycler to perform multiple overnight exchanges that drain into the toilet, sink, or bathtub while the patient sleeps, rather than into a bag as in CAPD. As a result, patients may not notice that the dialysate is cloudy. (See "Evaluating patients for chronic peritoneal dialysis and selection of modality", section on 'Available modalities'.)

The severity of abdominal pain varies with the culprit organism [17,18]. Streptococcal and fungal peritonitis are associated with particularly severe pain. However, the character of the abdominal pain is not specific and cannot be differentiated from other causes of abdominal pain.

Physical exam reveals abdominal tenderness and rebound tenderness, though guarding is rarely present. Occasionally systemic signs of sepsis, including hypotension, may be present.

The physical examination may reveal the likely cause of peritonitis. Patients with secondary peritonitis are more likely to have systemic manifestations of sepsis [19]. There may be more precise localization of pain or tenderness among patients with specific underlying pathology resulting in secondary peritonitis [20].

Patients with secondary peritonitis may demonstrate feculent material in the drained dialysate.  

EVALUATION — To evaluate possible peritonitis, the peritoneal fluid should be sent for cell count and differential, gram stain and culture. Among patients who are febrile or appear septic, we also check a complete blood count and blood cultures. Radiographic studies are not routinely performed [20].

Peritoneal fluid analysis — To evaluate possible peritonitis, the peritoneal fluid should be sent for cell count and differential, gram stain, and culture.

Method for obtaining peritoneal fluid — Special techniques improve the yield when obtaining peritoneal fluid for gram stain and culture and from patients using automated peritoneal dialysis.

An optimal technique for culturing peritoneal fluid among chronic ambulatory peritoneal dialysis (CAPD) and automated peritoneal dialysis (APD) patients is the combination of sediment culturing of 50 mL effluent and bedside inoculation of 3 to 5 mL of effluent dialysate in each of two blood culture bottles [8].

To perform sediment culturing, 50 mL of dialysate fluid is centrifuged at 3000 g (ie, relative centrifugal force) for 15 minutes and the supernatant decanted off. The sediment is resuspended in 3 to 5 mL of sterile saline, and the suspension is inoculated on solid culture medium and into standard blood culture bottles, which should be expeditiously transported to the microbiology laboratory. This method has been shown to be that most likely to identify the causative organism [21-23]. The solid media may be incubated in aerobic, microaerobic, and anaerobic environments. This technique generally results in a culture-negative rate of 20 percent or less.

To enhance the recovery of peritoneal cells among automated peritoneal dialysis (APD) patients who do not use a daytime exchange, we generally infuse 1 liter of dialysate and allow it to dwell for a minimum of two hours; the dialysate is then drained and examined for turbidity and sent for cell count and cell differential, and culture [20].

Cell count and differential — The major laboratory finding in bacterial peritonitis is an increase in the peritoneal fluid leukocyte count, usually to above 100 cells/mm3. By comparison, peritoneal dialysis patients without peritonitis typically have fewer than 8 leukocytes/mm3 in the peritoneal fluid [24]. Among patients with a peritoneal fluid leukocyte count that is elevated but not above 100 cells/mm3, we treat patients as having peritonitis if more than 50 percent of the leukocytes are neutrophils [18,25].

Approximately 10 percent of peritoneal dialysis patients with bacterial peritonitis have dialysate white cell counts below 100/mm3. A low white cell count with peritonitis is usually due to a short dwell time, as is observed among patients on APD. A poor host immune response may also cause a delayed or diminished increase in the peritoneal fluid white cell count [26].

Neither the number of white cells nor the differential is useful in predicting the causative micro-organism [27]. Increased lymphocytes may be seen with fungal and mycobacterial infections [28] although neutrophils usually predominate even in these infections [29-32]. A predominance of eosinophils may also be observed in bacterial peritonitis. In one review of 42 cases of eosinophilic peritonitis, 20 were culture negative and 22 had a bacterial pathogen identified [33]. There was no difference in the spectrum of bacterial pathogens identified between patients with eosinophilic bacterial peritonitis and those with noneosinophilic bacterial peritonitis. Among patients with eosinophilic nonbacterial peritonitis, compared with eosinophilic bacterial peritonitis, there was a slight statistical but clinically insignificant increase in the percentage of blood and dialysate eosinophil counts on initial presentation.  

Gram stain and culture — Peritoneal fluid culture is positive in approximately 80 to 95 percent of peritonitis cases provided that proper culture technique is followed [15,18,20].

The organisms that are cultured from peritoneal fluid are generally different in peritoneal dialysis-related and secondary peritonitis. In peritoneal dialysis-related peritonitis, gram-positive organisms (usually coagulase-negative Staphylococcus species) are the most common organisms, whereas enteric organisms (such as Bacteroides) or culture of multiple organisms are often observed in secondary peritonitis. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Microbiology'.)

The gram stain is usually negative; however, the identification of any organisms is a helpful guide to therapy since the Gram stain is predictive of the culture results [27]. Gram stain may be particularly useful in the early diagnosis of fungal peritonitis.

Culture of exit site — Culture of any purulent drainage from the exit site should be performed since isolation of the same organism as from peritoneal fluid suggests that the exit-site infection may be the cause of peritonitis. (See "Peritoneal catheter exit-site and tunnel infections in peritoneal dialysis in adults".)

Blood cultures and complete blood count (CBC) — Among patients who are febrile or appear septic, we check blood cultures and complete blood count, although we do not perform these tests in the absence of fever or signs of sepsis. In the absence of fever or signs of sepsis, blood cultures are generally negative among patients with both PD-related and secondary peritonitis [34].

A peripheral leukocytosis of 10,000 to 15,000/mm3 is often seen.

When to suspect secondary peritonitis — The culture of multiple enteric organisms suggests secondary peritonitis from a gastrointestinal source, including the possibility of a perforated viscus. For such patients, imaging and additional analysis of serum and peritoneal fluid are required.

At our center, we obtain peritoneal fluid amylase levels when secondary causes of peritonitis are suspected. Peritoneal fluid amylase levels are low (usually less than 10 to 15 international units/L) in the absence of peritonitis and only minimally elevated in bacterial peritonitis (<50 international units/L). However, among patients with secondary peritonitis (perforated viscus, pancreatitis), peritoneal fluid amylase levels can be >50 international units/L and are often in the range of 500 to 1000 international units/L [35]. If secondary peritonitis is suspected, then surgical consultation should be obtained.

Aspects of peritoneal dialysis that may complicate assessment of secondary peritonitis include the following:

Free air is commonly observed on imaging of PD patients in the absence of perforation.

Icodextrin dialysate decreases serum and peritoneal fluid amylase levels [36].  

The evaluation of secondary peritonitis is discussed elsewhere. (See "Spontaneous bacterial peritonitis in adults: Diagnosis", section on 'Distinguishing spontaneous from secondary bacterial peritonitis'.)

Unresolving, recurring, or relapsing peritonitis suggests a catheter or tunnel infection. (See "Peritoneal catheter exit-site and tunnel infections in peritoneal dialysis in adults", section on 'Routine monitoring' and "Peritoneal catheter exit-site and tunnel infections in peritoneal dialysis in adults", section on 'Treatment'.)

DIAGNOSIS

Presumptive diagnosis — Because untreated bacterial peritonitis is associated with morbidity and mortality, a presumptive diagnosis is made as quickly as possible and the patient is treated empirically pending confirmation of the diagnosis. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Antimicrobial therapy'.)

The diagnosis of peritonitis should be suspected in a peritoneal dialysis patient with abdominal pain or cloudy effluent. Patients with cloudy effluent should be presumed to have peritonitis, even in the absence of other findings on history and physical. Such patients should be empirically treated until the diagnosis is confirmed or excluded [8]. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Antimicrobial therapy'.)

In patients on automated peritoneal dialysis (APD), a presumptive diagnosis may be made in the presence of greater than 50 percent polymorphonuclear cells (PMNs), independent of the absolute white cell count [18,20]. The total white cell count is often low in APD patients with peritonitis because of the rapid exchanges and short dwell times, as described above. (See 'Cell count and differential' above.)

Among patients who are not on APD (ie, chronic ambulatory peritoneal dialysis [CAPD] patients), a presumptive diagnosis of peritonitis may also be made if there is a consistent clinical history and physical exam, even if the peritoneal leukocyte count is low (especially if >50 percent of the leucocytes are neutrophils), providing other causes of abdominal pathology have been excluded. This is because a small percentage of CAPD patients with infectious peritonitis do not have cloudy effluent, and it is important to make an early presumptive diagnosis of peritonitis and initiate antibiotics in order to prevent serious sequelae.

In this setting, clinical judgment is essential. Some clinicians would observe such a patient in clinic for a few hours and repeat the cell count and differential. In many such cases, the dialysate becomes cloudy on subsequent exchanges. During this observation period, the patient should be closely monitored and antibiotics initiated if signs, symptoms, and a repeat cell count are consistent with peritonitis. If this observation period cannot be conducted, the patient should be presumed to have peritonitis and empiric antibiotics initiated. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Initial empiric therapy'.)

Confirmed diagnosis — The diagnosis of peritonitis is confirmed by a positive dialysate culture. The culture is positive in approximately 80 to 95 percent of cases if proper culture technique is followed [15,18,20]. (See 'Method for obtaining peritoneal fluid' above.)  

If the dialysate effluent culture is negative but clinical signs and symptoms are otherwise consistent, a diagnosis of peritonitis may still be made. Peritonitis should be diagnosed if two or more of following are present [8]:

Consistent clinical features (abdominal pain or cloudy effluent).

Peritoneal fluid white count is greater than 100 cells/mm3 (or 0.1 x 109/L after dwell time of at least two hours) and the percentage of neutrophils is greater than 50 percent.

Positive effluent culture.

If the patient truly has an infectious cause of peritonitis, the culture may be negative for one or more of the following reasons:

The culture is obtained early in the course, before colony counts are high enough for isolation.

Microbiologic culture technique is incorrect, usually consisting of the collection of too little effluent [37].

Antibiotics are present, having been given for other reasons and not appreciated at the time of culturing [37,38].

If cultures are negative after three to five days, peritoneal dialysis fluid should be sent for repeat cell count and differential and fungal and mycobacterial cultures [8].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of peritonitis in peritoneal dialysis patients includes all the causes of abdominal pain without peritonitis in the general population and all the causes of noninfectious cloudy peritoneal fluid in the absence of or with variable amounts of abdominal pain.

Abdominal pain — The differential diagnosis is extensive among patients with abdominal pain and unremarkable peritoneal dialysate fluid. In these instances, one must evaluate for other causes of gastrointestinal pathology, particularly including pancreatitis, which, like peritonitis, may cause cloudy peritoneal fluid. (See "Causes of abdominal pain in adults".)

Cloudy peritoneal effluent — Multiple conditions may cause cloudy effluent. The differential diagnosis can be narrowed based upon analysis of the effluent. Conditions that cause cloudy effluent may be classified according to noncellular or cellular substance.

Noncellular — The following conditions should be considered among patients who have cloudy effluent but few cells [39,40]:

Excessive fibrin production. This may occur at initiation of peritoneal dialysis and occasionally after peritonitis. Excessive fibrin may be recognized by the appearance of filaments that eventually form a clot in the dialysis bag [39].

Effluent was obtained after a prolonged period of peritoneal rest (ie, no peritoneal dialysis or "dry" abdomen).

There is triglyceride or lipid leakage (chylous ascites). This could be related to lymphatic obstruction due to malignancy (especially lymphoma), acute pancreatis, superior vena cava syndrome, and has been reported with the use of dihydropyridine calcium channel blockers [41-44]. The presence of lipids can frequently be verified with inspection by an experienced clinician. The fluid can also be sent for triglyceride and/or lipid analysis.

Severe constipation and a prolonged dwell time [39-41].

Cellular — A cloudy effluent may be caused by a large number of cells of any type in the absence or presence of infection. Among patients with cloudy effluent, the predominant cell type is generally quickly identified by cellular analysis of the fluid. Cellular causes of cloudy effluent may be classified based upon the type of cell:

Atypical cells – Lymphoma or other malignancy.

Neutrophils – In addition to bacterial infection, exposure to certain drugs (amphotericin, vancomycin), renal cell carcinoma [40,45,46], pancreatitis and other retroperitoneal disease, leukemia, intra-abdominal disease, lymphoma [40], and icodextrin dialysate [47-50].

Eosinophils – In addition to bacterial infection, fungal and viral infections, allergic reactions, drug effects (such as vancomycin), early after catheter placement as a result of CO2 insufflation during laparoscopy, following peritonitis [51,52], icodextrin dialysate [33,47-50], intraperitoneal vancomycin [51-53].

Monocytes – In addition to bacterial infection, mycobacterial infection, and icodextrin dialysate.

Erythrocytes – Trauma during placement of the dialysis catheter and gynecologic disorders, ovulation, or menses. Bloody dialysate can occasionally occur with routine infectious peritonitis. (See "Bloody peritoneal dialysate (hemoperitoneum)".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dialysis".)

SUMMARY AND RECOMMENDATIONS

Causes of peritonitis – Among patients on peritoneal dialysis (PD), peritonitis may be directly related to peritoneal dialysis (ie, due to contamination with pathogenic skin bacteria during exchanges or to an exit-site or tunnel infection), or secondary to a nondialysis-related intra-abdominal or systemic process. Most cases are peritoneal dialysis-related. (See 'Causes' above.)

Clinical presentation – The most common symptoms are abdominal pain and cloudy peritoneal effluent. Exceptions are patients undergoing automated peritoneal dialysis (APD) who often do not state that they have had cloudy fluid. Among all patients, physical exam reveals abdominal tenderness, rebound tenderness, and occasionally systemic signs, including hypotension. (See 'Clinical presentation' above.)

Evaluation – Among all patients on PD who are suspected of having peritonitis, the peritoneal fluid should be sent for cell count and differential, gram stain and culture. Culture of any purulent drainage from the exit site should be performed.

If the patient is febrile or appears septic, we also check a complete blood count (CBC) and blood cultures. (See 'Evaluation' above.)

Diagnosis

Patients with cloudy effluent should be presumed to have peritonitis, even in the absence of other findings on history and physical. Such patients should be empirically treated until the diagnosis is confirmed or excluded. (See 'Presumptive diagnosis' above and "Microbiology and therapy of peritonitis in peritoneal dialysis".)

Peritonitis should be diagnosed if two or more of following are present:

-Consistent clinical features (abdominal pain or cloudy effluent).

-Peritoneal fluid white count is greater than 100 cells/mm3 (or 0.1 x 109/L after dwell time of at least two hours) and the percentage of neutrophils is greater than 50 percent.

-Positive effluent culture.

The diagnosis of peritonitis is confirmed by a positive dialysate culture. (See 'Diagnosis' above.)

Differential diagnosis – The differential diagnosis of peritonitis in peritoneal dialysis patients includes all the causes of abdominal pain without peritonitis in the general population and all the causes of cloudy peritoneal fluid in the absence of or with variable amounts of abdominal pain. (See 'Differential diagnosis' above.)

  1. Holley JL, Praino BM. Complications of peritoneal dialysis: Diagnosis and management. Semin Dial 1990; 3:245.
  2. Schreiber M, Burkart JM, et al. Peritonitis remains the leading cause of transfer from PD to HD (abstract). Perit Dial Int 1996.
  3. Woodrow G, Turney JH, Brownjohn AM. Technique failure in peritoneal dialysis and its impact on patient survival. Perit Dial Int 1997; 17:360.
  4. Pérez Fontan M, Rodríguez-Carmona A, García-Naveiro R, et al. Peritonitis-related mortality in patients undergoing chronic peritoneal dialysis. Perit Dial Int 2005; 25:274.
  5. Sipahioglu MH, Aybal A, Unal A, et al. Patient and technique survival and factors affecting mortality on peritoneal dialysis in Turkey: 12 years' experience in a single center. Perit Dial Int 2008; 28:238.
  6. Bunke CM, Brier ME, Golper TA. Outcomes of single organism peritonitis in peritoneal dialysis: gram negatives versus gram positives in the Network 9 Peritonitis Study. Kidney Int 1997; 52:524.
  7. Tzamaloukas AH, Obermiller LE, Gibel LJ, et al. Peritonitis associated with intra-abdominal pathology in continuous ambulatory peritoneal dialysis patients. Perit Dial Int 1993; 13 Suppl 2:S335.
  8. Li PK, Chow KM, Cho Y, et al. ISPD peritonitis guideline recommendations: 2022 update on prevention and treatment. Perit Dial Int 2022; 42:110.
  9. Yip T, Tse KC, Lam MF, et al. Risks and outcomes of peritonitis after flexible colonoscopy in CAPD patients. Perit Dial Int 2007; 27:560.
  10. Poortvliet W, Selten HP, Raasveld MH, Klemt-Kropp M. CAPD peritonitis after colonoscopy: follow the guidelines. Neth J Med 2010; 68:377.
  11. Machuca E, Ortiz AM, Rabagliati R. Streptococcus viridans-associated peritonitis after gastroscopy. Adv Perit Dial 2005; 21:60.
  12. Tzamaloukas AH, Murata GH, Fox L. Peritoneal catheter loss and death in continuous ambulatory peritoneal dialysis peritonitis: correlation with clinical and biochemical parameters. Perit Dial Int 1993; 13 Suppl 2:S338.
  13. Harwell CM, Newman LN, Cacho CP, et al. Abdominal catastrophe: visceral injury as a cause of peritonitis in patients treated by peritoneal dialysis. Perit Dial Int 1997; 17:586.
  14. Kern EO, Newman LN, Cacho CP, et al. Abdominal catastrophe revisited: the risk and outcome of enteric peritoneal contamination. Perit Dial Int 2002; 22:323.
  15. Vas, SI. Peritonitis. In: Peritoneal Dialysis, 3rd ed, Nolph, KD (Eds), Kluwer Academic Publishers, Dordrecht 1989. p.261.
  16. Oliveira LG, Luengo J, Caramori JC, et al. Peritonitis in recent years: clinical findings and predictors of treatment response of 170 episodes at a single Brazilian center. Int Urol Nephrol 2012; 44:1529.
  17. Voinescu CG, Khanna R. Peritonitis in peritoneal dialysis. Int J Artif Organs 2002; 25:249.
  18. Piraino B, Bailie GR, Bernardini J, et al. Peritoneal dialysis-related infections recommendations: 2005 update. Perit Dial Int 2005; 25:107.
  19. Shrestha BM, Brown P, Wilkie M. Surgical peritonitis in patients on peritoneal dialysis. Perit Dial Int 2008; 28:331.
  20. Li PK, Szeto CC, Piraino B, et al. Peritoneal dialysis-related infections recommendations: 2010 update. Perit Dial Int 2010; 30:393.
  21. Sewell DL, Golper TA, Hulman PB, et al. Comparison of large volume culture to other methods for isolation of microorganisms from dialysate. Perit Dial Int 1990; 10:49.
  22. Lye WC, Wong PL, Leong SO, Lee EJ. Isolation of organisms in CAPD peritonitis: a comparison of two techniques. Adv Perit Dial 1994; 10:166.
  23. Alfa MJ, Degagne P, Olson N, Harding GK. Improved detection of bacterial growth in continuous ambulatory peritoneal dialysis effluent by use of BacT/Alert FAN bottles. J Clin Microbiol 1997; 35:862.
  24. Tranaeus A, Heimbürger O, Lindholm B. Peritonitis in continuous ambulatory peritoneal dialysis (CAPD): diagnostic findings, therapeutic outcome and complications. Perit Dial Int 1989; 9:179.
  25. Flanigan MJ, Freeman RM, Lim VS. Cellular response to peritonitis among peritoneal dialysis patients. Am J Kidney Dis 1985; 6:420.
  26. Koopmans JG, Boeschoten EW, Pannekeet MM, et al. Impaired initial cell reaction in CAPD-related peritonitis. Perit Dial Int 1996; 16 Suppl 1:S362.
  27. Keane WF, Bailie GR, Boeschoten E, et al. Adult peritoneal dialysis-related peritonitis treatment recommendations: 2000 update. Perit Dial Int 2000; 20:396.
  28. Twardowski ZJ, Schreiber MJ Jr, Burkart JM. A 55-year-old man with hematuria and blood-tinged dialysate. Perit Dial Int 1992; 12:61.
  29. Eisenberg ES, Leviton I, Soeiro R. Fungal peritonitis in patients receiving peritoneal dialysis: experience with 11 patients and review of the literature. Rev Infect Dis 1986; 8:309.
  30. Cheng IK, Fang GX, Chan TM, et al. Fungal peritonitis complicating peritoneal dialysis: report of 27 cases and review of treatment. Q J Med 1989; 71:407.
  31. Holley HP Jr, Tucker CT, Moffatt TL, et al. Tuberculous peritonitis in patients undergoing chronic home peritoneal dialysis. Am J Kidney Dis 1982; 1:222.
  32. Dunmire RB 3rd, Breyer JA. Nontuberculous mycobacterial peritonitis during continuous ambulatory peritoneal dialysis: case report and review of diagnostic and therapeutic strategies. Am J Kidney Dis 1991; 18:126.
  33. Fontán MP, Rodríguez-Carmona A, Galed I, et al. Incidence and significance of peritoneal eosinophilia during peritoneal dialysis-related peritonitis. Perit Dial Int 2003; 23:460.
  34. Morduchowicz G, van Dyk DJ, Wittenberg C, et al. Bacteremia complicating peritonitis in peritoneal dialysis patients. Am J Nephrol 1993; 13:278.
  35. Burkart J, Haigler S, Caruana R, Hylander B. Usefulness of peritoneal fluid amylase levels in the differential diagnosis of peritonitis in peritoneal dialysis patients. J Am Soc Nephrol 1991; 1:1186.
  36. Rubinstein S, Franjul R, Surana S, Fogel J. Icodextrin-induced acute pancreatitis in a peritoneal dialysis patient: a case report and literature review
. Clin Nephrol 2016; 86 (2016):283.
  37. Szeto CC, Wong TY, Chow KM, et al. The clinical course of culture-negative peritonitis complicating peritoneal dialysis. Am J Kidney Dis 2003; 42:567.
  38. Eisele G, Adewunni C, Bailie GR, et al. Surreptitious use of antimicrobial agents by CAPD patients. Perit Dial Int 1993; 13:313.
  39. Rocklin MA, Teitelbaum I. Noninfectious causes of cloudy peritoneal dialysate. Semin Dial 2001; 14:37.
  40. de Freitas DG, Gokal R. Sterile peritonitis in the peritoneal dialysis patient. Perit Dial Int 2005; 25:146.
  41. Yoshimoto K, Saima S, Nakamura Y, et al. Dihydropyridine type calcium channel blocker-induced turbid dialysate in patients undergoing peritoneal dialysis. Clin Nephrol 1998; 50:90.
  42. Bargman JM, Zent R, Ellis P, et al. Diagnosis of lymphoma in a continuous ambulatory peritoneal dialysis patient by peritoneal fluid cytology. Am J Kidney Dis 1994; 23:747.
  43. Pérez Fontán M, Pombo F, Soto A, et al. Chylous ascites associated with acute pancreatitis in a patient undergoing continuous ambulatory peritoneal dialysis. Nephron 1993; 63:458.
  44. Rocklin MA, Quinn MJ, Teitelbaum I. Cloudy dialysate as a presenting feature of superior vena cava syndrome. Nephrol Dial Transplant 2000; 15:1455.
  45. Streather CP, Carr P, Barton IK. Carcinoma of the kidney presenting as sterile peritonitis in a patient on continuous ambulatory peritoneal dialysis. Nephron 1991; 58:121.
  46. Vlahakos D, Rudders R, Simon G, Canzanello VJ. Lymphoma-mimicking peritonitis in a patient on continuous ambulatory peritoneal dialysis (CAPD). Perit Dial Int 1990; 10:165.
  47. MacGinley R, Cooney K, Alexander G, et al. Relapsing culture-negative peritonitis in peritoneal dialysis patients exposed to icodextrin solution. Am J Kidney Dis 2002; 40:1030.
  48. Tintillier M, Pochet JM, Christophe JL, et al. Transient sterile chemical peritonitis with icodextrin: clinical presentation, prevalence, and literature review. Perit Dial Int 2002; 22:534.
  49. Boer WH, Vos PF, Fieren MW. Culture-negative peritonitis associated with the use of icodextrin-containing dialysate in twelve patients treated with peritoneal dialysis. Perit Dial Int 2003; 23:33.
  50. Glorieux G, Lameire N, Van Biesen W, et al. Specific characteristics of peritoneal leucocyte populations during sterile peritonitis associated with icodextrin CAPD fluids. Nephrol Dial Transplant 2003; 18:1648.
  51. Johnson CA. Intraperitoneal vancomycin administration. Perit Dial Int 1991; 11:9.
  52. Charney DI, Gouge SF. Chemical peritonitis secondary to intraperitoneal vancomycin. Am J Kidney Dis 1991; 17:76.
  53. Ejaz AA, Fitzpatrick PM, Durkin AJ, et al. Pathophysiology of peritoneal fluid eosinophilia in peritoneal dialysis patients. Nephron 1999; 81:125.
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