Fungal peritonitis in peritoneal dialysis

INTRODUCTION — 

Infections of the peritoneal space are a common complication of peritoneal dialysis [1]. Among patients undergoing peritoneal dialysis, peritonitis is more commonly caused by bacteria than fungi. However, peritonitis caused by fungi carries a higher morbidity and mortality than bacterial infections.

An overview of fungal peritonitis in patients undergoing peritoneal dialysis is presented in this topic review. A general overview of peritonitis, including bacterial peritonitis, in patients on peritoneal dialysis is presented separately. (See "Microbiology and therapy of peritonitis in peritoneal dialysis".)

EPIDEMIOLOGY

Incidence — Fungal peritonitis in patients on peritoneal dialysis is less common than bacterial peritonitis. Pooled data suggest an absolute incidence of 0.01 to 0.09 episodes per patient-year [2].

The highest rates of fungal peritonitis have been reported in tropical countries, such as India and Thailand, and in Australia [2,3]. Rates have been found to vary by season in such countries, with the highest rates associated with the wettest seasons, as further discussed below. (See 'Risk factors' below.)

Risk factors — Fungi may contaminate the usually sterile peritoneum via the same pathways as bacteria (see "Risk factors and prevention of peritonitis in peritoneal dialysis"):

●Breaks in sterile technique when connecting peritoneal catheters to bags of dialysate

●Catheter exit site or tunnel infections

●Intestinal perforation, appendicitis, necrotizing pancreatitis [4], abdominal surgery, peritoneovaginal fistulae, or catheter perforation of the bowel wall

However, several factors are associated specifically with a high risk of fungal peritonitis:

●Recent exposure to antibacterial agents, particularly for bacterial peritonitis – Most published series have found an association with recent antibacterial use and episodes of fungal peritonitis [1,2,5-11]. When these series are combined, 65 percent of patients were exposed to antibiotics within 30 days of the onset of fungal peritonitis, and 48 percent experienced an episode of bacterial peritonitis within the same time frame.

It is difficult to determine whether antibiotic exposure and peritoneal inflammation actually predispose to fungal infections or whether these factors merely identify a high-risk group of patients prone to peritonitis because of poor technique. Recent exposure to antibiotics may predispose to fungal peritonitis by shifting the balance of the patients' endogenous skin and bowel microbiota towards yeast species, thereby increasing the chances of contamination during catheter manipulation.

●Use of emergency peritoneal dialysis – A trend towards infection with fungal organisms has been observed in association with acute or emergent peritoneal dialysis performed in the hospital; this may be due to the severity of illness of these patients, concurrent treatment with antibacterial agents, or the administration of dialysis by personnel unfamiliar with the optimal techniques for peritoneal dialysis.

●Human immunodeficiency virus (HIV) infection – Patients with HIV who receive chronic peritoneal dialysis have a higher frequency of peritonitis with yeasts when compared with other patients receiving chronic peritoneal dialysis. (See "Human immunodeficiency virus and dialysis".)

●Extraperitoneal fungal infection (eg, fungemia)

●Environmental exposures – There are reports of outbreaks of Candida peritonitis associated with contamination of water baths used to warm dialysate solutions and even with environmental contact with pigeon guano [12,13]. In addition, contact with soil during gardening or recreation has been associated with peritonitis caused by molds.

In tropical locales, the incidence of fungal peritonitis has been found to increase during the wet seasons, perhaps due to increased perspiration and outdoor exposure in locales with optimal growth conditions for environmental molds [2,3].

MICROBIOLOGY — 

Although bacteria are the most common cause of peritoneal dialysis-associated peritonitis, fungal organisms account for a significant proportion of infections. In case series, the proportion of infections causes by fungi has ranged from 1 to 24 percent [2,14-16].

Most fungal peritoneal dialysis-associated infections are due to Candida species, especially C. albicans and C. parapsilosis [2,16,17].

Assorted molds and yeasts are occasionally observed, such as species of Aspergillus, Fusarium, Mucorales (eg, Rhizopus, Mucor, Cunninghamella), dematiaceous molds, and Trichosporon [2,18-22].

Fungi may also be identified as part of polymicrobial peritonitis and are a predictor of poor response to therapy in such cases [23].

Further discussion of the microbiology of peritoneal dialysis-associated peritonitis can be found separately. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Microbiology'.)

CLINICAL MANIFESTATIONS — 

The symptoms and signs of fungal peritonitis in patients on peritoneal dialysis are the same as those of bacterial peritonitis. (See "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis".)

The most consistent findings are a cloudy dialysate and abdominal pain, which occur in approximately 90 and 75 percent of patients, respectively. Abdominal pain is usually diffuse and may be associated with nausea, vomiting, and diarrhea. In some patients, symptoms may be subtle, consisting of only mild abdominal pain and low-grade fever.

Most patients have an elevated temperature. Examination of the abdomen typically displays signs of peritonitis, including diffuse tenderness with guarding, rebound tenderness, abdominal distention, and decreased bowel sounds.

DIAGNOSIS

When to suspect fungal peritonitis — Fungal peritonitis should be suspected in any patient on peritoneal dialysis who has peritonitis and who has had recent exposure to antibacterial antibiotics, especially if the antibiotics were given to treat bacterial peritonitis. (See 'Risk factors' above.)

Fungal peritonitis also should be considered in patients on peritoneal dialysis who have culture-negative peritonitis or peritonitis refractory to antibacterial antibiotics. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Culture-negative peritonitis'.)

Establishing the diagnosis — Sampling of dialysate fluid for cell count, microbiologic staining, and culture is necessary to establish the diagnosis of peritonitis and to confirm a fungal etiology. (See "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis", section on 'Evaluation'.)

Peritoneal cell count — Regardless of cause, peritonitis is diagnosed in a patient with characteristic clinical features and a peritoneal fluid white cell count >100/microL (after a dwell time of at least two hours) with >50 percent polymorphonuclear cells (see "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis", section on 'Diagnosis'). Among patients with fungal peritonitis, the peritoneal fluid white cell count is almost always >200 cells/microL, with a polymorphonuclear cell predominance.

In patients on peritoneal dialysis with suspected peritonitis, the finding of eosinophils in the peritoneal fluid should raise suspicion for a fungal etiology, especially mold [24]. A predominance of eosinophils may also be observed in bacterial peritonitis but is less common than in fungal peritonitis. (See "Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis", section on 'Cell count and differential'.)

Microbiologic tests

●Cultures and stains – The diagnosis of fungal peritonitis is confirmed by a peritoneal fluid culture that grows a fungus. Sometimes, an early diagnosis of fungal peritonitis can be made if the initial Gram stain of the peritoneal fluid reveals yeasts consistent with Candida or if a calcofluor white and/or KOH stain shows fungal elements.

For fungal culture, at least 10 mL of peritoneal fluid should be sent to optimize the yield from culture. Although Candida species usually grow quickly in culture, other fungi may require weeks to emerge. The diagnosis therefore requires a high level of suspicion, with some cases presenting as culture-negative peritonitis. (See 'When to suspect fungal peritonitis' above.)

●Fungal biomarkers – Biomarkers for fungal infections (eg, beta-D-glucan, galactomannan) have become important tests for early detection of invasive fungal infections, but their role in the diagnosis of fungal peritonitis is uncertain.

Elevated beta-D-glucan or galactomannan in serum and/or peritoneal fluid has been reported in case reports and small case series of patients with peritoneal dialysis-associated fungal peritonitis [2,17,25-28].

It is important to note that both beta-D-glucan and galactomannan tests can be falsely positive, including in patients with gram-negative bacterial infection or receiving certain antimicrobials [2,17,27]. Therefore, these tests may provide clues to the presence of a fungal infection, but confirmation of fungal peritonitis requires a positive stain or culture of peritoneal fluid.

MANAGEMENT — 

Treatment for fungal peritonitis should commence as soon as fungal organisms are identified by Gram stain, fungal stain, or culture (see 'Microbiologic tests' above). The goals of treatment are to eradicate infection and preserve the peritoneum for future use in peritoneal dialysis.

Key components of management include the following (algorithm 1):

Determining the site of care — In contrast to most patients with bacterial peritonitis, who ideally are managed as outpatients (see "Microbiology and therapy of peritonitis in peritoneal dialysis"), many patients with fungal peritonitis require, at least initially, management in the inpatient setting.

Indications for hospitalization in patients with fungal peritonitis include:

●Sepsis

●Severe abdominal pain

●Inability to administer promptly appropriate antifungal therapy as an outpatient (see 'Initial empiric therapy' below)

●Inability to expedite peritoneal dialysis catheter removal as an outpatient (see 'Immediate catheter removal' below)

●Anticipated delays in obtaining hemodialysis access or hemodialysis as an outpatient

Peritoneal lavage — If the dialysate is grossly cloudy or turbid, peritoneal lavage should be performed until the returning fluid is clear (algorithm 1). Lavage is thought to prevent adhesions and lower the fungal burden (algorithm 1).

Immediate catheter removal

●Prioritize rapid catheter removal – Once fungi are identified by stain or culture, the peritoneal dialysis catheter should be removed as soon as possible, and the patient should be placed on hemodialysis [17,29] (algorithm 1).

Delay or lack of catheter removal is a risk factor for increased mortality and loss of peritoneal membrane function [2,29,30]. In an observational study of over 300 patients with fungal peritonitis, leaving the catheter in place during therapy was associated with a six-times higher rate of death (adjusted HR [hazard ratio] 6.15; 95% CI 2.86-13.23) [2]. In another study of 70 patients with fungal peritonitis, the mortality rate in patients whose catheter was left in place was 91 percent (10 of 11 patients), whereas the mortality rate in patients whose catheter was removed was 31 percent [29].

●Patients with delayed catheter removal – In some settings, removal of the peritoneal dialysis catheter may be delayed because a timely transition to hemodialysis is impossible. Most well dialyzed patients on peritoneal dialysis, especially those with residual kidney function, can stop dialysis safely for at least two to three days. However, in patients with fungal peritonitis who have an anticipated lengthy delay in hemodialysis initiation and must continue peritoneal dialysis in the interim, the following issues may arise:

•Patients may experience catheter dysfunction. Poor return of the dialysate occurs frequently with infections by molds, which can potentially block the catheter [2]. To prevent this, we add intraperitoneal heparin (500 to 1000 units/L of dialysate) when fibrin strands are observed in dialysate or when there is a history of catheter clogging. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Dialysis prescription'.)

•Patients may become volume overloaded because of decreased ultrafiltration. Decreased ultrafiltration is due to an increase in the solute transport rate that results in rapid equilibration of fluid and solute across the inflamed peritoneal membrane. Our approach to volume overload in this setting is detailed elsewhere. (See "Microbiology and therapy of peritonitis in peritoneal dialysis", section on 'Dialysis prescription'.)

Antifungal therapy — Systemic antifungal therapy should be initiated as soon as peritoneal fluid reveals a fungus by stain or culture (algorithm 1). We favor systemic administration (instead of intraperitoneal administration) because immediate catheter removal should be prioritized in all patients with fungal peritonitis.

We also favor systemic therapy for the minority of patients who must temporarily continue peritoneal dialysis due to an anticipated lengthy delay in hemodialysis initiation; intraperitoneal heparin is often needed to maintain catheter patency in such patients, and the compatibility of antifungal agents and heparin in peritoneal fluid is uncertain. (See 'Immediate catheter removal' above.)

Delayed antifungal therapy is associated with poor outcomes, including mortality and loss of peritoneal membrane function [2,17].

Initial empiric therapy — In many cases, a fungal organism is revealed on a microbiology stain or culture before the actual species is identified. Often, the microbiology laboratory can differentiate yeast (eg, Candida) from molds (eg, Aspergillus) by microscopic appearance, which can guide antifungal selection while awaiting definitive identification of the organism.

Ultimately, empiric antifungal selection depends on the suspected organism and patient factors (eg, severity of illness, recent antifungal exposure, ability to take or absorb oral medications) (algorithm 1):

●Yeast (eg, Candida spp) suspected – For patients who are septic or are severely ill with a suspected yeast infection, antifungals should be administered intravenously (algorithm 1). For empiric intravenous therapy, we favor amphotericin B or an echinocandin rather than an azole (eg, fluconazole) until susceptibility testing reveals susceptibility to azoles. Resistance of Candida species to amphotericin B or echinocandins is rare, whereas fluconazole resistance is common in some Candida species.

For patients without sepsis or severe illness, we administer oral fluconazole for initial empiric therapy.

For patients who have had recent antifungal exposure, we avoid that antifungal class until susceptibility results return from the microbiology laboratory.

For all Candida isolates, we ask the microbiology laboratory to perform susceptibility testing for fluconazole, voriconazole, and an echinocandin.

Once the yeast is identified, the antifungal agent should be tailored to target the specific organism, as described in detail below. (See 'Subsequent therapy' below.)

The dosing for our preferred antifungal agents is as follows:

•Oral fluconazole (200 mg orally on day 1, then 100 mg orally once daily)

•Intravenous amphotericin B

-Amphotericin B deoxycholate (0.7 to 1.0 mg/kg/day intravenously, infused over 4 to 6 hours)

-Liposomal amphotericin B (3 to 5 mg/kg/day intravenously)

•An intravenous echinocandin

-Anidulafungin (200 mg intravenously on day 1, then 100 mg intravenously once daily)

-Micafungin (100 mg intravenously once daily)

-Caspofungin (70 mg intravenously on day 1, then 50 mg intravenously once daily)

Amphotericin B is typically used for treatment of azole-resistant candidal peritonitis. For most patients, we select intravenous amphotericin B deoxycholate (0.7 to 1 mg/kd/day intravenously, infused over four to six hours). However, for patients with residual kidney function (ie, >100 mL of urine daily), we select intravenous liposomal amphotericin B (3 to 5 mg/kg/day intravenously) to limit nephrotoxicity; this agent may also be used in patients who experience severe infusion-related reactions to the deoxycholate formulation or when the deoxycholate formulation is unavailable [31,32].

Echinocandins have proven efficacy for treatment of candidemia and invasive candidiasis (including peritoneal infections), but experience with echinocandins for peritoneal dialysis-associated fungal peritonitis is limited [33-37].

●Mold (eg, Aspergillus) suspected – For empiric therapy of mold peritonitis, we recommend intravenous amphotericin B (algorithm 1).

For most patients, we select intravenous amphotericin B deoxycholate (0.7 to 1 mg/kd/day intravenously, infused over four to six hours). However, for patients with residual kidney function (ie, >100 mL of urine daily), we select intravenous liposomal amphotericin B (3 to 5 mg/kg/day intravenously) to limit nephrotoxicity; this agent may also be used in patients who experience severe infusion-related reactions to the deoxycholate formulation or when the deoxycholate formulation is unavailable [31,32].

Once the mold is identified, the antifungal agent should be tailored to target the specific organism, as described in detail below. (See 'Subsequent therapy' below.)

Consultation with an infectious diseases expert is recommended in patients with suspected or confirmed peritonitis due to mold. In patients with fungal peritonitis, mold infections have been associated with higher mortality rates than yeast infections [2].

Subsequent therapy — Once the species of fungus has been identified, antifungal therapy should be tailored to target the specific organism (algorithm 1). In many cases, the initial agent can be changed to an oral agent or one with less toxicity.

●Candida spp – As stated above, once a Candida species is identified, we request susceptibility testing for fluconazole, voriconazole, and an echinocandin (eg, micafungin, anidulafungin, caspofungin) to help direct therapy.

Generally, C. albicans, C. parapsilosis, and C. tropicalis are susceptible to fluconazole, so we treat these organisms with fluconazole until susceptibility results return [1,29,38-40]. (See "Antifungal susceptibility testing", section on 'Candida spp' and "Management of candidemia and invasive candidiasis in adults", section on 'Management approach'.)

C. krusei is resistant to fluconazole, and C. glabrata has variable susceptibilities but is generally resistant. For these species, we suggest intravenous amphotericin B or an intravenous echinocandin [33-37]. (See "Antifungal susceptibility testing", section on 'Candida spp' and "Management of candidemia and invasive candidiasis in adults", section on 'Management approach'.)

The doses of our preferred agents are listed above. (See 'Initial empiric therapy' above.)

●Molds – Molds include organisms such as Aspergillus spp, Fusarium, Mucorales, and dematiaceous molds. Unlike Candida species, susceptibility testing is not readily available. Instead, antifungal selection is based on the organism, and susceptibility testing is generally not performed except in patients with clinical failure. (See "Antifungal susceptibility testing", section on 'Molds'.)

If the fluid shows hyphal forms or cultures reveal an unidentified mold, we suggest intravenous amphotericin B until the specific organism is identified, as described above. (See 'Initial empiric therapy' above.)

Once the organism is identified, the most appropriate antifungal agent can be given. Example organism-based regimens include the following:

•For Aspergillus spp or Scedosporium apiospermum complex, oral voriconazole (200 mg orally every 12 hours) is the treatment of choice [41,42]. Oral voriconazole is also suggested for infections due to dematiaceous molds (eg, Alternaria, Curvularia), although some patients have been reported to have responded to intravenous amphotericin B [43,44]. (See "Treatment and prevention of invasive aspergillosis", section on 'Antifungal therapy' and "Treatment of Scedosporium and Lomentospora infections", section on 'Antifungal therapy'.)

Patients receiving voriconazole should have serum levels checked to avoid toxicity and ensure adequate absorption, as discussed separately. Although voriconazole can be administered intravenously, oral administration is preferred because it is more convenient, has high oral bioavailability, and the intravenous formulation contains cyclodextrin, which may accumulate and lead to toxicity in patients with kidney dysfunction. (See "Pharmacology of azoles", section on 'Voriconazole'.)

•Mucorales (eg, Rhizopus, Mucor, Cunninghamella) infections should be treated with amphotericin B for the full course. (See "Mucormycosis (zygomycosis)", section on 'Antifungal drugs'.)

Duration of therapy — The optimal duration of therapy for fungal peritonitis in patients on peritoneal dialysis is unknown.

Although the 2022 International Society for Peritoneal Dialysis (ISPD) guidelines recommend two to four weeks of therapy from the date of catheter removal [17], more recent observational data including over 300 patients with peritoneal dialysis-associated peritonitis suggested that mortality from fungal peritonitis decreased by 2 percent for each additional day of antifungal therapy beyond a minimum 14-day duration [2].

●Candida peritonitis – For Candida peritonitis, two weeks of antifungal therapy after catheter removal is typically adequate, though some patients may require up to four weeks for complete resolution of symptoms [17].

●Mold peritonitis – For mold infections, we suggest continuing antifungal therapy for at least four weeks from the date of catheter removal, and until all symptoms and signs have resolved.

Timing of catheter replacement — The patient should be maintained with hemodialysis during treatment with systemic antifungal agents. After peritoneal dialysis catheter removal, the catheter may be reinserted after the completion of antifungal therapy and resolution of peritoneal symptoms.

However, the timing of replacement is complex and depends on the response to therapy and the severity of the initial event. In a study of 36 episodes of fungal peritonitis, peritoneal dialysis was eventually resumed in 12 cases, and the median time to catheter reinsertion was 15 weeks [45].

PREVENTION — 

Prevention of fungal peritonitis in patients on peritoneal dialysis involves antifungal prophylaxis in certain situations, limiting unnecessary antibiotic use, and nonpharmacologic interventions.

Antifungal prophylaxis — To prevent fungal peritonitis, we administer antifungal prophylaxis for all patients on peritoneal dialysis who receive a course of antibiotic therapy lasting longer than three days, regardless of the site of infection; the antifungal agent should be prescribed concurrently with the course of antibiotics. Our approach to antifungal prophylaxis is discussed elsewhere. (See "Risk factors and prevention of peritonitis in peritoneal dialysis", section on 'Antifungal prophylaxis during antibiotic therapy'.)

Other experts favor administration of antifungal prophylaxis with any antibiotic course lasting longer than one day [46-53]. Routine prophylaxis for all peritoneal dialysis patients (ie, in the absence of antibiotic therapy) is not recommended.

Limiting antibiotic exposure — Recent antibacterial antibiotic use is a major risk factor for the development of fungal peritonitis, as discussed above. (See 'Risk factors' above.)

Minimizing the use of unnecessary antibiotics and avoiding overly broad-spectrum antibiotics is of particular importance for preventing fungal peritonitis in patients on peritoneal dialysis.

Nonpharmaceutical interventions — As with bacterial peritonitis, a key to prevention of fungal peritonitis is proper training and technique for performance of peritoneal dialysis exchanges and catheter care. In-depth discussion of such preventive interventions is found separately. (See "Risk factors and prevention of peritonitis in peritoneal dialysis", section on 'Prevention' and "Peritoneal catheter exit-site and tunnel infections in peritoneal dialysis in adults", section on 'Prevention'.)

MORBIDITY AND MORTALITY — 

Complications of fungal peritonitis in patients on peritoneal dialysis include sclerosing peritonitis, adhesions with resulting bowel obstruction or stricture, invasion of the bowel wall, and abscess formation [54]. Extraperitoneal spread of infection, including candidemia, is unusual.

Compared with other causes of peritonitis, fungal peritonitis in peritoneal dialysis is associated with increased mortality [55,56]. Reported all-cause mortality rates have ranged from 15 to 45 percent [2,23,29,55,57]. Attributable mortality rates (ie, rate of death due to fungal peritonitis rather than underlying illness) have been difficult to determine.

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

●Epidemiology – The major risk factor for fungal peritonitis is recent exposure to antibacterial agents, particularly for bacterial peritonitis. The highest rates of fungal peritonitis are in tropical countries. (See 'Epidemiology' above.)

●Microbiology – Most fungal peritoneal dialysis-associated infections are due to Candida species. Non-candidal yeast and molds can also cause peritonitis. (See 'Microbiology' above.)

●Clinical manifestations – The symptoms and signs of fungal peritonitis in peritoneal dialysis patients are the same as those for bacterial peritonitis. The most consistent findings are a cloudy dialysate and diffuse abdominal pain. (See 'Clinical manifestations' above.)

●Diagnosis – Fungal peritonitis is confirmed by culturing fungus from dialysate fluid in a patient who meets criteria for peritoneal dialysis-associated peritonitis (ie, cell count >100 cells/microL with >50 percent polymorphonuclear cells). (See 'Diagnosis' above.)

●Management – Many patients are managed initially in the hospital. (See 'Determining the site of care' above.)

•Peritoneal lavage – For patients with fungal peritonitis who have cloudy or turbid peritoneal fluid, we suggest peritoneal lavage until the returning fluid is clear (Grade 2C). Peritoneal lavage may prevent adhesions and lower fungal burden. (See 'Peritoneal lavage' above.)

•Immediate catheter removal – For patients with fungal peritonitis, we recommend catheter removal as soon as possible (Grade 1B). Delay or lack of catheter removal is a risk factor for increased mortality. (See 'Immediate catheter removal' above.)

For patients with an anticipated delay in catheter removal who have fibrin strands in their peritoneal fluid or a history of catheter occlusion, we administer intraperitoneal heparin (500 to 1000 units/L of dialysate). Intraperitoneal heparin may prevent catheter dysfunction until the catheter is removed. (See 'Immediate catheter removal' above.)

•Antifungal therapy – Systemic antifungal therapy should be initiated as soon as peritoneal fluid reveals a fungus by stain or culture.

-Yeast identified on stain – For patients with sepsis or severe illness, we suggest initial empiric therapy with intravenous amphotericin B (Grade 2C). However, intravenous echinocandin is a reasonable alternative. These agents cover almost all candidal species and many non-candidal yeasts. (See 'Initial empiric therapy' above.)

For most patients without sepsis or severe illness, we suggest initial empiric therapy with oral fluconazole (Grade 2C). This agent covers most candida spp. (See 'Initial empiric therapy' above.)

-Mold identified on stain – For patients with mold infection, we suggest initial empiric therapy with intravenous amphotericin B (Grade 2C). This agent covers most molds. (See 'Initial empiric therapy' above.)

Therapy should be tailored once identification and susceptibility results are available. (See 'Subsequent therapy' above.)

•Duration of therapy – For Candida peritonitis, two weeks of therapy after catheter removal is usually adequate, though some patients may require up to four weeks for complete resolution. For mold infection, at least four weeks of therapy is appropriate from the date of catheter removal and until all symptoms have resolved. (See 'Duration of therapy' above.)

•Timing of catheter replacement – The patient should be maintained with hemodialysis during treatment with systemic antifungal agents. After peritoneal dialysis catheter removal, the catheter may be reinserted after completion of antifungal therapy and complete resolution of peritoneal symptoms. (See 'Timing of catheter replacement' above.)

●Prevention – For patients on peritoneal dialysis who receive a course of antibiotic therapy longer than three days, we administer antifungal prophylaxis to prevent fungal peritonitis. (See 'Prevention' above and "Risk factors and prevention of peritonitis in peritoneal dialysis", section on 'Antifungal prophylaxis during antibiotic therapy'.)

ACKNOWLEDGMENT — 

The UpToDate editorial staff acknowledges Steve J Schwab, MD, who contributed to earlier versions of this topic review.