(See also Introduction to Urinary Tract Infections [UTIs].)
Species of Candida, the most common cause, are normal commensals in humans. Candida colonization differs from infection in that infection produces tissue reaction. All invasive fungi (eg, Cryptococcus neoformans, Aspergillus species, Mucoraceae species, Histoplasma capsulatum, Blastomyces species, Coccidioides immitis) may infect the kidneys as part of systemic or disseminated mycotic infection. Their presence alone indicates infection.
Lower urinary tract infection (UTI) with Candida usually occurs in patients with urinary catheters, typically after antibiotic therapy, although candidal and bacterial infections frequently occur simultaneously. C. albicans prostatitis occurs infrequently in patients with diabetes, usually after instrumentation.
Renal candidiasis is usually spread hematogenously and commonly originates from the gastrointestinal tract. Ascending infection is possible and occurs mainly in patients with nephrostomy tubes, other permanent indwelling devices, and stents. At high risk are patients with diabetes and those who are immunocompromised because of tumor, AIDS, chemotherapy, or immunosuppressants. A major source of candidemia in such high-risk hospitalized patients is an indwelling intravascular catheter. Renal transplantation increases the risk because of the combination of indwelling catheters, stents, antibiotics, anastomotic leaks, obstruction, and immunosuppressive therapy.
Complications of candidal infection can include emphysematous cystitis or pyelonephritis and fungus balls in the renal pelvis, ureter, or bladder. Bezoars may form in the bladder. Lower or upper urinary tract obstruction may occur. Papillary necrosis and intrarenal and perinephric abscesses may form. Although renal function often declines, severe renal failure is rare without postrenal obstruction.
Most patients with candiduria are asymptomatic. Whether Candida can cause urethral symptoms (mild urethral itching, dysuria, watery discharge) in men is uncertain. Rarely, dysuria in women is caused by candidal urethritis, but it may result from the urine coming into contact with periurethral tissue that is inflamed due to candidal vaginitis.
Among lower urinary tract infections, cystitis due to Candida may result in frequency, urgency, dysuria, and suprapubic pain. Hematuria is common. In patients with poorly controlled diabetes, pneumaturia due to emphysematous cystitis has occurred. Fungus balls or bezoars may cause symptoms of urethral obstruction.
Most patients with renal candidiasis that is hematogenously spread lack symptoms referable to the kidneys but may have antibiotic-resistant fever, candiduria, and unexplained deteriorating renal function. Fungus ball elements in the ureter and renal pelvis frequently cause hematuria and urinary obstruction. Occasionally, papillary necrosis or intrarenal or perinephric abscesses cause pain, fever, hypertension, and hematuria. Patients may have manifestations of candidiasis in other sites (eg, central nervous system, skin, eyes, liver, spleen).
Candida urinary tract infection (UTI) is considered in patients with predisposing factors and symptoms suggesting UTI and in all patients with candidemia. Candida should be suspected in men with symptoms of urethritis only when all other causes of urethritis have been excluded.
Diagnosis of Candida UTI is by culture, usually from urine. The level at which candiduria reflects true Candida UTI and not merely colonization or contamination is unknown. Differentiating Candida colonization from infection requires evidence of tissue reaction.
Cystitis is usually diagnosed in high-risk patients with candiduria by the presence of bladder inflammation or irritation, as evidenced by pyuria. Cystoscopy and ultrasonography of the kidneys and bladder may help detect bezoars and obstruction.
Renal candidiasis is considered in patients with fever, candiduria, or passage of fungus balls. Severe renal failure suggests postrenal obstruction. Imaging of the urinary tract may help reveal the degree of involvement. Blood cultures for Candida are often negative.
Unexplained candiduria should prompt evaluation of the urinary tract for structural abnormalities.
Fungal colonization of catheters does not require treatment. Asymptomatic candiduria rarely requires therapy. Candiduria should be treated in the following:
Urinary stents and Foley catheters should be removed (if possible). For symptomatic cystitis, treatment is with fluconazole 200 mg orally once a day. For pyelonephritis, fluconazole 200 to 400 mg orally once a day is preferred. Therapy in both cases should be for 2 weeks. For fungi resistant to fluconazole, amphotericin B is recommended at a dose of 0.3 to 0.6 mg/kg IV once a day for 2 weeks for cystitis and 0.5 to 0.7 mg/kg IV once a day for 2 weeks for pyelonephritis.
For resistant pyelonephritis, flucytosine 25 mg/kg orally 4 times a day is added to the regimen if patients have adequate renal function; if not, the dose should be modified based on creatinine clearance (see Antifungal Drugs).
Flucytosine may help eradicate candiduria due to non-albicans species of Candida; however, resistance may emerge rapidly when this compound is used alone. Bladder irrigation with amphotericin B may transiently clear candiduria but is no longer indicated for cystitis or pyelonephritis. Even with apparently successful local or systemic antifungal therapy for candiduria, relapse is frequent, and this likelihood is increased by continued use of a urinary catheter. Clinical experience with using voriconazole to treat urinary tract infections (UTIs) is scant.
Fungal UTI affects mainly patients who have urinary tract obstruction or instrumentation, immunocompromise (including diabetes), or both.
Suspect fungal UTI in patients at risk or with candidemia who have clinical or laboratory findings consistent with UTI.
Use antifungal drug therapy only if patients will undergo urologic manipulation or have symptoms, neutropenia, or renal allografts.