Since the early 1980s, the prevalence of candiduria in hospitals has increased by 200% to 300% such that in a community hospital, 5% of urine cultures may yield Candida, and in tertiary care centers, Candida accounts for almost 10% of urinary isolates, including a quarter of Foley catheter-associated infections. Most positive Candida urine cultures are isolated or transient findings of little significance and represent colonization of catheters rather than true infection. Although less than 10% of candidemias are the consequence of candiduria, Candida urinary tract infections (UTIs) have emerged as important nosocomial infections.
Candida albicans is the most common species isolated from the urine, whereas non-albicans Candida species account for almost half the Candida urine isolates. Candida glabrata is responsible for 25% to 35% of infections.
Candiduria is rare in the absence of predisposing factors. Most infections are associated with use of Foley catheters, internal stents, percutaneous nephrostomy tubes, and age extremes of life. Diabetic patients, especially when their diabetes is poorly controlled, are particularly at risk primarily because of increased instrumentation, urinary stasis, and obstruction secondary to autonomic neuropathy. Concomitant bacteriuria is common and bacterial adherence to bladder epithelium may play a key role in the pathogenesis of Candida infection. Antimicrobials similarly play a critical role in that candiduria almost always emerges during or immediately after antibiotic therapy. Antibiotics, especially broad-spectrum agents, act by suppressing protective indigenous bacterial flora in the gastrointestinal (GI) tract and lower genital tract, facilitating Candida colonization of these sites with ready access to the urinary tract. Nosocomial candiduria is more common in intensive care unit (ICU)-based catheterized women with concomitant contributory vaginal Candida colonization. The pool of critically ill, immunosuppressed medical, and surgical patients has increased, and this increase, together with improved technology, provides an expanded population at risk of developing Candida infection.
Most lower UTIs are caused by retrograde infection from an indwelling catheter or genital or perineal colonization. Biofilm formation contributes to Candida persistence in the presence of catheters and stents. The upper urinary tract is uncommonly involved during ascending retrograde infection and then only in the presence of urinary obstruction, reflux, or diabetes. Renal candidiasis is usually the consequence of secondary hematogenous seeding of the renal parenchyma; Candida species have a unique tropism for the kidney and result in anterograde candiduria.
Most adult patients with candiduria are asymptomatic, especially those with indwelling bladder catheters. Only 4% to 14% of patients with candiduria have symptoms of urinary infection. Clinical manifestations depend on the site of infection. Candida cystitis may present with frequency, dysuria, urgency, hematuria, and pyuria. Ascending infection resulting in Candida pyelonephritis is characterized by fever, leukocytosis, and rigors and is indistinguishable from bacterial pyelonephritis. Excretory urography may reveal ureteropelvic fungus balls or papillary necrosis. Renal candidiasis is difficult to diagnose when secondary to hematogenous spread and presents with fever and other signs of sepsis. By the time renal candidiasis is considered, blood cultures are usually no longer positive; however, unexplained deteriorating renal function is often evident.
In contrast to adult patients, candiduria in low-birth-weight infants, especially extreme low weight (<1000 g), is synonymous with disseminated Candida infection and is associated with high mortality. This patient population is not further considered in this review.
Because isolation of Candida from a urine specimen may represent contamination, colonization, or superficial or deep infection of the lower or upper urinary tract, diagnosis is difficult and management depends on the site of infection. Contamination of the sample is particularly common in women with vulvovaginal colonization and may be excluded by repeating urine culture with special attention to proper collection techniques. Differentiating infection from colonization may be extremely difficult if not impossible in some patients, especially if they are catheterized. Accordingly, I often rely on accompanying clinical features to determine the significance of candiduria; unfortunately these are often nonspecific in critically ill patients, and fever and leukocytosis may have several other sources.
Quantitative urine colony counts have some value in separating infection from colonization but only in the absence of a Foley catheter. The latter negates any diagnostic value of quantitative cultures. In noncatheterized patients, counts greater than 104 colony-forming units (CFU)/mL are usually associated with infection. It is rare for patients with invasive disease of the kidney, pelvis, or bladder to have 103 CFU/mL or less. No definitive cutoffs for defining candiduria have been substantiated. Most patients with urinary tract Candida infection have pyuria, but the value of this finding is similarly diminished in the presence of a catheter or concomitant bacteriuria and in neutropenic subjects. Serologic tests of Candida