Chronic Kidney Disease Is a Potential Risk Factor for the Development of Purple Urine Bag Syndrome

To the Editor: Purple urine bag syndrome (PUBS) refers to purple discoloration of the urinary drainage bag after chronic urinary catheterization and was first described in 1978.1 This condition appears hours or days after catheterization. The pathogenesis of PUBS is that intestinal bacteria metabolize tryptophan, and then indoxyl sulfate is excreted into the urine and digested into indoxyl by sulfatase and phosphatase produced by bacteria. Indoxyl turns into indigo and indirubin in alkaline urine. Indigo is blue and indirubin is red. As they mix together, they become purple.2 According to a few previous reports, PUBS often occurred in elderly women who are bedridden, chronically catheterized, and constipated.3 In addition, PUBS was found in alkaline urine and with higher bacterial counts.3,4 Because of lack of significant patient numbers, the clinical background, underlining diseases, urinanalysis, and incidence of PUBS have not been well documented. To clarify uncertainty regarding this condition, especially risk factors, a cohort study was performed in a Taiwan hospital that included a 20-bed respiratory care ward and a 128-bed hospital-affiliated nursing home. The study was performed from June 2008 to September 2008. All consecutively catheterized patients were divided into a PUBS group and a non-PUBS group. For the enrolled patients, balloon catheters and urine bags were replaced every month. The included parameters of both groups included sex, age, living site, feeding route, and consciousness status. Underlying diseases, especially diabetes mellitus, hypertension, chronic obstructive pulmonary disease, previous cerebral vascular accident, dementia, chronic kidney disease, liver cirrhosis, hypoalbuminemia (<3 mg/dL), cancer, cervical spine injury, posttracheostomy status, and constipation were also documented. Chronic kidney disease (CKD) was defined as a glomerular filtration rate (GFR) of less than 60 mL/min per 1.73 m2 according to the clinical practice guidelines recommended by the Kidney Disease Outcomes Quality Initiative of the Nation Kidney Foundation.5 Urinanalysis included pH, glucose, protein, nitrite, leukocyte count, and urine crystal. Individual urine isolated bacterial species and colony counts were also recorded. The isolation and identification of bacteria were all sent to the laboratory immediately and cultured using a standard medium. Categorical variables were compared using the Mann-Whitney U-test or Fisher exact test, and continuous variables were compared using the Student t-test. P-values <.05 were considered to be statistically significant. There were 40 chronically foley catheterized patients enrolled in the study. All patients were disabled and bedridden. Of the 40 catheterized patients, 10 (25%) had PUBS, and 30 (75%) did not. As shown in Table 1, there were no significant differences in their basic information, including age, living site, sex, and underlying disease, with the exception of CKD; it was found that CKD was the only significant risk factor (P=.04, odds ratio=6.00, 95% confidence interval=1.27–28.25) for PUBS. In the urinanalysis, alkaline urine (pH≥7.5) and the presence of urine phosphate crystal (amphorous, phosphate, and triple phosphate) also indicated a trend toward the development of PUBS, although this did not reach a significant level. The most common pathogen in both groups was Escherichia coli. PUBS occurring in patients with CKD or uremia has been frequently reported,6–8 although the pathogenesis is not clear. Some hypotheses have been proposed. First, based on previous reports, it is known that indoxyl sulfate is mainly excreted into urine. The impaired renal clearance causes higher serum and urine concentration of indoxyl sulphate in uremic patients.7,8 This phenomenon contributed to the development of PUBS in uremic patients. The same phenomenon may also occur in patients with CKD. Second, PUBS is associated with urinary tract infection. Large bacterial colonies in urinanalysis were found to be related to the development of PUBS in a case control study.3 The urinary tract maybe a significant reservoir for infection in patients undergoing hemodialysis, and pyuria was more frequent in oliguric patients with CKD;9 the condition may be related to the development of PUBS. In Taiwan, many case reports of PUBS have been documented,7,8 with greater frequency than in other countries, according to a Medline search. This may be due to the high prevalence of CKD there, up to 6.4%, much greater than in the United States.10 The high prevalence of CKD may partially contribute to the development of PUBS in Taiwan. In conclusion, we performed a hospital-based cohort study and demonstrated that CKD is a potential risk factor in the development of PUBS. We appreciate the assistance of Miss Huang Shu-Xing, nutritionist, Wen-Hsuing Hospital, Kaohsiung, Taiwan. Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this letter. Author Contributions: Po-Liang Lu: plan design. Ying-Ming Tasi and Chi-Tun Lien: data collection. Tun-Chieh Chen: statistical analysis. Inn-Wen Chong: interpretation, consultant. Ming-Shyan Huang: corresponding author, letter preparation, consultant. Chih-Jen Yang: preparation of manuscript. Sponsor's Role: None.