Background/Aims: Purple urine bag syndrome (PUBS) is an uncommon clinical entity characterized by purple urine discoloration in the setting of urinary tract infections. Pa-thophysiology of PUBS has been correlated to aberrant metabolism of tryptophan. Multiple predisposing factors have been recognized, namely: female gender, advanced age, constipation, institutionalization, long-term catheter-ization, dementia and chronic kidney disease. Herein, we present a comprehensive review of all PUBS cases reported in PubMed, focusing on the predisposing factors and the microorganisms related to PUBS. Methods: We performed a search in PubMed database for articles referring to PUBS, published in English, French, Spanish and German from January 1978 until November 2017. The literature recruitment strategy was based on several keywords and Medical Subject Heading combination such as “purple urine bag syndrome” or PUBS or “urine discoloration”. The finally selected articles were categorized into case reports/series (88 articles including 112 patients) and studies (10 articles including 134 patients). Demographical data as well as predisposing factors were recorded and further analyzed. Results: According to our findings, mean age of PUBS patients was 78.9 ± 12.3 years, 70.7% were female while 90.1% were suffering from constipation, 76.1% were in a bedridden situation, 45.1% were experiencing long-term catheterization, 42.8% had been diagnosed with dementia, 14.3% had recurrent urinary tract infections and 14.1% were chronic kidney disease patients. 91.3% of patients presenting with PUBS alkaline urine were observed while the most common microbe in urine cultures was E. coli. Conclusions: PUBS is considered benign process in the majority of catheterized patients. Clinicians should be aware of the syndrome that may indicate serious comorbidities.

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IgA nephropathy (IgAN) is one of the most common recurrent glomerulonephritis after renal transplantation. Rarely, it is accompanied with the presence of crescents that leads to rapid deterioration of renal function and graft loss. We present a 54-year-old patient with IgAN that received a cadaveric kidney allograft, but developed biopsy proven recurrent IgAN 7 months after renal transplantation. He was treated with intravenous steroids and angiotensin-converting enzyme inhibitor and remission was achieved. 4 years later, he presented again with heavy proteinuria, hematuria and deterioration of renal function. Allograft biopsy revealed recurrent IgAN with crescents, which was successfully treated with pulse intravenous steroids and six monthly doses of intravenous cyclophosphamide. This regime resulted in long-term sustained remission with a stable functioning graft 3 years later. Although it is not an established treatment as in native kidneys, intravenous cyclophosphamide should probably be considered in kidney transplants with potentially reversible recurrent crescentic IgAN.

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Statins and colchicine co-administration consists of a potentially catastrophic drug-drug interaction since it provokes myotoxicity, myopathy and various degrees of rhabdomyolysis. Lipophilic statins and colchicine are biotransformed in the liver, primarily via CYP3A4 enzyme system leading to elevated blood levels of both agents and resulting in increased potential for combined myotoxicity. Hence, it would be of great clinical importance not only the awareness of this devastating complication but also the more advantageous type of statin that we should choose to achieve the recommended therapeutic goals regarding LDL levels with minimal myopathy risk. Therefore, once colchicine's use is commenced, a hydrophilic statin selection, such as rosuvastatin, seems favorable regarding the risk of myotoxicity. Herein, we aim to describe a patient with chronic kidney disease stage III and nephrotic syndrome that developed acute rhabdomyolysis soon after the administration of rosuvastatin while receiving colchicine. To the best of our knowledge, this is the first report of the combined effect of rosuvastatin and colchicine in the setting of chronic kidney disease leading to myotoxicity.