A 68-year-old man on peritoneal dialysis (PD) was hospitalized with the clinical picture of peritonitis. The patient was diagnosed with peritonitis caused by nontuberculous mycobacteria (NTM) according to positive Ziehl-Neelsen staining and negative Mycobacterium tuberculosis polymerase chain reaction results. Oral levofloxacin and clarithromycin, and later intraperitoneal imipenem were started. According to the anti-NTM susceptibility test results, oral minocycline was administered. The patient was treated for 6 months. He recovered without PD catheter removal; thus, PD was successfully continued. A genetic analysis identified the isolate as Mycobacterium iranicum. This is the first report of PD-related peritonitis caused by M. iranicum.

A 32-year-old man on peritoneal dialysis (PD) was hospitalized for seven days due to fever. A diagnosis of yeast-like fungal peritonitis was made by Gram staining. The patient was started on intravenous micafungin and oral fluconazole therapy following removal of the PD catheter. A fungal pathogen was isolated from the peritoneal fluid and identified as Cryptococcus species. Based on antifungal susceptibility testing, the treatment was changed to voriconazole and continued for 3 months. A genetic analysis identified the isolate as Cryptococcus laurentii (C. laurentii). This patient was diagnosed with C. laurentii PD-related peritonitis and was successfully treated with voriconazole and removal of the PD catheter.

D/Ps of some molecules did not correlate with D/P creatinine. Factors other than molecular weight, such as charge and protein binding rate, are involved in peritoneal transport rates. Metabolomic analysis appears useful to analyze small molecular uremic toxins, which could accumulate in PD patients, and the status of peritoneal membrane transport for each molecule.

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A 17-year-old lady was diagnosed with proteinuria and microscopic hematuria within the prior 2 years to this presentation. Further tests revealed nephrotic syndrome with hematuria and hypocomplementemia. Renal histopathology showed membranoproliferative glomerulonephritis. Immunostaining and electron microscopy, suggested C3 glomerulonephritis (C3GN). Nephritis-associated plasmin receptor (NAPlr) and plasmin activity (PA), markers of infection-related glomerulonephritis, were identified in the aforementioned pathology specimens. There are several reports suggesting a causal relationship between group A streptococcal infection and C3 glomerulopathy (C3G). There are many intractable cases, whereas some have responded to immunosuppressive therapy, as did our case. However, there is currently no established gold standard treatment for this disease. We herein report a case of C3G with glomerular positive NAPlr and PA despite the absence of a streptococcal infection. Accumulation of cases such as this may help advance treatment by clarifying the etiology and pathogenic mechanism of C3G and future prognosis.