Water avoidance and modification of exit-site care with stoma bag results in reduced exit-site infection rate in peritoneal dialysis patients.

AIM: Infection is one of the drawbacks associated with peritoneal dialysis (PD) and is related to significant morbidity. After we experienced an increase in exit-site infection (ESI) rate, mostly derived from environmental and water-derived organisms, we hypothesized that preventing exit-site exposure to water and narrowing local antibiotics range will reduce colonization and subsequent infection. MATERIALS AND METHODS: In this study, we aimed to estimate PD-related infections after exit-site policy change in a prospective study cohort of 27 participants compared to a control group of 58 participants. The modification of exit-site care consisted of applying a stoma bag during daily shower to prevent water exposure and conversion of local antibiotic from gentamycin to mupirocin. Primary outcome was catheter-related infection. Secondary outcomes were peritonitis rate and infection-related outcomes. RESULTS: The study group had a significantly lower ESI and ESI from environmental organisms' free probability. Rate of ESI from all causes was 0.054 ± 0.09 vs. 0.031 ± 0.09 episodes per patients' month for the control and study group, respectively (p = 0.049). Rate of environmental organism-related ESI was 0.047 ± 0.07 vs. 0.015 ± 0.08 episodes per patients' months for control and study group, respectively (p = 0.042). A higher risk of ESI from all organisms, and specifically from environmental organisms, was associated with being in the control group and a longer follow-up period. Rate of peritonitis was similar in both groups. CONCLUSION: The adjusted exit-site care policy significantly lowered ESI incidence. Avoidance of water exposure may have contributed to lessen bacterial colonization.

Nontuberculous mycobacteria infections of peritoneal dialysis patients: A multicenter study.

OBJECTIVES: Nontuberculous mycobacteria (NTM) infections pose a diagnostic challenge in peritoneal dialysis (PD) patients. In this study, we sought to identify findings that are suggestive of NTM infection in PD adult patients. METHODS: All patients with NTM exit-site infection (ESI) with/without tunnel infection and peritonitis identified during the last decade in eight medical centers in Israel were included. Clinical, microbiological, and outcome data were collected and analyzed. RESULTS: Thirty patients were identified; 16 had ESI (53%) and 14 had peritonitis (47%). Median age was 65 years (interquartile range 52-76). Abdominal pain and cloudy PD fluid were reported in all patients with peritonitis, whereas exit-site discharge and granulation tissue were common in patients with ESI. Fourteen patients (47%) had negative cultures prior NTM diagnosis, and isolation of diphtheroids or Corynebacterium spp. was reported in 9 of 30 patients (30%). Antimicrobial treatment prior to diagnosis was documented in 13 of 30 patients (43%). Delayed diagnosis was frequent. Treatment regimens and duration of therapy varied widely. In 26 of 30 (87%) patients, catheter was removed and 19 of 30 patients (63%) required permanent transition to hemodialysis. Two patients with peritonitis (2 of 14, 14%) and seven with ESI (7 of 16, 44%) were eligible for continuation of PD. CONCLUSIONS: Culture negative peritonitis, isolation of diphtheroids or Corynebacterium spp., previous exposure to antibiotics, and/or a refractory infection should all prompt consideration of PD-related NTM infection and timely workup. Catheter removal is recommended aside prolonged antimicrobial therapy. In select patients with ESI, continuation of PD may be feasible.

Attenuated glomerular arginine transport prevents hyperfiltration and induces HIF-1α in the pregnant uremic rat.

Pregnancy worsens renal function in females with chronic renal failure (CRF) through an unknown mechanism. Reduced nitric oxide (NO) generation induces renal injury. Arginine transport by cationic amino acid transporter-1 (CAT-1), which governs endothelial NO generation, is reduced in both renal failure and pregnancy. We hypothesize that attenuated maternal glomerular arginine transport promotes renal damage in CRF pregnant rats. In uremic rats, pregnancy induced a significant decrease in glomerular arginine transport and cGMP generation (a measure of NO production) compared with CRF or pregnancy alone and these effects were prevented by l-arginine. While CAT-1 abundance was unchanged in all experimental groups, protein kinase C (PKC)-α, phosphorylated PKC-α (CAT-1 inhibitor), and phosphorylated CAT-1 were significantly augmented in CRF, pregnant, and pregnant CRF animals; phenomena that were prevented by coadministrating l-arginine. α-Tocopherol (PKC inhibitor) significantly increased arginine transport in both pregnant and CRF pregnant rats, effects that were attenuated by ex vivo incubation of glomeruli with PMA (a PKC stimulant). Renal histology revealed no differences between all experimental groups. Inulin and p-aminohippurate clearances failed to augment and renal cortical expression of hypoxia inducible factor-1α (HIF-1α) significantly increased in CRF pregnant rat, findings that were prevented by arginine. These studies suggest that in CRF rats, pregnancy induces a profound decrease in glomerular arginine transport, through posttranslational regulation of CAT-1 by PKC-α, resulting in attenuated NO generation. These events provoke renal damage manifested by upregulation of renal HIF-1α and loss of the ability to increase glomerular filtration rate during gestation.