SummaryPatient safety is the foundation of high-quality health care. More than 350,000 patients receive dialysis in the United States, and the safety of their care is ultimately the responsibility of the facility medical director. The medical director must establish a culture of safety in the dialysis unit and lead the quality assessment and performance improvement process. Several lines of investigation, including surveys of patients and dialysis professionals, have helped to identify important areas of safety risk in dialysis facilities. Among these are lapses in communication, medication errors, patient falls, errors in machine and membrane preparation, failure to follow established policies, and lapses in infection control. The quality assessment and performance improvement process should include a dedicated safety team to focus on specifically identified areas of risk and to establish outcome goals guided by best practices and agreed-upon measures of success. A safety questionnaire can be given to patients and staff and the responses evaluated to improve understanding of the prevailing attitudes and concerns about safety. By sharing these results, openly acknowledging the challenges, and using a blame-free root cause process to identify action plans, the facility can begin to establish a culture of safety.

The INK4a proteins p16(INK4a) and p19(ARF) regulate cell cycle arrest and senescence. However, the role of these proteins in controlling these processes in the normal kidney and following injury is unknown. We performed unilateral ureteral obstruction (UUO) to induce fibrosis in 2- to 3-mo-old wild-type (WT) C57/B6 and INK4a knockout mice. By quantitative RT-PCR, p16(INK4a) levels were increased sixfold in WT mice 7 days after UUO and p19(ARF) remained undetectable. Kidney sections were examined to determine levels and localization of p16(INK4a), apoptosis, fibrosis, and senescent cells. INK4a knockout mice displayed mesangial cell proliferation, increased matrix deposition, and myofibroblast differentiation under normal conditions. Following UUO, INK4a knockout mice displayed 10-fold increased tubular and interstitial cell proliferation, 75% decreased collecting duct apoptosis, 2-fold greater collagen and fibronectin deposition, and no cell senescence by senescence-associated β-galactosidase staining compared with WT mice. Both INK4a knockout mesangial cells and kidney lysates from knockout mice following injury showed elevated levels of IL-6 by ELISA compared with WT samples. INK4a knockout epithelial cell cultures displayed increased mesenchymal cell markers when exposed to transforming growth factor-β. These results confirm that p16(INK4a) controls cell proliferation and matrix production and mitigates fibrosis following injury and suggest that the mechanism involves a role in limiting inflammation and cell proliferation.

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