Publications

BACKGROUND AND OBJECTIVES

Little is known about geographic differences in the incidence of AKI. The objective of this study was to determine if regional variation exists in the population incidence of dialysis-requiring AKI in the United States.

DESIGN, SETTING, PARTICIPANTS, & METHODS

Data from the Nationwide Inpatient Sample, a US nationally representative sample of hospitalizations, were used to determine the incidence rates of dialysis-requiring AKI between 2007 and 2009 among the four US Census-designated regions. Cases were identified using validated discharge codes. Poisson regression models were used to estimate overall regional rates, accounting for the data's sampling scheme.

RESULTS

In 2007-2009, the population incidence rates of dialysis-requiring AKI differed across the four Census-designated regions (P=0.04). Incidence was highest in the Midwest (523 cases/million person-yr, 95% confidence interval=483 to 568) and lowest in the Northeast (457 cases/million person-yr, 95% confidence interval=426 to 492). The pattern of regional variation in the incidence of dialysis-requiring AKI was not the same as the pattern of regional variation in the incidence of renal replacement therapy-requiring ESRD (obtained from the US Renal Data System). In-hospital mortality associated with dialysis-requiring AKI differed across the four regions, with the highest case fatality in the Northeast (25.9%) and the lowest case fatality in the Midwest (19.4%).

CONCLUSIONS

Significant regional variation exists in the population incidence of dialysis-requiring AKI in the United States, and additional investigation is warranted to uncover potential causes behind these geographic differences.

Arg1 is produced by AAMs and is proposed to have a regulatory role during asthma and allergic inflammation. Here, we use an Arg1 reporter mouse to identify additional cellular sources of the enzyme in the lung. We demonstrate that ILC2s express Arg1 at rest and during infection with the migratory helminth Nippostrongylus brasiliensis. In contrast to AAMs, which express Arg1 following IL-4/IL-13-mediated STAT6 activation, ILC2s constitutively express the enzyme in a STAT6-independent manner. Although ILC2s deficient in the IL-33R subunit T1/ST2 maintain Arg1 expression, IL-33 can regulate total lung Arg1 by expanding the ILC2 population and by activating macrophages indirectly via STAT6. Finally, we find that ILC2 Arg1 does not mediate ILC2 accumulation, ILC2 production of IL-5 and IL-13, or collagen production during N. brasiliensis infection. Thus, ILC2s are a novel source of Arg1 in resting tissue and during allergic inflammation.