Background The epidemic of COVID-19 presents a special threat to elderly adults. However, information on kidney damage in elderly patients with COVID-19 is limited. Acute kidney injury (AKI) is common in hospitalized adults and associated with a poor prognosis. We sought to explore the association between AKI and mortality in elderly patients with COVID-19. Methods We conducted a retrospective, observational cohort study in a large tertiary-care university hospital in Wuhan, China. All consecutive inpatients elderly than 65 years with COVID-19 were enrolled in this cohort. Demographic data, laboratory values, comorbidities, treatments, and clinical outcomes were all collected. Data were compared between patients with AKI and without AKI. The association between AKI and mortality was analyzed. Results Of 1764 in-hospital patients, 882 elderly cases were included in this cohort. The median age was 71 years (interquartile range [IQR]: 68-77), 440 (49.9%) were man. The most presented comorbidity was cardiovascular diseases (58.2%), followed by diabetes (31.4%). Of 882 elderly patients, 115 (13%) developed AKI and 128 (14.5%) died. Patients with AKI had higher mortality than those without AKI (68 [59.1%] vs 60 [7.8%]; P < 0.001). Multivariable Cox regression analysis showed that increasing odds of in-hospital mortality associated with higher interleukin-6 on admission, myocardial injury and AKI. Conclusion AKI is not an uncommon complication in elderly patients with COVID-19 but is associated with high risk of death. Physicians should aware the risk of AKI in elderly patients with COVID-19.

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Following a chronic insult, renal tubular epithelial cells (TECs) contribute to the development of kidney fibrosis through dysregulated lipid metabolism that lead to lipid accumulation and lipotoxicity. Intracellular lipid metabolism is tightly controlled by fatty acids (FAs) uptake, oxidation, lipogenesis, and lipolysis. Although it is widely accepted that impaired fatty acids oxidation (FAO) play a crucial role in renal fibrosis progression, other lipid metabolic pathways, especially FAs uptake, has not been investigated in fibrotic kidney. In this study, we aim to explore the potential mechanically role of FAs transporter in the pathogenesis of renal fibrosis. In the present study, the unbiased gene expression studies showed that fatty acid transporter 2 (FATP2) was one of the predominant expressed FAs transport in TECs and its expression was tightly associated with the decline of renal function. Treatment of unilateral ureteral obstruction (UUO) kidneys and TGF-β induced TECs with FATP2 inhibitor (FATP2i) lipofermata restored the FAO activities and alleviated fibrotic responses both in vivo and in vitro. Moreover, the expression of profibrotic cytokines including TGF-β, connective tissue growth factor (CTGF), fibroblast growth factor (FGF), and platelet-derived growth factor subunit B (PDGFB) were all decreased in FATP2i-treated UUO kidneys. Mechanically, FATP2i can effectively attenuate cell apoptosis and endoplasmic reticulum (ER) stress induced by TGF-β treatment in cultured TECs. Taking together, these findings reveal that FATP2 elicits a profibrotic response to renal interstitial fibrosis by inducing lipid metabolic reprogramming including abnormal FAs uptake and defective FAO in TECs.