Nanomedicine (Lond.) (Epub ahead of print) ISSN 1743-5889 part of Research Article 10.2217/nnm-2017-0256 © 2017 Future Medicine Ltd Aim: We used resveratrol (Res)-loaded nanoparticles (Res NPs) as a novel method for improving the pharmacokinetic properties of Res and analyzed the effect of Res NPs in chronic kidney disease (CKD). Materials & methods: We coupled anti-kidney injury molecule-1 antibodies to Res NPs and analyzed safety and efficacy. Results: Res NPs had low toxicity and induced autophagy. Res NPs inhibited the NLRP3 inflammasome and IL-1β secretion. Higher NLRP3 expression levels were observed in peripheral blood monocytic cells of CKD patients than healthy individuals. Treatment with kidney injury molecule-1-Res NPs significantly reduced creatinine and protected against tubulointerstitial injury in a murine model of CKD. Conclusion: Res NPs through NLRP3 inflammasome attenuation and autophagy induction may be as a strategy to prevent CKD. First draft submitted: 14 August 2017; Accepted for publication: 31 August 2017; Published online: 8 September 2017 Keywords:฀ autophagy฀•฀chronic฀kidney฀disease฀•฀infammasome฀•฀kidney฀injury฀molecule-1฀ •฀resveratrol Chronic kidney disease (CKD) is a progres- sive and irreversible loss of renal function characterized by a decreased glomerular fil- tration rate. CKD is becoming one of the most important health problems worldwide and greatly affects patients’ quality of life [1,2] . Rates of CKD in the population are increas- ing, largely because of increasing prevalence of associated comorbidities such as cardio- vascular disease, diabetes, hypertension and obesity. Furthermore, untreated CKD can result in end-stage renal disease and neces- sitate dialysis or kidney transplantation [3] . In CKD, several features might contribute to a persistent state of inflammation and its pro- oxidant effects, such as proteinuria, reduced cytokine clearance and infections [4] . Patients with CKD demonstrate antioxidant defense deficiency because of the reduced consump- tion of vitamins and minerals containing antioxidants [5] . Therefore, chronic inflam- mation and oxidative stress features play a key role in the development and progression of CKD and related disorders [6] . Based on previous studies, kidney injury molecule-1 (KIM-1), a recently discovered transmem- brane protein with extracellular mucin and immunoglobulin domains, is believed to play a role in tubulointerstitial damage [7] . KIM-1 is not detectable in normal human or rodent kidneys but KIM-1 expression is increased more than that of any other protein in injured kidneys, and it is localized predominantly to the apical membrane of surviving proximal epithelial cells [7,8] . Therefore, upregulation of renal KIM-1 expression is located in dedif- ferentiated proximal tubular cells and is asso- ciated with fibrosis and inflammation [9,10] . The incidence of CKD has increased dramat- ically over the past 10 years, and new strate- gies for slowing its progression are urgently needed [2] . Accumulated evidence has revealed that persistent inflammation leads to progressive Resveratrol-loaded nanoparticles conjugated with kidney injury molecule-1 as a drug delivery system for potential use in chronic kidney disease Yuh-Feng Lin ‡,1,2 , Yu-Hsuan Lee 3 , Yung-Ho Hsu 1,4 , Yi- Jie Chen 1 , Yuan-Feng Lin 2 , Fong-Yu Cheng ‡,5 & Hui-Wen Chiu* ,1,2 1 Division฀of฀Nephrology,฀Department฀of฀ Internal฀Medicine,฀Shuang฀Ho฀Hospital,฀ Taipei฀Medical฀University,฀Taiwan 2 Graduate฀Institute฀of฀Clinical฀Medicine,฀ College฀of฀Medicine,฀Taipei฀Medical฀ University,฀Taipei,฀Taiwan 3 Department฀of฀Food฀Safety/Hygiene฀&฀ Risk฀Management,฀College฀of฀Medicine,฀ National฀Cheng฀Kung฀University,฀Tainan,฀ Taiwan 4 Department฀of฀Internal฀Medicine,฀ School฀of฀Medicine,฀College฀of฀Medicine,฀ Taipei฀Medical฀University,฀Taipei,฀Taiwan 5 Department฀of฀Chemistry,฀Chinese฀ Culture฀University,฀Taipei,฀Taiwan *Author฀for฀correspondence:฀ Tel.:฀+886฀2฀22490088฀ext.฀8884 leu3@tmu.edu.tw Authors฀contributed฀equally For reprint orders, please contact: reprints@futuremedicine.com