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Background: Information on kidney impairment in patients with coronavirus disease 2019 is limited. This study aims to assess the prevalence and impact of abnormal urine analysis and kidney dysfunction in hospitalized COVID-19 patients in Wuhan. Methods:We conducted a consecutive cohort study of COVID-19 patients admitted in a tertiary teaching hospital with 3 branches following a major outbreak in Wuhan in 2020. Hematuria, proteinuria, serum creatinine concentration and other clinical parameters were extracted from the electronic hospitalization databases and laboratory databases. Incidence rate for acute kidney injury (AKI) was examined during the study period. Association between kidney impairment and in-hospital death was analyzed. Results:We included 710 consecutive COVID-19 patients, 89 (12.3%) of whom died in hospital. The median age of the patients was 63 years (inter quartile range, 51-71), including 374 men and 336 women. On admission, 44% of patients have proteinuria hematuria and 26.9% have hematuria, and the prevalence of elevated serum creatinine and blood urea nitrogen were 15.5% and 14.1% respectively. During the study period, AKI occurred in 3.2% patients. Kaplan-Meier analysis demonstrated that patients with kidney impairment have higher risk for in-hospital death. Cox proportional hazard regression confirmed that elevated serum creatinine, elevated urea nitrogen, AKI, proteinuria and hematuria was an independent risk factor for in-hospital death after adjusting for age, sex, disease severity, leukocyte count and lymphocyte count. : medRxiv preprint Conclusions: The prevalence of kidney impairment (hematuria, proteinuria and kidney dysfunction) in hospitalized COVID-19 patients was high. After adjustment for confounders, kidney impairment indicators were associated with higher risk of inhospital death. Clinicians should increase their awareness of kidney impairment in hospitalized COVID-19 patients. Wu, M.; Guo, J.; Yao, J.; Liao, X.; Song, S.; Han, M.; Li, J.; Duan, G.; Zhou, Y.; Wu, X.; Zhou, Z.; Wang, T.; Hu, M.; Chen, X.; Fu, Y.; Lei, C.; Dong, H.; Zhou, Y.; Jia, H.; Chen, X.; Yan, J., Caution on Kidney Dysfunctions of 2019-nCoV Patients. 2020 23. Kumar, A.; Zarychanski, R.; Pinto, R.; Cook, D. J.; Marshall, J.; Lacroix, J.; Stelfox, T.; Bagshaw, S.; Choong, K.; Lamontagne, F.; Turgeon, A. F.; Lapinsky, S.; Ahern, S. P.; Smith, O.; Siddiqui, F.; Jouvet, P.; Khwaja, K.; McIntyre, L.; Menon, K.; Hutchison, J.; Hornstein, D.; Joffe, A.; Lauzier, F.; Singh, J.; Karachi, T.; Wiebe, K.; Olafson, K.; Ramsey, C.; Sharma, S.; Dodek, P.; Meade, M.; Hall, R.; Fowler, R. A.; Canadian Critical Care Trials Group, H. N. C., Critically ill patients with 2009 influenza A(H1N1) infection in Canada.

Background and objectivesSince December 2019, coronavirus disease 2019 (COVID-19) outbreak occurred and has rapidly spread worldwide. However, little information is available about the AKI in COVID-19. We aimed to evaluate the incidence, risk factors, and prognosis of AKI in adult patients with COVID-19.Design, setting, participants, & measurementsThis was a retrospective cohort study of 1392 patients with COVID-19 admitted to a tertiary teaching hospital. Clinical characteristics and laboratory data were extracted from electronic hospitalization and laboratory databases. AKI was defined and staged according to the 2012 Kidney Disease: Improving Global Outcomes criteria. Risk factors for AKI and the association of AKI with in-hospital mortality were assessed.ResultsA total of 7% (99 of 1392) of patients developed AKI during hospitalization, 40% (40 of 99) of which occurred within 1 week of admission. Factors associated with a higher risk of AKI include severe disease (odds ratio [OR], 2.25; 95% confidence interval [CI], 1.37 to 3.67), higher baseline serum creatinine (OR, 2.19; 95% CI, 1.17 to 4.11), lymphopenia (OR, 1.99; 95% CI, 1.12 to 3.53), and elevated D-dimer level (OR, 2.68; 95% CI, 1.07 to 6.70). The in-hospital mortality in patients with AKI stage 1, stage 2, and stage 3 was 62%, 77%, and 80%, respectively. AKI was associated with in-hospital mortality even after adjustment for confounders (OR, 5.12; 95% CI, 2.70 to 9.72).ConclusionsAKI is uncommon but carries high in-hospital mortality in patients with COVID-19.

Complement synthesis in cells of origin is strongly linked to the pathogenesis and progression of renal disease. Multiple studies have examined local C3 synthesis in renal disease and elucidated the contribution of local cellular sources, but the contribution of infiltrating inflammatory cells remains unclear. We investigate the relationships among C3, macrophages and Th17 cells, which are involved in interstitial fibrosis. Here, we report that increased local C3 expression, mainly by monocyte/macrophages, was detected in renal biopsy specimens and was correlated with the severity of renal fibrosis (RF) and indexes of renal function. In mouse models of UUO (unilateral ureteral obstruction), we found that local C3 was constitutively expressed throughout the kidney in the interstitium, from which it was released by F4/80+macrophages. After the depletion of macrophages using clodronate, mice lacking macrophages exhibited reductions in C3 expression and renal tubulointerstitial fibrosis. Blocking C3 expression with a C3 and C3aR inhibitor provided similar protection against renal tubulointerstitial fibrosis. These protective effects were associated with reduced pro-inflammatory cytokines, renal recruitment of inflammatory cells, and the Th17 response. in vitro, recombinant C3a significantly enhanced T cell proliferation and IL-17A expression, which was mediated through phosphorylation of ERK, STAT3, and STAT5 and activation of NF-kB in T cells. More importantly, blockade of C3a by a C3aR inhibitor drastically suppressed IL-17A expression in C3a-stimulated T cells. We propose that local C3 secretion by macrophages leads to IL-17A-mediated inflammatory cell infiltration into the kidney, which further drives fibrogenic responses. Our findings suggest that inhibition of the C3a/C3aR pathway is a novel therapeutic approach for obstructive nephropathy.

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BackgroundRecent studies have shown associations between contrast-induced acute kidney injury (CI-AKI) and increased risk of adverse clinical outcomes in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI); however, the estimates are inconsistent and vary widely. Therefore, this meta-analysis aimed to evaluate the precise associations between CI-AKI and adverse clinical consequences in patients undergoing PCI for ACS.MethodsEMBASE, PubMed, Web of Science™ and Cochrane Library databases were systematically searched from inception to December 16, 2016 for cohort studies assessing the association between CI-AKI and any adverse clinical outcomes in ACS patients treated with PCI. The results were demonstrated as pooled risk ratios (RRs) with 95% confidence intervals (CI). Heterogeneity was explored by subgroup analyses.ResultsWe identified 1857 articles in electronic search, of which 22 (n = 32,781) were included. Our meta-analysis revealed that in ACS patients undergoing PCI, CI-AKI significantly increased the risk of adverse clinical outcomes including all-cause mortality (18 studies; n = 28,367; RR = 3.16, 95% CI 2.52–3.97; I2 = 56.9%), short-term all-cause mortality (9 studies; n = 13,895; RR = 5.55, 95% CI 3.53–8.73; I2 = 60.1%), major adverse cardiac events (7 studies; n = 19,841; RR = 1.49, 95% CI: 1.34–1.65; I2 = 0), major adverse cardiovascular and cerebrovascular events (3 studies; n = 2768; RR = 1.86, 95% CI: 1.42–2.43; I2 = 0) and stent restenosis (3 studies; n = 130,678; RR = 1.50, 95% CI: 1.24–1.81; I2 = 0), respectively. Subgroup analyses revealed that the studies with prospective cohort design, larger sample size and lower prevalence of CI-AKI might have higher short-term all-cause mortality risk.ConclusionsCI-AKI may be a prognostic marker of adverse outcomes in ACS patients undergoing PCI. More attention should be paid to the diagnosis and management of CI-AKI.Electronic supplementary materialThe online version of this article (10.1186/s12882-018-1161-5) contains supplementary material, which is available to authorized users.

NNWarp is a highly re-usable and efficient neural network (NN) based nonlinear deformable simulation framework. Unlike other machine learning applications such as image recognition, where different inputs have a uniform and consistent format (e.g. an array of all the pixels in an image), the input for deformable simulation is quite variable, high-dimensional, and parametrization-unfriendly. Consequently, even though the neural network is known for its rich expressivity of nonlinear functions, directly using an NN to reconstruct the force-displacement relation for general deformable simulation is nearly impossible. NNWarp obviates this difficulty by partially restoring the force-displacement relation via warping the nodal displacement simulated using a simplistic constitutive model-the linear elasticity. In other words, NNWarp yields an incremental displacement fix per mesh node based on a simplified (therefore incorrect) simulation result other than synthesizing the unknown displacement directly. We introduce a compact yet effective feature vector including geodesic, potential and digression to sort training pairs of per-node linear and nonlinear displacement. NNWarp is robust under different model shapes and tessellations. With the assistance of deformation substructuring, one NN training is able to handle a wide range of 3D models of various geometries. Thanks to the linear elasticity and its constant system matrix, the underlying simulator only needs to perform one pre-factorized matrix solve at each time step, which allows NNWarp to simulate large models in real time.

• Conventional MRI failed to predicted microscopic infiltration of the retinoblastoma. • Scleral and ciliary body invasion could be excluded with high NPV. • ADC values correlated well with some high-risk pathological prognostic parameters.