Introduction Some patients with COVID-19 pneumonia present systemic disease involving multiple systems. There is limited information about the clinical characteristics and events leading to acute kidney injury (AKI). We described the factors associated with the development of AKI and explored the relation of AKI and mortality in Mexican population with severe COVID-19. Methods We retrospectively reviewed the medical records of individuals with severe pneumonia caused by SARS-CoV-2 hospitalized at the largest third-level reference institution for COVID-19 care in Mexico between March and April 2020. Demographic information, comorbidities, clinical and laboratory data, dates of invasive mechanical ventilation (IMV) and hospitalization, mechanical-ventilator settings and use of vasoactive drugs were recorded. Results Of 99 patients studied, 58 developed AKI (58.6%). The risk factors for AKI were older age (OR = 1.07, 95% CI = 1.01–1.13, p = 0.024); obesity (OR = 6.58, 95% CI = 1.8–24.05, p = 0.040); and the need for IMV (OR = 6.18, CI = 1.29–29.58, p = 0.023). The risk factors for mortality were obesity (OR = 5.57, 95% CI = 1.48–20.93, p = 0.011); requirement of vasoactive drugs on admission (OR = 5.35, 95% CI = 1.16–24.61, p = 0.031); and AKI (OR = 8.61, 95% CI = 2.24–33.1, p = 0.002). In-hospital mortality was significantly higher in patients with AKI stage 3 (79.3%) and AKI stage 2 (68.7%) compared with those with AKI stage 1 (25%; p = 0.004). Fifty-three patients underwent the furosemide stress test (FST) to predict progression to AKI stage 3. Of those, 12 progressed to AKI stage 3 (22%). The ROC curve for the FST had an AUC of 0.681 (p = 0.009); a sensitivity of 81.6% and a specificity of 54.5%. Conclusions AKI was common in our cohort of patients with severe pneumonia caused by SARS-CoV-2 infection. The risk factors for AKI were older age, obesity and the need for of IMV on admission. The risk factors for mortality were obesity, requirement of vasoactive drugs on admission and AKI. Mortality was more frequent in patients with AKI stages 2–3. The FST had an acceptable predictive capacity to identify patients progressing to AKI stage 3.

A high proportion of critically ill patients with COVID-19 develop acute kidney injury (AKI) and die. The early recognition of subclinical AKI could contribute to AKI prevention. Therefore, this study was aimed at exploring the role of the urinary biomarkers NGAL and [TIMP-2] × [IGFBP7] for the early detection of AKI in this population. This prospective, longitudinal cohort study included critically ill COVID-19 patients without AKI at study entry. Urine samples were collected on admission to critical care areas for determination of NGAL and [TIMP-2] × [IGFBP7] concentrations. The demographic information, comorbidities, clinical, and laboratory data were recorded. The study outcomes were the development of AKI and mortality during hospitalization. Of the 51 individuals that were studied, 25 developed AKI during hospitalization (49%). Of those, 12 had persistent AKI (23.5%). The risk factors for AKI were male gender (HR = 7.57, 95% CI: 1.28–44.8; p = 0.026) and [TIMP-2] × [IGFBP7] ≥ 0.2 (ng/mL)2/1000 (HR = 7.23, 95% CI: 0.99–52.4; p = 0.050). Mortality during hospitalization was significantly higher in the group with AKI than in the group without AKI (p = 0.004). Persistent AKI was a risk factor for mortality (HR = 7.42, 95% CI: 1.04–53.04; p = 0.046). AKI was frequent in critically ill COVID-19 patients. The combination of [TIMP-2] × [IGFBP7] together with clinical information, were useful for the identification of subclinical AKI in critically ill COVID-19 patients. The role of additional biomarkers and their possible combinations for detection of AKI in ritically ill COVID-19 patients remains to be explored in large clinical trials.

IntroductionFluid accumulation is associated with adverse outcomes such as acute kidney injury (AKI) in critically ill patients. This study aimed to describe the factors associated with AKI in individuals with influenza A H1N1 severe pneumonia, and explore the relation of fluid accumulation with AKI and mortality.Material and methodsWe reviewed medical records of individuals with influenza A H1N1 severe pneumonia and no history of chronic kidney disease, attending a national referral center for respiratory diseases between November 2014 and May 2015. Demographic information, risk factors for AKI, physiologic and laboratory data, outcomes and information on fluid intake and output were recorded. Categorical variables were compared using the chi-square test. Quantitative variables were compared using the Mann-Whitney test. Factors associated with AKI and mortality were identified by binary logistic regression. Linear models of fluid accumulation rates for individuals and groups were estimated using segmented linear regression.ResultsOf 60 patients studied, 43 developed AKI (71.6%). Male gender was protective for AKI (p = 0.019). AKI was associated with nephrotoxic drugs (p = 0.016); PEEP>10 cm H2O on admission (p = 0.031); mortality (p = 0.037); and fluid accumulation ≥10% (fluid overload) at day 7 of hospitalization (p = 0.00026). Mortality was associated with older age (p = 0.009); nephrotoxic drugs (p = 0.034); and higher Pneumonia Severity Index score (112 vs. 76, p = 0.008) on admission. The Deceased-AKI group had a higher rate of fluid accumulation (expressed as ml/kg/body weight) than the Survivors-No AKI group during the study period of 7 days (Survivors-No AKI = 13.31 vs. Deceased-AKI = 22.76, p = 0.019). During the highest phase of fluid accumulation, the Survivors-No AKI group had a slower rate of fluid accumulation than the Survivors-AKI group (14.91 vs. 28.49, p = 0.001).ConclusionsA high rate of fluid accumulation was associated with AKI and mortality. We support the approach of resuscitation in acute illness, with an early transition to neutral and then negative fluid balances.

Introduction: Some patients with COVID-19 pneumonia present systemic disease involving multiple systems. There is limited information about the clinical characteristics and events leading to acute kidney injury (AKI). We described the factors associated with the development of AKI and explored the relation of AKI and mortality in Mexican population with severe COVID-19. Methods: We retrospectively reviewed the medical records of individuals with severe pneumonia caused by SARS-CoV-2 hospitalized at the largest third-level reference institution for COVID-19 care in Mexico between March and April 2020. Demographic information, comorbidities, clinical and laboratory data, dates of mechanical ventilation and hospitalization, mechanical-ventilator settings and use of vasoactive drugs were recorded. Results: Of 99 patients studied, 58 developed AKI (58.6%). The group with AKI had higher body mass index (p=0.0003) and frequency of obesity (p=0.001); a higher requirement of invasive mechanical ventilation (p=0.008) and vasoactive drugs (p=0.004); greater levels of serum creatinine (p<0.001) and D-dimer on admission (p<0.001); and lower lymphocyte counts (p=0.001) than the non-AKI group. The multivariate analysis indicated that risk factors for AKI were obesity (adjusted hazard ratio (HR)=2.71, 95% confidence interval (CI)=1.33-5.51, p=0.005); higher serum creatinine (HR=1.44, CI=1.02-2.02, p=0.035) and D-dimer levels on admission (HR=1.14, CI=1.06-1.23, p<0.001). In-hospital mortality was higher in the AKI group than in the non-AKI group (65.5% vs. 14.6%; p=0.001). Conclusions: AKI was common in our cohort of patients with severe COVID-19 and it was associated with mortality. The risk factors for AKI were obesity, elevated creatinine levels and higher D-dimer levels on admission. Key words: Acute kidney injury; AKI; acute renal failure; COVID-19; SARS-CoV-2.

In hospitalized COVID-19 patients, disease progression leading to acute kidney injury (AKI) may be driven by immune dysregulation. We explored the role of urinary cytokines and their relationship with kidney stress biomarkers in COVID-19 patients before and after the development of AKI. Of 51 patients, 54.9% developed AKI. The principal component analysis indicated that in subclinical AKI, epidermal growth factor (EGF) and interferon (IFN)-α were associated with a lower risk of AKI, while interleukin-12 (IL-12) and macrophage inflammatory protein (MIP)-1β were associated with a higher risk of AKI. After the manifestation of AKI, EGF and IFN-α remained associated with a lower risk of AKI, while IL-1 receptor (IL-1R), granulocyte-colony stimulating factor (G-CSF), interferon-gamma-inducible protein 10 (IP-10) and IL-5 were associated with a higher risk of AKI. EGF had an inverse correlation with kidney stress biomarkers. Subclinical AKI was characterized by a significant up-regulation of kidney stress biomarkers and proinflammatory cytokines. The lack of EGF regenerative effects and IFN-α antiviral activity seemed crucial for renal disease progression. AKI involved a proinflammatory urinary cytokine storm.