Kidney Recovery and Death in Critically Ill Patients With COVID-19–Associated Acute Kidney Injury Treated With Dialysis: The STOP-COVID Cohort Study

Abstract

Rationale & Objective Acute kidney injury treated with kidney replacement therapy (AKI-KRT) occurs frequently in critically ill patients with COVID-19. We examined the clinical factors that determine kidney recovery in this population. Study Design Multicenter cohort study. Setting & Participants 4221 adults with COVID-19 not receiving kidney replacement therapy who were admitted to intensive care units at 68 US hospitals with COVID-19 from March 1 to June 22, 2020 (the “ICU cohort”). Among these, 876 developed AKI-KRT after admission to the ICU (the “AKI-KRT subcohort”). Exposure(s) The ICU cohort was analyzed using AKI severity as the exposure. For the AKI-KRT subcohort, exposures included demographics, comorbidities, initial mode of KRT, and markers of illness severity at the time of dialysis initiation. Outcome(s) The outcome for the ICU cohort was estimated glomerular filtration rate (GFR) at hospital discharge. A three-level outcome including death, kidney nonrecovery, and kidney recovery at discharge, was analyzed for the AKI-KRT subcohort. Analytical approach The ICU cohort was characterized using descriptive analyses. The AKI-KRT subcohort was characterized with both descriptive analyses and multinomial logistic regression to assess factors associated with kidney nonrecovery while accounting for death. Results Among a total of 4221 patients in the ICU cohort, 2361 (56%) developed AKI, including 876 (21%) who received KRT. More severe AKI was associated with higher mortality. Among survivors, more severe AKI was associated with an increased rate of kidney nonrecovery and lower kidney function at discharge. Among the 876 patients with AKI-KRT, 588 (67%) died, 95 (11%) had kidney nonrecovery, and 193 (22%) had kidney recovery by the time of discharge. The odds of kidney nonrecovery was greater for lower estimated GFR with odds ratios (ORs) of 2.09 (95% CI, 1.09-4.04), 4.27 (95% CI, 1.99-9.17), and 8.69 (95% CI, 3.07-24.55) for CKD GFR categories 3, 4, and 5, respectively, compared to estimated GFR > 60 mL/min/1.73 m2. Oliguria at the time of KRT initiation was also associated with nonrecovery (OR 2.10 [95% CI, 1.14-3.88] and 4.02 [95% CI, 1.72-9.39] for patients with 50-499 and <50 mL urine/day respectively, compared to ≥500 mL urine/day). Limitations Later recovery events may not have been captured due to lack of post-discharge follow-up. Conclusions Lower baseline eGFR and reduced urine output at the time of KRT initiation are each strongly and independently associated with kidney nonrecovery among critically ill patients with COVID-19.

Fluid Overload is Associated with Poor Prognosis in Hospitalized Patients with Covid-19 and Acute Kidney Injury

“…Patients at the lowest global uid overload quartile had lower D-Dimer, LDH, C-RP and ferritin levels (p<0.001) and tended to have lower need for RRT than the other three quartiles, but it was not statistically signi cant (4.3% vs 9.0% vs 14.1 vs 11.5% for 1 st , 2 nd , 3 rd , and 4 th uid overload quartiles, respectively; p= 0.148). On the other hand, patients at 4 th uid overload quartile had longer hospital stay than the other groups (9 [6-17] vs 9.5 [6-16] vs 9 [6-14] vs 11 [7][8][9][10][11][12][13][14][15][16][17][18] days for 1 st , 2 nd , 3 rd , and 4 th uid overload quartiles, respectively, p<0.001). Figure 3 shows the Kaplan-Meier plots for 28-day mortality according to global uid overload quartiles, and for categorical >1000 cc global volume overload.…”

“…Acute Kidney Injury is one of the most common complications of Covid-19 and it has been associated with increased risk of death, prolonged stay in hospital, and need for RRT 2,3,14 . Although age, male sex, and previous uncontrolled comorbidities, such as cardiovascular disease, diabetes and CKD, have been independently associated with worst outcomes among patients with Covid-19 and AKI, few of them are relatively modi able during hospitalization that could improve prognosis 7,[14][15][16][17][18][19][20][21][22][23][24][25][26] . Likewise, data from previous studies have only focused on clinical and biochemical characteristics and have not widely analyzed patient's volume status in non-acute heart failure context and/or previously treated with RRT 6,15,27 .…”

Predictors of Poor Outcome among Critically Ill COVID-19 Patients: A Nationally Representative Sample of the Saudi Arabian Population

“…In comparison to our results, Al Sulaiman et al found that 46% of their patients had AKI [ 18 ]. Similarly, a large multicenter study in the US with 4221 critically ill patients found that AKI occurred in 56% of their patients [ 38 ]. Several studies have proposed the mechanisms of AKI development in COVID-19 patients, which include a higher level of soluble tumor necrosis factor, stimulation of inflammatory mediators and cytokine storms, which can cause a microvascular injury and AKI; moreover, the virus can target angiotensin-converting enzyme 2, which is found in the kidney, and can even directly infect the kidney [ 39 , 40 ].…”

Mechanisms of SARS-CoV-2 Infection-Induced Kidney Injury: A Literature Review

“…We performed a systematic search in PubMed to identify recently published large cohort studies related to AKI in patients with COVID-19. We used the search terms “Coronavirus”, “COVID-19”, “SARS-CoV-2”, “acute kidney damage”, “acute kidney injury”, “AKI” and found that the incidence of AKI was higher in severe COVID-19 patients and AKI was strongly associated with high mortality ( Table 1 ) ( Bell et al., 2021 ; Chen et al., 2021 ; Jewell et al., 2021 ; Kilis‐pstrusinska et al., 2021 ; Marques et al., 2021 ; Procaccini et al., 2021 ; Rahimzadeh et al., 2021 ; Scarpioni et al., 2021 ; Sullivan et al., 2021 ; Strohbehn et al., 2021 ; Wan et al., 2021 ; Hung et al., 2022 ; Hsu et al., 2022 ; Sindhu et al., 2022 ). Many possible mechanisms for COVID-19-induced kidney injury have been proposed, including the direct kidney injury mediated by the combination of virus and ACE2.…”