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Patients who develop acute kidney injury (AKI) while hospitalized with COVID-19 experienced a significantly faster decline in kidney function and a slower recovery after hospital discharge compared with patients with AKI that was not related to COVID-19, new research shows.
Importantly, the greater decline occurred independently of AKI severity and patient comorbidities, underscoring a unique ― and troubling ― effect of COVID-19, senior author F. Perry Wilson, MD, told Medscape Medical News.
“It’s another sign that COVID-AKI is a particularly nasty form of AKI,” said Wilson, a nephrologist at Yale University School of Medicine, New Haven, Connecticut. “It hits the kidneys pretty hard, even in people without many comorbidities, and, we now believe, may have lasting effects.”
The study, by James Nugent, MD, MPH, Yale University School of Medicine, and colleagues, was published March 10 in JAMA Network Open.
First Look at Long-term Effects of COVID-19 on the Kidneys
AKI is a known complication among patients hospitalized with COVID-19. It occurs in a quarter to about a half of those hospitalized with the virus and in up to 78% of those with COVID-19 who require treatment in the intensive care unit. Cases have been shown to be more severe than AKI that is not associated with COVID-19, and patients are less likely to experience in-hospital kidney recovery, the authors report.
The longer-term effects of COVID-19 on the course of kidney function following discharge after AKI have not been well documented.
To investigate the question, Nugent and colleagues evaluated 182 patients from five hospitals in Connecticut and Rhode Island who developed AKI after testing positive for COVID-19 from March 10 to August 31, 2020, and who survived after discharge and did not require dialysis within 3 days.
The patients were compared with 1430 patients who developed AKI that was not associated with COVID-19.
Overall, 50.4% of the patients were women; the median age was 69.7 years. Consistent with patterns observed with COVID-19 hospitalization, patients with COVID-19-associated AKI were more likely to be Black (40.1% vs 15.7%) or Hispanic (22% vs 8.8%) than White.
Patients with COVID-19 had fewer comorbidities than patients who did not have COVID-19. Rates of preexisting chronic kidney disease and hypertension were similar.
Outpatient creatinine level measurements in the first 6 months following discharge showed that among patients with AKI associated with COVID-19, the mean rate of decline in estimated glomerular filtration rate (eGFR) after discharge was significantly faster compared with patients who did not have COVID-19, after adjusting for baseline characteristics and comorbidities, which included congestive heart failure, hypertension, diabetes, baseline eGFR, and Elixhauser comorbidity score (-12.4 mL/min/1.73 m2 per year; P = .030).
The difference remained significant after adjusting for other factors, including peak creatinine level and the need for in-hospital dialysis (-14.0 mL/min/1.73 m2 per year; P = .01).
At the time of hospital discharge, 82.4% of patients with COVID-19-associated AKI and 79.9% of those without COVID-19 had recovered from AKI.
In a subanalysis that assessed the time to recovery among 319 patients who had not fully recovered from AKI at the time of discharge, those with COVID-19-related AKI were found to be significantly less likely to have experienced kidney recovery at the outpatient follow-up (adjusted hazard ratio, 0.57).
Monitor Kidney Function After Discharge Following COVID-19
It is thought that in COVID-19 patients, AKI may result from either direct or indirect effects on the kidneys.
The causes of the continued kidney dysfunction after discharge observed in the current study are not well understood. The authors note that evidence from studies of other coronavirus strains show that lung fibrosis after pulmonary infections may give rise to tubulointerstitial fibrosis, which could lead to progression of AKI to chronic kidney disease.
Wilson said the known hyperinflammatory state that is associated with COVID-19 is a prime suspect.
“We are still speculating, since we don’t have direct measurements for some of these things, but my gut is that inflammation is playing a big role here,” he said.
“We know that kidneys tend to be quite susceptible to inflammatory conditions, and we know that inflammation is a characteristic of severe COVID-19 disease. But clearly we need more direct measurements of inflammatory state to draw firm conclusions,” he noted.
Until more is known, there is a need to closely monitor patients’ kidney status after COVID-19.
“The most important thing is that patients hospitalized with COVID should have their kidney function followed, particularly if they had AKI during that hospitalization,” Wilson emphasized.
“In terms of management, we don’t yet know what specific therapies (if any) will help in this condition, so the best advice we can give is to do those things that are good for all patients with kidney disease: keep blood pressure controlled, keep diabetes controlled (if present), and refer to nephrology if there is ongoing decline,” he said.
Wilson has received support from the National Institute of Diabetes and Digestive and Kidney Diseases and personal fees from Efference LLC, a medical communications company. He is the author of a blog for Medscape Medical News.
JAMA Netw Open. Published March 10, 2021. Full text
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