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Early diagnosis of chronic kidney disease (CKD) can help optimize treatment and manage the disease to prevent further decline.
COVID-19 infection has been found to be associated with acute kidney injury, though its effect on long-term kidney function is not well known. Authors of a study published in JAMA Network Open investigated whether kidney function decline accelerated following COVID-19 infection compared with after other respiratory tract infections, such as viral pneumonia. Additionally, because severe COVID-19 often presents as viral pneumonia, the investigators also assessed if the acceleration in kidney function decline differed from after pneumonia caused by other pathogens, and if pre-existing kidney disease is a risk factor.
Patients with linked health record data from the Stockholm Creatinine Measurements Project were included in this cohort study. Adults 18 years and older with their first recorded positive COVID-19 polymerase chain reaction (PCR) or antigen test result from February 1, 2020, to January 1, 2022, were enrolled and included in the study. In addition, patents with a pneumonia diagnosis between February 1, 2018, and January 1, 2020, were enrolled, because pneumonia is a predominant indication for hospitalization related to COVID-19. Further, the specific time period was selected to avoid the confusion of COVID-19 and pneumonia infections.
Study cohorts were not mutually exclusive, meaning that those who had pre-pandemic pneumonia were also eligible for inclusion in the COVID-19 cohort. Further, if a patient had more than 1 occurrence of either COVID-19 or pneumonia during the follow-up period, only the first episode was included.
According to the authors, the study’s primary outcome was the mean annual change in eGFR slopes prior to and following each infection, and the secondary outcome was the annual change in postinfection eGFR slops following COVID-19 or pneumonia. In addition, the authors noted that based on results, recommendations on monitoring, interventions, or the optimization of chronic kidney disease (CKD) treatment may be made.
Additionally, a tertiary study outcome—time to 25% reduction in eGFR, including incident kidney replacement therapy (eg, dialysis or kidney transplant)—was included. Kidney replacement therapy date was determined through the Swedish Renal Registry linkage, and to reduce outcome misclassification and to confirm that eGFR declines were sustained, a linear interpolation method was utilized. Covariates included demographic (eg, age, sex), socioeconomic (eg, highest education level, annual income), and clinical factors (eg, history of comorbid conditions such as diabetes, cardiovascular diseases, immunosuppression, among others).
A total of 134,565 patients with COVID-19 and 35,987 patients with pneumonia were included in the study. Most of the COVID-19 cohort were women (n = 74,819; 55.6%) and had a median age of about 51 years (IQR: 37-64 years). The pneumonia cohort was also primarily women (n = 19,359; 53.8%) and had a median age of 71 years (IQR: 61-92). Additionally, the median baseline eGFR was about 94 (IQR: 79-107) mL/min/1.73m2 for the COVID-19 cohort and 79 (IQR: 61-92) mL/min/1.73m2 for the pneumonia cohort. A total of 16,749 individuals (46.5%) in the pneumonia cohort required hospitalization compared with 17,871 (13.3%) in the COVID-19 cohort.
The authors noted that those who were hospitalized were more likely to be male, have a lower educational level and annual income, and more comorbidities with lower baseline kidney function compared with those who were not hospitalized. Among those who were hospitalized, approximately 19.0% (n = 3391) with COVID-19 and 22.7% (n = 3794) with pneumonia had concurrent acute kidney injury. The COVID-19 cohort had a median of 2 (IQR: 1-3) creatinine tests prior to infection compared with 3 (IQR: 2-6) tests before infection for the pneumonia cohort.
During a median follow-up of about 10.8 (IQR: 8.4-13.2) months for the COVID-19 group, 2061 (1.5%) individuals died at 17 (95% CI, 16-19) per 1000 person-years. For the pneumonia cohort, the median follow-up was also 10.8 (4.8-19.2) months, and 6091 (16.9%) individuals died at 175 (95% CI, 170-179) per 1000 person-years.
Prior to COVID-19 infection, individuals had little change in eGFR regardless of hospitalization status. Following infection, the mean decline was about 4.1 mL/min/1.73m2 (95% CI, 3.8-4.4) faster. Conversely, there was an observed decline in eGFR prior to pneumonia, and after, the mean decline was about 0.9 mL/min/1.73m2 (95% CI, 0.5-1.3) faster. After hospitalization, decline accelerated by about 2.4 mL/min/1.73m2 (95% CI, 1.9-2.9); however, there was no observed evidence of accelerated decline after non-hospitalized pneumonia (0.1 [95% CI, −0.7 to 0.6] mL/min/1.73m2 faster; P for interaction < .001).
Further, an approximate 25% reduction in eGFR occurred in 1051 patients (0.8%) who survived COVID-19 compared with 619 (1.7%) who survived pneumonia. After adjusting for covariates, the ratio for 25% reduction in eGFR was about 1.19 (95% CI, 1.07-1.34) overall for COVID-19 compared with pneumonia, increasing to 1.42 (95% CI, 1.22-1.64) among those who were hospitalized. Among those who were not hospitalized, there was no notable difference between COVID-19 and pneumonia (HR, 1.04; 95% CI, 0.88-1.24).
With these findings, the authors urge that individuals who are hospitalized for COVID-19 receive close monitoring of their kidney function. Doing so will allow health care professionals to make diagnoses quicker, while also optimizing management and treatment of CKD to prevent further decline or complications.
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