COVID-19 Infection Increases Likelihood of Kidney Function Decline

Rapid kidney function decline often follows COVID-19 infection, including in patients with moderate to severe chronic kidney disease (CKD), a new study finds. Other research identified plasma biomarkers that may predict major adverse kidney events (MAKE) in patients hospitalized with COVID-19.

Among 97,203 insured patients with CKD G3-4, a total of 8695 patients (8.9%) contracted SARS-CoV-2. Investigators propensity score matched 4475 patients with and 4426 patients without COVID-19. Of this subset, 63% had CKD G3a, 28% had CKD G3b, and 9% had CKD G4.

Rapid kidney function decline, defined as a 40% or greater annual decline in estimated glomerular filtration rate (eGFR), occurred in 2.5% of the COVID-19 group compared with 1.5% of the uninfected group, Clarissa Jonas Diamantidis, MD, MHS, of Duke University School of Medicine in Durham, North Carolina, and colleagues reported in Kidney Medicine. The COVID-19 group had significant 1.6-fold increased odds of rapid kidney function decline.

In the overall cohort, the eGFR slope was significantly steeper for patients with vs without COVID-19 during the pandemic: -2.94 vs -2.36 mL/min/1.73m², the investigators reported. For three-quarters of patients with CKD, kidney function worsened during the pandemic regardless of infection. Noninfection-related experiences of the pandemic may have indirectly contributed to rapid kidney function decline, the investigators suggested.

Patients with CKD stages G3b and G4 were twice as likely to experience rapid kidney function decline during the pandemic compared with patients with CKD stage G3a. Rapid progressors prior to the pandemic had 3-fold increased odds of rapid kidney function decline during the pandemic. Higher vs lower Charlson Comorbidity score also was significantly associated with 1.1-fold increased odds of rapid decline.

Dr Diamantidis’ team further found that Asian patients had 4.2-fold increased odds of rapid kidney function decline during the pandemic compared with White patients.

Separate research by Ashish Verma, MBBS, of Evans Biomedical Research Center in Boston, Massachusetts, published in Kidney Medicine, documents greater proportions of kidney-disease related deaths overall among Asian (and Black) adults compared with White adults in the United States. The highest kidney disease proportional mortality rate was among Filipino individuals aged 60 years or older (2.4%). The death rate was higher for South Asians than East Asians with CKD. The investigators noted that the COVID-19 pandemic may have led to early deaths in some groups.

“Taken together, these findings support CKD as both a risk factor for severe COVID-19 and a consequence of COVID-19. Therefore, close monitoring of the CKD population for long-term consequences of COVID-19 is warranted,” Dr Diamantidis’ team wrote.

She noted that adverse kidney outcomes after COVID-19 disease often follow acute kidney injury (AKI).

In another study, published in the American Journal of Kidney Diseases, Chirag R. Parikh, MD, PhD, of Johns Hopkins University School of Medicine in Baltimore, Maryland, and colleagues investigated the ability of 26 plasma biomarkers of injury, inflammation, and repair to predict COVID-19-associated major adverse kidney events (MAKE). Among 576 patients hospitalized with COVID-19 (30% with pre-existing stage 3 CKD or higher), 95 patients (16%) experienced MAKE, defined as KDIGO stage 3 AKI, dialysis-requiring AKI, or mortality within 60 days.

Each standard deviation increase in soluble tumor necrosis factor receptor 1 or 2 (sTNFR1 or sTNFR2) was significantly associated with a 2.3-fold increased risk for MAKE, the investigators reported. The C index of sTNFR1 and sTNFR2 was 0.80 and 0.81, respectively. Clinical models (including age, sex, race, baseline serum creatinine, diabetes, hypertension, obesity, and WHO COVID-19 severity score) yielded C indexes of 0.86 and 0.85 when sTNFR1 and sTNFR2 were added, respectively.

“Given their role in the body’s response to inflammation, elevations in sTNFR1 and sTNFR2 in the setting of COVID-19 may serve as markers of disease severity, with prolonged inflammation leading to worse kidney outcomes,” Dr Parikh and colleagues wrote.

The investigators proposed cutoffs for sTNFR1 and sTNFR2 of 2130 pg/mL and 14,670 pg/mL because they had high negative predictive values of 92% and 94%, respectively, for MAKE within 60 days.

Identification of high-risk patients who meet these cutoffs would allow outpatient nephrologists to take extra steps to slow or prevent CKD progression, according to Dr Parikh’s team.

Disclosure: The Kidney Medicine COVID-19 research was supported by OptumLabs. Please see the original reference for a full list of disclosures.

Disclosure: Some study authors in the American Journal of Kidney Diseases study declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.

This article originally appeared on Renal and Urology News