Nikhil Prasad Fact checked by:Thailand Medical News Team Sep 12, 2026 55 minutes ago
Kidney problems linked to COVID-19 may persist for at least six months, particularly among people sick enough to require hospitalization, according to a prospective Swedish study that tracked both filtering function and signs of tubular injury.
Hospitalized COVID-19 patients showed signs of impaired kidney function and persistent tubular injury for up to six months
after infection
Researchers followed 218 adults with COVID-19, including 77 hospitalized and 141 non-hospitalized patients. None had documented kidney disease at enrollment.
Researchers came from Umeå University, including its Departments of Clinical Microbiology, Medical Biosciences/Clinical Chemistry, Physics, Diagnostics and Intervention, and Public Health and Clinical Medicine; the Laboratory for Molecular Infection Medicine Sweden at Umeå University; and Örebro University’s Department of Infectious Diseases, Faculty of Medicine and Health.
Cystatin C Reveals a Persistent Gap
The clearest difference emerged when kidney filtration was estimated using cystatin C rather than creatinine. During acute COVID-19, median cystatin C-based estimated glomerular filtration rate, or eGFR, was 61 mL/min/1.73 m² in hospitalized patients versus 91 in non-hospitalized patients.
Both groups improved, but the gap remained striking six months later: median cystatin C-based eGFR reached 86 among hospitalized patients compared with 118 among those who had not been hospitalized. Creatinine-based eGFR was less effective at distinguishing the groups during acute illness, possibly because hospitalization-related muscle loss can alter creatinine levels.
More than half of hospitalized patients also met criteria for selective glomerular hypofiltration syndrome during acute infection, based on the ratio between cystatin C- and creatinine-derived eGFR. Median ratios later rose above the syndrome threshold, suggesting general recovery.
Tubular Injury Markers Stay Elevated
The study also looked beyond the kidney’s glomeruli to markers associated with tubular damage. KIM-1, a protein that rises after stress to proximal tubular cells, was higher in hospitalized patients at every assessment. Median KIM-1 was 135 ng/L versus 73 during acute illness and remained 114 versus 78 at six months.
VEGF-A showed a similar pattern. Hospitalized patients had a median level of 467 ng/L acutely, nearly three times the 164 recorded in non-hospitalized patients. At six months, levels had fallen to 258 but remained above 162 in the non-hospitalized group. The researchers said sustained KIM-1 and VEGF-A elevations may reflect persistent tubular injury, inflammation, or ongoing tissue repair.
Another marker, osteoactivin, was initially lower in hospitalized patients but became higher at follow-up, while TFF3 showed no significant unadjusted differences between groups. In this
Thailand Medical News report, the findings underscore why relying on creatinine alone may miss subtler kidney abnormalities after severe COVID-19.
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What the Findings Mean
The authors cautioned that the study lacked healthy controls, included only Swedish patients infected in 2020-2021, and could not establish participants’ pre-COVID kidney function. Steroid treatment may also have influenced cystatin C measurements.
Conclusion: The results indicate that severe COVID-19 can leave measurable glomerular and tubular abnormalities for months, supporting cystatin C-based filtration estimates and potentially closer kidney monitoring after hospitalization while longer-term studies determine whether these changes fully resolve.
The study findings were published in the peer reviewed Scandinavian Journal of Clinical and Laboratory Investigation.
https://www.tandfonline.com/doi/full/10.1080/00365513.2026.2724491
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