POST-ACUTE COVID-19 SYNDROME AND URINARY TRACT INFECTIONS
Keywords:
COVID-19, SARS-CoV-2, complicated urinary infections, urosepsisAbstract
The complications in the respiratory tract and cardiovascular events are the leading causes of death and
morbidity among COVID-19 patients but it was shown that nearly all other systems might be involved including the
urinary system. The post-acute COVID-19 syndrome is defined as the presence and/or persistence of symptoms 8–
12 weeks after the onset of COVID-19 unrelated to any other illness. The main pathophysiological mechanisms
underlying the post-acute COVID-19 syndrome depend on the organ system involved, virus-specific
pathophysiological alterations, immunological and inflammatory alterations, and other common post-infectious
sequelae. Urinary tract infections (UTIs) that affect the kidneys, and cause fever, stones, sepsis, urinary obstruction,
catheters, or immunocompromised patients are classified as complicated infections.
The objective of this study was to assess complicated urinary tract infections in patients who recently recovered
from COVID-19. It is an observational analysis of a case series of ten patients aged 22 to 71 years who had COVID-
19 one to six months before the urinary infection. Their radiographic images of the lungs had a finding suggesting
sequelae of respiratory infection. Urine cultures were positive for Escherichia coli in 5 patients, Enterococcus spp.
in 3 patients, and 2 patients had sterile findings but their urinalysis revealed the presence of leukocytes and bacteria.
Six patients were febrile and two patients had clinical signs of urosepsis (systolic pressure<100mm/hg, tachypnea
>22r/min, leukocytosis, and GSC<15) in two patients. All patients had elevated leukocyte counts and high CRP
serum levels, confirming acute inflammation. D-dimers were elevated in most patients (n=9), which could signal
active clotting issues—important in the context of infections and inflammatory processes. Serum creatine was
elevated in 4 patients possibly indicating renal stress or dysfunction. Elevated serum urea levels in more than half of
patients (n=6) indicate protein catabolism or decreased renal clearance. The study observed a higher incidence of
patients with elevated serum glucose (n=9), which could be stress-induced hyperglycemia or underlying metabolic
issues like diabetes.
Treatment was dual antibiotic therapy with intravenous cephalosporin and ciprofloxacin (n=6), intravenous
ertapenem and ciprofloxacin (n=3), and intravenous amikacin in one patient. The patients were discharged to home
treatment after 5 days (n=1), 10 days (n=4), 15 days (n=3) and 20 days (n=2) respectively. The average hospital stay
due to urinary infection was 13 (+/-10) days; male patients had a longer average hospital stay (20 days) compared to
female patients (12.22 days). Patients with urinary catheters had a longer hospital stay (15 days) unlike the others
(12.5 days), indicating more severe urinary issues or complications that might extend the hospital stay. Patients
requiring intensive care (n=2) had a longer average hospital stay (17.5 days) compared to those who did not need
intensive care (11.875 days), underscoring the impact of critical care needs on hospitalization length.
This case series concludes that in a certain number of patients, depending on the patient's age, gender, and
comorbidities, complicated urinary infections may occur after COVID-19. They should be recognized and treated in
time in order not to escalate into a life-threatening condition such as urosepsis.
References
El-Arif, G., Farhat, A., Khazaal, S., Annweiler, C., Kovacic, H., Wu, Y., Cao, Z., Fajloun, Z., Khattar, Z. A., & Sabatier, J. M. (2021). The Renin-Angiotensin System: A Key Role in SARS-CoV-2-Induced COVID-19. Molecules (Basel, Switzerland), 26(22). https://doi.org/10.3390/molecules26226945
Faix, J. D. (2013). Biomarkers of sepsis. Critical Reviews in Clinical Laboratory Sciences, 50(1), 23–36. https://doi.org/10.3109/10408363.2013.764490
Fehr, A. R., & Perlman, S. (2015). Coronaviruses: an overview of their replication and pathogenesis. Methods in Molecular Biology (Clifton, N.J.), 1282, 1–23. https://doi.org/10.1007/978-1-4939-2438-7_1
Frithiof, R., Bergqvist, A., Järhult, J. D., Lipcsey, M., & Hultström, M. (2020). Presence of SARS-CoV-2 in urine is rare and not associated with acute kidney injury in critically ill COVID-19 patients. Critical Care (London, England), 24(1), 587. https://doi.org/10.1186/s13054-020-03302-w
Gabarre, P., Dumas, G., Dupont, T., Darmon, M., Azoulay, E., & Zafrani, L. (2020). Acute kidney injury in critically ill patients with COVID-19. Intensive Care Medicine, 46(7), 1339–1348. https://doi.org/10.1007/s00134-020-06153-9
Lamb, L. E., Timar, R., Wills, M., Dhar, S., Lucas, S. M., Komnenov, D., Chancellor, M. B., & Dhar, N. (2022). Long COVID and COVID-19-associated cystitis (CAC). International Urology and Nephrology, 54(1), 17–21. https://doi.org/10.1007/s11255-021-03030-2
Lin, W., Fan, J., Hu, L.-F., Zhang, Y., Ooi, J. D., Meng, T., Jin, P., Ding, X., Peng, L.-K., Song, L., Tang, R., Xiao, Z., Ao, X., Xiao, X.-C., Zhou, Q.-L., Xiao, P., & Zhong, Y. (2021). Single-cell analysis of angiotensin-converting enzyme II expression in human kidneys and bladders reveals a potential route of 2019 novel coronavirus infection. Chinese Medical Journal, 134(8), 935–943. https://doi.org/10.1097/CM9.0000000000001439
Maillard, D., Delpuech, C., & Hatzfeld, C. (1990). Ventilatory adjustments during sustained resistive unloading in exercising humans. European Journal of Applied Physiology and Occupational Physiology, 60(2), 120–126. https://doi.org/10.1007/BF00846031
Nalbandian, A., Sehgal, K., Gupta, A., Madhavan, M. V, McGroder, C., Stevens, J. S., Cook, J. R., Nordvig, A. S., Shalev, D., Sehrawat, T. S., Ahluwalia, N., Bikdeli, B., Dietz, D., Der-Nigoghossian, C., Liyanage-Don, N., Rosner, G. F., Bernstein, E. J., Mohan, S., Beckley, A. A., … Wan, E. Y. (2021). Post-acute COVID-19 syndrome. Nature Medicine, 27(4), 601–615. https://doi.org/10.1038/s41591-021-01283-z
Parmar, M. S. (2021). Acute kidney injury associated with COVID-19-Cumulative evidence and rationale supporting against direct kidney injury (infection). Nephrology (Carlton, Vic.), 26(3), 239–247. https://doi.org/10.1111/nep.13814
Perlot, T., & Penninger, J. M. (2013). ACE2 - from the renin-angiotensin system to gut microbiota and malnutrition. Microbes and Infection, 15(13), 866–873. https://doi.org/10.1016/j.micinf.2013.08.003
Rello, J., Valenzuela-Sánchez, F., Ruiz-Rodriguez, M., & Moyano, S. (2017). Sepsis: A Review of Advances in Management. Advances in Therapy, 34(11), 2393–2411. https://doi.org/10.1007/s12325-017-0622-8
Rysz, S., Al-Saadi, J., Sjöström, A., Farm, M., Campoccia Jalde, F., Plattén, M., Eriksson, H., Klein, M., Vargas-Paris, R., Nyrén, S., Abdula, G., Ouellette, R., Granberg, T., Jonsson Fagerlund, M., & Lundberg, J. (2021). COVID-19 pathophysiology may be driven by an imbalance in the renin-angiotensin-aldosterone system. Nature Communications, 12(1), 2417. https://doi.org/10.1038/s41467-021-22713-z
Subramanian, A., Nirantharakumar, K., Hughes, S., Myles, P., Williams, T., Gokhale, K. M., Taverner, T., Chandan, J. S., Brown, K., Simms-Williams, N., Shah, A. D., Singh, M., Kidy, F., Okoth, K., Hotham, R., Bashir, N., Cockburn, N., Lee, S. I., Turner, G. M., … Haroon, S. (2022). Symptoms and risk factors for long COVID in non-hospitalized adults. Nature Medicine, 28(8), 1706–1714. https://doi.org/10.1038/s41591-022-01909-w
