ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO0197

Chikungunya Fever: A Trigger for Different Renal Disorders

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Costa, Denise MARIA DO NASCIMENTO, Universidade Federal de Pernambuco, Recife, PE, Brazil
  • Oliveira, Camila Barbosa Lyra, Universidade Federal de Pernambuco, Recife, PE, Brazil
  • Vajgel, Gisele, Universidade Federal de Pernambuco, Recife, PE, Brazil
  • Cavalcante, Maria Alina G.M., Universidade Federal de Pernambuco, Recife, PE, Brazil
  • Lages, Joyce Santos, Universidade Federal do Maranhao, Sao Luis, MA, Brazil
  • Neves, Precil D., Universidade de Sao Paulo, Sao Paulo, São Paulo, Brazil
  • Salgado Filho, Natalino, Universidade Federal do Maranhao, Sao Luis, MA, Brazil
  • Valente, Lucila Maria, Universidade Federal de Pernambuco, Recife, PE, Brazil
  • Barros-Silva, Gyl, Universidade Federal do Maranhao, Sao Luis, MA, Brazil
Background

Prevalence of chikungunya fever (CHIK)-related kidney injury (KI) is variable, but data are scarce and limited to the acute phase of the disease. Necropsies performed in fatal acute cases of CHIK show that viral RNA can be found in renal tissue, but clinical and histopathological aspects poorly characterized. This study aimed to describe renal histopathological features and to detect viral antigens in renal tissue in patients affected by CHIK in different phases of infection.

Methods

This was an exploratory study, conducted between 2016 and 2020. Patients followed in six nephrology reference centers due to KI with onset after different phases of CHIK infection were evaluated. These patients had hematuria, proteinuria and/or renal dysfunction after a common history of CHIK infection and were referred for renal biopsy. Viral antigens were investigated by electron microscopy, immunohistochemistry and PCR in renal tissue.

Results

Sixteen patients (aged 10-59years) had KI 0.5 to 24months after CHIK, with predominance of glomerular lesions. Initial creatinine ranged from 0.2 to 22.3mg/dl (median 3.9mg/dl; IQR 1.0-5.5). Proteinuria and hematuria were initially detected in 94% and 81% of patients, respectively. Histopathological findings comprised diagnoses of focal segmental glomerulosclerosis (FSGS) (3), class IV lupus nephritis (3), crescentic glomerulonephritis (2), atypical hemolytic uremic syndrome (aHUS) (2), pauci-immune vasculitis (1), PLA2R-positive membranous nephropathy (2), collapsing glomerulosclerosis (CG) (2). One patient was diagnosed with collagen IV-related nephropathy in renal biopsy performed due to macroscopic hematuria after CHIKV infection. No viral antigens were detected in renal tissue. The 2 patients with aHUS included in the study carry heterozygosis mutations associated with increased risk of developing the disease. APOL1 high-risk genotypes were identified in 2 patients with CG (G1/G2 and G2/G2) and 1 patient with FSGS (G1/G2). Nine (56%) patients progressed to chronic kidney disease after a median follow-up of 12 months.

Conclusion

Our findings reveal the potential of CHIK virus to directly cause and/or trigger KI. These effects can be translated into a variety of renal lesions potentially with significant severity.