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Kidney Week

Abstract: FR-PO104

B Cells Are Associated with Renal Recovery After AKI

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Coelho, Silvia, Hospital Prof. Dr. Fernando Fonseca, Amadora, Portugal
  • Salvador, Rute, CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisbon, Portugal
  • Cabral, M. guadalupe, CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisbon, Portugal
  • Corte-Real, Ana Sacchetti, Hospital Prof. Dr. Fernando Fonseca, Amadora, Portugal
  • Martins, Ana, Hospital Prof. Dr. Fernando Fonseca, Amadora, Portugal
  • Matos, Filomena Isabel, Hospital Prof. Dr. Fernando Fonseca, Amadora, Portugal
  • Freitas, Paulo, Hospital Prof. Dr. Fernando Fonseca, Amadora, Portugal
  • Jacinto, Antonio, Nova Medical School, Lisboa, Portugal

Group or Team Name

  • Tissue Repair and Inflammation
Background

The mechanisms associated with renal recovery after an episode of Acute Kidney Injury (AKI) are still poorly understood but immune factors seem to play a role. We aim to determine the association between the urinary immune profile of AKI patients and renal recovery.

Methods

Adult patients with AKI >stage 2 by KDIGO and sterile leukocyturia at admission in 2 Intensive Care Units (ICUs) of a Portuguese tertiary Hospital were prospectively included in a consecutive way. Anuria, CKD > stage 3, dialysis one week previous admission and absence of informed consent were exclusion criteria. Urinary flow cytometry was performed at Day 1 (D1) and 3 (D3). Renal recovery was defined as a decreased of at least one stage of AKI classification by KDIGO at 7days of ICU admission.

Results

From January to September 2018, a total of 552 patients were admitted in both ICUs, 108 with AKI >stage 2 by KDIGO at admission. Of these, 18 had sterile leukocyturia and no exclusion criteria. Median age was 75 years, 83.3% male, 88.9% caucasian, 33.3% diabetic and 66.7% hypertensive. Median baseline serum creatinine was 1.14mg/dl. APACHE II score was 30.5, 66.7% medical and 33.3% surgical admissions. Sepsis alone 44.4% or sepsis+hypoperfusion 38.9% were the most common causes of AKI, 33.3% needing Renal Replacement Therapy. Mortality at ICU and hospital discharge was 25.0% and 38.9%, respectively.
Half the patients recovered renal function (REC) and half did not (NREC). Serum creatinine and cystatin C at admission did not differ between REC and NREC groups (3.06 SD0.56 vs 3.74 SD1.90 mg/dl, NS; and 3.25 SD1.24 vs 4.08 SD1.21mg/dl, NS, respectively). At D1, REC patients had similar % of T Cells (CD45+CD3+) (0.5 vs 0.6%, NS) and more B Cells (CD45+CD19+) (19.6 vs 4.3%, p=0.046), NK Cells (CD45+CD161+) (4.5 vs 1.1%, NS), neutrophils (28.7 vs 16.5%, NS) and dendritics (CD45+CD1c+) (4.9 vs 1.7%, NS). Patients who recovered also had a higher macrophages M1 (CD45+CD11b+CD68+) ratio D1/D3 (3.4 vs 1.3%, NS).

Conclusion

Immune mechanisms seem to play a role in renal regeneration and recovery after an episode of AKI. In our critically ill population, urinary B Cells were statistically significantly associated with renal recovery at 7 days after AKI at ICU admission.