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Abstract: SA-PO217

Persistence of CKD and Hypertension at 12 Months After Cisplatin Therapy in Children

Session Information

  • Onco-Nephrology: Clinical
    November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Onco-Nephrology

  • 1500 Onco-Nephrology

Authors

  • Lebel, Asaf, The Hospital for Sick Children, Toronto, Ontario, Canada
  • McMahon, Kelly, McGill University Health Centre, Montreal, Quebec, Canada
  • Cockovski, Vedran, The Hospital for Sick Children, Toronto, Ontario, Canada
  • Lee, Jasmine, The Hospital for Sick Children, Toronto, Ontario, Canada
  • Yordanova, Mariya, Montreal Children's Hospital, Montreal, Quebec, Canada
  • Huynh, Louis, Queen's University, Kingston, Ontario, Canada
  • Crépeau-Hubert, Frédérik, McGill University, Montreal, Quebec, Canada
  • Blydt-Hansen, Tom D., University of British Columbia, Vancouver, British Columbia, Canada
  • Mammen, Cherry, British Columbia Children's Hospital, Vancouver, British Columbia, Canada
  • Pinsk, Maury N., University of Manitoba, Winnipeg, Manitoba, Canada
  • Rassekh, Shahrad Rod, British Columbia Children's Hospital, Vancouver, British Columbia, Canada
  • Schultz, Kirk Raymond, British Columbia Children's Hospital, Vancouver, British Columbia, Canada
  • Tsuyuki, Ross T., University of Alberta, Edmonton, Alberta, Canada
  • Zappitelli, Michael, The Hospital for Sick Children, Toronto, Ontario, Canada
Background

Cisplatin (CisP) commonly causes acute kidney injury (AKI). Late CisP-nephrotoxicity (chronic kidney disease (CKD); hypertension (HTN)) is poorly characterized in children. We determined prevalence and progression of CKD and HTN 3 and 12 months (m) post-CisP therapy, and if CisP-AKI is associated with these outcomes.

Methods

12 Canadian-site prospective cohort study. Protocol: Children treated with CisP were followed during cancer therapy (labs, clinical data) and at 3 and 12m post-CisP therapy completion (blood pressure [BP], blood and urine collection). AKI during cancer therapy: defined per KDIGO serum creatinine criteria. Outcomes: a) CKD: eGFR <90ml/min/1.73m2 or urine albumin/creatinine ratio ≥3mg/mmol; b) elevated BP and HTN, per 2017 child HTN guidelines. Paired t-tests and McNemar’s test used to determine if outcome prevalence differed from 3 to 12 m. Logistic regression (odds ratio [OR], 95% CI) used to determine relation of AKI with 3 and 12m CKD and HTN.

Results

Of 159 patients (50.3% male; median age 5.5 [IQR 2.4–11.9] yrs), 37 % developed AKI. Figure (1): There was no significant change in 3 vs. 12m prevalence (McNemar p-values all >0.05) of any outcomes (CKD: 44% and 39%, respectively; HTN: both 17%). eGFR was significantly lower at 12 vs. 3m (Figure (2), median [IQR] 135.8 [52.1] vs. 120.6 [37.4], respectively, p-value <0.001). AKI during CisP therapy was associated with 3 and 12m CKD (OR 2.2 [95% CI 1.2-4.4] and 2.8 [95% 1.4-5.6], respectively) but not HTN (OR 1.6 [95% CI 0.7-3.9] and 2.1 [95% CI 0.9-5.1], respectively).

Conclusion

CKD and HTN were common and persisted from 3m to 12m after cancer therapy completion. AKI was associated with later CKD but not HTN. Research on interventions to prevent AKI and reduce post-CisP CKD and HTN is needed.

Funding

  • Government Support - Non-U.S.