Supplementary Materials

The PDF file includes:

  • Supplementary Materials and Methods
  • Fig. S1. The flowchart illustrates the selection criteria for the single-center study population.
  • Fig. S2. The flowchart illustrates the selection criteria for the study population from the Danish National Registry of Patients.
  • Fig. S3. The flowchart illustrates the selection criteria for the multicentric study population.
  • Fig. S4. AKI-driven papillary tumors originate from clonal proliferation of single TECs in mice.
  • Fig. S5. NICD1 overexpression in mouse tubular cells induces papillary tumors and CKD.
  • Fig. S6. AKI accelerates clonal type 2 papillary tumor development in mice.
  • Fig. S7. NOTCH1 overexpression enhances cell division and promotes aberrant mitosis.
  • Fig. S8. AKI induces papillary tumors by promoting clonal expansion of renal progenitors in mice.
  • Fig. S9. AKI induces papillary tumors from renal progenitors in a NOTCH1-dependent manner.
  • Table S1. Postoperative AKI is a risk factor for the development of pRCC recurrence in humans in a single-center study.
  • Table S2. The preoperative characteristics of 594 patients treated with partial nephrectomy for kidney tumors and clinical details of 89 patients with pRCC (the RECORd1 project).
  • Table S3. Postoperative AKI is a risk factor for the development of pRCC recurrence in humans in a multicentric study (RECORd1 project).
  • Table S4. AKI-activated pathways are overexpressed in human pRCC in a subtype-specific manner.
  • Table S5. Multivariate analysis indicates NOTCH1 as a risk factor for pRCC prognosis.
  • References (5379)

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Other Supplementary Material for this manuscript includes the following:

  • Movie S1 (.mp4 format). 3D reconstruction of a papillary tumor in Pax8/NICD1/Confetti kidney at 36 weeks.