ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

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


The Latest on Twitter

Kidney Week

Abstract: TH-PO908

Multiparametric MRI for Assessment of CKD: Correlation with Histology and Progression

Session Information

Category: CKD (Non-Dialysis)

  • 1903 CKD (Non-Dialysis): Mechanisms


  • Buchanan, Charlotte Elizabeth, University of Nottingham , Nottingham, United Kingdom
  • Mahmoud, Huda, Royal Derby Hospital Renal Unit, Derby, United Kingdom
  • Cox, Eleanor, University of Nottingham , Nottingham, United Kingdom
  • Prestwich, Benjamin L., University of Nottingham , Nottingham, United Kingdom
  • Selby, Nicholas M., Royal Derby Hospital Renal Unit, Derby, United Kingdom
  • Taal, Maarten W., Royal Derby Hospital Renal Unit, Derby, United Kingdom
  • Francis, Susan, University of Nottingham , Nottingham, United Kingdom

Multiparametric Magnetic Resonance Imaging (MRI) allows non-invasive assessment of renal structure and function in CKD. Here, MR results are correlated with biopsy and clinical measures at baseline, with repeat scanning after 1 year to assess progression.


26 CKD patients (Stage 3-4, eGFR 20–59ml/min/1.73m2, 19M, 56±15yrs) were scanned within a median 53 days from renal biopsy, data were also collected on age-matched healthy volunteers (HVs). At baseline, patients were scanned twice, two weeks apart, to assess reproducibility. Histological fibrosis quantification was performed on renal biopsies with sirius red staining to measure % interstitial fibrosis (IF). GFR was determined using Iohexol clearance and urine PCR was measured. Clinical and MRI assessments were repeated at 1 year. Scanning was performed on a 3T Philips Ingenia scanner and included T1 mapping and diffusion weighted imaging as markers of fibrosis and inflammation, arterial spin labelling to assess perfusion, T2* mapping as a marker of oxygenation, and measures of kidney volume and renal artery flow. Analysis was performed using in-house software to create multiparametric maps. Baseline MR data were assessed against clinical measures and biopsy results, year 1 data was analysed to assess progression.


Cortex T1 was significantly increased in CKD patients compared to HVs (CKD:1559±18,HV:1435±19ms, p<0.001). Cortex diffusion was reduced in CKD patients, but not significantly. There was no significant difference in kidney volume or T2* between CKD patients and HVs. Cortex perfusion (CKD:86.8±10,HV:199.5±12ml/100g/min) and renal artery flow (CKD:156.9±10,HV:227.4±10ml/100g/min) were significantly lower in CKD (p<0.001). GFR was correlated with cortex perfusion, diffusion, T1 and renal artery flow. The strongest MRI measure to correlate with IF score was perfusion, whilst glomerular sclerosis correlated with cortex T1. The mean GFR did not vary significantly across 1 year, however patients fell into 2 groups; those with improved (n=8) and declined (n=12) renal function. There was a trend for change in T1 to be associated with progression of disease severity.


This work demonstrates MRI can differentiate pathophysiological changes in CKD and can be used as a method to assess progression of CKD.