Diffusion-weighted magnetic resonance imaging (DWI) is a non-invasive method sensitive to local water motion in the tissue. As a tool to probe the microstructure, including the presence and potentially the degree of renal fibrosis, DWI has the potential to become an effective imaging biomarker. The aim of this review is to discuss the current status of renal DWI in diffuse renal diseases. DWI biomarkers can be classified in the following three main categories: (i) the apparent diffusion coefficient—an overall measure of water diffusion and microcirculation in the tissue; (ii) true diffusion, pseudodiffusion and flowing fraction—providing separate information on diffusion and perfusion or tubular flow; and (iii) fractional anisotropy—measuring the microstructural orientation. An overview of human studies applying renal DWI in diffuse pathologies is given, demonstrating not only the feasibility and intra-study reproducibility of DWI but also highlighting the need for standardization of methods, additional validation and qualification. The current and future role of renal DWI in clinical practice is reviewed, emphasizing its potential as a surrogate and monitoring biomarker for interstitial fibrosis in chronic kidney disease, as well as a surrogate biomarker for the inflammation in acute kidney diseases that may impact patient selection for renal biopsy in acute graft rejection. As part of the international COST (European Cooperation in Science and Technology) action PARENCHIMA (Magnetic Resonance Imaging Biomarkers for Chronic Kidney Disease), aimed at eliminating the barriers to the clinical use of functional renal magnetic resonance imaging, this article provides practical recommendations for future design of clinical studies and the use of renal DWI in clinical practice.

Rates of cardiovascular mortality are disproportionately high in patients with end stage kidney disease receiving dialysis. However, it is now generally accepted that patient survival is broadly equivalent between the two most frequently used forms of dialysis, in‐center hemodialysis (HD) and peritoneal dialysis (PD). This equivalent patient survival is notable when considering how specific aspects of HD have been shown to contribute to morbidity and mortality. These include more rapid loss of residual renal function (RRF), HD‐induced myocardial and cerebral ischemia, and risk factors associated with the intermittent delivery of HD. Potential mechanisms specific to PD that may drive cardiovascular disease include the metabolic consequences of excessive absorption of glucose and glucose degradation products (GDPs), inadequate volume control, and high rates of hypokalemia. The aim of this review is to compare and contrast the different drivers of adverse outcomes between the dialysis modalities, as greater understanding of this may help in patient‐centered decision‐making when considering options for renal replacement therapy.

IDH remains a significant clinical problem. Recent evidence from the last 2 years does not support any major changes to current practice, with cooling of the dialysate and reduction of IDWG remaining cornerstones of management.

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Twelve patients underwent serial cardiac, cerebral and renal multiparametric 3T MRI scans before, during and after haemodialysis. During dialysis, there was a significant decline in cardiac and stroke index and myocardial strain, with increased diastolic dysfunction. This was accompanied by a reduction in blood flow to both the heart and brain. White matter T1 increased during dialysis suggesting fluid shifts increasing water content resulting in local oedema. Total kidney volume, renal cortex T1 and T2* all reduced during dialysis likely reflecting reduced renal blood volume and change in renal tissue water. These results highlight the acute multi-organ effects of dialysis.

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Background and Aims Chronic kidney disease (CKD) progression is currently monitored using estimated GFR (eGFR) and albuminuria but these are relatively crude measures with multiple limitations. Multiparametric renal magnetic resonance imaging (MRI) combines several MR measures into a single scan session, offering the potential to assess severity, progression and response to therapy in CKD in a novel, non-invasive way. Previous studies have focussed on cross-sectional comparisons of MRI and clinical measures. In this study we sought to investigate the ability of MRI variables to predict and monitor progression of CKD over two years. Method Persons with CKD stage 3-4 (eGFR 15-59ml/min/1.732) who had undergone renal biopsy were recruited. Participants underwent multiparametric renal MRI scans on a 3T Philips Ingenia scanner at baseline, one and two years. In addition demographic data, medical history, eGFR and urine protein:creatinine ratio (uPCR) was collected. Multiparametric renal MRI comprised longitudinal relaxation time (T1 using SE-EPI and bFFE readouts), Diffusion Weighted Imaging, renal blood flow (Phase Contrast MRI), renal cortex perfusion (Arterial Spin Labelling), and Blood Oxygen Level Dependent (BOLD) relaxation rate (R2*). CKD progression was defined as participants having a slope in eGFR of -5ml/min/yr or greater over 2 years. Interstitial fibrosis was quantified on renal biopsy samples. Results 22 participants underwent MRI scanning at baseline (7 participants were classified as ‘progressors’ and 15 as ‘stable’), while 13 completed all three scans (4 of whom were ‘progressors’). At baseline, cortex T1 was significantly higher for ‘progressors’ compared to ‘stable’ participants (p=0.02), and renal cortex perfusion was significantly lower (p=0.03). There was no significant difference in total kidney volume (TKV), ADC, renal cortex or medulla R2*, or renal biopsy measures of interstitial fibrosis between ‘progressor’ and ‘stable’ CKD participants. At Year 1 and Year 2 compared to baseline, a decrease in total kidney volume (TKV) was found, with a significantly greater decrease in TKV in the ‘progressor’ group (p=0.04). Over time, T1 increased in the ‘progressor’ group versus baseline, particularly in the cortex which showed a significant difference at year 1 (p=0.034) and year 2 (p=0.053). There was a trend for a reduction in ADC in ‘progressors’ versus stable participants over time. There was no significant change over time or between groups in renal cortex perfusion, renal cortex or medulla T2*, or renal biopsy measures of interstitial fibrosis. Conclusion Our results show that at baseline lower renal cortex perfusion and higher renal cortex T1 were associated with progression of CKD over 2 years suggesting that these MRI parameters may be a predictors of progression. On the other hand, cortex T1, TKV and ADC changed more in ‘progressors’ than in ‘stable’ participants over time (TKV and ADC decreased, T1 increased), suggesting that they may be useful MRI measures to monitor progression. Further studies are required to confirm these findings in a larger cohort of patients before renal MRI can be recommended for clinical use.

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