3 research outputs found

    Kidney biopsy

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    The causes of acute and chronic decline in kidney function are vast. Understanding the underlying diagnosis is essential to slow the progression of the kidney disease or achieve recovery. Detailed clinical assessment and simple investigations can help identify the nature of kidney injury (pre-renal, intrinsic, post-renal). Used appropriately, kidney biopsy has the potential to generate valuable information to aid diagnosis, guide prognosis and management, and identify relapse of intrinsic kidney disease. However, kidney biopsy is an invasive procedure with significant, albeit small, complications because of the risk of bleeding. The decision to proceed should be led by the nephrology team and requires a careful risk–benefit assessment and close discussion with the patient

    Association between native T1 mapping of the kidney and renal fibrosis in patients with IgA nephropathy.

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    INTRODUCTION: IgA nephropathy (IgAN) is the commonest global cause of glomerulonephritis. Extent of fibrosis, tubular atrophy and glomerulosclerosis predict renal function decline. Extent of renal fibrosis is assessed with renal biopsy which is invasive and prone to sampling error. We assessed the utility of non-contrast native T1 mapping of the kidney in patients with IgAN for assessment of renal fibrosis. METHODS: Renal native T1 mapping was undertaken in 20 patients with IgAN and 10 healthy subjects. Ten IgAN patients had a second scan to assess test-retest reproducibility of the technique. Native T1 times were compared to markers of disease severity including degree of fibrosis, eGFR, rate of eGFR decline and proteinuria. RESULTS: All patients tolerated the MRI scan and analysable quality T1 maps were acquired in at least one kidney in all subjects. Cortical T1 times were significantly longer in patients with IgAN than healthy subjects (1540 ms ± 110 ms versus 1446 ± 88 ms, p = 0.038). There was excellent test-retest reproducibility of the technique, with Coefficient-of-variability of axial and coronal T1 mapping analysis being 2.9 and 3.7% respectively. T1 correlated with eGFR and proteinuria (r = - 0.444, p = 0.016; r = 0.533, p = 0.003 respectively). Patients with an eGFR decline > 2 ml/min/year had increased T1 times compared to those with a decline  0, compared to those with a 'T'-score of 0 (1575 ± 106 ms versus 1496 ± 105 ms, p = 0.131), though not to significance. CONCLUSIONS: Cortical native T1 time is significantly increased in patients with IgAN compared to healthy subjects and correlates with markers of renal disease. Reproducibility of renal T1 mapping is excellent. This study highlights the potential utility of native T1 mapping in IgAN and other progressive nephropathies, and larger prospective studies are warranted
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