Abstract

Pathophysiological abnormalities in early diabetic nephropathy are poorly understood. We employed MRI to characterise renal perfusion, tissue oxygenation and kidney size in non-diabetic volunteers and type 1 diabetic patients without and with early renal disease. We studied ten control participants (C; age 40.0 [range 31-54] years), nine longstanding normotensive type 1 diabetic patients (T1Normo; age 40.1 [31-50] years, estimated glomerular filtration rate [eGFR] 83.4 ± 10.6 ml min(-1) 1.73 m(-2)) and eight microalbuminuric type 1 diabetic patients (T1Micro; age 42.4 [33-52] years, eGFR 71.6 ± 13.7 ml min(-1) 1.73 m(-2)). Six microalbuminuric patients were restudied after 4 weeks without renin-angiotensin-aldosterone system inhibitors. Phase contrast angiography and kidney blood oxygen level dependent (BOLD) (R(2)(*)) MRI were performed, before and during water diuresis. Contrast-enhanced MRI was performed at baseline urine flow rate. Renal artery flow, renal vascular resistance (RVR), cortical and medullary volumes, and R(2)(*) were determined. Renal cortical and medullary volumes were similar in all groups (cortex: C 108 ± 16, T1Normo 112 ± 21, T1Micro 111 ± 10 cm(3)/1.73 m(2); medulla: C 35 ± 14, T1Normo 29 ± 10, 33 ± 6 cm(3)/1.73 m(2)). RVR increased from control to normoalbuminuric to microalbuminuric type 1 diabetic patients (C 0.061 ± 0.018, T1Normo 0.077 ± 0.014, T1Micro 0.093 ± 0.024 mmHg ml(-1) min(-1) 1.73 m(-2), ANOVA p = 0.012). RVR correlated inversely with eGFR in normoalbuminuric, but not in microalbuminuric diabetic patients. Renal artery flow was lower in the whole diabetes cohort (control 740 ± 205 vs diabetes 591 ± 128 ml min(-1) 1.73 m(-2), p = 0.035). Cortical and medullary volumes remain normal in early diabetic nephropathy. Decreased renal flow in longstanding normoalbuminuric type 1 diabetic patients may reflect intrarenal vascular stiffening, whereas in the microalbuminuric patients it may also reflect increased intraglomerular pressure.

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