The burden of diabetes mellitus is on the rise, largely driven by increasing obesity, with an estimated global prevalence of 366 million in 2011 and expected to affect 552 million people by 2030.1 As a result, the morbidity and mortality associated with diabetic complications is expected to rise.
Diabetic nephropathy is one of the most significant complications of diabetes mellitus and is the most common cause of worldwide end-stage kidney disease. The UK renal registry data suggests that 25.3 per cent of end-stage kidney disease patients in the UK have a primary diagnosis of diabetic nephropathy.2
Diabetic nephropathy is characterised by persistent albuminuria, progressive reduction in glomerular filtration rate (GFR) and characteristic pathological changes on histology. The earliest clinical evidence of diabetic nephropathy is the presence of persistent low levels of albumin in the urine (30-300 mg/day or 3.4-34 mg/mmol albumin to creatinine ratio), referred to as microalbuminuria.
Microalbuminuria cannot be detected by standard urine dipstick tests but by special dipsticks. The urine albumin concentration can be measured using 24-hour urine collections or, more commonly, using a spot urine sample to calculate the urine albumin to creatinine ratio.
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