Long-standing proteinuria and poor glycaemic control make diabetic nephropathy (increased urinary albumin excretion in the absence of other causes) the most likely diagnosis. However, alternative diagnoses such as structural renal disease, childhood reflux nephropathy, membranous nephropathy, immunoglobulin A nephropathy or glomerulonephritis should be considered. The stage of renal disease should be identified so that appropriate action can be taken to treat complications of renal failure and plan for renal replacement therapy. Nephropathy in type 1 diabetes is almost invariably associated with retinopathy and frequently associated with neuropathy, so these should be specifically identified.

Diabetic nephropathy is marked by progression from normal urinary albumin excretion (UAE), through increased UAE, to reduced glomerular filtration rate (GFR) and finally, end-stage renal failure. Approximately one in three people who have had type 1 diabetes for 20 years will develop persistent microalbuminuria (UAE 30-300 mg/24 h), of whom half will already have gone on to develop persistent macroalbuminuria (>300 mg/24 h).1 The DCCT/EDIC (Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications) study cohort2 demonstrated that poor glycaemic control is the major modifiable risk factor associated with increased UAE in type 1 diabetes. Studies in the 1980s suggested that progression from microalbuminuria to macroalbuminuria occurred eventually in approximately 80% of patients. However, aggressive intervention, as described below, can halt or reverse progression of micro-albuminuria in up to 60% of patients.3 Where macroalbuminuria or reduced GFR are already established, aggressive intervention can substantially slow progression of renal disease. However, at least one in five people receiving renal replacement in industrialized nations have diabetes.

Advancing renal failure

GFR (ml/min/1.73m2)





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