Diabetic nephropathy is the leading cause of kidney disease in patients starting renal replacement therapy and affects ϳ40% of type 1 and type 2 diabetic patients. It increases the risk of death, mainly from cardiovascular causes, and is defined by increased urinary albumin excretion (UAE) in the absence of other renal diseases. Diabetic nephropathy is categorized into stages: microalbuminuria (UAE Ͼ20 g/min and Յ199 g/min) and macroalbuminuria (UAE Ն200 g/min). Hyperglycemia, increased blood pressure levels, and genetic predisposition are the main risk factors for the development of diabetic nephropathy. Elevated serum lipids, smoking habits, and the amount and origin of dietary protein also seem to play a role as risk factors. Screening for microalbuminuria should be performed yearly, starting 5 years after diagnosis in type 1 diabetes or earlier in the presence of puberty or poor metabolic control. In patients with type 2 diabetes, screening should be performed at diagnosis and yearly thereafter. Patients with micro-and macroalbuminuria should undergo an evaluation regarding the presence of comorbid associations, especially retinopathy and macrovascular disease. Achieving the best metabolic control (A1c Ͻ7%), treating hypertension (Ͻ130/80 mmHg or Ͻ125/75 mmHg if proteinuria Ͼ1.0 g/24 h and increased serum creatinine), using drugs with blockade effect on the reninangiotensin-aldosterone system, and treating dyslipidemia (LDL cholesterol Ͻ100 mg/dl) are effective strategies for preventing the development of microalbuminuria, in delaying the progression to more advanced stages of nephropathy and in reducing cardiovascular mortality in patients with type 1 and type 2 diabetes. Diabetes Care 28:176 -188, 2005DEFINITION AND EPIDEMIOLOGY -Diabetic nephropathy is the leading cause of chronic kidney disease in patients starting renal replacement therapy (1) and is associated with increased cardiovascular mortality (2). Diabetic nephropathy has been classically defined by the presence of proteinuria Ͼ0.5 g/24 h. This stage has been referred to as overt nephropathy, clinical nephropathy, proteinuria, or macroalbuminuria. In the early 1980s, seminal studies from Europe revealed that small amounts of albumin in the urine, not usually detected by conventional methods, were predictive of the later development of proteinuria in type 1 (3-5) and type 2 (6) diabetic patients. This stage of renal involvement was termed microalbuminuria or incipient nephropathy.The cumulative incidence of microalbuminuria in patients with type 1 diabetes was 12.6% over 7.3 years according to the European Diabetes (EURODIAB) Prospective Complications Study Group (7) and ϳ33% in an 18-year follow-up study in Denmark (8). In patients with type 2 diabetes, the incidence of microalbuminuria was 2.0% per year and the prevalence 10 years after diagnosis 25% in the U.K. Prospective Diabetes Study (UKPDS) (9). Proteinuria occurs in 15-40% of patients with type 1 diabetes, with a peak incidence around 15-20 years of diabetes (8,10,11). In patients with t...

Diabetic nephropathy is the leading cause of chronic renal disease and a major cause of cardiovascular mortality. Diabetic nephropathy has been categorized into stages: microalbuminuria and macroalbuminuria. The cut-off values of micro- and macroalbuminuria are arbitrary and their values have been questioned. Subjects in the upper-normal range of albuminuria seem to be at high risk of progression to micro- or macroalbuminuria and they also had a higher blood pressure than normoalbuminuric subjects in the lower normoalbuminuria range. Diabetic nephropathy screening is made by measuring albumin in spot urine. If abnormal, it should be confirmed in two out three samples collected in a three to six-months interval. Additionally, it is recommended that glomerular filtration rate be routinely estimated for appropriate screening of nephropathy, because some patients present a decreased glomerular filtration rate when urine albumin values are in the normal range. The two main risk factors for diabetic nephropathy are hyperglycemia and arterial hypertension, but the genetic susceptibility in both type 1 and type 2 diabetes is of great importance. Other risk factors are smoking, dyslipidemia, proteinuria, glomerular hyperfiltration and dietary factors. Nephropathy is pathologically characterized in individuals with type 1 diabetes by thickening of glomerular and tubular basal membranes, with progressive mesangial expansion (diffuse or nodular) leading to progressive reduction of glomerular filtration surface. Concurrent interstitial morphological alterations and hyalinization of afferent and efferent glomerular arterioles also occur. Podocytes abnormalities also appear to be involved in the glomerulosclerosis process. In patients with type 2 diabetes, renal lesions are heterogeneous and more complex than in individuals with type 1 diabetes. Treatment of diabetic nephropathy is based on a multiple risk factor approach, and the goal is retarding the development or progression of the disease and to decrease the subject's increased risk of cardiovascular disease. Achieving the best metabolic control, treating hypertension (<130/80 mmHg) and dyslipidemia (LDL cholesterol <100 mg/dl), using drugs that block the renin-angiotensin-aldosterone system, are effective strategies for preventing the development of microalbuminuria, delaying the progression to more advanced stages of nephropathy and reducing cardiovascular mortality in patients with diabetes.

Albumin measurements (UAC and UACR) in an RUS presented almost perfect accuracy for the screening of micro- and macroalbuminuria and UAC measured in an RUS is simpler and less expensive than UACR and UAER. It is suggested as a valid test for use in screening for diabetic nephropathy.