Abstract
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.
Highlights
Diabetic nephropathy (DN) is the leading cause of chronic renal disease in patients starting renal replacement therapy [1] in the United States as well as in Brazil [2]
African-Brazilians are more susceptible to progress to end-stage renal disease (ESRD) than people of European ancestry, but there appears to be a similar prevalence of micro- or macroalbuminuria [13]
The increased incidence of ESRD attributable to diabetes mellitus (DM) suggests that other factors are involved in the etiology of DN, since a putative improvement in blood pressure (BP) levels, increased use of angiotensin converting enzyme (ACE) inhibitors and better glucose control due to lower glycemic targets have been frequent in recent years
Summary
It is essential to have a better understanding of it, especially in relation to prevention and aggressive management to avoid progression to ESRD. Its direct association with cardiovascular complications makes it imperative to perform intensive, early management of the risk factors. Detection of DN, the multifactorial approach targeting the main risk factors (hyperglycemia, hypertension, dyslipidemia and smoking), and the use of renoprotective agents such as the drugs that act on the renin-angiotensin-aldosterone system, may delay progression of kidney disease in DM, besides reducing cardiovascular mortality. ACE: angiotensin convertin enzyme; ARB: angiotensin receptor blocker; BP: blood pressure; DM: diabetes mellitus; DN: diabetic neprhopathy; ESRD: end-stage renal disease; ET-1: endothelin-1; GFR: glomerular filtration rate; HbA1c: glicohemoglobin A1c; MDRD: Modification of Diet in Renal Disease; RAS: renin-angiotensin system; UAE: urinary albumin excretion
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