Diabetes is defined as failure of the b-cells of the pancreas to secrete sufficient insulin to satisfy body requirements and is one of the most common complications of obesity (see 6.19 Diabetes/Syndrome X). Diabetes can be classified into two main types: type 1 and 2. Type 1 generally shows a marked hyperglycemia with diabetic ketoacidosis. In contrast to type 1, type 2 diabetes shows less hyperglycemia and ketoacidosis. The incidence of diabetes has increased enormously in this decade. Diabetes can be diagnosed by determining blood glucose level where 8-h fasting blood glucose is X 126 mg dL _ 1 or 2-h postprandial blood glucose X 200 mg dL _ 1 following an oral glucose tolerance test. Additionally, symptoms of marked hyperglycemia include polyuria and polydipsia.12
Type 1 diabetes is defined as the failure of pancreatic b-cells to secret insulin and can be subdivided into type 1A and 1B diabetes. Type 1A results from chronic, progressive T cell-mediated autoimmune destruction of the b-cells of the pancreas, eventually leading to severe insulin deficiency. The rate of b-cell destruction is quite variable, being rapid in some individuals, especially infants and young children, and slower in adolescents and adults. The disease occurs throughout childhood and adolescence in genetically predisposed individuals. Type 1A diabetes predominantly affects European Caucasians and is less frequent in African Americans, Asians, and Native North Americans. Type 1B diabetes has a low prevalence rate with unknown etiology and it is strongly inherited. There is no evidence of b-cell autoimmunity associated with type 1B diabetes. Patients with type 1 diabetes should receive insulin frequently and do not respond well to oral hypoglycemic drugs.13
Type 2 diabetes occurs as a result of a decrease in insulin secretion and/or insulin resistance due to lack of exercise and increased body weight gain. The increased incidence of type 2 diabetes parallels the worldwide obesity epidemic. A family history of type 2 diabetes has repeatedly been reported in patients with this disease and patients often have other independent risk factors for cardiovascular disease, including hypertension, dyslipidemia, and microalbuminuria. Until recently, children virtually always had type 1 diabetes mellitus caused by absolute deficiency of insulin secretion, whereas type 2 diabetes was predominantly a disease of middle-aged and elderly. Nowadays, type 2 diabetes accounts for 45% of the new diabetic cases in children and adolescents in the USA. There is a greater occurrence of type 2 diabetes in African American, Hispanic, and Native American adolescents.12 Children and adolescents with newly diagnosed type 2 diabetes are virtually always overweight or obese. Therefore, children and adolescents with type 2 diabetes may develop both renal micro- and macrovascular complications at a young age due to inadequate treatment. Patients with type 2 diabetes can be treated with oral hypoglycemic drugs and/or insulin.
There is a strong correlation between diabetes and the incidence of renal dysfunction. Diabetes mellitus is the most common cause of end-stage renal disease. Hyperglycemia itself can cause glomerular hyperfiltration, endothelial dysfunction, and albuminuria. Albumin constitutes about 40% of total urinary protein excreted in most patients with kidney disease and diabetes. Both albuminuria and proteinuria are early markers of kidney damage, particularly in diabetic kidney disease.14 The high prevalence of abnormal albuminuria in individuals with diabetes suggests that hyperglycemia is often associated with renal abnormalities in some subjects and that these abnormalities precede the onset of diabetes. Microalbuminuria is also an independent risk factor for renal disease in both diabetic and nondiabetic individuals. Many diabetic patients will progress from renal dysfunction that is characterized by glomerular hyperfiltration and albuminuria to diabetic nephropathy. Diabetic nephropathy is one of the most common complications of diabetes, occurring in 57% of diabetic subjects and may increase morbidity rate due to severe organ damage. Diabetic nephropathy shows functional and structural changes in the kidney including decrease in glomerular filtration rate and renal fibrosis. Taken together, it is well established that diabetes can lead to renal dysfunction and without pharmacological intervention, 20% to 40% of patients with type 2 diabetes progress to severe nephropathy and about 20% of these patients will eventually develop end-stage renal disease.15
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