Advanced glycosylation end products in patients with diabetic nephropathy

Article Abstract:

Patients with diabetes develop a number of long-term complications of this disorder, but the factors responsible for these complications are poorly understood. At least some of the chronic problems associated with diabetes may due to the accumulation of what biochemists call advanced glycosylation end products (AGEs). Many proteins are glycosylated as a part of their normal synthesis; specific sugar molecules are added to the protein structure by specific enzymes in the cell. However, sugar molecules may chemically react with proteins without the help of enzymes. Since diabetic patients may have high levels of blood sugar for decades, the production of non-enzymatic glycosylated proteins is much greater among these patients. It is thought that these substances, also known as AGEs, may be eliminated from the body in healthy people, but may accumulate to a pathological degree in patients with diabetes. Some cells in the body apparently recognize AGEs and begin the process of their disposal, but the details of this process remain unclear. The kidneys may serve to complete the disposal process; if this is the case, AGEs would accumulate faster in patients with kidney disease. The development of a new method for measuring AGEs now permits this theory to be examined. The amount of AGEs was measured in autopsy tissue obtained from 9 patients with diabetes and 18 nondiabetic patients. The amount of AGEs was almost four times greater in the tissue from the diabetic patients. Furthermore, the diabetics who had end-stage kidney disease had about twice the amount of AGEs than diabetic patients without kidney disease. When AGEs were measured in the blood of living diabetic patients with kidney disease, it was found that the amount of AGEs decreased during dialysis. However, the decrease was less than the decrease in creatinine, an indicator of dialysis effectiveness. In two patients, AGE levels in the blood returned to normal after kidney transplantation. These results indicate that the kidneys play a role in the elimination of advanced glycosylation end products from the body. Apparently healthy kidneys are important in this regard and dialysis does not perform this function satisfactorily. (Consumer Summary produced by Reliance Medical Information, Inc.)

Glycosylation

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Toward a basic understanding of diabetic complications

Article Abstract:

Although type I and type II diabetes (insulin-dependent and non-insulin dependent diabetes, respectively) have different causes, they both result in long-term complications which seriously affect the health of diabetic patients. These complications include blindness and kidney failure; the complications affecting diabetics have in common that they involve damage to nerves and tiny blood vessels. This damage is believed to be the result of years of exposure to high amounts of glucose in the blood. Despite efforts at control, the blood sugar levels of diabetic patients never remain within the physiological limits achieved by healthy people. This extra glucose permits the chemical reaction of glucose with proteins, without the help of enzymes. The presence of the proteins chemically modified with glucose, called glycosylated proteins, correlates strongly with tissue damage in cases of long-standing diabetes. However, evidence is still lacking to indicate that the presence of these proteins in the blood and connective tissues actually causes the complications of diabetes. These non-enzymatically glycosylated proteins are called advanced glycosylation end products, or AGEs. These products are also found to increase with age in healthy individuals, and it is therefore tempting to speculate that the complications of diabetes may be related to some of the effects of normal aging. However, such analogies must be taken with a grain of salt. Closer physiological examination reveals many disparities between the effects of diabetes and normal aging. For example, several structures in the kidney enlarge in some diabetic patients. The increase in volume of the mesangium and the widening of the glomerular basement membrane correlate closely with kidney disease. No such changes are observed in the course of normal aging. Therefore, while both advanced diabetes and normal aging are associated with an increase in AGEs, other physiological factors must be at work as well. (Consumer Summary produced by Reliance Medical Information, Inc.)

Editorial

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Glomerular lesions and urinary albumin excretion in type I diabetes without overt proteinuria

Article Abstract:

Several studies have suggested that small amounts of albumin protein in the urine (microalbuminuria) of diabetic patients is a sign of degenerative kidney changes. This study tested the relation of albumin urine excretion to the microscopic appearance of kidney tissues in 48 patients with insulin-dependent (Type 1) diabetes, as evaluated with light and electron microscopes, which allow cells to be examined at very high magnification. The results were also correlated with other clinical and laboratory findings. The authors conclude that finding traces of albumin by itself is insufficient to predict accurately the level of anatomic kidney damage. However, when this condition is present with high blood pressure and

Analysis, Kidneys, Creatinine, Pathological histology, Urine, Urinalysis, Albumin, Kidney biopsy, Kidney glomerulus

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