Urinary albumin and diabetic nephropathy

Laboratory criterion characterizing the development of the pronounced stage of diabetic nephropathy is proteinuria (usually with unchanged urine sediment), decreased SCF and increasing azotemia (concentration of urea and creatinine in the blood serum). In 30% of patients, nephrotic syndrome develops (massive proteinuria - more than 3.5 g / day, hypoalbuminemia, hypercholesterolemia, edema). From the moment of the appearance of constant proteinuria, the rate of decrease in SCF is on average 2 ml / min. month, which leads to the development of terminal chronic renal failure already 5-7 years after the detection of proteinuria.

Stages of development of diabetic nephropathy

Stage	Clinical and laboratory characteristics	Development timeframes
Hyperfunction of the kidneys	Increase in SCF more than 140 ml/min Increased renal blood flow Renal hypertrophy Normoalbuminuria (less than 30 mg/day)	At the beginning of the disease
Initial structural changes in kidney tissue	Thickening of the glomerular capillary basement membranes Expansion of the mesangium High SCF persists Normoalbuminuria (less than 30 mg/day)	2-5 years
Incipient nephropathy	Microalbuminuria (30-300 mg/day) SCF is high or normal. Intermittent increase in blood pressure.	5-15 years
Severe nephropathy	Proteinuria (more than 500 mg/day) SCF normal or moderately reduced Arterial hypertension	10-25 years
Uremia	Decrease in SCF to less than 10 ml/min	More than 20 years from the onset of diabetes mellitus or 5-7 years from the appearance of proteinuria
	Arterial hypertension Symptoms of intoxication

At the stage of chronic renal failure, laboratory tests allow us to determine the tactics for managing patients with diabetes mellitus.

• With the development of chronic renal failure in patients with type 1 diabetes mellitus, the daily requirement for insulin decreases sharply, and as a result, the frequency of hypoglycemic conditions increases, which requires a reduction in the insulin dose.
• Patients with type 2 diabetes mellitus taking oral hypoglycemic drugs are recommended to be switched to insulin therapy if chronic renal failure develops, since most of these drugs are metabolized and excreted by the kidneys.
• If the serum creatinine concentration is more than 500 μmol/L (5.5 mg%), it is necessary to consider preparing the patient for hemodialysis.
• Serum creatinine concentration of 600-700 μmol/L (8-9 mg%) and glomerular filtration rate (GFR) of less than 10 ml/min are considered indications for kidney transplantation.
• An increase in the concentration of creatinine in the blood serum to 1000-1200 μmol/l (12-16 mg%) and a decrease in SCF to less than 10 ml/min are considered an indication for programmed hemodialysis.

Renal failure associated with diabetic nephropathy is the direct cause of death in approximately half of cases of type 2 diabetes mellitus. It is very important for the clinician to conduct laboratory tests frequently to monitor the dynamics of diabetic nephropathy. According to the recommendations of WHO experts, in the absence of proteinuria, microalbuminuria testing should be performed:

• in patients with type 1 diabetes mellitus, at least once a year after 5 years from the onset of the disease (if diabetes mellitus occurs after puberty) and at least once a year from the moment of diagnosis of diabetes at the age of up to 12 years;
• in patients with type 2 diabetes mellitus at least once a year from the moment of diagnosis.

With normal excretion of albumin in urine, one should strive to maintain the fraction of glycosylated hemoglobin (HbA _1c) at a level of no more than 6%.

In the presence of proteinuria in patients with diabetes mellitus, the rate of increase in proteinuria (in daily urine) and the rate of decrease in SCF are examined at least once every 4-6 months.

At present, the microalbuminuria test should be considered as an indicator of the function of plasma membranes of highly differentiated cells. Normally, negatively charged albumin does not pass through the glomerular filter of the kidneys, primarily due to the presence of a high negative charge on the surface of epithelial cells. This charge is due to the structure of phospholipids of cell membranes, rich in polyene (polyunsaturated) fatty acids. A decrease in the number of double bonds in acyl residues of phospholipids reduces the negative charge, and albumin begins to be filtered into primary urine in increased quantities. All these changes occur during the development of atherosclerosis, so microalbuminuria develops in patients with hereditary forms of GLP, coronary heart disease (CHD), arterial hypertension, as well as in 10% of practically healthy people (in screening studies) and in patients with impaired glucose tolerance. Changes in the structure of phospholipids of plasma membranes of highly differentiated cells occur in atherosclerosis and immediately affect the charge of membranes, so a study of microalbuminuria allows us to identify the early stages of the disease.

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