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Diabetic Nephropathy - Overview of Information
Last reviewed: 12.07.2025
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Diabetic nephropathy is a specific lesion of the renal vessels in diabetes mellitus, accompanied by the formation of nodular or diffuse glomerulosclerosis, the terminal stage of which is characterized by the development of chronic renal failure.
Diabetes mellitus is a group of metabolic diseases characterized by the development of persistent hyperglycemia due to a defect in insulin secretion, insulin action, or both (World Health Organization, 1999). In clinical practice, the main group of patients with diabetes mellitus are patients with type 1 diabetes mellitus (insulin-dependent diabetes mellitus) and type 2 diabetes mellitus (non-insulin-dependent diabetes mellitus).
With prolonged exposure of hyperglycemia to the vessels and nervous tissue of the body, specific structural and functional changes in target organs occur, which is manifested by the development of complications of diabetes mellitus. Conventionally, these complications can be divided into microangiopathies (damage to small and medium-sized vessels), macroangiopathies (damage to large-caliber vessels) and neuropathy (damage to nervous tissue).
Diabetic nephropathy is classified as a microangiopathy. It is considered a late complication of diabetes mellitus of both type 1 and type 2.
Epidemiology of diabetic nephropathy
Throughout the world, diabetic nephropathy with the development of chronic renal failure is considered the main cause of death in patients with type 1 diabetes. In patients with type 2 diabetes, diabetic nephropathy is the second leading cause of death after cardiovascular diseases. In the United States and Japan, diabetic nephropathy is the most common kidney disease (35-40%), pushing primary kidney diseases such as glomerulonephritis, pyelonephritis, and polycystic kidney disease into second or third place. In European countries, the "epidemic" of diabetic nephropathy is less threatening, but it accounts for 20-25% of the causes of extracorporeal treatment of chronic renal failure.
In Russia, mortality from renal failure in type 1 diabetes, according to the State Register (1999-2000), does not exceed 18%, which is 3 times lower than the level registered in the world over the past 30 years. In type 2 diabetes, mortality from chronic renal failure in Russia is 1.5%, which is 2 times lower than the world level.
Diabetic nephropathy has become the most common cause of chronic renal failure in the United States and European countries. The reasons for this phenomenon are mainly the rapid growth of type 2 diabetes and the increase in life expectancy of patients with diabetes.
The prevalence of diabetic nephropathy depends primarily on the duration of the disease. This is especially evident in patients with type 1 diabetes mellitus, who have a relatively precise date of onset. Nephropathy rarely develops in the first 3-5 years in patients with type 1 diabetes mellitus, and is detected in almost 30% of patients after 20 years. Most often, diabetic nephropathy develops 15-20 years after the onset of the disease. For patients with type 1 diabetes mellitus, the age of onset of the disease is very important. The maximum frequency of diabetic nephropathy is in people with the onset of diabetes mellitus at the age of 11-20 years, which is determined by the pathological effect on the kidneys in combination with age-related hormonal changes in the body.
The prevalence of diabetic nephropathy in type 2 diabetes mellitus is less studied primarily due to the uncertainty of the onset time of type 2 diabetes mellitus, which usually develops after 40 years and often aggravates existing kidney diseases. Therefore, already at the time of diagnosis of type 2 diabetes mellitus, microalbuminuria can be detected in 17-30% of patients, proteinuria in 7-10%, and chronic renal failure in 1%.
Causes and pathogenesis of diabetic nephropathy
The development of kidney damage in diabetes mellitus is associated with the simultaneous influence of two pathogenetic factors - metabolic (hyperglycemia and hyperlipidemia) and hemodynamic (the influence of systemic and intraglomerular hypertension).
Hyperglycemia acts as the main initiating metabolic factor in the development of diabetic kidney damage. In the absence of hyperglycemia, changes in renal tissue characteristic of diabetes mellitus are not detected.
There are several mechanisms of the nephrotoxic effect of hyperglycemia:
- non-enzymatic glycosylation of renal membrane proteins, which changes their structure and function;
- direct toxic effect of glucose on kidney tissue, leading to activation of the enzyme protein kinase C, which increases the permeability of renal vessels;
- activation of oxidative reactions leading to the formation of a large number of free radicals, which have a cytotoxic effect.
Hyperlipidemia is another metabolic factor involved in the development and progression of diabetic nephropathy. Modified LDL damages the kidneys by penetrating through the damaged endothelium of the glomerular capillaries and promoting the development of sclerotic processes in them.
Intraglomerular hypertension (high hydrostatic pressure in the capillaries of the renal glomeruli) acts as the main hemodynamic factor in the development of diabetic nephropathy. This phenomenon in diabetes mellitus is based on an imbalance in the tone of the afferent and efferent arterioles of the renal glomerulus: on the one hand, there is a "gaping" of the afferent glomerular arteriole due to the toxic effect of hyperglycemia and activation of vasodilating hormones, and on the other hand, there is a constriction of the efferent renal arteriole due to the action of local angiotensin II.
However, in diabetes mellitus of both types 1 and 2, arterial hypertension is the most powerful factor in the progression of renal failure, which in terms of its damaging effect is many times greater than the influence of metabolic factors (hyperglycemia and hyperlipidemia).
Causes and pathogenesis of diabetic nephropathy
Symptoms of diabetic nephropathy
At the initial stages (I and II), the course of diabetic nephropathy is asymptomatic. When performing the Reberg test, an increase in SCF is noted (> 140-150 ml/min x 1.73 m2 ).
At stage III (the stage of incipient diabetic nephropathy), symptoms are also absent, microalbuminuria (20-200 mg/l) is determined with normal or increased SCF.
Starting from the stage of severe diabetic nephropathy (stage IV), patients develop clinical symptoms of diabetic nephropathy, which primarily include:
- arterial hypertension (appears and increases rapidly);
- swelling.
Where does it hurt?
Diagnosis of diabetic nephropathy
Diagnosis and staging of diabetic nephropathy are based on anamnesis data (duration and type of diabetes mellitus), laboratory test results (detection of microalbuminuria, proteinuria, azotemia and uremia).
The earliest method of diagnosing diabetic nephropathy is the detection of microalbuminuria. The criterion for microalbuminuria is highly selective excretion of albumin in urine in an amount of 30 to 300 mg/day or 20 to 200 mcg/min in the night portion of urine. Microalbuminuria is also diagnosed by the albumin/creatinine ratio in morning urine, which eliminates errors in daily urine collection.
Diagnosis of diabetic nephropathy
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Treatment of diabetic nephropathy
The basis of effective therapy of diabetic nephropathy is early diagnostics and treatment carried out in accordance with the stage of the disease. Primary prevention of diabetic nephropathy aims to prevent the occurrence of mycoalbuminuria, i.e. impact on its modifiable risk factors (level of carbohydrate metabolism compensation, intraglomerular hemodynamics, lipid metabolism disorder, smoking).
The main principles of prevention and treatment of diabetic nephropathy include:
- glycemic control;
- blood pressure control (blood pressure level should be < 135/85 mmHg in patients with diabetes mellitus in the absence of microalbuminuria, < 130/80 mmHg in the presence of microalbuminuria and < 120/75 mmHg in patients with proteinuria);
- control of dyslipidemia.
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