Diabetic kidney disease is the number one cause of chronic kidney failure in Western countries: 25 to 50 per cent and more than 90 per cent are type 2 diabetes.
Diabetic glomerulonephritis is the term used to refer to the secondary glomerular damage caused by diabetes. These glomerular lesions have morphological features described by Kimmelstiel and Wilson since 1936. However, diabetic nephropathy, in addition to glomerular damage, has other lesions caused by diabetes itself. should be in the kidneys such as tubular damage or manifestations of necrosis of the kidney radio or bladder neuropathy caused by diabetes.
Diabetic glomerulonephritis is a typical complication of insulin-dependent type I diabetes that occurs in people with diabetes from a very young age. However, it can also occur in patients with type II diabetes that is not insulin-dependent.
Nowadays, in the European and American countries, end-stage chronic kidney failure due to diabetes accounts for a high rate and is increasing.
Diabetic glomerulonephritis (defined by frequent proteinuria in people with diabetic retinopathy or in people with kidney biopsy results in fibrosis - glomerular fibrosis) often occurs. is currently starting in year 10 in Insulin-dependent diabetic patients. The annual incidence rate peaks between the 15th and 20th year of diabetes. The duration of Insulin-dependent diabetes is a major risk factor for developing diabetic nephropathy as well as diabetic retinopathy, in addition to hyperglycaemia, hypertension is also factors. Another risk factor for kidney complications in diabetic patients.
A lifetime in patients with diabetic nephropathy is greatly reduced. Without effective treatment, half of all patients die after 7 years of proteinuria. The mortality rate in this group of patients is 37 times higher than in the general population. In contrast, diabetic patients without proteinuria have an almost normal lifespan. It should also be noted that the majority of the causes of death in insulin-dependent diabetes are less associated with kidney failure, which is often associated with cardiovascular disease, especially coronary artery disease.
Diabetic kidney disease is the number one cause of chronic kidney failure in Western countries: 25 to 50% and more than 90% are type 2 diabetes.
Mechanism of pathogenesis
The mechanism for secondary glomerulonephritis after insulin-dependent diabetes is under discussion, but the more recent theories are interesting because they may have beneficial consequences for the prevention and or treatment of kidney disease. diabetes.
The role of hemodynamic abnormalities observed at the onset of diabetes has not been known recently. Increased filtration and increased pressure account for microalbuminuria and also possible loosening of the vasculature can cause glomerular fibrosis. Factors that cause the increase in filtration are many: first of all, chronic hyperglycaemia but also due to increased secretion of insulin-antagonistic hormones (glucagon, growth hormone) and active substances that alter arterioles. the renal arrival and arterioles of the kidneys (especially PGE2 and PGI2).
The increase in blood flow through the capillaries plays a major role in vascular pathology (retina and other capillaries).
Secondary metabolic disorders following hyperglycaemia are also involved in the development of kidney disease by altering the molecular structure of glomerular components, especially the basal membrane, by increasing stool glucose and decreasing sulphate process. Polyol metabolic sugar alterations (increased production of sorbitol and fructose) whose role in diabetic cataract development are certain, may also be involved in proteinuria. It results in increased glomerular filtration of macromolecules and accumulation in the glomeruli of circulating proteins causing glomerular damage.
Implementing the quadrants
The definitive diagnosis of diabetic nephropathy is based on cytology. However, in most cases, a positive diagnosis is usually based on proteinuria (mainly albumin), increased blood pressure, and decreased glomerular filtration rate.
Albuminuria: Can be quantified by special immunological techniques (radioactive immunity, ELISA ...). Allows the determination of albuminuria in a very small amount in urine. In normal human’s albumin excreted in urine does not exceed 20-30 mg/day or 15-20 μg / min. When the urine contains albumin from 30mg to 300 mg/day (from 20 to 200 μg / min) called microalbuminuria: this is an early abnormal marker in the kidney, valuable in diagnosis in the early stage of urinary tract diabetes on the kidneys. When albuminuria is 300 mg / 24 hours or more, it is called gross albuminuria (corresponding to 0.5 g / 24 hours of protein). It should be noted that the urinary albumin excretion is very different from time to time on the same individual, so several albumin urinary tests are required for evaluation.
Blood pressure: Hypertension is a symptom of diabetic kidney disease. However, arterial blood pressure depends on the stage of renal complications. In the stage of microalbuminuria, the systolic blood pressure at night decreases slightly and this phenomenon no longer exists when there is macroscopic albumin.
Decreased glomerular filtration rate: Decreased glomerular filtration rate is a symptom of kidney failure, a complication of end-stage diabetes. The glomerular filtration rate is assessed by creatinine clearance coefficient. However, it should be noted that creatinine measurement may be incorrect due to hyperglycaemia. Some other substances are also used to evaluate the clearance coefficient in diabetic nephropathy such as inulin, radioisotopes 125Iodothalamate, 51Cr - EDTA.
In addition to the three signs mentioned above, to evaluate the glomerular damage in diabetic nephropathy, when the diagnosis is based on:
Time of diabetes: being sick for many years, dependent on insulin.
Symptoms of microscopic vascular disease (especially in diabetic retinopathy).
In diabetic patients with trisomy of glomerulonephritis with years of disease and retinopathy, the probability of having diabetic nephropathy is greater than 95%.
Clinical and experimental studies (especially in patients with insulin-dependent type I diabetes, followed for a long time) have shown that characteristic diabetic nephropathy has morphological abnormalities and Functioning very early, Mogensen was divided into 5 phases:
Stage 1: The period of hyperfunction and hypertrophy, which occurs immediately after diabetes mellitus. Increased kidney stimulation, enlarged glomeruli, but their structure is normal.
The level of glomerular filtration increases, blood flow through the kidney increases in parallel, can increase urinary albumin. Glomerular filtration decreased after several weeks or months of insulin treatment, but the size of the kidneys remained unchanged.
Stage 2: Can persist for many years and 60% of type I diabetes lasts for life. Glomerular filtration rate may increase. This increase is correlated with kidney size and diabetes control. Perhaps increased filtration and poor diabetes control are needed to develop diabetic nephropathy. Urinary albumin secretion is normal but may be increased in stressful situations. The thickness of the glomerular basal membrane increases, the intervascular stroma increases more and these lesions are irreversible.
Stage 3: The initial diabetic kidney disease stage. Occurs only in 40% of patients with diabetes. It lasts 11-20 years, albumin urinary excretion increases frequently for several years from 10-200 μg / min. The increase infiltration persisted, but it began to decrease as urinary microalbuminuria increased. Blood pressure readings often rise higher than the average person. It is not known (according to current reviews) whether therapeutic interventions at this stage (good control of hyperglycaemia, antihypertensive treatment) allow delaying progression; However, microalbuminuria is also significantly reduced.
Stage 4: Is the established diabetic kidney disease stage with proteinuria regularly over 0.5g / 24 hours, arterial hypertension is constant. The nephrotic syndrome often occurs. Complications other than diabetic nephropathy are also common, especially retinopathy (often blind), peripheral neuropathy and or autonomic neuropathy. Glomerular filtration rate decreased by an average of 1ml / month; Effective antihypertensive treatment can slow this progression.
In contrast, it is not yet certain whether strict blood sugar control affects the progression of kidney failure.
Glomerular damage is characteristic: diffuse glomerular fibrosis exists, consisting of progressive basal membrane thickening and an increase in the intervascular stroma, in 10-20% of cases there are nodules stained by accumulating PAS convergence in the adjacent space of the glomeruli is called nodular glomerular fibrosis of Kimmelstiel and Wilson.
Stage 5: Is the stage of end-stage renal failure. These patients make up an important part of the patient population receiving treatment in non-kidney dialysis centres and kidney transplants.
With diabetes that is not insulin-dependent (10 times more common than the other group), kidney disease is also a common complication, occurring in
20-40% of this type of diabetes mellitus; 3-8% progress to end-stage chronic renal failure. In this diabetic nephropathy, there is no increase in glomerular filtration.
In practice insulin-dependent diabetic patients, a kidney biopsy is not required to confirm the diagnosis if the duration of the diabetes mellitus is more than 10 years and there is diabetic retinopathy. In contrast, a kidney biopsy is necessary if these two factors are inadequate and or the clinical picture is leading to another etiologic.
Comparing two factors albuminuria and blood pressure often allows to distinguish between diabetic and diabetic patients with renal complications, when comparing these 2 factors in diabetes with 6 conditions the following scenario occurs:
Table: Correlation situations between hypertension, albuminuria in diabetes mellitus.
Diabetes + primary hypertension
Diabetes + severe hypertension (1)
Diabetes and severe hypertension (1.2)
Diabetic kidney disease in early stage
Diabetic kidney disease
(1: There is left ventricular hypertrophy; 2: There is damage to many other organs of hypertension)
Prevent diabetic kidney disease
Primary prophylaxis of type 1 diabetes is likely to be with an immunosuppressive treatment because it is an autoimmune disease.
Type 2 diabetes: need to combat risk factors (too much weight gain and sedentary lifestyle).
Primary and secondary prophylaxis of diabetic nephropathy includes:
Ideal blood sugar control: Normalization of blood sugar is a top priority in treatment. Conventional insulin therapy (3.4 injections a day) is commonly used. This reduces the risk of kidney disease in type 1 diabetes. The benefits of strict glycaemic control in type 2 diabetes are probably equally worthwhile. The required metabolic target is HbA1c <7%.
Usually, in diabetes with kidney complications, it is more difficult to keep blood sugar stable than without kidney complications.
Antihypertensive treatment may prevent diabetic nephropathy or slow its progression. In type 2 diabetes, angiotensin II receptor blockers reduce the risk of gross proteinuria and chronic renal failure. In patients with type 1 diabetes, treatment with conventional ACE inhibitors to normalize blood pressure may have similar effects.
Smoking cessation reduces the risk of occurrence and severity of microalbuminuria in both forms of diabetes by 30%.
Treat diabetic nephropathy when confirmed
For all stages of diabetic nephropathy, the goal of treatment is control of metabolism by secretory secretion and Insulin therapy. hypoglycaemia is not prescribed any more as soon as the CRC is below 30 ml/min (risk of hypoglycaemia with Sulfamide and acidosis with Biguanide)
In type 1 diabetes ACE inhibitors (including about 25% of people with normal blood pressure) are indicated as there is evidence of their effectiveness in slowing the progression of diabetic nephropathy. Unlink type 1.
In type 2 diabetic nephropathy, angiotensin sine II receptor inhibitors (Losartan, Irbesartan) slow the progression of kidney disease.
Attention when giving ACE inhibitors and angiotensin II receptor inhibitors.
Study on renal artery stenosis in patients with type 2 diabetes.
Regular monitoring of biological tests, which take into account blood potassium and serum creatinine.
The ideal blood pressure goal is 130/80 mm Hg or even 125/75 mmHg if the urinary protein is more than 1 g / 24 h, with ACE inhibitors or angiotensin II receptor inhibitors.
To achieve blood pressure within the normal range in diabetic nephropathy requires a combination of 2, 3, or 4 antihypertensive drugs. Diuretics are often combined with ACE inhibitors or receptor blockers. The angiotensin II form because it increases the antihypertensive and anti-proteinuria effect. A moderate salt restriction (6 g / day) is required with antihypertensive therapy.
When using a diet high in protein, which increases proteinuria and affects kidney function, a portion of about 0.8 g protein/kg/day is needed. In practice, the risk of malnutrition appears without careful monitoring.
Vascular risk factors should be considered because cardiovascular complications are increased in this patient population.
Treatment for end-stage chronic renal failure
Dialysis treatment is usually earlier than for non-diabetic chronic renal failure (when the creatinine clearance coefficient calculated by Cockcroft is about 15 ml/min).
Due to the rapid progression of kidney disease and complications in peripheral blood vessels (calcification of the arteries), the creation of blood vessels for haemodialysis (vasculature) must be performed earlier (when the creatinine purification by Cockcroft about 20-25 ml/min).
In general, diabetic nephropathy treated with extra-renal dialysis or kidney transplant has a worse prognosis than non-diabetic patients, mainly due to cardiovascular complications.
The prognosis of life is bad in patients who have had an end-stage chronic renal failure due to diabetic nephropathy because of other complications such as cardiovascular disease, infection ... To prevent these complications, it is necessary to intervene. At an early stage in the risk factors such as hypertension, saltwater stasis, anaemia, blood vessel calcification and hyperlipidaemia ...
Kidney transplant: Consider young people and can pair (kidney, pancreas) at the same time.
Cyclic dialysis: There are difficulties in creating dynamic-venous probes because the pathology of the blood vessels of diabetes makes the vein openings more susceptible to failure and inoperability.
Peritoneal dialysis: Used in cases of dialysis problems.