Diabetic nephropathy
Diabetic nephropathy is the most common cause of end-stage renal failure and the need for dialysis.
The following factors contribute to the development of diabetic nephropathy: poorly regulated glycemia, hypertension, elevated LDL cholesterol values and tobacco smoking. The basic function of the kidneys is to remove harmful metabolic products and excess fluid from the blood through the filtration process.
The kidneys are made up of millions of glomeruli, a ball of capillaries that filter the blood and the urine created comes through the ureters into the bladder and is removed from it through the urethra. In the early phase of diabetic nephropathy, the glomeruli are enlarged, probably as a result of early hemodynamic changes and increased pressure within the glomeruli (glomerular hypertension). Damage to the glomerular membrane occurs and it begins to leak albumins and other proteins into the urine. Otherwise, the pores on the glomerular membranes in a healthy kidney let in a very small amount of some proteins.
The glomerular membrane is up to three times thicker, especially in patients with microalbuminuria. As the disease progresses, glomerular sclerosis occurs which manifests itself in the deterioration of kidney function. The method of early detection of nephropathy is based on the finding of microalbumin in the first morning urine sample and in further monitoring, the finding of albumin in the 24-hour urine sample is necessary. The finding of serum creatinine is a good indicator of kidney function. Since blood pressure can be slightly elevated in the early stages of the disease, it is necessary to do a 24-hour Holter of blood pressure, so it can be discovered that the pressure does not decrease at night which can often be the first sign of diabetic nephropathy.
The onset and progression of nephropathy can be prevented or delayed by good regulation of glycemia and elevated blood pressure. ACE inhibitors have not only an antihypertensive but also a renoprotective effect because they primarily dilate the efferent arterioles of the glomerulus and thereby reduce the pressure in the glomerulus. All patients with type 1 diabetes who have microalbuminuria should take ACE inhibitors, regardless of whether they have normal or elevated blood pressure. In the final stage of diabetic nephropathy, complete kidney failure occurs.
The first complaints associated with the deterioration of kidney function are the ability loss to concentrate urine which is manifested by frequent urination of large amounts of urine, nighttime urination, morning thirst, morning sickness and sometimes vomiting. In the advanced stage of renal failure, symptoms of disturbed homeostasis may appear, i.e. salt and water retention (swelling, increased blood pressure and heart decompensation), metabolic acidosis with deep breathing. The skin is pale grayish in color, excoriations due to itching, bleeding, smell of ammonia. Anemia, tendency to infections, disorders of sexual functions, absence of menstruation, fatigue, weakening of intellectual functions, peripheral neuropathy, accumulation of fluid in the pericardium and lungs (uremic lung). Collapsed kidney function should best be replaced with kidney transplantation, hemodialysis or peritoneal dialysis.
The occurrence and development of diabetic nephropathy can be prevented by the following measures: optimal glycemic control in the early stage of renal insufficiency, the target value can be HbA1c 6.5 - 7% and in the advanced stage of diabetic kidney disease the acceptable value is HbA1c 7%. Optimal control of blood pressure < 130/80 mmHg and with the presence of proteinuria < 125/75 mmHg. There is an opinion that there is no single target value that would suit all patients, but the treatment of hypertension should be individual. Optimal regulation of blood fats (LDL cholesterol < 3.00 mmol/L. Diet with little protein. Stopping smoking.
