Primary and secondary dysmetabolic nephropathy is distinguished, depending on the causes.
In the first case, the disease is hereditary and is characterized by development in the early stages of urolithiasis and a progressive course. The development of chronic kidney failure is also observed.
Secondary dysmetabolic nephropathy can be associated with excessive intake of any substances or with diseases of the gastrointestinal tract. The most common secondary dysmetabolic nephropathy.
Diseases in the form of calcium oxalate nephropathy are more common in children. The cause of the occurrence is, as a rule, a violation of the exchange of oxalates and calcium. The causes of oxalate formation can be intestinal anastomoses, ulcerative colitis, Crohn's disease, as well as excessive intake of oxalates from food. Oxalate dysmetabolic nephropathy in children in most cases is hereditary. An important role, in addition to genetic factors, is played by an unfavorable environmental situation, unbalanced nutrition and stress. The first signs may appear even in newborns, but are more often detected at the age of 6-7 years. For children with this disease, vegetovascular dystonia, obesity, allergies are characteristic. The overall development of the child with this disease does not suffer. The progression of nephropathy can lead to the development of urolithiasis, and with layering of a bacterial infection, to kidney inflammation.
Phosphate dysmetabolic nephropathy is a sign of a violation of phosphorus-calcium metabolism. The main cause of its occurrence are chronic urinary tract infections. Urate nephropathy is a violation of the metabolism of uric acid. A characteristic feature in this disease is brick-colored urine.
Treatment of dysmetabolic nephropathy consists in the use of specific methods of therapy, diet and proper drinking regimen, in the general normalization of lifestyle. A universal method of treating nephropathy is the use of a large amount of fluid, as this reduces the concentration of soluble substances in the urine. Taking fluid at bedtime increases the volume of nighttime urination. Take preferably plain or mineral water. The purpose of the diet is to reduce the salt load on the kidneys. Specific therapy is aimed at normalizing metabolic processes, eliminating salts and preventing crystallization processes.
In the treatment of oxalate nephropathy, patients are prescribed a cabbage-potato diet. Strong meat broths, jellied meat, chocolate, cocoa, sorrel and spinach, carrots, beets and cranberries are excluded from the diet. The use of pears, prunes and dried apricots is recommended. Drug therapy consists of taking antioxidants and membranotropic drugs. The treatment will be long. Vitamin B6 (pyridoxine) is prescribed for a monthly course, as well as vitamin A, which normalizes the interaction of lipids and cell membrane proteins . Vitamin E (tocopherol acetate) is a powerful antioxidant and also strengthens lipid-protein bonds of cell membranes. Xidiphon and dimephosphon are also used as membrane stabilizers. In the treatment of crystalluria, the effectiveness of cystone and magnesium oxide has been shown.
Foods rich in purine bases, such as kidneys, liver, nuts, beans, peas, should be excluded from the diet. It is necessary to use mainly products of plant and dairy origin. Good results are obtained with a large amount of fluids, including decoctions of herbs such as horsetail, clover, knotweed. Mineral water is recommended slightly alkaline, slightly mineralized.