Dysmetabolic nephropathy: symptoms manifestation, treatment

Dysmetabolic nephropathy is a group of diseases with metabolic disorders and renal tubular lesions. This group includes oxalate, urate and other nephropathies.

Oxalatnaja nefropatija happens primary (hereditary) and secondary (got). Primary oxaluria is inherited by autosomal recessive, less often dominant types. The inadequacy of the enzyme, the accumulation and increased amount of excretions in the urine of glycolate, glyoxylate and oxalic acid salts (the first type of disease) are ascertained.

The second type is associated with the deficiency of the enzyme D-glycerate dehydrogenase and there is increased urinary excretion of glyoxylate, hydroxypyruvate, calcium oxalate, l-glycerate. These metabolic disturbances lead to the deposition of calcium oxalate crystals in the proximal tubules and interstitium. Then the processes of calcification acquire generalized character (bones, cartilage, vessel walls, lymph nodes, spleen and other organs), nephrolithiasis, hydronephrosis, interstitial nephritis, and later chronic renal failure.

Clinical manifestations



Painful urination, colic, nausea, vomiting, erythrocyturia or hematuria, sometimes secondary pyelonephritis. Laboratory concluded hyperoxaluria (> 40 mg /day), increased amount of glyoxylate (> 5 mg /day), glycolate (> 15 mg /day), l-glycerate (up to 300-600 mg /day). With ultra-sound examination of the kidneys is the expansion of the cup-and-pelvis system, echopositive shadows.

Treatment of dysmetabolic nephropathy



Potato-cabbage diet, cocoa exception, chocolate, sorrel, spinach, parsley, beets, celery, etc. You can include butter, butter, boiled meat, pumpkin, cucumbers, pears, prunes, dried apricots in the diet. Magnesium oxide, vitamin B6 A, E, essential, unitiol, lipoic acid are shown.

Urinary nephropathy



It is primary (hereditary) and secondary (with myeloma, hemolytic anemia, in the treatment of cytostatics, diuretics and salicylates, etc.). Violation of purine metabolism, and as a result of xanthinuria, is caused by a defect of the enzyme xanthine oxidase (the defective gene is localized in the 2-nd chromosome). Crystals of uric acid are deposited in the interstitial medulla of the kidneys, tubules. Interstitial nephritis arises, urate stones are formed.

Clinical manifestations:

Dysuric syndrome, pain syndrome, erythrocyturia, hematuria, crystalluria, secondary pyelonephritis. With the progression of sclerotic changes in the kidneys, chronic renal failure occurs. Laboratory criteria: hyperuricemia more than 0350 mmol /l, hyperuricosuria more than 4 mmol /l, with xantynuria, the level of xanthine in the blood is more than 1 μmol /l.

Treatment



Milk and vegetable diet, the exclusion of foods containing a lot of purine (liver, kidneys, brains, broths, pates, sprats, peas, beans, beans, nuts, cocoa). It is recommended to include in the diet vegetables (potatoes), cereals, fruits, milk, eggs. Lemons, citrate mixture, sodium bicarbonate prevents the formation of urate salts and urate stones. Shows of unloading days (fruit, potato-vegetable, lactic acid) and providing sufficient liquid (1 -2 L per day) are shown. Assign orotova acid 2-6 mg per day, allopurinol 5 mg per kg per day, colchicine 05-2 mg per day.