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Dysmetabolic( exchange) nephropathy - Causes, symptoms and treatment. MF.

  • Dysmetabolic( exchange) nephropathy - Causes, symptoms and treatment. MF.

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    Dysmetabolic or metabolic nephropathy is a kidney damage caused by a metabolic disorder. Dysmetabolic nephropathy occupies a significant place in the structure of morbidity in pediatric practice, metabolic disorders in the urine are detected in every third child.

    Causes of metabolic nephropathy

    Primary and secondary dysmetabolic nephropathy is isolated depending on the cause of the onset. The primary form arises from hereditary metabolic disorders, characterized by early manifestation, progressive course, rapid formation of kidney stones, and the development of renal failure. Secondary dysmetabolic nephropathies are associated either with a large intake of certain substances into the body, or with a violation of their secretion.

    Normally, the salts in the urine are in a dissolved state. Under the influence of certain factors, the salts crystallize and precipitate them out. These factors are divided into environmental factors and internal factors associated with a violation in the work of certain body systems. Predisposing factors of the external environment include dry hot climate, hard water, vitamin deficiency, abuse of foods containing large amounts of protein, purines, oxalic acid, alcoholism, frequent sauna visits, taking diuretics, cytotoxic drugs, sulfonamide drugs.

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    Internal factors include congenital anomalies of the kidneys and ureters, especially those associated with urinary passage disorders, urinary tract infections, hormonal changes, for example, hyperparathyroidism, prolonged bed rest and immobilization, genetically caused metabolic disorders.

    Thus, under the influence of the above factors, crystallization of salts occurs, the deposition of crystals in the kidney tissue with the development of inflammation, and also, with local accumulation of salts, stones are formed.

    Symptoms of dysmetabolic nephropathy

    Most secondary dismetabolic nephropathies are associated with a disruption in calcium metabolism( 70-90%), urate-5%, and cystinuria occurs in 3% of cases.

    1. Oxalate-calcium nephropathy is the most common disease in childhood. The cause of its development is a violation of the exchange of calcium and oxalates. Normally, oxalates enter the body with food or are formed during metabolism. Oxalates have a great ability to crystallize, so even a slight increase in their concentration in the urine leads to precipitation. The causes of an increase in the concentration of oxalates are:

    • Increased intake of food for the abuse of products such as cocoa, chocolate, beets, celery, spinach, rhubarb, parsley, broths, especially vegetable.
    • Increased absorption due to inflammatory bowel diseases, such as Crohn's disease, ulcerative colitis and others.
    • Increased synthesis in the body in conditions of excess ascorbic acid, lack of pyridoxine, or with a genetically determined exchange defect of oxalates.

    Crystals of oxalates fall in the tubules of the kidneys, causing their inflammation. With prolonged current inflammation, the functional tissue of the kidneys is replaced by a scar tissue.

    The disease is most often detected at the age of 7-8 years. Specific symptoms are absent. There may be mild abdominal pains without clear localization, passing alone, burning with urination. In the analysis of urine draws attention to oxalate-calcium crystalluria, hematuria of varying severity, there may be a small proteinuria and / or leukocyturia in the absence of bacteria.

    Children with oxalate nephropathy grow and develop normally. During puberty, the disease usually worsens. This is probably due to hormonal imbalance. With the progression of nephropathy, it is possible to form urolithiasis, tubulointerstitial nephritis, and with the attachment of bacterial infection-pyelonephritis.

    2. The main cause of secondary phosphaturia is an infection of the urinary system. Microorganisms break down uric acid, the urine becomes alkaline, this promotes the crystallization of phosphorus salts. Diagnosis is based on the presence of phosphate-calcium crystals in the urine.

    3. Uric acid is identified by the final product of purine metabolism. Therefore, uricosuric nephropathy occurs with excessive consumption of products rich in purines( alcoholic beverages, broths, offal, mushrooms, asparagus, cauliflower), as well as increased uric acid production in the body. Crystallization of urates is facilitated by an acidic urine environment, as well as a decrease in its quantity. Primary urate nephropathies are caused by a genetic defect in the exchange of uric acid. Manifestations of urate nephropathy complicate such diseases as myeloma, erythremia, hemolytic anemia. The cause of secondary urate nephropathy is also the long-term use of diuretics, cytostatics, and chronic urinary tract infections, for example, pyelonephritis.

    Urinary nephropathy is characterized by a long asymptomatic course. Changes in the urine are manifested by crystalluria, small proteinuria, hematuria. With pronounced crystalluria urine acquires a brick color. Over time, urate or mixed stones are formed.

    4. Cystine is the most insoluble of amino acids. The formation of crystals arises from the accumulation of cystine in the kidney cells or the disruption of the reverse absorption of cystine in the tubules. Both causes are due to hereditary disorders of the kidney structure. When the renal tubules are damaged as a result of pyelonephritis or tubulointerstitial nephritis, secondary cystinuria develops. Cystinuria is characterized by the development of kidney fibrosis, the formation of stones. With the infection, pyelonephritis develops.

    Examination for suspected dysmetabolic nephropathy

    To confirm the diagnosis, it is not enough to find some crystals in the urine. It should be borne in mind that the appearance of urate or oxalate in the urine may indicate failure to comply with the diet and subsequently disappear without a trace. The appearance of cystine crystals in urine is always regarded as a pathology. In addition, biochemical analysis of urine is necessary to identify salts, as well as assess the function of the kidneys based on the concentration in urine of some standard substances. Kidney ultrasound can determine the compaction of kidney structures, kidney stones, and signs of inflammation.

    Treatment of dismetabolic nephropathy

    Treatment of dismetabolic nephropathies is a multicomponent process. The patient shows the use of a sufficient amount of fluid, since the release of urine in large amounts reduces the concentration of salts and thereby reduces the risk of their crystallization. Especially topical is the intake of fluid before bedtime in order to prevent stagnant phenomena. It is recommended to use simple or mineral water.

    The goal of the diet is the complete or partial cessation of the intake of salt precursors into the body with food.

    When oxalate nephropathy is recommended cabbage and potato diet with restriction of products containing oxalate.

    Kind of nephropathy Nephropathy Prohibited products
    Oxalate nephropathy Meat dishes, sorrel, spinach, cranberries, beets, carrots, cocoa, chocolate
    Urinary nephropathy Liver, kidneys, meat broths, peas, beans, nuts, cocoa, alcoholic beverages
    Phosphate nephropathy Cheese, liver, caviar, chicken, beans, chocolate
    Cystine nephropathy Cottage cheese, fish, eggs, meat

    It also shows the use of foods that make alkalinizing urine: dried apricots, prunes, pears, alkaline mineral waters. From drug therapy, the use of vitamins and antioxidants( tocopherol, pyridoxine, vitamin A) is necessary.

    The diet with urate nephropathy provides for the rejection of products containing purines. Products of dairy and vegetable origin are considered as priority. The amount of liquid used should be increased to two liters. The means that alkalinize urine are used: decoctions of herbs( dill, horsetail, oats, a leaf of a birch), and also slightly alkaline mineral waters. To reduce the concentration of uric acid, allopurinol is used. As a means of strengthening the membranes of the kidney cells, xidiphon and vitamin B6 are used.

    Phosphoric crystals of exclude phosphorus-containing products. Particular attention is paid to acidification of urine( mineral water, ascorbic acid).To reduce the absorption of phosphorus in the intestine is used Almagel. An important condition is the treatment of foci of chronic infection of the urinary tract.

    The diet for cystinuria is aimed at restricting foods containing methionine( the precursor of cystine), consuming a large amount of liquid, and applying a means alkalinizing urine. The courses use membrane stabilizing drugs and nephroprotectors. The method of treatment in the development of renal failure is a kidney transplant. Unfortunately, after 10-15 years, nephropathy develops in the transplanted kidney.

    In primary nephropathy, the prognosis is unfavorable due to the rapid development of renal failure. Secondary nephropathy is characterized by a more favorable course. Compliance with diet, water and drinking regimen, drug therapy, as well as timely treatment of urinary tract infection often allows to achieve the normalization of the main indicators in urine.

    Physician therapist, nephrologist Sirotkina EV