Dangerous kidney disease: what is nephrocalcinosis and how to get rid of it. Renal nephrocalcinosis treatment with folk remedies Primary nephrocalcinosis in children

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Many different factors of the environment in which humanity lives, provokes the occurrence of metabolic changes in the body. As a result of such violations, new compounds are formed, which eventually accumulate in various organs and lead to the development of various diseases.

Renal nephrocalcinosis - what is it?

Nephrocalcinosis is a pathological inflammatory process characterized by diffuse precipitation of calcium phosphate salts on the walls of the renal tubules or in their parenchyma itself.

This disease often develops as a result of a violation of calcium metabolism in the human body for any reason. Calcium salts crystallize and are deposited in the tissues of organs, mainly in the renal tissue, sclerosis (scarring) develops. Nephrocalcinosis in almost all variants of development leads to renal failure (chronic).

Types of pathogenetic aspects of the development of the disease

There are two types of nephrocalcinosis, which are distinguished by etiological factors:

• With the development of sclerosis and the deposition of calcium elements on the previously unchanged renal parenchyma, one can speak of the primary form of nephrocalcinosis;
• In the secondary form of the disease, the sediment is fixed on the scar tissue of the kidney. This type of nephrocalcinosis begins simultaneously both from the cortical part and from the epithelium of the tubules.

According to the localization of calcifications in the kidney, the disease is classified:

• Cortical nephrocalcinosis (calcium deposits are formed mainly in the cortical layer of the kidney);
• Medullary (calcium precipitates in the areas of the renal pyramids).

The formation of calcium phosphate and its fixation in the kidneys is due to hypercalcemia and hypercalciuria (increased calcium concentration in the blood and urine). Due to the increased load, the kidneys do not cope with their basic functions; sediment is fixed inside the epithelial cells of the renal tubules.

Then dystrophic changes in the epithelium occur, calcium salts pass into the interstitial part of the renal tissue or into the lumen of the tubules, blocking them (cylinders). In the parenchyma, metastatic foci of calcium fixation provoke the activation of the immune system, which leads to the replacement of normal kidney tissue with connective tissue.

Inflammatory changes occur due to blockage of the tubules of the kidneys and disruption of the normal passage of urine. Often as a complication, pyelonephritis occurs, as well as hydronephrosis of the kidney.

The reasons

Causal factors in the development of primary nephrocalcinosis:

1. Increasing the intake of calcium in the human body. The cause may be congenital tubulopathy in children, neonatal nephropathy, Burnett's syndrome and Lightwood-Fanconia, some other diseases.
2. Pathological conditions in which calcium is strongly excreted from the bones: osteoporosis, hormonal imbalance (hyperparathyroidism), metastatic processes in the bone system and multiple myeloma, increased levels of thyroid hormones.
3. Increasing the level of vitamin D in the body, which is responsible for increasing the concentration of calcium in the blood.

Reasons for the development of a secondary form of nephrocalcinosis:

1. Acute violation of the blood supply to the cortical layer of the kidneys.
2. Radiation damage to the kidneys.
3. Toxic effects on the body of mercury.
4. Overdose or use of excessive amounts of phenacetin, sulfonamides.
5. Abuse of various diuretics.
6. Violations associated with changes in the acid-base balance of the blood.

Signs and symptoms

Nephrosclerosis and precipitation of calcium salts in the renal parenchyma can have many different clinical manifestations.

First of all, there are signs of calcium intoxication of the body:

• Nausea, bouts of vomiting;
• Weakness and malaise, feeling thirsty;
• Headaches and pains in the region of the heart;
• Heart rhythm disturbances, changes in the ECG (shortening the period of contraction of the heart);
• Itching of the skin, dryness and signs of peeling;
• The joints are deformed, painful sensations appear in them when moving;
• The motility of the intestines and stomach is disturbed, this causes painful abdominal cramps and constipation.
• emotional lability;
• Signs of hypertension may appear;

If the tubules of the kidneys and their epithelial cells are affected, then pain occurs in the lumbar region, pyelonephritis or hydronephrosis may develop.

In case of blockage of the urinary tract, clinical signs of urolithiasis appear.

Due to pathological calcification of the tubules of the kidneys, their sensitivity to the influence of antidiuretic hormone decreases, as a result, the following symptoms appear:

• Persistent decrease in the osmotic pressure of urine;
• Increase in daily diuresis;
• Polydipsia (resulting from intense thirst).

Diagnostics

Necessary laboratory and instrumental methods for diagnosing kidney nephrocalcinosis:

1. Nephrocalcinosis at the initial stages of its development has practically no clinical manifestations. In the early stages of the development of the disease, the most informative diagnostic method, but also the most invasive, is a kidney biopsy using a puncture technique.
2. Ultrasound examination (ultrasound) is considered a fairly informative method for diagnosing kidney calcification in the early stages. On the obtained image, when scanning in various planes and sections, one can see a symptom of perimedullary rings of high echogenicity. Also, nephrocalcinosis of the kidneys on ultrasound is expressed by the following signs: (with a cortical form) linear hyperechoic neoplasms or a diffuse nature of the inclusion.
3. Radiography and CT are effective already in the late stages of the development of calcification, when triangular-shaped pyramids or linear calcifications in the cortical layer of the kidney are clearly visualized in the picture.
4. To determine the etiological and pathogenetic conditions for the development of the disease in children and adults, blood and urine are taken to determine the content of calcium and phosphorus in them.
5. A general analysis of biological fluids (urine and blood), their biochemistry and the Sulkovichka test (calciuria level) are carried out.
6. It is very important to assess the functional state of the kidneys, for this, creatinine clearance is determined, and the level of alkaline phosphatase is assessed.
7. In order to determine the form of the disease (primary or secondary), the level of parathyroid hormone in the patient's blood is examined.

On the video, signs of early kidney nephrocalcinosis:

Treatment

The attending physician, having fully studied all the results of the patient's research, prescribes medication, the purpose of which is to eliminate the root cause of the disease:

• With severe dehydration of the body and violation of the acid-base balance, it is necessary to carry out intravenous drip infusion of solutions (sodium or potassium citrate, potassium aspartate, sodium bicarbonate or sodium chloride).
• If hypercalcemia is not significant, treatment with folk remedies is acceptable, which necessarily include a diet.
• Assign the intake of B vitamins orally or in injectable form.
• With the progression of renal failure or the development of a coma, hemodialysis is performed.
• A solution of magnesium sulfate or sodium phosphate is administered intravenously for hypercalcemia.
• Perhaps the appointment of hormonal drugs (prednisolone or thyrocalcitonin).
• When signs of pyelonephritis appear, treatment is appropriate for this disease.

Features of diet therapy

To reduce the level of calcium in the blood, it is very important to exclude the following foods: sunflower oil, mustard, sesame seeds, various types of cheeses. You can not eat wheat flour, bran, almonds, dairy products, oatmeal.

You should adhere to diet number 7, which causes the removal of toxins from the body.

Of the folk methods of treating kidney diseases, strawberries, strawberry leaves in the form of a decoction can be noted. The decoction is taken orally for about 10 days daily.

Gooseberries, viburnum and sea buckthorn have a good effect (anti-inflammatory and diuretic effect).

A decoction prepared for warm sitz baths of birch and sage leaves improves blood circulation in the vascular bed of the kidneys, relieves inflammation.

Forecast

With the progression of renal nephrocalcinosis, the prognosis for the future is unfavorable, since the development of renal failure and uremia is inevitable. With timely diagnosis of the disease and proper treatment, the prognosis for the development of the disease is more favorable. It is impossible to cure nephrocalcinosis with folk remedies, so it is very important to see a doctor in time.

Metabolic disorders lead to the failure of all internal organs. The kidneys are no exception. In violation of calcium metabolism, a disease can develop - nephrocalcinosis. Renal pathology in a neglected state often leads to serious consequences. To prevent such an outcome, it is important to know the symptoms of the disease, treatment methods and prevention rules.

What is nephrocalcinosis in children and adults

Nephrocalcinosis is characterized by the deposition of calcium salts in the parenchyma (tissue that fills the organ) and the tubules of the kidneys. As a result, calcifications are formed - a dense stone sediment, under which the kidney tissue dies.

With nephrocalcinosis, calcium salts accumulate in the body

The disease can occur in both adults and children, including infants.

Pathology is accompanied by the following disorders:

• deterioration of blood circulation in the kidney;
• an increase in the load on the organs of urination;
• acute inflammatory process in the organ;
• scarring of the renal tissue;
• development of renal failure.

In medicine, the disease has other names:

• kidney calcification;
• metastatic calcification of the kidney;
• calcareous metastases in the kidney;
• calcareous degeneration of the kidney.

Types of nephrocalcinosis

Depending on the causes of nephrocalcinosis, it happens:

• primary - accompanied by the deposition of calcium salts in healthy renal tissues. Occurs as a result of various diseases and disorders of metabolic processes in the body;
• secondary - fixation of calcium deposits occurs on the scar tissues of the kidney. Scars are formed as a result of exposure to the kidney tissue of chemical and toxic substances.

Based on the number of affected organs, nephrocalcinosis is divided into two types:

• unilateral,
• bilateral.

Depending on the location of calcifications in the kidney, nephrocalcinosis occurs:

• medullary - calcium salts are located in the renal pyramids;
• cortical - calcium salts are formed in the cortical layer of the kidney.

Causes of the development of pathology in children and adults

The main reserves of calcium are in the bone tissue, where the chemical element binds to proteins. And also calcium is found in the blood, lymph and intercellular fluid. Calcium is excreted from the body by the colon and kidneys. The following substances affect calcium metabolism in the body:

• vitamin D, which is produced under the influence of ultraviolet radiation from the sun, and also enters the body with food. Vitamin D stimulates the resorption (release) of calcium from bone tissue. With an excess of vitamin D, the calcium content in the blood also increases, which leads to the development of nephrocalcinosis. Most often, an excess of vitamin D is observed with the abuse of drugs containing this substance;
  
• parathyroid hormone produced by the parathyroid glands. There is a "double feedback" between parathyroid hormone and calcium. If the level of calcium in the blood decreases, the parathyroid glands increase the production of parathyroid hormone. This increases the amount of calcium in the blood. In turn, calcium acts on the receptors of the parathyroid glands, which causes them to stop the release of parathyroid hormone. In the presence of various pathologies of the parathyroid glands, the production of parthormone can be impaired, the amount of calcium in the blood increases, and prerequisites for the development of nephrocalcinosis arise;
  The work of the parathyroid glands affects the level of calcium in the blood
• calcitonite is a thyroid hormone that stimulates the absorption of calcium by bone tissue, as well as accelerating the removal of the trace element from the body by the intestines and kidneys. Calcitonite is produced in small quantities during strong physical exertion, which leads to an increase in the level of calcium in the blood;
  The thyroid hormone calcitonitis helps to reduce the amount of calcium in the blood.
• phosphorus, which enters the body with food. With a deficiency of phosphorus, the calcium content in the blood increases, calcium salts accumulate in the vessels, internal organs, including the kidneys.

Other factors affecting the development of nephrocalcinosis:

• congenital renal pathologies;
• (inflammatory process in the tubules of the kidney);
• (inflammatory process in the renal glomeruli);
• hereditary predisposition;
• exposure to radiation, toxins, mercury on the kidneys;
• abuse of antibiotics, diuretics and other drugs.

Video: excess calcium in the body

Symptoms of the disease

In the initial stage of development, the disease may not manifest itself in any way and not bother a person. With the progression of the pathology, when calcium deposits begin to affect the urinary function of the kidneys, symptoms appear:

• frequent urination;
• an increase in daily diuresis (the amount of urine excreted by the kidneys per day);
• lethargy and fatigue;
• loss of appetite;
• increased gas formation;
• nausea:
• swelling of the hands and feet;
• high blood pressure;
• constant thirst;
• pain syndrome in the region of the heart;
• arrhythmia;
• itching of the skin.

Symptoms in infants have some features:

• the child often spit up;
• urine becomes dark and cloudy;
• the baby can be capricious and refuse to breastfeed.

In older children, the signs of nephrocalcinosis are similar to the general symptoms.

Dangerous symptoms

If the calcifications have reached a large size and an obstruction (blockage) of the ureter has occurred, an attack of renal colic may occur, which is accompanied by severe symptoms:

• a sharp pain syndrome appears in the kidney area, then spreads to the upper abdomen. And also pain can be localized in the back, legs, groin, under the ribs, in the area of ​​the ureter;
• a person develops profuse vomiting, which contributes to rapid dehydration of the body;
• blood appears in the urine;
• there is severe dizziness;
• body temperature rises to 38-40 degrees.

During renal colic, the pain in a person is so severe that a pain shock can occur. With symptoms characteristic of an attack, it is urgent to call an ambulance.

Diagnosis of nephrocalcinosis

If nephrocalcinosis is suspected, laboratory tests are prescribed:

• general urine analysis;
• Sulkovich's test, which determines the content of calcium in the urine;
• general blood analysis;
• with the determination of the content of calcium and phosphorus;
• blood test for thyroid and parathyroid hormones.

Instrumental diagnostic methods are also used:

Diagnosis of the disease in children and adults is carried out according to the same scheme.

Differential Diagnosis

Nephrocalcinosis should be differentiated with a spongy kidney - a congenital pathology in which small cysts form in the area of ​​the renal pyramids. The internal contents of the cysts are a condensate of calcium salts.

Treatment

Surgical intervention is not used to treat nephrocalcinosis, preference is given to conservative methods.

Medical therapy

The following drugs can be used to treat nephrocalcinosis in children and adults:

• anti-inflammatory drugs (Canephron, Cyston);
• antibiotics (Cefotaxime, Augmentin) - are prescribed for a bacterial infection that often accompanies progressive nephrocalcinosis;
• to restore metabolism, infusions of bicarbonate or sodium citrate are used;
• diuretics (Veroshpiron, Furosemide, Urakton) - contribute to an increase in diuresis, due to which excess calcium is excreted from the body;
• B vitamins - improve kidney function.

Diuretics are very rarely used to treat children under 1 year of age. An exception is the appearance of severe edema.

Photo gallery: medicines used for nephrocalcinosis

Kanefron eliminates inflammatory processes in the kidneys Cefotaxime is used for bacterial infections in the kidneys B vitamins improve kidney function Furosemide enhances the excretory function of the kidneys

Physiotherapy

Physiotherapy is used at the initial stage of the development of the disease and can significantly improve the physical performance of the patient. The following physiotherapy procedures are among the most effective:

• phonophoresis - relieves pain, eliminates inflammation in the kidneys. Under the influence of ultrasound, drugs penetrate deep into the tissues, which speeds up the healing process. The procedure has no contraindications and does not cause side effects;
• magnetotherapy - helps to strengthen the body's defenses, improves blood circulation in the kidneys, enhances the excretory and filtration functions of the organ, reduces pain. There are no contraindications to the procedure, so magnetotherapy is suitable for both adults and children.

Diet and drinking regimen

With nephrocalcinosis, treatment table No. 7, developed by the Soviet nutritionist M. I. Pevzner, is used. Basic rules of the diet:

• you need to eat often (4-5 times a day) and in small portions so as not to overload the work of the kidneys;
• the amount of fluid consumed per day should be at least two liters;
• the use of salt in the diet, which contributes to dehydration, is reduced;
• spicy, pickled, smoked, fried, fatty foods are not used in the diet;
• food is boiled, stewed, steamed, baked;
• alcoholic and carbonated drinks, coffee, strong black tea are excluded.

And also with the disease, the use of foods high in calcium is limited:

• dairy products - cottage cheese, kefir, cheese, milk, yoghurts;
• legumes - soybeans, lentils, peas, beans;
• some vegetables - parsley, dill, basil, broccoli, white cabbage, potatoes;
• dried apricots;
• oatmeal;
• sesame;
• pistachios.

Photo gallery: prohibited foods for nephrocalcinosis

Vegetables with a spicy taste are prohibited with nephrocalcinosis Fast food increases the burden on the kidneys Alcoholic beverages are toxic to the kidneys Dairy products are high in calcium
Sesame seeds contain a lot of fat and calcium,

• any cereals, except oatmeal;
• pasta;
• fruit;
• berries;
• vegetables (except prohibited);
• lean meats and fish;
• green tea;
• drink with chicory;
• herbal decoctions and infusions.

Photo gallery: useful products for nephrocalcinosis

Green tea detoxifies the body Fruits contain all the vitamins necessary for the body With nephrocalcinosis, give preference to lean meats
With nephrocalcinosis, you can use any cereal, except for oatmeal Feel free to use cucumbers and tomatoes in the diet

Folk remedies

Some medicinal herbs can improve kidney function in nephrocalcinosis. However, it should be remembered that any plant has contraindications and you should consult your doctor before using it.

Remedy for nephrocalcinosis with flax seeds

The decoction helps to remove calcifications from the kidneys, and also relieves pain symptoms.

Step-by-step instructions for preparing the product:

1. Pour one tablespoon of flax seeds into a glass of water.
2. Bring the mixture to a boil, cool.
3. Add a few drops of lemon juice to the solution.
4. Use the remedy for two days every 2 hours (sleep time is not taken into account). Single dosage - 50 ml.

Infusion of rose hips

The tool has a diuretic, and also helps to increase immunity.

Cooking process:

1. Three tablespoons of rose hips pour 0.5 liters of boiling water.
2. Cook over low heat for 10 minutes.
3. Infuse the decoction for an hour, then filter.
4. Consume three times a day, one hour after meals. At one time, take 150 ml of decoction, the course of treatment is two weeks.

Anti-inflammatory infusion of corn stigmas, birch leaves and burdock root

The infusion relieves inflammation in the kidneys, increases the excretion of urine.

Step by step recipe:

1. Place two teaspoons of corn stigmas, the same number of birch leaves, and a teaspoon of burdock root in a glass container.
2. Pour raw materials with 300 ml of boiling water, close the jar with a lid.
3. Insist for an hour, then filter.
4. Take three times a day 30 minutes before meals. Single dosage - two tablespoons. The course of treatment is two weeks.

Photo gallery: medicinal plants for nephrocalcinosis

Corn silk has a diuretic effect Birch leaves eliminate inflammatory processes in the kidneys
Flax seeds improve kidney function and reduce pain Burdock root enhances the excretory function of the kidneys
Rose hips improve blood circulation in the kidneys, increase their filtration function

Treatment prognosis and possible complications

With timely diagnosis and proper treatment, the outcome of the disease is often positive: nephrocalcinosis can be defeated. If the pathology is in an advanced stage, the prognosis is very sad: renal failure develops, in which the kidneys completely lose their excretory and filtration functions. There are only two ways out of this situation: lifelong use of hemodialysis or organ transplantation.

Prevention

Rules for the successful prevention of nephrocalcinosis:

• watch your diet - eat healthy and high-quality foods, do not abuse spicy and salty foods;
• drink clean water;
• lead an active lifestyle - physical activity improves blood circulation in the kidneys, which prevents stagnant processes;
• complete the treatment of all infectious and inflammatory diseases in the body;
• give up bad habits - drinking alcohol and smoking;
• regularly undergo preventive medical examinations;
• Properly use antibacterial agents and other medicines.

It is impossible to completely protect yourself from nephrocalcinosis. However, if simple rules of prevention are followed, the risk of developing pathology is reduced. If the diagnosis has already been made, do not be discouraged. Contact a competent specialist and follow his instructions.

Nephrocalcinosis or calcifications in the kidneys are characterized by abundant deposition of calcium salts in the tissues of the urinary organ. Calcification can occur in both kidneys or in one. The pathological process occurs due to deviations in the metabolic process. In the treatment of calcifications in the kidney, it is important first of all to prevent the source of the pathological reaction. To do this, normalize metabolic processes in the body.

Calcification in the kidneys: how to recognize?

Pathological processes of varying severity regularly occur in the kidneys. Nephrocalcinosis is diagnosed if calcium phosphate is deposited in or on the walls of the tubules of the organ. With calcification, an inflammatory reaction is noted in the urinary organ. A failure occurs if, for some reason, there has been a deviation in the calcium exchange process. In case of violation, scars form on healthy kidney tissue, which damages their function.

Calcifications pose a threat to human health and in most cases provoke chronic kidney failure.

Types of nephrocalcinosis

Nephrocalcinosis of the kidneys is manifested by different symptoms. Sometimes calcifications are diagnosed in the right or left kidney, less often the deposition of calcium salts is observed in both organs at the same time. The table shows the main types of calcifications in the kidneys, which have their own characteristics:

Classification	Type of nephrocalcinosis	a brief description of
By etiology	Primary	Calcifications appear against the background of congenital anomalies, an excess of vitamin D
	Secondary	The sediment is formed on the sclerosed tissues of the organ due to pathologies of an acquired nature
With the flow	Asymptomatic	Pathological signs are absent or appear dimly
	With severe symptoms	Symptoms are pronounced
According to the location of the pathological process	Cortical	The cortical layer of the organ is affected
	Medullary	Precipitation of salts in the zones of the renal pyramids
	Independent	Occurs when the metabolic process is disturbed

Why do they appear?

Pathological deposits in the kidneys occur for various reasons. All sources of nephrocalcinosis are divided into primary and secondary. The primary sources of calcification in the kidneys include:

Uncontrolled intake of vitamin D leads to the formation of kidney stones.

• A large intake of a substance in the body:
  • unbalanced diets;
  • taking vitamin D without a doctor's prescription for prevention.
• Impaired function of the musculoskeletal system, due to the leaching of salts into the bloodstream:
  • osteoporosis.
• Pathologies in the urinary organ, in which the tubules of the kidneys, which are responsible for the release of calcium ions into the urine, do not function properly.
• Hormonal disorders that negatively affect the process of release of substances from the human body.
• Thyroid dysfunction.
• Sarcoidosis.

There are such secondary causes of the formation of calcifications in the kidneys:

• death of the tissues of the internal organ;
• impaired flow of blood fluid in the kidney area;
• mercury intoxication;
• exposure;
• long-term use of certain medications.

Signs to look out for

In children and adults, calcifications in the kidneys are characterized by special symptoms. But sometimes it happens that the filtration process does not decrease in the bladder and kidneys, which is why pathological manifestations are not observed for a long time. The clinical picture manifests itself when the bile excretion pathways are blocked and is characterized by the following symptoms:

A symptom of pathology can be pain in the joints.

• constant fatigue;
• dizziness;
• lack of appetite;
• disturbed sleep;
• itchy feeling;
• soreness in the joints;
• mucous impurities in urine;
• impaired function of the digestive tract.

With the formation of calcifications of large sizes or a large number, the following manifestations occur:

• pain in the lumbar region;
• constant feeling of thirst;
• yellowing of the epidermis;
• frequent trips to the toilet, in which the daily volume of urine increases;
• swelling of the lower and upper extremities;
• the smell of acetone from the oral cavity;
• increase in blood pressure.

With impaired renal function against the background of nephrocalcinosis, pyelonephritis, hydronephrosis, or the formation of stones in the urinary organs develop.

A cyst with calcifications: how dangerous is it?

Cystic formation is formed when salts accumulate in the renal parenchyma and healthy cells die. In this case, the tubules become clogged and the connective tissue grows, replacing the parenchyma of the organ. With a cyst with calcifications, an inflammatory reaction and an infectious lesion occur, provoking insufficiency of the organ of the urinary system. On average, the size of the cyst is no more than 0.5 cm. If the patient is not operated on in time and the cyst is not removed, then nephrosclerosis will appear.

Dangerous consequences of calcifications

A neglected pathology can cause cancerous tumors in the kidney.

The greatest threat of calcifications is organ dysfunction and the development of renal failure. If nephrocalcinosis does not progress, then it is not particularly dangerous. But with the development of pathology, calcifications eventually affect more and more healthy tissue of the organ, causing disturbances in the urinary tract. Violated with calcifications and water-salt balance. Also, nephrocalcinosis can provoke cancerous tumors or benign neoplasms.

What to do with calcifications in the kidneys?

The need for early diagnosis

It is impossible to detect calcifications on your own, for this you need to consult a doctor and undergo a comprehensive diagnosis, including laboratory and instrumental manipulations:

• general analysis of urine and blood;
• biochemistry of blood fluid;
• radiograph;
• kidney diagnostics by ultrasound;
• analysis of the concentration of parathyroid hormone and vitamin D;
• CT and/or MRI;
• biopsy.

Effective treatment methods

What drugs will help?

Drugs for the treatment of nephrocalcinosis are used in the early stages of the disease to eliminate unpleasant manifestations. It is possible to treat calcifications in such medical ways:

Sodium bicarbonate is used at the initial stage of stone formation.

• The use of sodium citrate, potassium, sodium bicarbonate. Solutions are administered intravenously, the procedure is carried out to remove hazardous substances.
• The introduction of vitamin B.
• The use of magnesium sulfate or sodium phosphate. The procedure is necessary if the potassium content has increased.
• Taking hormonal medications:
  • "Prednisolone";
  • "Thyrocalcitonin".

In especially severe cases, when renal failure rapidly develops and becomes chronic, extrarenal blood purification is required through. If these procedures do not help to partially restore the function of the organ, then doctors prescribe surgery with a transplant of a donor organ.

Complete collection and description: nephrocalcinosis of the kidneys in children, treatment and other information for the treatment of man.

• Date: 17-02-2015
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• Stages of development of pathology

Nephrocalcinosis of the kidneys is called the deposition of calcium salts in a scattered manner in the tissues of the kidneys. This disease, related to calcifications (better known as renal dystrophy), is characterized by the presence of disturbances in the processes of calcium metabolism. Calcium salts contained in the liquids in the dissolved state settle and are deposited in the intercellular environment of the kidney and directly in its cells.

Kidney nephrocalcinosis is usually accompanied by the occurrence of inflammatory and sclerotic changes in combination with renal failure. Doctors singled out only two stages of the disease: primary nephrocalcinosis, which occurs in the kidney, which has not yet undergone any structural changes, and also secondary, in which deposits of calcium salts occur with subsequent modifications in the structure of the organ tissue.

Stages of development of pathology

There are two main stages of the disease: primary and secondary, which have different symptoms.
Primary nephrocalcinosis is characterized by:

• violation in the bones of the process of Ca binding;
• active release of Ca from bones;
• tumor changes in a number of organs and the skeletal system;
• metastasis of malignant neoplasms of bone tissue;
• corticosteroid and postcastration osteoporosis;
• hyperparathyroidism;
• numerous injuries in many bones at the same time;
• osteomyelitis;
• thyrotoxicosis and others;
• pathologies leading to the accumulation of excess calcium in tissues and its deposition;
• conditions causing the ingestion of excess calcium into the body;
• a variety of disease states, the course of which causes acidosis.

Features of the secondary stage The occurrence of secondary nephrocalcinosis of the kidneys is due to:

• misuse of amphotericin;
• mercury fumes;
• uncontrolled use of phenacetin, anthranil and thiazide diuretics, sulfonamides and ethacrine diuretics;
• ischemic cortical necrosis of the kidneys. Due to the fact that during the development of the disease, the underlying disease and hypercalcemia, which is accompanying, are distinguished, two categories of symptoms are distinguished.

Signs caused by excess calcium: malaise, weakness, increased fatigue, nausea and vomiting, drying of the skin, constant thirst, pain and shaped changes in the joints, convulsions, nervous disorders, disturbances in the processes of digestion of food, changes in the systolic wave on the cardiogram, keratoconjunctivitis. Pathological changes in the structure of the body and the cessation of their normal functioning leads to:

• short-term attacks of renal colic;
• polyuria;
• pain in the lumbar region;
• isosthenuria;
• polydipsia.

Sometimes, in addition to the listed symptoms, specialists detect red blood cells, white blood cells, bacteria and salt formations in the composition of the urinary sediment in large quantities. At later stages, arterial hypertension, edema, and proteinuria are found in the patient.

Back to index

Therapeutic procedures and preventive measures

To prevent the development of kidney nephrocalcinosis, it is necessary to monitor the amount of calcium supplied with fluids consumed. It should remain within the normal range. Do not use calcium-containing drugs without consulting a doctor. It is required to pay due attention to the ailments associated with the excretory system, in time to seek help from a specialist.

http://youtu.be/hjR-DTYKotA

Timely detection of the disease guarantees half the success in further treatment.

At the initial stages, nephrocalcinosis is diagnosed using a method such as puncture biopsy of the kidneys. In a more serious condition, they resort to plain radiography, which helps to detect salt neoplasms in the inner region of the kidneys. To identify the detailed causes of the pathology, a blood and urine test is prescribed to detect Ca and P, some hormones and other substances in them.

With kidney nephrocalcinosis, treatment is facilitated by the rapid elimination of the causes that caused disturbances in the metabolic processes of calcium in the body.

In the simplest cases, treatment is based only on dietary restrictions, namely, the doctor requires that foods containing calcium be excluded from the diet for a while. Severe dehydration is treated with infusions of sodium citrate and bicarbonate solution. Asparaginate and potassium citrate will help to cope with acidosis, and preparations of sodium chloride and ammonium will relieve alkalosis. The attending physician prescribes hemodialysis in cases with progressive renal failure.

http://youtu.be/QE5YJt8XkQo

Self-treatment attempts are strictly prohibited. With kidney nephrocalcinosis, treatment with folk remedies is inappropriate, since there are no specific recommendations in the medical literature in the fight against this disease. By observing the correct diet and doctor's recommendations, you can forget about this disease forever.

• Causes of nephrocalcinosis
• What happens to the kidneys with nephrocalcinosis?
• Clinical manifestations
• How to establish a diagnosis?
• Principles of treatment

Nephrocalcinosis or kidney calcification is the deposition of calcium salts in the parenchyma of an organ, which has a diffuse (common) character and is accompanied by the development of inflammatory, sclerotic processes in the kidney tissue, which can ultimately lead to chronic renal failure.

Causes of nephrocalcinosis

Depending on the causes of development, there are 2 types of kidney calcification:

• primary, which develops in a healthy kidney;
• secondary, which affects the pathologically altered organ.

Primary nephrocalcinosis

This is not an independent disease, this pathological condition is a symptom of diseases that are accompanied by disorders of calcium-phosphorus metabolism with the development of hypercalcemia (increased calcium concentration in the blood) and hypercalciuria (active excretion of calcium in the urine). The most common cause of primary kidney calcification is:

• excessive intake of calcium ions in the body (diet enriched with this element, drugs with calcium);
• lesions of bone tissue with the release of calcium from its depot (bones) into the blood (bone tumors, osteoporosis, bone metastases);
• malignant tumors of various localization, which have the ability to synthesize parathyroid hormone;
• violation of calcium excretion from the body (hormonal diseases, kidney pathology);
• kidney diseases in which the function of the renal tubules, which are responsible for the release of calcium ions into the urine, is impaired (congenital and acquired tubulopathies);
• hypervitaminosis D (leads to hypercalcemia and related consequences);
• sarcoidosis;
• hyperparathyroidism (increased secretion of parathyroid hormone by the parathyroid glands), in 90% of cases this disease is caused by a hormone-producing tumor of the gland.

Secondary nephrocalcinosis

The reasons that contribute to the development of secondary calcification of the kidneys include:

• necrosis of kidney tissue;
• circulatory disorders in the organ (atherosclerosis, thrombosis, embolism of the renal arteries);
• radiation damage to the kidneys;
• mercury intoxication;
• continuous use of sulfa drugs, phenacetin, thiazide, anthranilic, ethacrine diuretics, amphotericin B.

Regulation of calcium metabolism in the body

Normally, calcium metabolism in the body is regulated by 3 hormones: vitamin D, parathyroid hormone and calcitonin. The reservoir of this element is the bones, where calcium is stored and, if necessary, enters the blood.

Vitamin D enters the body with food and is formed in the skin under the influence of ultraviolet radiation. It increases the concentration of calcium in the blood by:

• activation of calcium absorption from food in the intestine;
• increase the reabsorption of ions in the kidneys;
• increased resorption of calcium from bones.

Accordingly, with a pathology such as hypervitaminosis D (an excess of vitamin in the body), hypercalcemia will also develop with calcification of the kidneys and other organs.

Parathyroid hormone is produced in the parathyroid glands. Its synthesis is regulated by the concentration of calcium in the blood - with a high content of calcium in the blood, the synthesis of parathyroid hormone decreases and vice versa. Parathyroid hormone increases the concentration of calcium in the blood in the following ways:

• leaches calcium from bones;
• increases the reabsorption of the element in the kidneys;
• activates the synthesis of vitamin D;
• enhances the absorption of calcium from food in the intestines.

Leaving the physiological mechanisms of the influence of parathyroid hormone, with an increase in its concentration, hypercalcemia and nephrocalcinosis develop.

Calcitonin is a hormone produced by the thyroid gland. The function of the hormone is to reduce the concentration of calcium in the blood by:

• suppression of the process of calcium resorption in bone tissue;
• in the kidneys inhibits the reabsorption of ions, which leads to an increase in the excretion of calcium in the urine.

• general weakness, fatigue, inability to concentrate, drowsiness, depression;
• skeletal muscle weakness, muscle and joint pain, bone pain;
• nausea, vomiting, spastic abdominal pain, constipation, lack of appetite, pancreatitis;
• thirst and dry mouth;
• cardiac arrhythmias, pain in the region of the heart, hypertension, during examination, a shortening of the QT interval is found on the ECG, on ultrasound - calcification of the heart valves and blood vessels, with severe hypercalcemia - cardiac arrest;
• signs of urolithiasis, frequent pyelonephritis, pain in the lumbar region, signs of progressive renal failure.

When kidney damage is already irreversible, edema, increased blood pressure, proteinuria and other signs of terminal renal failure appear.

How to establish a diagnosis?

It is important! The earlier the diagnosis of nephrocalcinosis is established, the greater the chance of saving kidney function. At an early stage of the disease, the only diagnostic method is a puncture biopsy of the kidney, since the changes are not yet visible either with radiography or ultrasound.

Radiographic signs of nephrocalcinosis appear only in advanced cases, when most of the parenchyma of the organs is pathologically changed. Ultrasound will also help to suspect calcification, but the scans are very similar to such a congenital pathology as a spongy kidney, which requires differential diagnosis.

Methods such as determining the concentration of calcium in the blood and urine, the concentration of parathyroid hormone, vitamin D, a general and biochemical analysis of blood, urine, and an examination aimed at finding the root cause of hypercalcemia will also help in establishing the diagnosis.

Principles of treatment

Treatment of kidney calcification, first of all, should be aimed at eliminating the cause of this pathological condition.

In order to correct the level of calcium in the blood, apply:

• the introduction of solutions of citrate and sodium bicarbonate;
• aspartate and potassium citrate in acidosis (shift of the acidic balance of the blood to the acid side) and sodium or ammonium chloride - in alkalosis (to the alkaline side);
• a diet with a restriction of calcium intake in the body;
• B vitamins;
• the abolition of drugs that contain calcium;
• hemodialysis with hypercalcemic crisis and the threat of cardiac arrest;
• therapy of concomitant pyelonephritis, urolithiasis, high blood pressure, renal failure;
• in the terminal stage of renal failure, treatment is carried out by program hemodialysis or kidney transplantation.

The prognosis for nephrocalcinosis depends on the stage of the disease and the treatments that are used. Most often, at the initial stages of the pathology, with timely diagnosis and effective, intensive treatment, the patient's condition improves, kidney function is restored, and the organ can be saved. But with the progression of calcification and the development of renal failure, severe complications are possible, which, if not treated with hemodialysis or kidney transplantation, lead to death.

Nephrocalcinosis as a symptom complex of a heterogeneous group of diseases is one of the urgent problems in the practice of pediatricians and pediatric nephrologists. International reliable data on the prevalence of nephrocalcinosis, including in combination with nephrolithiasis, are currently not available. According to some authors, in Ukraine the incidence of urolithiasis in children is relatively low and ranges up to 0.1%. At the same time, there is an increase in the incidence of this pathology, which makes this problem relevant, since pathological calcification itself entails a progressive deterioration in renal functions.

Nephrocalcinosis is manifested by diffuse deposition of calcium salts in the interstitium, glomeruli and walls of the renal arterioles and is accompanied by inflammatory-sclerotic changes and renal failure. For the first time this condition was described by R. Virchow as "calcium metastases", and the term "nephrocalcinosis" was introduced by F. Albright et al. in 1934 when describing the deposition of calcium salts in the renal parenchyma in hyperparathyroiditis.

Nephrocalcinosis can be cortical, which is most often the outcome of acute tubular necrosis, and medullary, which may be a continuation of cortical nephrocalcinosis, but more often develops independently due to a number of metabolic disorders. Cortical nephrocalcinosis is less common and covers the entire renal parenchyma. It is associated with metabolic defects, such as primary hyperoxaluria, or is the end stage of chronic renal failure. The causes of the development of cortical nephrocalcinosis can be:

Acute corticonecrosis against the background of acute dehydration, shock of various origins, hectic fever, blood transfusion, sepsis, poisoning with salts of heavy metals, hemolytic-uremic syndrome;

Chronic glomerulonephritis;

Oxalosis I and II types;

Alport syndrome;

Pyelonephritis in HIV-infected patients;

Chronic pyelonephritis;

Autosomal recessive polycystic disease;

Vesicoureteral reflux;

sickle cell anemia;

Pyridoxine deficiency.

Medullary nephrocalcinosis is much more common than cortical nephrocalcinosis. At the same time, the deposition of calcium salts mainly in the area of ​​the pyramids develops with various disorders of phosphate-calcium metabolism occurring with hypercalcemia and hypercalciuria (osteogenic nephropathy, various tubulopathies). Hypercalciuria as a cause of the development of medullary nephrocalcinosis is observed in the following conditions:

Idiopathic hyperoxaluria;

Idiopathic hypercalcemia;

Hypothyroidism;

Spongy kidney;

Some types of tubulopathies.

Currently, there are up to 32 hereditary syndromes, the symptom complex of which includes nephrocalcinosis.

There are 3 stages of development of nephrocalcinosis. The first stage is the so-called "chemical nephrocalcinosis", or hypercalcemic nephropathy, when the content of serum calcium is increased, but there is no evidence of its deposition in the renal interstitium. In this case, the main pathological effect is on the distal nephron, the ascending part of the loop of Henle and the collecting ducts, which is manifested by a decrease in the concentration function of the kidneys and an increase in resistance to vasopressin. The second stage is called "microscopic nephrocalcinosis", when an increased influx of calcium to the kidneys is accompanied by its accumulation inside the cells of the renal epithelium. When the concentration of intracellular calcium reaches a certain limit, cell dystrophy occurs, and calcium deposits move into the interstitial space or into the lumen of the tubules. The cylinders formed at the same time clog the tubules, which leads to their dilatation and atrophy. Salt deposits in the interstitium cause a lymphoproliferative reaction with subsequent nephrosclerosis.

The third stage is “macroscopic nephrocalcinosis”, which is visualized using ultrasound diagnostics, computed tomography, and survey Ro-graphy of the abdominal organs. In this case, the deposition of calcifications can be detected both in the cortical and in the medullary zone. When examining a macropreparation, stones in the pyelocaliceal system and linear white stripes and spots are determined on the cut surface.

The clinical picture of nephrocalcinosis is determined primarily by the signs of the underlying disease. Nephrocalcinosis itself in most cases is asymptomatic and is detected as an accidental finding (with ultrasound or x-ray of the abdominal organs). With mild hypercalcemia (< 2,9 ммоль/л) клинические симптомы обычно отсутствуют. При умеренной или тяжелой степени появляются симптомы со стороны ЦНС (сонливость, изменения психического статуса), желудочно-кишечного тракта (анорексия, тошнота, запор), почек (полиурия, почечнокаменная болезнь), костно-мышечной (артралгии, миалгии, слабость) и сосудистой систем (артериальная гипертензия). Изменения на ЭКГ могут быть в виде укорочения интервала QT, аритмии, депрессии сегмента ST, слабости синусового узла, нарушения атриовентрикулярной проводимости. При мозговом нефрокальцинозе могут быть боли в поясничной области, связанные с прохождением почечных конкрементов по мочевым путям, гематурия, лейкоцитурия, цилиндрурия.

Diagnosis of nephrocalcinosis includes a study of the level of serum calcium, phosphorus, albumin. Determination of serum calcium levels is necessary to clarify the association of nephrocalcinosis and hypercalcemia/normocalcemia. In blood plasma, calcium is found in the free (ionized) and associated with proteins and anions (citrate, phosphate) state. The content of ionized calcium is from 0.98 to 1.13 mmol/l (physiological constant). Even a slight increase in ionized calcium leads to functional changes in the myocardium (shortening of the ST interval) and calcification of the walls of blood vessels and body tissues. The level of total calcium in the blood plasma of healthy children is 2.2–2.8 mmol/l. In the case of changes in blood pH and albumin concentration, the level of total calcium also changes. Therefore, when assessing the concentration of calcium, it is necessary to take into account the level of albumin in the blood. To recalculate the true calcium content depending on the concentration of albumin (g / l), there is a formula:

Ca (corrected) = Ca (measured) + 0.02 x (40-albumin).

A study of the acid-base balance of the blood is necessary to clarify the shifts towards acidosis / alkalosis and the blood pH, since in cases where the blood pH deviates from normal values, a recalculation according to the formula is also required to determine the concentration of total Ca:

Ca (corrected) = Ca (measured) + 0.05 (7.40 = actual pH).

The level of blood electrolytes must be investigated for the differential diagnosis of diseases that occur with electrolyte disturbances and nephrocalcinosis. For example, hyperkalemia is observed in distal renal tubular acidosis, Barter's syndrome, Liddle's syndrome, and primary hyperaldosteronism.

Neuroendocrine regulation of calcium-phosphorus metabolism is carried out by parathyroid hormone. A decrease in the concentration of ionized calcium in the blood serum leads to an increase in the secretion of parathyroid hormone, which enhances the reabsorption of calcium in the renal tubules and increases its entry into the blood. Another mechanism for increasing the concentration of ionized calcium is bone resorption with increased secretion of parathyroid hormone. In such patients, densitometry is indicated to detect signs of osteoporosis. Parathyroid hormone antagonist is calcitonin, which reduces the level of ionized calcium by enhancing the processes of bone mineralization and increasing renal excretion of calcium, which can lead to hypercalciuria.

The study of the level of thyroid hormones is necessary to identify its hyperfunction. In hyperthyroidism, hypercalcemia is observed, which is associated with both increased calcium filtration and a decrease in its tubular reabsorption. It is necessary to monitor the daily excretion of calcium, phosphate, citrate, oxalates, hydroxyproline and magnesium, as well as daily protein excretion (excluding nephrotic syndrome) and endogenous creatinine clearance.

Hypocitraturia, according to various sources, in 50% of cases leads to calcium nephrolithiasis in patients with normal daily calcium excretion. Citrate is freely filtered by the glomeruli of the kidneys, and 75% of it is reabsorbed by the proximal convoluted tubules. The excretion of citrate is small. In addition to primary, idiopathic hypocitraturia, most secondary causes result in a decrease in urinary citrate excretion by increasing reabsorption in the proximal renal tubules. The reasons for the low content of citrate may be metabolic acidosis, hypokalemia, taking thiazide diuretics, carbonic anhydrase inhibitors, magnesium deficiency, renal tubular acidosis, diarrhea.

To exclude urinary tract infection in children with nephrocalcinosis, it is necessary to study the dynamics of general and quantitative urine tests, urine cultures for sterility.

Ultrasound examination of the kidneys is the leading method for diagnosing nephrocalcinosis. With cerebral nephrocalcinosis, 3 stages are distinguished: I - hyperechogenicity of the pyramids; II - "white garlands", total hyperechogenicity of the pyramids; III - the presence of an acoustic shadow. With cortical nephrocalcinosis, 3 ultrasound types are also distinguished. In the first type, a thin band of calcification is determined. The second type is characterized by the presence of two thin parallel hyperechoic tracks (the so-called "tram lines"). In the third type, patchy calcification with a random distribution in the renal cortex is detected. However, none of these types is pathognomonic for any of the causes of nephrocalcinosis.

Plain radiography of the kidneys reveals advanced cases with significant calcification of the renal pyramids. Computed tomography is most effective in detecting areas of calcification and may help differentiate between cerebral and cortical nephrocalcinosis. Magnetic resonance imaging is not an effective study to establish a diagnosis. If it is necessary to establish the cause of nephrocalcinosis, it is possible to perform a puncture biopsy of the renal tissue.

Treatment of nephrocalcinosis is a very difficult task due to the fact that a large number of causes leads to its formation. The fundamental principles of treatment are the elimination of the identified causes of nephrocalcinosis and disorders of calcium-phosphorus homeostasis. In addition to well-known methods of treatment, special attention is paid to the treatment of pyelonephritis, which contributes to the progression of renal failure in children with nephrocalcinosis. In these cases, longer courses of antibiotic therapy may be used. Long-term prophylactic treatment with uroseptics is often used. In the case of acute occlusion of the urinary tract by stones in the combination of nephrocalcinosis with nephrolithiasis, surgical intervention is indicated, which was undertaken in our patient with bilateral nephrolithiasis.

We present a case from practice. Girl T. was born from the 2nd pregnancy, which occurred in the mother with a threatened miscarriage at 9 weeks, anemia, 1st term delivery, with double entanglement of the umbilical cord around the neck, Apgar score 6–7 points. Birth weight - 3330 g, height - 53 cm, head and chest circumference 42 cm each. When examined by a doctor in the delivery room, the child was found to have no anus. Diagnosed with rectovaginal fistula, atresia of the anus and rectum. She was urgently operated on - a colostomy was placed on the ascending colon. The postoperative period proceeded without complications. She received antibiotics (gentamicin, cefazolin), prozerin, immunoglobulin, lactobacterin, rheopolyglucin, vikasol, etamzilat, festal, linex, trental, contrykal, chimes, eufillin, riboxin. Discharged at the age of 1 month in a satisfactory condition with a weight of 3200 g, with a normally functioning colostomy: stool through the stoma and fistula mushy, yellow.

2 days after discharge, her condition deteriorated sharply: she began to vomit, she developed vomiting, high fever, loose stools. She was hospitalized in a local hospital, where the first urinalysis revealed: leukocyturia (1-2 in the field of view), single unchanged erythrocytes, proteinuria - 0.1 g/l of protein. Pseudomonas aeruginosa 106, citrobacter 108, sensitive to cefuroxime, was isolated in stool culture.

On ultrasound of the kidneys: the right kidney is 66 x 32 x 38 mm in size, normal location; the entire collecting system is performed by a coral calculus; the calyces are dilated to 11 mm, the average thickness of the parenchyma is up to 5 mm; the left kidney is 56 x 25 x 30 mm in size, normal location, the pelvicalyceal complex is not changed; in the pelvis calculus 6 x 9 mm. Bladder of the correct form, normal size. Against the background of antibiotic therapy, signs of intoxication and pyuria persisted.

At the age of 2.5 months, the child developed acute renal failure due to obturation of the right ureter, left kidney and left ureter with calculi. In an urgent order, an operation was performed - lumbotomy on the right, removal of a coral-like stone of the right kidney, imposition of a nephrostomy. A week later, a lumbotomy was performed on the left, the calculus of the left kidney was removed, and a nephrostomy was placed on the left. She was treated for a long time with courses of antibiotic therapy, and was discharged with improvement. At discharge, a rectovaginal fistula was preserved up to 0.3 cm in diameter, the anus was absent in the usual place. At the age of 6 months, the child underwent abdominoperineal proctoplasty according to Romualdi. The postoperative period proceeded without complications. Subsequently, again at 9 and 11 months, she was treated for exacerbation of secondary chronic pyelonephritis, acetonemic state, intestinal dysbacteriosis. In repeated crops of feces - Staphylococcus aureus with continuous growth, Proteus vulgaris 108. At the age of one, an operation was performed - closure of the colostomy, which was complicated by a paraligature abscess of the postoperative scar of the abdominal wall, an abscess was opened, the ligature was removed, but compensated stenosis of the anus and rectum remained. Permanent finger bougienage of the anus is recommended. In sowing feces, St. aureus 106, resistant to many antibiotics, and Pseudomonas aeruginosa 106, sensitive to gentamicin, stood out. There was no diarrhea syndrome. Cicatricial insufficiency of the anus, enuresis, encopresis persisted. There was no urge to empty the stool on his own.

She was repeatedly treated in different hospitals in Ukraine, and then in Russia (parents changed their place of residence) due to exacerbation of secondary chronic pyelonephritis, chronic renal failure, cicatricial insufficiency of the anus. At the age of 5.5 years, an intestinal amoeba was found in the feces, she was treated for this, but was not detected in the reanalysis. In urine tests, a slight leukocyturia and oxaluria persisted, and a hyporeflex bladder was diagnosed.

At the age of six, chronic erythematous hypoacid antrum-gastritis was diagnosed (according to esophagogastroduodenoscopy), prolapse of the gastric mucosa into the esophagus up to 1 cm. The tone of the left half of the colon (descending and sigma) is increased; the rest of the length - reduced. Emptying is incomplete: contrast delay in all departments. The lumen of the output section of the large intestine is up to 0.5 cm. The transverse colon is located in the small pelvis. Data in favor of diffuse dystonic colitis, prolapse of the transverse colon, stenosis of the output sections of the colon. The elongation of the sigmoid colon is determined - dolichosigma.

In dynamics at the age of 8, repeated ultrasound revealed echo-signs of gallbladder deformity with bile stasis, splenomegaly; the bile ducts are sealed, an enlarged duodenal ring is visualized; echogenicity of the pancreas is moderately increased. Ultrasound of the kidneys: dimensions: right 6.9 x 2.6 cm, reduced; left 9.8 x 4.3 cm, unchanged. The contours are even and clear. The parenchyma is homogeneous, echogenicity is normal. The thickness of the parenchyma is somewhat reduced in the right kidney. Parenchymal constriction in the left kidney. The area of ​​the renal sinus is relatively expanded in the right kidney. The structure of the renal sinus is heterogeneous due to salt inclusions in both kidneys. The bladder is not changed. Conclusion: hypoplasia of the right kidney, saline diathesis, echo-signs of chronic pyelonephritis.

On renography at the age of 10: the secretory-excretory function of the kidneys is not impaired. Static scintigraphy of the kidneys at 10 years old: the left kidney is of normal shape, 97 x 58 mm, with a good concentration of the radiopharmaceutical (RP) and its homogeneous distribution in the parenchyma. The right kidney has a scintigraphically irregular round shape, reduced (65 x 47 mm), with a satisfactory concentration of radiopharmaceuticals and its uniform distribution in the parenchyma. The functionally active parenchyma of the right kidney is 39% compared to the left one. Diffuse decrease in the volume of the functioning parenchyma (hypoplasia) of the right kidney.

During the last 2 years, she suffered repeated seasonal respiratory infections 4-5 times a year. In 2011, she was treated in the hospital of the Central City Clinical Hospital No. 3 in Donetsk for acute bronchitis, bilateral purulent sinusitis, and infiltrative-plaque psoriasis. In the department, she was examined for TORCH infection: antibodies (enzymatic immunoassay) to cytomegalovirus (IgG) - 44.47 (positive) were detected. Serum urea - 4.9 mmol / l, creatinine - 0.054 mmol / l. Protein and protein fractions, transaminases, bilirubin, cholesterol are normal. At the same time, the content of high-density lipoproteins was reduced - 0.78 mmol / l (at a rate of 1.20-1.70 mmol / l) and ionized calcium - 1.20 mmol / l (at a rate of 1.29-1.31 mmol/l).

The ventilation function of the lungs is not impaired. Repeated urine tests without pathology. On ultrasound of the abdominal organs: echocardiography of cholecystitis; Ultrasound of the kidneys: the right kidney is reduced (8.0 x 3.2 cm), the parenchyma is not thinned, up to 1.6 cm, the pelvicalyceal system (PCS) is not expanded, cortico-medullary differentiation is somewhat reduced; the structure of the renal sinuses of normal echogenicity; left kidney: not enlarged (1.0 x 4 cm), the parenchyma is not thinned, up to 1.6 cm; ChLS is not dilated, renal sinuses are of normal echogenicity. The parenchyma is heterogeneous due to calcifications. Echo signs of hypoplasia and dysplasia of the right kidney. Nephrocalcinosis.

Based on the anamnesis, data from objective and additional research methods in the clinic of the Central City Clinical Hospital No. 3 in Donetsk, the diagnosis was made: chronic CMV infection, hypoplasia and dysplasia of the right kidney, secondary chronic pyelonephritis, remission. Encopresis, condition after bilateral nephrolithotomy. Nephrocalcinosis, nephrolithiasis, cholecystopathy, psoriasis.

She received augmentin orally, licopid, ventolin, pulmicort through a nebulizer, bifiform, enterosgel, reosorbilact IV, bioaron-S. Discharged with improvement for outpatient follow-up care.

Thus, the presence of congenital malformations of the gastrointestinal tract, early detection of nephrocalcinosis and nephrolithiasis, timely surgical intervention and treatment of exacerbations of chronic pyelonephritis with repeated courses of antibiotic therapy, preventive treatment with uroseptics could prevent a progressive decline in renal function in our patient. Timely appointment of therapy that prevents the progression of both the underlying disease and nephrocalcinosis is necessary to correct this pathology.

Nephrocalcinosis (oxalosis) is a consequence of impaired metabolism of oxalic acid and increased synthesis of oxalates, which are deposited in the kidneys.

Nephrocalcinosis is more common in children under 3 years of age. For some time the disease is asymptomatic, but then kidney failure develops, from which children die. The situation is aggravated by joining the main suffering of pyelonephritis.

The diagnosis is made on the basis of the abundant content of crystals of oxalate salts in the urine, with the obligatory condition that exogenous sources of these substances (vegetables, etc.) be excluded from food. A peculiar change in the functions of the distal parts of the nephron tubules is noteworthy - a decrease in the secretion of ammonia and reabsorption of phosphorus, as well as excessive excretion of alkalis.

An X-ray examination reveals calcified areas of the kidneys. Along with them, it is possible to identify stones of different sizes, in which sometimes surgical intervention is required, which is generally useless in case of nephrocalcinosis.

The course of nephrocalcinosis is long, and the prognosis is doubtful, since children die from the associated severe pyelonephritis and (and) kidney failure. Prevention and treatment should mainly be directed against these complications.

Tubulopathy with polyuria

Renal melituria is a group of tubulopathies, which are mainly manifested by the excretion of sugars (glucose, sucrose, galactose, etc.) in the urine. Of these, non-diabetic glucosuria is observed in most cases. In general, the entire group of melituria in children is much more common than diabetes mellitus.

The essence of this tubulopathy lies in a hereditary disorder of the enzyme systems responsible for the reabsorption of sugars in the kidneys, although the more intimate aspects of these disorders are not well understood. Inheritance occurs in an autosomal recessive manner.

The main clinical manifestation of melituria is a constant, uniform, independent of the intake of carbohydrates, excretion of sugars in the urine. Even with a load of glucose, the sugar curve remains normal. A constant and significant loss of sugars weakens the child, causing symptoms of hypoglycemia. Concomitant severe polyuria causes exicosis of the child, hypokalemia, polydipsia is pronounced.

The diagnosis is made on the basis of laboratory data, taking into account that with renal melituria, the functional ability of the kidneys is not impaired, and the level of sugars in the urine is not affected (diet, insulin, etc.).

In uncomplicated cases, treatment is not necessary. With a large loss of sugars in the urine and hypoglycemia, a diet rich in carbohydrates is necessary.

Nephrogenic diabetes insipidus This tubulopathy decreases the sensitivity of the renal tubules to vasopressin (VP) and reduces the reabsorption of water, resulting in the release of a large amount of unconcentrated urine; significant polyuria is accompanied by polydipsia.

In nephrogenic diabetes insipidus, antidiuretic activity plasma is preserved, but the receptors located in the epithelium of the distal part of the nephron tubules are unable to respond to vasopressin. In neurohypophyseal diabetes, which has similar clinical manifestations, on the contrary, the state of the receptors is not disturbed, but the level of vasopressin secretion is reduced. Therefore, in nephrogenic diabetes insipidus, the administration of this hormone to a patient does not reduce polyuria. This phenomenon is used for the differential diagnosis of these two types of diabetes insipidus.

The anomaly is inherited by recessive type, predominantly boys get sick. Polyuria appears already at an early age, then polydipsia joins. A large loss of water leads to a violation of the mineral and acid-base balance, exicosis, and a lag in physical and mental development. Often the body temperature rises.

Severe polyuria

There are also milder, latent forms of this disease with moderate polyuria and mild disturbance of homeostasis. Such forms are mainly observed at the age of 8-12 years.

Severe polyuria (up to 5-6 liters) causes overdistension of the bladder - hydrokinetic bladder, which is sometimes the reason for visiting a urologist.

Treatment should be directed to the regulation of water-salt metabolism, the introduction of a sufficient amount of fluid. There are reports that diuretics from the group of benzothiazine derivatives slightly increase the osmolarity of urine and reduce polyuria, thereby contributing to the normal development of the child.

Jade with loss of salt. This tubulopathy is also called salt diabetes, although the first name (soltloosingnephritis) is more common. Its main clinical manifestation is the excretion of a large amount of sodium chloride in the urine - hypernatriuria. With this tubulopathy, the sensitivity of the tubules to aldesterone is reduced, the release of which by the adrenal glands is not disturbed. In this regard, sodium reabsorption in the tubules of nephrons decreases, which leads to its increased excretion and hyponatremia. In the first days of a child's life, there is a deterioration in appetite, vomiting, adynamia, malnutrition; then muscle hypotonia, slowing down of ossification, dehydration appear; even later, a lag in physical and mental development becomes noticeable, and the filtration function of the kidneys decreases. In such children, resistance to infection is reduced, and its addition, in turn, aggravates the depletion of the body in sodium. In untreated cases, this pathology leads to cachexia of the child, frequent collapses and ends in death.

Nephrocalcinosis is an ailment characterized by an inflammatory process: calcium salts are deposited in the kidney tissues. The disease is included in the calcific group of pathologies (called renal dystrophy). The disease begins its development when there is a violation in the body of the metabolic process of calcium.

Diluted calcium salts in the composition of liquids begin to crystallize and accumulate in the cellular and intercellular space, with subsequent inflammation and the development of scarring in the tissues (sclerosis). Next comes kidney failure. As a rule, nephrocalcinosis of the kidneys begins to develop in damaged areas of the kidneys that have suffered from other diseases and (or) infections. The disease can develop both in an adult and in a newborn child.

Types and pathogenetic aspects of the disease

According to the clinical manifestations of the disease, two main forms of kidney nephrocalcinosis are distinguished:

• primary;
• Secondary.

With the primary manifestations of nephrocalcinosis, no changes in the tissue of the kidneys are observed (an absolutely healthy organ is affected).

The causes of the development of the primary form of this disease are:

• Vitamin D intoxication or hypervitaminosis;
• milk-alkaline syndrome, which develops with prolonged use of milk and alkaline preparations;
• Lightwood-Fanconi disease;
• Addison's syndrome;
• inflammatory sarcoidosis disease;
• excessive intravenous administration of calcium salts.

Removal of calcium from bone tissue and as a result:

• Swelling of bone tissue and internal organs;
• disease of the parathyroid glands;
• metastatic foci in the bones;
• plasmacytoma;
• various types of osteoporosis;
• inflammation of the bone marrow (osteomyelitis);
• frequent bone fractures;
• Paget's disease;
• high levels of thyroid hormones.

The secondary form of the disease is accompanied by damage to the damaged organ. Reasons for the secondary form:

1. The death of nephrons (functional kidney cells) and a decrease in the size of the organ. The cause of death was radiation exposure of the body.
2. Ischemic necrosis of the renal cortex: rapid necrosis due to acute, insufficient blood supply to the organ.
3. Prolonged and (or) excessive use of antimicrobial (sulfonamides), diuretic (thiazide, ethacrynic and anthranilic diuretics) drugs and analgesics (phenacitine).
4. Uncontrolled use of the antibiotic amphotericin.
5. mercury intoxication.

11 main symptoms and signs of the disease

During this kidney disease, the following symptoms occur:

1. There is a rapid fatigue of the human body, reduced endurance;
2. frequent appearance of weakness in the body;
3. possible nausea and vomiting;
4. signs of dehydration (dizziness and pain, dark circles under the eyes, dark yellow urine, decreased urine output, dry mouth, feeling thirsty);
5. constipation;
6. skin itching;
7. pain in the joints appears;
8. seizures;
9. psychological unstable state of a person;
10. lack of coordination;
11. trembling of the legs and arms.

The above symptoms are characteristic of calcium intoxication.

• Pain and cramps in the lumbar region;
• renal colic appears;
• isosthenuria (low specific gravity of urine);
• polyuria (large amount of urine, above 1,000 - 1,600 ml.);
• intense thirst is experienced.

In a clinical study in the urine sediment, a change in its structure will be observed. Most often, this is a high content of bacteria, erythrocytes and leukocytes. Then swelling, high blood pressure will begin to appear, and at this stage, kidney failure is detected, which leads to serious complications:

• Can go into a chronic form of renal failure;
• manifest an acute form of renal failure;
• the appearance of kidney stones (as a result of urolithiasis);
• obstructive uropathy may occur (urinary fluid will not go out through the urethra, but will go back to the kidneys).

Why is nephrocalcinosis dangerous?

The accumulation of calcium salts, calcification, in the tissues of the kidneys negatively affects the organ - there is a malfunction. But it is also important to know that the impact of the disease will affect other urinary organs. Deposition can also occur in the bladder. There is a water-salt imbalance. The formation of numerous calcifications may indicate the development of malignant (rarely benign) neoplasms.

Features of the development of the disease

The above reasons increase the influx of calcium to the organs. The kidneys cannot cope with the increased load, and calcium elements begin to accumulate in the cells of the kidney tissue. The concentration of calcium in the cells of the kidneys goes beyond the permissible limits, inflammatory phenomena are triggered, which will lead to further death of the cells of the organ. Degeneration occurs at the cellular level. Calcium begins to be deposited in the renal tubules themselves.

As a result of such a pathological change in the organ, the so-called calcium cylinders are formed. The tubules become clogged and cease to perform their function in the kidneys. Due to calcium deposits, the connective tissue of the kidneys increases and grows. The parenchyma (the name of the kidney tissue) ceases to maintain the required balance of fluids and electrolytes and is replaced by unnecessary scar tissue (the development of sclerosis). Calcifications are formed.

Most often, their formation begins to manifest itself in areas of accumulation of fluids and substances that are unnecessary to the body. Then there are signs of nephrocalcinosis. The kidneys begin to decrease in size and wrinkle. The process then progresses to kidney failure. The disease can often be accompanied by urolithiasis and pyelonephritis (kidney infections). This worsens the disease even more and gives the development of serious complications, with the subsequent progression of renal failure.

Diagnostics

If signs of nephrocalcinosis disease are found, it is necessary to contact a general practitioner (if the child is a pediatrician) and a nephrologist.

Most often, at the initial stages of diagnosing nephrocadcinosis, the patient's blood and urine are taken for examination. After collecting tests, identifying symptoms, possible causes and examining the patient, the following diagnostic stage is used to confirm the diagnosis, at which instrumental studies of the disease are used by the doctor:

• Ultrasound procedure;
• survey radiography;
• magnetic resonance imaging (MRI);
• computed tomography (CT);
• biopsy.

Ultrasound of the kidneys may not be an effective method of diagnosing: deposits can be very small and not always detected. A more accurate and detailed picture is given by MRI and CT. A biopsy is used as a last resort, if previous methods do not give an accurate picture of the course of the disease.

Prevention and the basics of treatment

Therapeutic treatment of nephrocalcinosis begins with a decrease in calcium in the patient's blood. At the initial stage of the development of the disease, it is enough to introduce the right diet and adjust your lifestyle. In more advanced cases, serious treatment is required.

The doctor may prescribe treatment with the following medications:

• citrate and sodium bicarbonate (they will more effectively remove unnecessary substances from the body);
• sodium chloride (contributes to the balance of the alkaline environment);
• potassium citrate (contributes to the balance of the acidic environment);
• vitamin b.

In the treatment of nephrocalcinosis, the diet should be aimed at reducing vitamin D, it is excluded to use dairy products, sesame and sunflower seeds, almonds, walnuts, halva, legumes, pastries from wheat flour, black bread. But you need to eat foods rich in magnesium. Be sure to drink the highest quality water.

It is necessary to begin to lead a more active and healthy lifestyle, to engage in physical exercises, this will positively affect the outflow of urine and will reduce the concentration of harmful substances.