What is Nephrocalcinosis?
Nephrocalcinosis is a disease that belongs to the group of calcifications. Calcifications, also known as calcareous dystrophy, are a form of pathology for calcium metabolism in the body: calcium salts (they were dissolved in liquids) precipitate from liquids, deposited in the interstitial tissue and cells.
Nephrocalcinosis is a variant of metastatic calcification in which calcium salts are diffusely deposited in the kidney tissue, which causes their inflammatory-sclerotic changes and renal failure.
Types of nephrocalcinosis according to clinical manifestations:
At primary changes in the kidneys are not observed, and at secondary, pathology of the kidneys occurs along with the processes of precipitation of calcium salts. Nephrocalcinosis can occur, for example, with alkaline-milk syndrome or Burnett’s syndrome. It is likely in children who are transferred from natural feeding to cow’s milk with herbal supplements. Read more about the reasons below.
Causes of Nephrocalcinosis
Among the causes of primary nephrocalcinosis are:
- conditions in which too much calcium gets into the body (familial and idiopathic hypercalcemia of newborns, hypervitaminosis D, Burnett’s syndrome, Lightwood-Fanconi syndrome, Addison’s disease, sarcoidosis, excessive intravenous administration of calcium salts)
- conditions in which there is mobilization of calcium from bones (tumors of bones and certain organs, hyperparathyroidism, myeloma, bone metastases of tumors, postcastration and corticosteroid osteoporosis, postmenopausal osteoporosis, osteomyelitis, multiple bone fractures, Paget’s disease, neuroplegia, thymotobia, imotobiosis, thymotobiosis, immobilization)
- hypophosphatasia (calcium binding in the bones is broken)
- oxalosis, cystinosis, calciphylaxis, in which in the tissues calcium unnecessary there is deposited normally
- tubulopathies and various diseases that occur with acidosis (Battler-Albright chronic tubular acidosis, Lightwood’s transient tubular acidosis, Low-oculocerebrorenal syndrome, de Tony-Debreu-Fanconi glucose-phosphatioaciduria, hyperchloretic aza)
Secondary nephrocalcinosis: causes
Among the most likely reasons are called:
- radiation nephrosclerosis
- ischemic cortical necrosis of the kidneys
- abuse of sulfonamides, thiazide diuretics, phenacetin, ethacrine diuretics, anthranilic diuretics
- uncontrolled use of amphotericin
- mercury salt poisoning
Nephrocalcinosis can be caused by renal and extrarenal disorders of acid-base balance. This is mainly metabolic and respiratory acidosis, in rare cases, it is metabolic alkalosis. With these diseases, the level of calcium in the blood rises, its excretion in the urine increases. The degree of calciuria can be a maximum of 400-600 milligrams in 24 hours.
Pathogenesis during Nephrocalcinosis
The pathogenesis of calcifications
The matrix for calcium salts inside the cells is lysosomes and mitochondria. Outside the cells, these are collagen and elastic fibers plus glycosaminoglycans of the main substance of the interstitial tissue. Calcium salts can be deposited in the form of grains, foci of lime, which are more or less common in different cases. Bone tissue may form in areas with lime, and around it there will be inflammation and a fibrous capsule.
Local and general factors play a role in the pathogenesis of calcifications. Therefore, forms of calcification, in addition to the criterion for the location of calcifications, are distinguished by pathogenetic factors. Calcification can be metastatic, metabolic and dystrophic, which is also known as (petrification).
Pathogenesis of nephrocalcinosis
An abnormally large influx of calcium occurs to the kidneys, it accumulates in the cells of the epithelium of the human kidneys. When too much intracellular calcium is collected, cell dystrophy occurs. The deposited calcium enters the interstitial space or into the lumen of the tubules. In this process, cylinders are formed that overlap the canaliculi; therefore, they dilate and atrophy. Salt deposits in the interstitium cause a lymphoproliferative reaction, then nephrosclerosis occurs.
With nephrocalcinosis, infection and the formation of stones occur, because this disease becomes the source of pyelonephritis and / or hydronephrosis. The pathogenesis of primary nephrocalcinosis in children and adults is characterized by the fact that the proximal nephron is first affected, and the glomerulus and distal are affected later. If the nephrocalcinosis is secondary, then calcium is deposited simultaneously in the distal nephron.
Symptoms of Nephrocalcinosis
With nephrocalcinosis, there is usually a underlying disease. Therefore, two groups of symptoms appear immediately, as well as concomitant hypercalcemia. Calcium intoxication causes the following symptoms:
- general weakness
- dry skin
- joint deformity
- joint pain
- mental instability
- convulsive seizures
- shortening the duration of systole on an electrocardiogram
With kidney damage, when the transport of substances in the tubules is disrupted and their sensitivity to antidiuretic hormone is lost, there are:
- bouts of renal colic are likely (when calculi go away)
- lower back pain
Often there are persistent changes in the urinary sediment, it contains a large number of bacteria, white blood cells, salt cylinders and red blood cells. Later, edema, proteinuria, arterial hypertension are recorded. In this period, as a rule, symptomatic and laboratory signs of kidney failure already appear.
- Chronic renal failure
- Acute renal failure
- Obstructive uropathy
- Stones in the kidneys
Diagnosis of Nephrocalcinosis
Diagnosis of nephrocalcinosis at the stage of its appearance is based on information obtained using a puncture biopsy of the kidney. Such a method as survey radiography is relevant only in severe cases, when calcification of the renal pyramids is significantly expressed.
To approximately determine the degree of calciuria, diagnosticians sometimes use the Sulkovich test. To clarify the cause of the disease, examine the patient’s urine and blood for the content of calcium and phosphorus, determine the activity of parathyroid hormone in the blood, alkaline phosphatase. It is necessary to identify the discharge of oxyproline with urine, acid-base balance, clearance of creatinine and phosphate.
Diagnostic nephrocalcinosis is distinguished from a spongy kidney, in which the cystic spaces are filled with a condensate of calcium salts.
It is necessary to eliminate as early as possible the cause of the violation of calcium metabolism in the body. With a severe degree of dehydration, an infusion is made by infusion of a solution of sodium bicarbonate or sodium citrate, potassium citrate and asparaginate with acidosis, and with alkalosis, infusions of sodium chloride and ammonium are made.
If hypercalcemia is moderate, the patient is advised to adhere to a food regimen in foods in which there is little or no calcium. Vitamin B6 and an infusion of magnesium sulfate solution are attributed. The treatment of acute hypercalcemia consists in the infusion of a solution of magnesium sulfate, sodium phosphate, EDTA-sodium. Doctors may prescribe the administration of thyrocalcitonin or prednisone.
Treatment of progressive renal failure is mandatory with hemodialysis. It is important to adequately treat pyelonephritis, which causes progression of kidney failure. With secondary nephrocalcinosis, it is important to identify and cure the underlying disease, which is an etiological factor.
The prognosis for effective treatment at the beginning of the disease is good. An unfavorable prognosis in patients with progressive nephrocalcinosis, because in advanced cases there is uremia, which threatens the health and life of the patient.
Prevention of Nephrocalcinosis
- You should get the optimal amount of calcium (no more and no less) with daily nutrition.
- You can not take calcium preparations without a doctor’s prescription.
- It is important to treat kidney diseases on time.
- If you experience suspicious symptoms and any health problems, you should urgently consult a therapist, family or highly specialized doctor.