Total calcium in the urine

In metabolic equilibrium, the daily excretion of calcium in the urine corresponds to the absorption of calcium in the intestine. Calcium excretion in the urine depends on the amount of filtered calcium in the glomeruli and tubular reabsorption. Filtration in the glomeruli of ionized calcium and calcium in a complex with low-molecular anions( approximately 60% of the total in the blood serum).The kidneys re-absorb 87-98% of filtered calcium. Reabsorption of calcium occurs passively throughout the nephron. The proximal convoluted tubules reabsorb 60%, the Henle loop 30%, the distal part of the nephron 10% calcium. Reabsorption of calcium in the distal tubules of the kidneys stimulates PTH.To fully understand the metabolism of calcium in the patient's body, it is necessary to study it in the urine. The reference limits for the release of total calcium in the urine, depending on the diet, are presented in Table.[Tiz U., 1986].

Table Reference limits for the release of total calcium in the urine

Table Reference limits for the release of total calcium in the urine

Normal mechanisms of calcium homeostasis prevent hypercalcemia by increasing the release of calcium in the urine. In connection with this, any non-renal-related increase in serum calcium concentration causes an increase in calcium filtration and an increased release of calcium in the urine. An increase in the intake of sodium to the Henle loop and the distal renal tubules( for example, in the administration of furosemide) also leads to an increase in the excretion of calcium in the urine. Hypercalciuria leads to a violation of calcium reabsorption in any part of the nephron. Understanding these mechanisms is important for the treatment of nephrolithiasis associated with hypercalciuria.

Hypercalciuria - urinary excretion of more than 300 mg / day of calcium in men and more than 250 mg / day in women, or more accurately - the release of calcium in the urine in an amount of more than 4 mg / kg of ideal body weight per day in either sex.

Calcium stones account for 70-80% of all kidney stones. Approximately 40-50% of patients with calcium stones observe hypercalciuria. In 40% of these patients idiopathic hypercalciuria is detected, in 5% - primary hyperparathyroidism, in 3% - renal-calcium acidosis. Other causes of hypercalciuria include excessive intake of vitamin D, calcium and alkali, sarcoidosis, Itenko-Ku-shing syndrome, hyperthyroidism, Paget's disease and immobilization.

Elevated calcium excretion in the urine is observed with hypercalciemia associated with malignant neoplasms, osteoporosis, proximal tubule dysfunction, the use of diuretics( furosemide, ethacrynic acid).

Most often, in kidney stones, idiopathic hypercalciuria is detected. This is a heterogeneous disorder associated with increased release of calcium in the urine with intestinal hyperabsorption( absorbent hypercalciuria) or reduced reabsorption of calcium in the renal tubules( loss through the kidneys).Absorptive hypercalciuria is possible with primary intestinal anomaly with hyperabsorption due to increased intestinal reactivity to calcitriol( type I) or elevated calcitriol in blood( type II).An increase in the concentration of calcitriol can cause phosphate loss through the kidneys, which in the future will cause a decrease in inorganic phosphorus in the blood serum, increased production of calcitriol, increased intestinal calcium absorption, increased serum calcium and hypercalciuria( type III).The primary loss of calcium through the kidneys disrupts its reabsorption in the tubules and can also cause hypercalciuria( renal hypercalciuria).Idiopathic hypercalciuria can be hereditary. The change in laboratory parameters for different types of idiopathic hypercalciuria is presented in the table.

Table Changes in laboratory parameters for different types of idiopathic hypercalciuria [McDermot MT, 1998]

Table Changes in laboratory indicators for various types of idiopathic hypercalciuria [McDermott M.T., 1998]

Note: AbG is an absorbent hypercalciuria;PG - renal hypercalcusuria.

Note: AbG is an absorbent hypercalciuria;PG - renal hypercalcusuria.

The concentration of inorganic phosphorus in the serum is reduced in case of ab-sorptive hypercalciuria of type III due to the primary loss of phosphates through the kidneys. The concentration of PTH in renal hypercalciuria is increased, because the primary disorder is a decrease in re-absorption of calcium, which causes relative hypocalcemia and stimulates PTH release by the principle of negative feedback. With absorption type II hypercalciuria, the calcium content in daily urine is normal, as in patients on a diet with a calcium restriction( 400 mg per day), because the absorption excess is not so significant. Nevertheless, the amount of calcium in the daily urine with a restriction of calcium intake for absorbent hypercalciuria I and III type, renal hypercalciuria remains high. Normal daily excretion of calcium in the urine with calcium restriction in food up to 400 mg per day is less than 200 mg / day. The concentration of calcium in urine on an empty stomach is normally less than 0.11 mg / 100 ml of GFR.The normal ratio of calcium and creatinine in the urine is less than 0.2 after taking 1 g of calcium as a load.

The establishment of the type of idiopathic hypercalciuria is important for the selection of adequate pharmacological therapy for nephrolithiasis.

Hypocalcauria - decrease in the concentration of calcium in the urine - occurs with nephritis, expressed hypoparathyroidism, hypovitaminosis D, hypothyroidism.

Urinary calcium is essential for the diagnosis of familial hypercalcemia-hypocalciuria, in which excretion of calcium with urine is less than 5 mmol / day in the presence of hypercalcemia.