What Is Hypercalciuria?

Hypercalciuria is the most common metabolic abnormality in patients with calcium urinary stones, accounting for about 30% to 60% of patients with calcium stones. If normal people limit daily intake of 400 mg of calcium and 100 mg of sodium, 100 mg of urine is excreted in 24 hours. If this diet is continued for 1 week, the 24-hour urine calcium is still greater than 200 mg, which is called hypercalciuria; if the normal diet, the 24-hour urine calcium excretion is greater than 4 mg / kg body weight, or the 24-hour urine calcium excretion is greater than 300 mg in men Women greater than 250 mg are called hypercalciuria. There are three types of hypercalciuria: absorptive hypercalciuria, renal hyperuricemia, and reabsorbent hypercalciuria.

Hypercalciuria

[span] According to the mechanism of the occurrence of hypercalciuria, it is divided into three types of reabsorption, absorptive and renal hypercalciuria. Other metabolic diseases with well-defined etiology can also lead to hypercalciuria and urinary calcium stones, such as distal renal tubular acidosis, sarcoidosis, long-term bed rest, osteopenic disease, glucocorticoid excess, Renal tubular acidosis accounts for 0.5% to 3% of patients with calcium stones, such as hyperthyroidism and high vitamin D. Others are rare.

Resorbable hypercalciuria

The basic exception is

Absorptive hypercalciuria

The primary metabolic disease is due to an abnormal increase in intestinal calcium absorption, followed by a slight increase in blood calcium, which increases the glomerular filtration calcium and inhibits the secretion of PTH. Due to reduced PTH secretion, renal tubular calcium reabsorption is reduced, so hypercalciuria is due to increased glomerular filtration calcium and decreased renal tubular calcium reabsorption (Figure 5). The balance between increased intestinal calcium absorption and increased renal calcium excretion can maintain blood calcium in the normal range.

Absorptive hypercalciuria is divided into 3 types:

Type hypercalciuria appears in high and low calcium diets;

Type hypercalciuria only occurs in a high calcium diet, and in a calcium limited diet (400 mg / d), urine calcium is normal, and the clinical symptoms of type are milder than those of type ;

Type is secondary to high phosphorus excretion in the kidney, and is also known as hypophosphatemic absorbable hypercalciuria.

The exact mechanism of increased intestinal calcium absorption in absorbable hypercalciuria is unknown. In some patients, intestinal calcium absorption is not directly related to blood 1,25- (OH) ₂ D ₃ concentrations. Intestinal perfusion studies have shown that the site of high calcium absorption is in the jejunum and not in the ileum, and magnesium absorption is normal. This selective jejunal high calcium absorption suggests that vitamin D has no important pathogenic effect, because one of the effects of vitamin D and its metabolites is to increase the absorption of calcium and magnesium in the two sections of the jejunum and ileum.

However, an increase in blood 1,25- (OH) ₂ D ₃ concentrations in approximately one-third of patients with absorbable hypercalciuria suggests that increased intestinal calcium absorption is vitamin D-dependent. To explain the reason, hypophosphatemia was proposed as an important factor. These patients with absorptive hypercalciuria have a primary renal phosphorus leak, followed by hypophosphatemia that stimulates the kidneys to synthesize 1,25 (OH) ₂ D ₃ . Although orthophosphate treatment can reduce blood 1,25- (OH) ₂ D ₃ concentration, it cannot reduce intestinal calcium absorption.

The primary cause is impaired renal calcium reabsorption and leakage of renal calcium, followed by a slight decrease in blood calcium, stimulation of parathyroid glands, increased PTH secretion, mobilization of bone calcium, and increased intestinal calcium absorption. These effects make blood calcium Return to normal range (Figure 6). Although clinical bone disease is rare, the bone density has been significantly reduced with ¹²⁵ I-photon absorber. Intestinal calcium absorption is increased in some patients with renal hypercalciuria, but not all of them. Intestinal calcium absorption fractions have been found to be higher in 70% of patients, and urine calcium increased significantly after oral calcium loading. These results suggest that intestinal hyperabsorption of renal hypercalciuria is not a primary disorder and may be a secondary change. Treatment of renal hypercalciuria with thiazide diuretics can reduce blood PTH and 1,25 (OH) ₂ D ₃ concentrations to normal and restore normal calcium absorption.