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Renal deposition of calcium-phosphate or calcium-oxalate re­sults in nephrocalcinosis. This disorder is more frequently found in children and preterm newborns and deposits are more frequently composed by apatite and begins within medulla. In rare patients with primary hyperoxaluria (type 1 or 2) deposits are cortical and composed by calcium-oxalate. Nephrocalcinosis may occur in the course of many hereditary tubular disorders having hypercalciuria as the common alter­ation: Dent’s disease, Bartter’s disease (type 1 and 2), distal tubular acidosis, primary hypomagnesemia-hypercalciuria- nephrocalcinosis syndrome. These tubular disorders are mono- genic and were found in 33% of newborn with nephrocalcinosis. Conversely, iatrogenic causes were responsible of 30­50% of infant nephrocalcinosis. Furosemide and vitamin D are the most frequently implicated drugs, probably due to their capability to increase calcium excretion. Nephrocalci­nosis was also associated to the use of gentamicine, extreme prematurity and severe respiratory disease. Vitamin D, with calcium or phosphate salts, is used to maintain normal plasma concentrations of calcium and phosphate in children with hypoparathyroidism or renal rickets, in their different forms. Because these patients are predisposed to lose calcium in urine, therapy with bivalent ions and vitamin D increases their calcium excretion to an extent that greatly amplifies the risk for renal calcium-phosphate precipitation. Hypercalciuria was observed in 34% of newborns with nephro- calcinosis, but increased oxalate and urate excretions and decreased citrate excretion were also described. Plasma calcium concentrations, calcium and phosphate intake were found increased in newborns with nephrocalcinosis. Nephrocalcinosis can solve in 50% of infants, but resolution is less probable in children with hypercalciuria. Discount drugs online canadian-healthcare-shop.com

In adults, nephrocalcinosis usually occurs in patients with pri­mary hyperparathyroidism or sarcoidosis or in patients chroni­cally taking calcium or phosphate salts and vitamin D for con­trol of hypocalcemia or hypophosphatemia. In addition, nephro- calcinosis can develop in patients with medullary sponge kid­ney and severe infectious or ischemical diseases of kidney. Nephrocalcinosis can progressively damage kidney function, impairing glomerular filtration rate and urinary concentration capacity. Deterioration of renal function may be slight with time, but it is correlated with the degree of nephrocalcinosis and to severity of the underlying disorder. Nephrolithiasis may complicate nephrocalcinosis and was reported in 14% of chil­dren. It may occur when an interstitial deposit erupts into urinary tract and becomes a site for salt deposition open to the urinary tract.

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Kidney stone disease may be considered as the main compli­cation of hypercalciuria. Despite the amount of research, the first evidence that hypercalciuric subjects are predisposed to kidney stones was recently provided in a work, displaying that the risk to produce stones increased with calcium excretion in general population. Previous studies had limited their ob­servation to the higher frequency of hypercalciuria in calcium stone forming patients and the larger calcium excretion in re­lapsing compared to non-relapsing stone formers. In spite of these findings, the real role of calcium in stone for­mation has not been yet understood. Calcium stone-promoting activity may be due to the effect of calcium ions on urinary sta­bility and saturation for calcium salts. However, when tested in vitro, the effect of calcium ions on the activity product of calci- um-oxalate or calcium-phosphate was much less remarkable than that of phosphate, oxalate or water; thus, calcium concen­tration did not appear as the main determinant of salt solubility. Therefore, other aspects of calcium activity in stone for­mation have been explored. It was observed that the intrinsic urinary power to inhibit salt precipitation decreased when calci­um was added to urine. This effect was attributed to calcium-in­duced alterations in molecular structure of Thamm-Horsfall pro­tein, that reduced its efficacy to inhibit calcium-oxalate and cal­cium-phosphate crystal nucleation and growth. cad pharmacy 1 internet online drugstore

Uncertainty about the role of calcium is also justified by the fact that the pathogenetic mechanism for stone production is un­known. The current theories hypothesize that initial events in stone formation can develop in tubules or, alternatively, in pap­illary interstitium. According to the tubular theory (Fig. 2), a stone can develop from crystal agglomerates retained within the lumen of a renal tubule. Physical-chemical characteris­tics of tubular fluid can promote the precipitation of calcium- phosphate within the ascending Henle’s loop and calcium-ox- alate in the collecting tubule. Crystals can grow and aggre­gate in supersaturated fluids and can be retained within the tubular lumen due to their capability to adhere to the tubular wall. Studies in animals showed that oxalate, under the form of ions or crystals, can cause tubular cell injury, necrosis or apop- tosis with release of cell debris in tubular lumen and exposure of basement membrane to the tubular fluid. These events may be crucial for macroaggregate development and stone forma­tion, because crystals can easily attach to the injured tubular wall and calcium-oxalate can precipitate on cell debris, espe­cially membrane fragments rich of phospholipids, even in the presence of stable urine. The final pathway for stone production may be the retention of a crystal macroagglomerate within papillary Bellini’s ducts, which may become a stone after ulceration of the papilla and its exposition to the urinary tract.

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In most of patients, primary hypercalciuria results from an in­crease of intestinal calcium absorption (absorptive hypercalci­uria). In less than 5% of patients, primary hypercalciuria may be caused by a primary defect in tubular calcium reab- sorption (renal hypercalciuria). These different forms of hypercalciuria are clinically distinguished with the measure­ments of fasting calcium excretion and plasma PTH. In absorp­tive hypercalciuria, fasting calcium excretion is normal, while circulating levels of PTH are low. In renal hypercalciuria, both fasting calcium excretion and circulating PTH are high. In spite of these simple criteria, the real mechanisms leading to hypercalciuria remain unclear and around one-third of patients remain unclassifiable because they exhibit fasting hypercalci- uria and normal plasma PTH. Furthermore, contrarily to expectations, patients with absorptive hypercalciuria often have a deficit in bone mineral density, similar to that observed in re­nal hypercalciuria. Recently, we found that hypercalci- uric stone-forming women with low bone mineral density at vertebral sites presented the highest values of intestinal calcium absorption. This observation suggests that the defect causing hypercalciuria could be expressed in bones and intes­tine, where it could activate calcium absorption and bone me­tabolism and ultimately increase calcium excretion. Many pro­teins with a relevant role in calcium metabolism, like calcium- sensing receptor, vitamin D receptor or calcium pump, are ex­pressed in bone, tubular and enteral cells. In case of their alter­ation, the effect on calcium excretion should result from the combination of their influences in bones, intestine and kidney. Therefore, in some groups of patients, pathogenesis of hyper­calciuria could be more complex than proposed till now. canadian medshop 247 canadian drugstore

Urinary alterations associated to primary hypercalciuria

Increased excretions of sodium, sulphate, urate, urea and phosphate may be found in hypercalciuric patients and also in their relatives and were justified with a high dietary intake of these substances or their precursors. Further studies ex­ploring the effect of nutrients on ion excretion displayed that animal proteins and sodium are important determinants of uri­nary calcium and that their excess in diet increases the values of excreted calcium.

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Introduction

Primary hypercalciuria is a defect of calcium metabolism, char­acterized by increased 24 hour urinary calcium excretion which is not justified by any apparent metabolic alteration. Its prevalence is 5-10% in the general population, but is signifi­cantly higher in patients with calcium kidney stones, nephrocalcinosis, arterial hypertension and osteoporosis. Online Canadian pharmacy mycanadianhealthcare.com

Primary hypercalciuria has a familial distribution displaying a complex transmission pattern due to a polygenic substrate. In addition to the family history, large body mass and high in­take of animal proteins and salt predispose to hypercalciuria. Therefore, primary hypercalciuria appears as a multifactori­al disorder determined by the interaction of different genetic and environmental factors (Fig. 1).

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