Bisphosphonates are widely used to prevent osteoporosis and, among these, alendronate and risedronate, exhibit a favourable efficacy/safety profile over long-term use. Theoretically, if increased bone resorption partly explained id- iopathic hypercalciuria, it follows that drugs capable of reduc­ing the rate of bone turnover should also have some effect on calcium excretion. Alendronate, 20 mg daily, had been shown to prevent hypercalciuria and the calcium-stone forming propensity induced by prolonged bed-rest. Independently of immobilization, genetic hypercalciuric rats reduced both cal­cium excretion and urine saturation with calcium salts upon al- endronate administration. The effects of bisphosphonates on calcium excretion was studied in the phosphate depletion induced hypercalciuria, which is referred to as being caused by increased efflux of calcium from bone. Phosphate depleted rats developed hypophosphatemia, hypercalcemia and hypercalci- uria, but failed to respond to pamidronate, despite an improved bone histology. canadian-healthcare-shop.com cheap generic drugs online

Recently we have reported similar results in patients with fast­ing hypercalciuria who had been given alendronate 10 mg/daily and re-studied after a three-month course. There was a signifi­cant decrease in both fasting and 24-hour calcium excretion and, consequently, a 43% reduction in urine saturation with calcium oxalate. These changes were obtained in the face of normal levels of plasma calcium and only minor and tran­sient increases in serum PTH, and maintained over a two-year follow-up (Figure 3). From these results bisphosphonates ap­pear as promising new tools in the management of hypercalci­uria, namely in the fasting hypercalciuria or in patients with bio­chemical (and clinical) evidence of increased bone resorption.

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Citrate supplementation, as alkaline potassium salt, was for­merly introduced in the treatment of distal renal tubular acido- sis and subsequently extended to idiopathic hypocitraturic calcium nephrolithiasis. Regardless of the accompanying cation (sodium, potassium, magnesium) citrate salts exhibit di­rect effects on calcium excretion, acting by two distinct mecha­nisms: first, citrate anion is a strong ligand of calcium, and this will result in a decrease in free ionised calcium concentration; second, alkalinisation is expected to reduce bone resorp­tion, thereby decreasing total calcium excretion. The principal effect of citrate on calcium excretion is due to its ability to bind calcium, so that the calcium-citrate soluble com­plex accounts for by about 10 to 40% of total urinary calcium (Figure 1). Therefore, an increase in urinary citrate will result in a decrease in the fraction of free-ionised calcium, which is the species thermodynamically important for the saturation of calci­um forming salts. Discount drugs online cad pharmacy

The effect of potassium citrate upon the skeleton is shared by other alkaline salts, such as potassium bicarbonate. In fact, in postmenopausal women, the oral administration of potassium bicarbonate, at a dose sufficient to neutralise endogenous acid, improved calcium balance, by reducing calcium excretion, through a reduction of bone resorption and an increase in the rate of bone formation. In a prospective short-term study, alkaline mineral water induced a significant reduction in the biochemical markers of bone resorption. There also are re­cent reports of a specific effect of potassium intake on calcium excretion, because it has been found that potassium deficiency increases, whereas potassium supplementation as either cit­rate or bicarbonate or chloride salts, decreases calcium excre­tion. Potassium citrate, given to healthy menopausal women decreased net acid excretion and concurrently de­creased markers of bone resorption (Figure 2). Percent varia­tions of urine citrate were inversely related to those of de- oxypyridinolines and hydroxyproline, whereas calcium excre­tion exhibited only minor decreases .

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The amazing advances in molecular genetics have also in­volved hypercalciuria, and at least three candidate genes were shown to arbour mutations leading to altered calcium excretion. The chloride channel 5 (ClC-5), the calcium sensing receptor and the paracellin-1 are proteins encoded by corresponding genes, whose mutations causing either loss or gain of function, lead to hypercalciuric syndromes (Table II). Transfection or gene-disruption studies with these genes not only contribute to clarify mechanisms of the underlying diseases, but also help to understand the pathophysiology of idiopathic hypercalciurias. Recent reports have addressed the issue of treatment of ge­netic hypercalciurias, namely, in the course of Dent’s syndrome and familial hypocalcemic hypercalciuria. The mechanism leading to hypercalciuria in Dent’s syndromes is as yet not fully elucidated, in that both intestinal hyperab- sorption and renal leak could contribute. Chlorthalidone, but not amiloride, was shown to reduce both calcium excretion and calcium oxalate and calcium phosphate supersaturation in Dent’s syndrome, yielding similar results as in patients with id- iopathic hypercalciuria. These results led authors to con­clude that the hypocalciuric response to thiazides indicates that inactivation of the ClC-5 does not impair calcium transport in the distal convoluted tubule and that thiazides should be effec­tive in reducing the risk of kidney stone recurrence in these pa­tients. cad-pharmacy.com canadian drugstore

Different approaches were tried in patients with CaR mutations with gain of function. These patients may present with hypocal- cemia of various severity, some of them presenting with major clinical signs of hypocalcemia. The classical treatment with ac­tive vitamin D derivatives, while relieving hypocalcemic symp­toms, induced significant increases in calcium excretion with an attendant risk of nephrocalcinosis. More recently, synthetic human PTH-(1-34) was shown to provide a safe and effective alternative to calcitriol therapy, able to maintain normal serum calcium levels without hypercalciuria. Similar encouraging results have been reported in two such patients by using hy- drochlorothiazide (1 mg/kg), which reduced urinary calcium ex­cretion and maintained serum calcium concentrations near the lower limit of normal, allowing the vitamin D doses to be re­duced, while alleviating symptoms. Finally, magnesium salts and thiazides were used to treat pa­tients with FHHNC (see Table II) caused by paracellin-1 muta­tions. While being of some efficacy to correct biochemical changes, treatment did not prevent, however, progression to chronic renal failure, which is a feature of this disease.

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Introduction

Idiopathic hypercalciuria is the most frequent metabolic abnor­mality since up to 40 to 60% of patients with nephrolithiasis are hypercalciuric. Fasting hypercalciuria, accompanies id­iopathic hypercalciuria in up to 50% of the patients. It is widely agreed that high calcium excretion may be causative for stone disease, because the higher calcium concentration, the higher the state of saturation with the calcium forming salts. However, a more general involvement of mineral metabolism, and in particular bone turnover, comes from the fact that virtu­ally all of these patients tend to develop a negative external balance of calcium, because renal loss overtakes net calcium absorption at the intestine. We care about you health canadian medshop 247 item

The mechanisms of hypercalciuria are complex and not fully clarified as yet, and this issue is the object of another article in the Journal. Anyway, a better understanding of the pathogene­sis of hypercalciuria represents the basis of the different thera­peutic options so far pursued, which will be the object of the present review. These are listed in Table I. The points concern­ing the dependence of calcium excretion on dietary factors will be omitted, being treated elsewhere in this issue. …Read the rest of this article

Pleural effusions in the yellow nail syndrome are thought to be secondary to dysfunction of pleural lymphatics. Once present, they tend to persist and may recur rapidly after therapeutic thoracentesis, making this an impractical option in many symptomatic patients. Chemical pleurodesis using quinacrine (Atabrine) and tetracycline has been successful in two patients. Nine patients have been treated successfully with open pleural abrasion, pleurectomy or decortica­tion. Unfortunately, chemical pleurodesis causes pain and discomfort and has an appreciable failure rate, and open pleural abrasion and pleurectomy, while very effective, are major surgical procedures associated with a perioperative morbidity of up to 10 percent.

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The triad of yellow nails, lymphedema and pleural effusion was first described by Emerson in 1966 and was labelled the yellow nail syndrome. Since then, more than 100 patients with the classic triad or variants thereof have been described. Pleural effusions in this syndrome range from small, unilateral and asymptomatic to large, bilateral and debilitating. We describe a patient with yellow пай syndrome and symptomatic chronic pleural effusion inadequately controlled with frequent thoracentesis but successfully treated with pleuroperitoneal shunting.

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