Calcium diuretic-induced

Diuretics have been shown to have variable effects in relationship to urinary calcium excretion and supersaturation, most notably including loop diuretic induced hypercalciuria and attenuation of urinary calcium excretion by thiazide diuretics. The factors contributing to nephrotoxicity are most commonly associated with multiple factors that favor calcium salt or uric acid deposition at the tubulo-interstitial level. Management of renal stone formation and nephrocalcinosis therefore presents a unique clinical challenge, balancing factors that increase risk for abnormal calcium salt deposition or crystallization, and factors that reduce this risk. 

Therapeutic measures that have been used to decrease the incidence of contrast-induced nephropathy include extracellular volume expansion, minimization of the amount of contrast administered, and treatment with oral acetylcysteine. Theophylline, fenoldopam, loop diuretics, mannitol, dopamine, and calcium antagonists have no effect or may worsen ARF. 

Might antagonize verapamil Might induce hypercalcemia with thiazide diuretics Fiber laxatives (variable), oxalates, phytates, and sulfates can decrease calcium absorption if given concomitantiy Phenytoin, barbiturates, carbamazepine, rifampin increase vitamin D metabolism... 

Drugs that may affect repaglinide include CYP 450 inhibitors (eg, clarithromycin, erythromycin, ketoconazole, miconazole), CYP 450 inducers (eg, barbiturates, carbamazepine, rifampin), beta blockers, calcium channel blockers, chloramphenicol, corticosteroids, coumarins, estrogens, gemfibrozil, isoniazid, itraconazole, levonorgestrel and ethinyl estradiol, MAOIs, nicotinic acid, NSAIDs, oral contraceptives, phenothiazines, phenytoin, probenecid, salicylates, simvastatin, sulfonamides, sympathomimetics, thiazides and other diuretics, and thyroid products. 

Hypercalcemia is a common clinical condition that can accompany a variety of other medical conditions, such as sarcoidosis, vitamin D toxicity, hyperparathyroidism, and malignancy. When calcium levels are exceptionally high, adjunctive measures for the control of plasma calcium levels are necessary, as this is a medical emergency. Various modalities in combination are used to treat this condition intravenous hydration with normal saline and the use of loop diuretics (e.g., furosemide) to induce calcium diuresis are the most important supportive measures. 

Certain foreign compounds may cause the retention or excretion of water. Some compounds, such as the drug furosemide, are used therapeutically as diuretics. Other compounds causing diuresis are ethanol, caffeine, and certain mercury compounds such as mersalyl. Diuresis can be the result of a direct effect on the kidney, as with mercury compounds, which inhibit the reabsorption of chloride, whereas other diuretics such as ethanol influence the production of antidiuretic hormone by the pituitary. Changes in electrolyte balance may occur as a result of excessive excretion of an anion or cation. For example, salicylate-induced alkalosis leads to excretion of Na+, and ethylene glycol causes the depletion of calcium, excreted as calcium oxalate. 

Calcium channel blockers are well known to cause peripheral oedema, in particular ankle oedema. This occurs as the vasodilatation induced by the drug tends to make the blood vessel walls leaky, and so fluid escapes to, and accumulates in the surrounding tissues. Unfortunately, this condition is unresponsive to diuretic therapy, and so the only way to reverse it is to discontinue the drug. 

BARBITURATES DIURETICS-CARBONIC ANHYDRASE INHIBITORS Risk of osteomalacia Barbiturates have a small risk of causing osteomalacia this may be T by acetazolamide-induced urinary excretion of calcium Be aware... 

Loop diuretic therapy has been implicated in the development of renal calcifications in both preterm and full-term infants [99-105]. In a study by Jacinto et al., nephrocalcinosis occurred in 20 of 31 (64%) of premature infants with birth weights less than 1500 g, with 65% of affected infants having received furo-semide [103]. Nephrocalcinosis was found in 14% of full-term infants with congestive heart failure receiving long-term furosemide therapy [104]- Furosemide may induce high urinary calcium excretion rates and low urinary citrate to creatinine ratio, risk factors for renal calcification [106]. 

Similar to the other high-ceiling diuretics, ethacrynic acid inhibits the NaVKV2CI symporter in the ascending limb of the loop of Henie to promote a marked diuresis. Sodium, chloride, potassium, and calcium excretion are increased following oral or intravenous administration of ethacrynic acid. Oral administration of ethacrynic acid results in diuresis within 1 hour and a duration of action of 6 to 8 hours. Toxicity induced by ethacrynic acid is similar to that induced by furosemide and bumetanide. Ethacrynic acid is not widely used, however, because it induces a greater incidence of ototoxicity and more serious gastrointestinal effects than those of furosemide or bumetanide. 

There is a strong correlation between hypercalcemia and hypertension (9,10). Black males may have a higher risk for this side effect (H). Caution must be used when treating hypercalcemia-induced hypertension since thiazide diuretics can transiently produce hypercalcemia. With long-standing hypercalcemia, calcium may be deposited on the cardiac valves and coronary arteries (12.). Another cardiovascular side effect of hypercalcemia is lengthening of the ECG OT interval. 

Ticlopidine-induced increases in bleeding times are opposed by methylprednisolone and prednisolone but its effects on platelet function are not affected. Ticlopidine decreases the clearance of phenazone (antipyrine), which suggests that it has mild enzyme-inhibiting effects. Beta blockers, calcium-channel blockers and diuretics are reported not to interact with ticlopidine. 

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