Aminoglycosides renal failure caused

Causes of hypocalcemia include hypoparathyroidism, hypomagnesemia, alcoholism, hyperphosphatemia, blood product infusion (due to chelation by the citrate buffers), chronic renal failure, vitamin D deficiency, acute pancreatitis, alkalosis, and hypoalbuminemia. Medications that cause hypocalcemia include phosphate replacement products, loop diuretics, phenytoin (Dilantin, available as generic), pheno-barbital (available as generic), corticosteroids, aminoglycoside antibiotics, and acetazolamide (available as generic).34,39,42... 

WARNING Renal impair is the major tox foUow administration instructions Uses CMV retinitis w/ HIV Action Selective inhibition of viral DNA synth Dose Rx 5 mg/kg IV over 1 h once/wk for 2 wk w/ probenecid Maint 5 mg/kg IV once/2 wk w/ probenecid (2 g PO 3 h prior to cidofovir, then 1 g PO at 2 h 8 h after cidofovir) X in renal impair Caution [C, -] Contra Probenecid or sulfa allergy Disp Inj SE Renal tox, chills, fever, HA, NA /D, thrombocytopenia, neutropenia Interactions t Nephrotox W/ aminoglycosides, amphot icin B, foscar-net, IV pentamidine, NSAIDs, vancomycin t effects W/zidovudine EMS Monitor ECG for hypocalcemia (t QT int val) and hypokalemia (flattened T waves) OD May cause renal failure hydration may be effective in reducing drug levels/effects Cilostazol (Pletal) TAntiplatelet, Arterial Vasodilator/ Phosphodiesterase Inhibitor] Uses Reduce Sxs of intermittent claudication Action Phosphodiesterase in inhibitor t s cAMP in pits blood vessels, vasodilation inhibit pit aggregation Dose 100 mg PO bid, 1/2 h before or 2 h after breakfast dinner Caution [C, +/-] Contra CHE, hemostatic disorders. 

Adults. 3 g PO q6h x 4 PRN Supl 1-2 g IM or IV repeat PRN Preeclampsia/pre-mature labor 4 g load then g/h IV inf Cardiac arrest 1-2 g IV push (2-4 mL 50% soln) in 10 mL DjW AMI Load 1-2 g in 50-100 mL D5W, over 5-60 min IV then 0.5-1.0 g/h IV up to 24 h (ECC 2005) Feds. 25-50 mg/kg/dose IM or IV q4-6h for 3-4 doses repeat PRN dose w/ low urine output or renal insuff Caution [B, +] Contra Heart block, renal failure Disp Inj 10, 20, 40, 80, 125, 500 mg/mL bulk powder SE CNS depression, D, flushing, heart block Interactions T CNS depression W/ antidepressants, antipsychotics, anxiolytics, barbiturates, hypnotics, narcotics EtOH T neuromuscular blockade Wf aminoglycosides, atracurium, gallamine, pancuronium, tubocurarine, vecuronium EMS Check for absent patellar reflexes this may indicate tox may cause hypokalemia (flattened T waves) and hypocalcemia OD May cause hypotension, resp arrest, T PR, QRS, and QT interval, AV block, and cardiac arrest calcium salts can be given to reverse resp depression... 

WARNING Systemic absorption of oral route may cause neuro/oto/nephrotox may result resp paralysis possible w/ any route of administration Uses Hepatic coma, bowel prq) Action Aminoglycoside, poorly absorbed PO -1- GI bacterial flora Dose Adults. 3-12 g/24- h PO in 3-4 doses Peds. 50-1 (X) mg/kg/24 h PO in 3-4 doses Caution [C, /-] Renal failure, neuromuscular disorders, hearing impair Contra Intestinal obst Disp Tabs, PO soln SE Hearing loss w/ long-term use rash, NA EMS Use neuromuscular blockers w/ caution, reduced dose may be necessary t bleeding risk w/ concurrent anticoagulant use OD May cause neuromuscular block and kidney failure calcium salts can be used to revise neuromuscular block... 

Renal failure will result in a diminished elimination of drugs that are primarily secreted, such as penicillins and aminoglycosides, and therefore in a longer half-life of the drug (45). Likewise, liver disease may result in a capacity-limited biotransformation, and consequently in a slower elimination of the drug. Bacterial pneumonia in calves may also result in increased serum oxytetracycline concentrations, a condition that can cause prolonged elimination (46). 

In studies of the etiology of acute renal failure, medication-induced renal injury is reported as a major cause. In an analysis of over 2000 hospitalized patients, almost 100 experienced renal insufficiency and seven episodes were attributed solely to aminoglycoside therapy [11]. A high percentage of neonatal patients are treated with aminoglycosides and in the involvement of drugs in neonatal acute renal failure has increased up to 8-fold in the last 10 years [12]. 

NAG, along with other urinary enzymes, has been used to evaluate drug induced tubular damage as in the case of acetaminophen [113], 5-aminosalicyate/ sulfasalazine in patients being treated for inflammatory bowel disease [114], and the relative nephrotoxicity of differing aminoglycoside dose schedules in neonates [115]. Assess of the urinary excretion of NAG have also been reported in hypertensive patients [116] and in patients with chronic renal failure due to various causes [117]. However, to date, it is considered to be an ancillary but non-definitive marker of renal disease. 

A study assessing the risk factors for nephrotoxicity with aminoglycosides (tobramycin and gentamicin) enrolled 1489 patients, 157 of whom developed clinical nephrotoxicity. Of these patients 118 had no immediately identifiable cause (sueh as acute renal failure) and further evaluation of other risk factors found that the concurrent use of amphotericin B significantly increased the risk of nephrotoxicity. ... 

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