Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content ++ Table Graphic Jump Location | Download (.pdf) | Print TABLE A6–1: Drug-Induced Kidney Structural–Functional Alterations Tubular epithelial cell damage Acute tubular necrosis Aminoglycoside antibiotics Radiographic contrast media Cisplatin, carboplatin Amphotericin B Cyclosporine, tacrolimus Adefovir, cidofovir, tenofovir Pentamidine Foscarnet Zoledronate Osmotic nephrosis Mannitol Dextran IV immunoglobulin Hemodynamically mediated kidney injury Angiotensin-converting enzyme inhibitors Angiotensin II receptor blockers Nonsteroidal anti-inflammatory drugs (NSAIDs) Cyclosporine, tacrolimus OKT3 Obstructive nephropathy Crystal nephropathy Acyclovir Sulfonamides Indinavir Foscarnet Methotrexate Nephrolithiasis Sulfonamides Triamterene Indinavir Nephrocalcinosis Oral sodium phosphate solution Glomerular disease Minimal change disease NSAIDs, COX-2 inhibitors Lithium Pamidronate Interferon-α and -β Membranous disease NSAIDs Penicillamine Captopril Focal Segmental Glomerulosclerosis Pamidronate Interferon-α and -β Lithium Sirolimus Anabolic steroids Tubulointerstitial disease Acute allergic interstitial nephritis Penicillins Ciprofloxacin NSAIDs, cyclooxygenase-2 inhibitors Proton pump inhibitors Loop diuretics Chronic interstitial nephritis Cyclosporine Lithium Aristolochic acid Papillary necrosis NSAIDs, combined phenacetin, aspirin, and caffeine analgesics Renal vasculitis, thrombosis, and cholesterol emboli Vasculitis and thrombosis Hydralazine Propylthiouracil Allopurinol Penicillamine Gemcitabine Mitomycin C Methamphetamines Cyclosporine, tacrolimus Adalimumab Bevacizumab Cholesterol emboli Warfarin Thrombolytic agents ++ Table Graphic Jump Location | Download (.pdf) | Print TABLE A6–2: Potential Risk Factors for Aminoglycoside Nephrotoxicity (A) Related to aminoglycoside dosing: Large total cumulative dose Prolonged therapy Trough concentration exceeding 2 mg/La Recent previous aminoglycoside therapy (B) Related to synergistic nephrotoxicity. Aminoglycosides in combination with Cyclosporine Amphotericin B Vancomycin Diuretics Iodinated radiographic contrast agents Cisplatin NSAIDs (C) Related to predisposing conditions in the patient Preexisting kidney disease Diabetes Increased age Poor nutrition Shock Gram-negative bacteremia Liver disease Hypoalbuminemia Obstructive jaundice Dehydration Hypotension Potassium or magnesium deficiencies aThe equivalent concentration in SI molar units are 4.3 μmol/L for tobramycin and 4.2 μmol/L for gentamicin. ++ Table Graphic Jump Location | Download (.pdf) | Print TABLE A6–3: Recommended Interventions for Prevention of Contrast Nephrotoxicity Intervention Recommendation Recommendation Gradea Contrast Minimize contrast volume/dose Use noniodinated contrast studies Use low- or iso-osmolar contrast agents A-1 A-2 A-2 Medications Avoid concurrent use of potentially nephrotoxic drugs, eg, NSAIDs, aminoglycosides A-2 Isotonic sodium chloride (0.9%) Initiate infusion 3–12 hours prior to contrast exposure and continue 6–24 hours postexposure Infuse at 1–1.5 mL/kg/h adjusting postexposure as needed to maintain a urine flow rate of 150 mL/h Alternatively, in urgent cases, initiate infusion at 3 mL/kg/h, beginning 1 hour prior to contrast exposure, then continue at 1 mL/kg/h for 6 hours postexposure A-1 N-acetylcysteine Administer 600–1200 mg by mouth (PO) every 12 hours, 4 doses beginning prior to contrast exposure (ie, 1 dose prior to exposure and 3 doses postexposure) B-1 aStrength of recommendations: A, B, and C are good, moderate, and poor evidence to support recommendation, respectively. Quality of evidence: 1, evidence from more than 1 properly randomized, controlled trial; 2, evidence from more than 1 well-designed clinical trial with randomization, from cohort or case-controlled analytic studies or multiple time series, or dramatic results from uncontrolled experiments; 3, evidence from opinions of respected authorities, based on clinical experience, descriptive studies, or reports of ... Your MyAccess profile is currently affiliated with '[InstitutionA]' and is in the process of switching affiliations to '[InstitutionB]'. Please click ‘Continue’ to continue the affiliation switch, otherwise click ‘Cancel’ to cancel signing in. Get Free Access Through Your Institution Learn how to see if your library subscribes to McGraw Hill Medical products. Subscribe: Institutional or Individual Sign In Username Error: Please enter User Name Password Error: Please enter Password Forgot Username? Forgot Password? Sign in via OpenAthens Sign in via Shibboleth