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Appendix 6: Drug-Induced Kidney Disease

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    AMA Citation
    Drug-Induced Kidney Disease. In: Wells BG, DiPiro JT, Schwinghammer TL, DiPiro CV. Wells B.G., DiPiro J.T., Schwinghammer T.L., DiPiro C.V. Eds. Barbara G. Wells, et al.eds. Pharmacotherapy Quick Guide New York, NY: McGraw-Hill; . http://accesspharmacy.mhmedical.com/content.aspx?bookid=2177&sectionid=165471272. Accessed April 18, 2019.
    MLA Citation
    . "Drug-Induced Kidney Disease." Pharmacotherapy Quick Guide Wells BG, DiPiro JT, Schwinghammer TL, DiPiro CV. Wells B.G., DiPiro J.T., Schwinghammer T.L., DiPiro C.V. Eds. Barbara G. Wells, et al. New York, NY: McGraw-Hill, , http://accesspharmacy.mhmedical.com/content.aspx?bookid=2177&sectionid=165471272.

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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

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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
a

The equivalent concentration in SI molar units are 4.3 μmol/L for tobramycin and 4.2 μmol/L for gentamicin.

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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
a

Strength 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 ...

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