From the Guidelines
Medications known to be nephrotoxic include nonsteroidal anti-inflammatory drugs (NSAIDs), certain antibiotics such as aminoglycosides and vancomycin, contrast dyes, ACE inhibitors, ARBs, chemotherapy drugs like cisplatin and methotrexate, calcineurin inhibitors, lithium, and proton pump inhibitors with long-term use. These medications can cause kidney damage through various mechanisms, including direct cellular toxicity, crystal formation in kidney tubules, altered kidney blood flow, and inflammatory responses. The nephrotoxicity risk increases with higher doses, longer duration of treatment, pre-existing kidney disease, older age, and dehydration 1. Patients with risk factors for kidney injury should have their kidney function monitored regularly when taking these medications. Some of the specific nephrotoxic medications and their effects include:
- Aminoglycosides, which can cause nephrotoxicity and ototoxicity 1
- Vancomycin, which can cause nephrotoxicity, especially when used in combination with other nephrotoxic agents 1
- Cisplatin, which can cause acute tubular injury and other kidney lesions 1
- Lithium, which can cause renal tubular dysfunction and nephrotoxicity with prolonged use 1
- Proton pump inhibitors, which can cause nephrotoxicity with long-term use 1. It is essential to weigh the benefits and risks of using these medications and to monitor kidney function regularly in patients with risk factors for kidney injury.
From the FDA Drug Label
Dose-related and cumulative renal insufficiency, including acute renal failure, is the major dose-limiting toxicity of cisplatin Nephrotoxicity Systemic vancomycin exposure may result in acute kidney injury (AKI).
Medications known to be nephrotoxic:
These medications can cause renal insufficiency, acute renal failure, or acute kidney injury.
From the Research
Nephrotoxic Medications
Medications that are known to be nephrotoxic include:
- Antibiotics and antimicrobials, which can cause acute kidney injury (AKI) through mechanisms such as acute interstitial nephritis, acute tubular necrosis, and intratubular crystal deposition 4, 5
- Aminoglycoside antibiotics, such as gentamicin, which can induce tubular necrosis, epithelial oedema of proximal tubules, and cellular desquamation 6, 7
- Other therapeutic classes of drugs, which can cause nephrotoxicity through various pathophysiological mechanisms 8
Mechanisms of Nephrotoxicity
The mechanisms of nephrotoxicity vary depending on the specific medication and can include:
- Glomerular injury
- Tubular injury or dysfunction
- Distal tubular obstruction from casts
- Acute interstitial nephritis (AIN) mediated by a type IV (delayed-type) hypersensitivity response 5
- Intratubular crystal deposition
- Proximal/distal tubulopathy with electrolyte wasting abnormalities 4
Clinical Manifestations
The clinical manifestations of nephrotoxicity can range from mild forms of tubular injury to significant deterioration of kidney function requiring acute renal replacement therapy, and can include:
- Acute tubular necrosis (ATN)
- Acute interstitial nephritis (AIN)
- Fanconi syndrome 5