Drug-Induced Kidney Injury Common in Cancer Patients
Drug-induced kidney injury (DIKI) refers to structural and functional damage to the kidneys caused directly or indirectly by drugs or their metabolites. It is one of the common causes of hospital-acquired (iatrogenic) acute kidney injury (AKI), and in severe cases can progress to chronic kidney disease (CKD) or even renal failure.
Both the Chinese and Western medicines commonly used by tumor patients can cause kidney damage. Aristolochiaceae plants in Chinese medicine (Xixin, Madouling, Guanmutong, Mufangji, etc.) and some heavy metals (such as Xionghuang, Zhusha, etc.) can cause irreversible chronic renal interstitial inflammation. Aminoglycoside antibiotics (gentamicin), vancomycin, and the chemotherapy drugs cisplatin and methotrexate can cause renal tubular epithelial cell injury and crystal nephropathy. The commonly used non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and diclofenac can cause acute interstitial nephritis and renal papillary necrosis. The immunosuppressants cyclosporine and tacrolimus cause renal vasoconstriction and chronic kidney disease. The diuretic furosemide causes electrolyte disturbances and induces kidney injury. Even the iodinated contrast media used in contrast-enhanced CT can induce contrast-induced nephropathy (acute kidney injury). Many targeted drugs are also nephrotoxic.
These are only some of the common drugs that may cause kidney damage. In fact, if we carefully read the package inserts of the drugs used by cancer patients, we will find that a considerable number of anti-cancer or anti-cancer adjunctive drugs have some nephrotoxicity. But cancer is a life-threatening chronic disease, and patients have no choice but to receive these drug treatments. Therefore, regularly re-examining renal function and closely monitoring the patient's clinical manifestations can better prevent patients from developing serious problems due to drug-induced kidney injury.
When a patient's kidneys suffer acute injury, they may present with oliguria, anuria, and edema, with elevated blood creatinine, uric acid, and urea nitrogen, and proteinuria, hematuria, or cast urine in urinalysis. Patients who take certain anti-cancer drugs long-term leading to renal interstitial fibrosis or chronic pyelonephritis may present with fatigue, anemia, hypertension, and slowly rising blood creatinine. Some patients may develop allergic interstitial nephritis, with fever, rash, limb and joint pain, elevated C-reactive protein, and eosinophilia. Patients with crystal nephropathy may show flank pain and hematuria, with drug crystals visible in the urine.
If the patient's renal function was normal before taking the medicine and the above problems appear after taking it, and examination confirms that renal function has been impaired, the medicine should be stopped immediately, and the prescribing doctor and a nephrology specialist should be consulted for joint assessment, with the doctor giving the corresponding management plan. Even for anti-cancer drugs that must be used, when drug-induced kidney injury occurs, continuing to take them or taking them alone is not recommended. Patients with kidney damage should not continue taking drugs that may worsen the kidney damage, so as to avoid life-threatening danger.
Patients with acute kidney injury should be hospitalized, while patients with chronic kidney injury may, depending on the situation, take medicine at home. The glucocorticoid prednisone has a certain effect on immune interstitial nephritis; N-acetylcysteine (NAC) can reduce the risk of contrast-induced nephropathy; patients with severe acute kidney injury may require dialysis; the patent medicine Yimucao granules and Zhibai Dihuang Wan also have a certain therapeutic effect on kidney damage. But whatever kind of kidney injury, it is a very serious problem requiring medication and treatment under a doctor's guidance; patients should not self-medicate.