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Case history

image A 57-year-old man presented with metastatic transitional cell cancer of the upper urinary tract, causing solitary hydronephrosis and flank pain. He had a history of severe anxiety and was taking 50 mg amitriptyline once daily and 400 mg ibuprofen three times daily.

The following details were noted: weight 62 kg; Na+ 138 mmol/l; K+ 5.3 mmol/l; urea 4.0 mmol/l; creatinine 108 μmol/l; estimated glomerular filtration rate (eGFR) 61 ml/min per 1.73 m2. His Eastern Cooperative Oncology Group performance status was 1 and he was keen to proceed with palliative chemotherapy.

What are the risk factors for developing kidney toxicity during anticancer treatment?

Can kidney function be accurately estimated?

Which anticancer treatments are commonly associated with kidney toxicity?

What steps may be taken to reduce the risk of anticancer drug-related kidney toxicity?

What could be done to reduce this man’s risk of kidney toxicity?

What are the long-term consequences?

What are the risk factors for developing kidney toxicity during anticancer treatment?

Nephrotoxicity is often a dose-limiting adverse effect of many anticancer therapies. Toxicity may be a result of damage to the microvasculature, the glomerulus or the tubules. The clinical manifestation may vary depending on the mechanism of kidney injury: from the presence of electrolyte abnormalities, to asymptomatic reduction in glomerular filtration rate (GFR), to overt renal failure requiring dialysis.1 Here, we focus on recognition of the at-risk patient and discuss how thorough assessment and clinical decision making may help to reduce the risk of nephrotoxicity related to oncological management.

When considering starting chemotherapy, it is important to consider the potential renal implications of the treatment. It is important to assess the patient for factors that may increase the risk of nephrotoxicity and address those that are modifiable. The key risk factors for chemotherapy-related kidney toxicity are:

  • Age >75 years.

  • Pre-existing chronic kidney disease (CKD; eGFR <60 ml/min per 1.73 m2).

  • Hypoalbuminaemia (alters drug handling).

  • Choice of chemotherapy.

  • Hypovolaemia, e.g. vomiting, diuretics.

  • Concomitant use of other nephrotoxins, e.g. NSAIDs, aminoglycosides, iodinated contrast.

  • Involvement of the urogenital tract and potential for obstruction.2

Can kidney function be accurately estimated?

Many chemotherapy drugs are excreted by the kidneys via glomerular filtration or tubular secretion. Where the drug and/or its active metabolites are excreted by the kidneys, an estimation of kidney function is essential to ensure safe dosing of treatment. Unfortunately, serum creatinine (dependent upon muscle mass) is a poor biomarker of kidney function in patients with cancer, owing to reduced muscle mass (sarcopenia). Equations such as Cockcroft–Gault, Wright’s or that of the Modification of Diet in Renal Disease (MDRD) study use serum creatinine to calculate kidney function and will therefore potentially overestimate GFR in patients with cancer. The gold standard investigation of renal function remains isotopic GFR measurement, which should be used to ensure safe treatment of patients whose estimated GFR is in ...

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