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Case History

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Image not available. A 76-year-old man with castrate refractory metastatic prostate cancer receiving palliative chemotherapy with docetaxel (75 mg/m2 day 1, three-weekly) is admitted unwell with a two-day history of vomiting and diarrhoea following his second cycle of chemotherapy. He has a history of hypertension and hypercholesterolaemia and is taking ramipril 2.5 mg once-daily and simvastatin 20 mg at night. He weighed 68kg and his vital signs are: temperature 37.2°C, pulse 105 bpm; blood pressure 92/60 mmHg. Urea and electrolytes: Na+ 136 mmol/l; K+ 6.5 mmol/l; urea 22 mmol/l; creatinine 245 µmol/l. Serum creatinine was 89 µmol/l two weeks previously.

What is the definition of acute kidney injury (AKI)?

What are the causes of AKI?

What are the risk factors for AKI and how can it be prevented?

What investigations should be performed in AKI?

What is the management of AKI?

What is the prognosis for AKI?

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Background

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What is the definition of acute kidney injury?

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Image not available. Acute kidney injury (AKI) can be considered a spectrum of injury, with even relatively minor rises in serum creatinine being associated with an increased morbidity and mortality. Recent definitions have been based upon rises in serum creatinine or falls in urine output and have been harmonized by the international guideline organization, Kidney Diseases: Improving Global Outcomes (KDIGO).

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Acute kidney injury is defined when one of the following criteria is met:

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  • Serum creatinine rises by 26 µmol/l within 48 hours;

  • Serum creatinine rises 1.5-fold from the reference value,* which is known or presumed to have occurred within 1 week;

  • Urine output is <0.5 ml/kg for more than six consecutive hours.

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*The reference serum creatinine should be the lowest creatinine value recorded within 3 months of the event.

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Patients with cancer may have a reduced muscle mass (sarcopenia) which can be a consequence of both cancer cachexia and treatment (e.g. with tyrosine kinase inhibitors). The result is a low baseline level of serum creatinine and the potential to overestimate the patient's kidney function, which may then lead to incorrect drug dosing. Such patients will have a reduced functional kidney reserve and be at risk of AKI.

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The recognition of AKI may be hampered because the reduced muscle mass and creatinine production will limit the rise in serum creatinine and mask the severity of the underlying injury.

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What are the causes of AKI?

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When a diagnosis of AKI is made it is essential to ascertain the cause as that will allow appropriate, prompt treatment (Table 17.1). The most common causes include sepsis, hypovolaemia and nephrotoxins, but AKI may also develop secondary to complications from oncological treatments or the disease process itself.

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Table Graphic Jump Location
Table 17.1Causes of acute kidney injury (AKI)

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