Drugs that can be continued safely in AKI
A number of medications are frequently prescribed to patients at risk of AKI and are worthy of comment.
In an ICU setting, high dose aspirin (1g iv) reversibly reduces GFR and reduces urinary PGE2 secretion (73) as would be expected. However, it has been suggested that oral aspirin spares the kidney (74) and the first UK Heart and Renal Protection study (75) recorded no cases of AKI in 120 pre-dialysis patients and 67 renal transplant recipients given aspirin 100mg daily. Furthermore, a recent retrospective cohort analysis has demonstrated a decreased risk of AKI for patients with CKD who were taking aspirin prior to cardiac surgery (76). Furthermore, aspirin may protect against endotoxin-induced AKI (77) and has been suggested to improve kidney transplant survival (78).
Although paracetamol inhibits cyclo-oxygenase, this is not its major mechanism of action and its effects are significantly different to those of NSAIDs (79). Accordingly, it does not affect glomerular autoregulation and can be used safely in CKD and AKI.
Statins do not accumulate in renal impairment, are not associated with acute kidney injury following cardiac surgery (80, 81) and may reduce the risk of contrast induced AKI (82, 83). Although none of these directly address the safety in AKI, they suggest strongly that statins do not need to be stopped if patients develop AKI. Furthermore, as for aspirin, no cases of AKI were noted following administration of simvastatin 20mg daily in the first UK Heart and Renal Protection study (75).
Interstitial nephritis is a cause of intrinsic kidney disease, present in 2-3% of biopsies performed (84), that may present as AKI. It is typically associated with proteinuria (often heavy) with or without haematuria (<50% of cases) (84). Drugs cause 60-70% of cases (85) with penicillins, ciprofloxacin, NSAIDs, COX-2 inhibitors, proton pump inhibitors and H2 antagonists being among the commonest causative agents (84, 86). If suspected, urgent referral to nephrology is appropriate. Importantly, if AKI is seen in the context of NSAID administration haemodynamic effects of the NSAID and acute interstitial nephritis (AIN) are both possible causes. In the former risk factors for AKI such as CKD, left ventricular failure, diabetes or hypovolaemia would be present and dipstick urinalysis will typically not reveal proteinuria and haematuria. In AIN, although any patient may be affected, the patient need not have any comorbid pathologies and urinalysis will be abnormal.