Management of AKI
Early recognition of the at risk patient, which inherently includes assessment of comorbities, underpins best care of AKI. There are then four pillars to management:
- Exclude intrinsic renal disease and obstruction
- Identify and treat precipitating disease (most often sepsis)
- Assess and correct volume status
- Stop medications that may either exacerbate AKI (most often ACEI/ARB, NSAID/COX-2 inhibitor or loop diuretic) or accumulate to toxic levels in AKI (most importantly metformin). Potassium sparing diuretics should be stopped also, given the risk of hyperkalaemia.
Even ‘mild’ illness in these at risk patients should be taken seriously. If recognised early management may consist simply of treating an underlying infection and temporarily stopping medications such as ACEI/ARB. In this way much significant AKI could be prevented.
The 2009 NCEPOD study into AKI (3) highlighted deficiencies in assessment of comorbidity, assessment of fluid status and assessment of medications as the main contributors to poor care.
Assessment of co-morbidity
Co-morbidity will be assessed as part of the identification of the at risk patient. Specifically with respect to AKI, any condition that reduces glomerular perfusion, either due to reduced cardiac output, hypovolaemia or vascular disease, will confer increased risk of AKI. Type 2 diabetes and left ventricular failure are the commonest conditions to be encountered in primary care.
Treatment of sepsis in patients at risk of AKI
Information on treatment of underlying conditions is not the focus of this document, but it is important to highlight sepsis as a frequent trigger for AKI. Infection need not affect the urinary tract, with for example ‘non-severe’ pneumonia being clearly documented as a trigger (34). It is important to reiterate that acute illness that might be considered minor in the patient not at risk of AKI, can still be sufficient to prompt an acute deterioration in kidney function in the at risk patient.
Detailed information on antibiotic prescribing in renal failure is available in the BNF (55). Local guidelines will also influence prescribing, but some general principles of relevance to patients with AKI should be considered. Parenteral antibiotics used primarily in secondary care (e.g. aminoglycosides) will not be considered here. Of the large number of antibiotics available for use in primary care, only trimethoprim, tetracyclines and nitrofurantoin have effects of particular concern in AKI.
The BNF recommends that nitrofurantoin should be avoided if eGFR is <60ml/min/1.73m2 and that tetracyclines (except doxycycline and minocycline) should be avoided in renal impairment. Trimethoprim is a useful antibiotic, in particular because of the low incidence of C. difficile diarrhoea. Although safe in most patients at full dose down to an eGFR of 30ml/min/1.73m2, the inevitable elevation in serum creatinine following it’s prescription may cause diagnostic confusion (48) and significant hyperkalaemia may be seen in up to 6% of patients. Still, it can be used safely in many patients with mildly impaired kidney function or who are at risk of AKI. However, in patients with established AKI it should be avoided. Trimethoprim is also, rarely, associated with interstitial nephritis. Similar considerations apply to co-trimoxazole.
Penicillins and cephalosporins in general are safe in AKI. Although cleared by the kidneys, the therapeutic window is large and therefore the higher serum concentrations achieved in patients with renal impairment are rarely of clinical significance. Dose reduction may be necessary as advised on an individual drug basis. Penicillins are also rarely associated with interstitial nephritis.
Quinolones in general are safe but dose reduction may be needed if GFR <60ml/min/1.73m2.
Macrolides are in general safe although erythromycin has been associated with reversible hearing loss in patients with severe renal impairment. Azithromycin can be used at full dose at all levels of kidney function.
Assessment of fluid status
Clinical assessment of fluid status may be difficult. Most important is to recognise when an at risk patient is at risk also of developing hypovolaemia. Given the poor sensitivity of clinical assessment for hypovolaemia doctors should have a low threshold for measurement of serum creatinine concentration. Furthermore, if an at risk patient has clinical signs of hypovolaemia it is very likely that they will have developed AKI and serum creatinine concentration must be measured with early review.