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Acute kidney injury 

Acute kidney injury

Chapter:
Acute kidney injury
Author(s):

J Firth

DOI:
10.1093/med/9780199204854.003.2105_update_001

Update:

Enhanced discussion on recognition and management of hypovolaemia; further comment on possible specific treatments for patients with or at risk of AKI (fenoldopam, growth factors, N-acetylcysteine).

Updated on 25 May 2011. The previous version of this content can be found here.
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date: 30 March 2017

Definition—for practical clinical purposes, acute kidney injury is defined as a significant decline in renal excretory function occurring over hours or days. This is usually detected by a rise in the serum concentration of creatinine. Oliguria—defined (arbitrarily) as a urinary volume of less than 400 ml/day—is usually present, but not always. More precise definitions, such as those of the Risk Injury Failure Loss and Endstage kidney disease (RIFLE) classification, or the modification of this definition as proposed by the Acute Kidney Injury Network (AKIN), are required for epidemiological or trial purposes.

Epidemiology—depending on precise definition, transient renal dysfunction complicates about 5% of medical and surgical admissions. Severe acute kidney injury (serum creatinine >500 µmol/litre) affects 200 to 750 per million adult population per year in the United Kingdom.

Clinical approach

Diagnosis—all patients admitted to hospital with acute illness, but particularly older people and those with pre-existing chronic kidney disease, should be considered at risk of developing acute kidney injury. The most common precipitant is volume depletion—early detection of which requires careful monitoring of fluid input and output, lying and standing (or sitting) pulse and blood pressure, and daily weighing. Serum creatinine and electrolytes should be measured on admission in all acutely ill patients, and repeated daily or on alternate days in those who remain so.

Assessment—after treatment of life-threatening complications, the initial assessment of a patient who appears to have acute kidney injury must answer three questions: (1) is the kidney injury really acute?—has serum creatinine been measured previously?; (2) is urinary obstruction a possibility?—renal ultrasonography is required urgently when the diagnosis of acute kidney injury is not clear cut (but remember that 5% of cases of obstruction will have a misleading initial ultrasound report); and (3) is there a renal inflammatory cause?—stick testing of the urine is mandatory in any patient with acute kidney injury, with urinary microscopy for cellular casts if this reveals significant proteinuria or haematuria. Red-ell casts are found in acute glomerulonephritis, renal vasculitis, accelerated-phase hypertension, and (sometimes) in interstitial nephritis—their presence indicates the need for urgent specialist renal referral.

General aspects of management

The immediate management of a patient with renal impairment is directed towards three goals: (1) recognition and treatment of any life-threatening complications of acute kidney injury; (2) prompt diagnosis and treatment of hypovolaemia; and (3) specific treatment of the underlying condition—if this persists untreated then renal function will not improve.

Life-threatening complications—the greatest danger is hyperkalaemia, which can cause cardiac arrest without any preceding symptoms whatsoever. All doctors who work with acutely ill patients should be able to recognize the characteristic ECG appearances, which are a better indicator of cardiac toxicity in the individual patient than the serum potassium level. As serum potassium rises, the following changes occur progressively: (1) ‘tenting’ of the T wave; (2) reduction in size of P waves, increase in the PR interval, widening of the QRS complex; (3) disappearance of the P wave, further widening of the QRS complex; (4) irregular ‘sinusoidal’ ECG; and (5) asystole. Severe hyperkalaemic changes require immediate treatment with intravenous calcium (usually given as calcium gluconate, 10 ml of 10% solution, intravenously over 60 s), after which intravenous insulin/glucose or nebulized salbutamol can be used to reduce the serum potassium for a few hours to allow time for renal excretion (in cases of renal failure that are rapidly treatable, e.g. bladder outflow obstruction) or initiation of renal replacement therapy.

Fluid management—a key part of the immediate assessment and management of any patient who is very ill, which will include many of those with acute kidney injury, is to make a correct assessment of their intravascular volume status and to resuscitate rapidly and effectively, as discussed in Chapter 17.3. Once this has been achieved, in the patient who remains oliguric, fluid intake should be limited to the volume of the previous day’s urine output and gastrointestinal losses, plus 500 ml, but this allocation may need to be substantially increased in the presence of fever or in hot environments, when insensible losses may be much increased. To keep the patient in the optimal state of fluid balance, there is no substitute for careful, twice-daily clinical examination for signs of intravascular volume depletion or excess, supplemented by accurate daily weighing, to gauge the overall net fluid balance, and an intelligent flexible response to the findings.

Renal replacement therapy—mandatory indications for immediate instigation are: (1) refractory hyperkalaemia; (2) intractable fluid overload; (3) metabolic acidosis producing circulatory compromise; and (4) overt uraemia manifesting as encephalopathy, pericarditis, or uraemic bleeding. Modern practice is (whenever possible) to begin renal replacement therapy when the serum creatinine reaches 500 to 700 µmol/litre, unless there is clear evidence that spontaneous recovery is occurring or there are other reasons to maintain a conservative approach.

Renal biopsy—should be considered when: (1) the history, examination, or laboratory tests suggest a systemic disorder that could cause acute kidney injury and could be diagnosed by renal biopsy; (2) the urinary sediment contains red cell casts; (3) the case history is atypical; and (4) renal failure is unusually prolonged (say beyond 6 weeks).

Specific causes of acute kidney injury

There are many possible causes of acute kidney injury, but in any given clinical context few of these are likely to require consideration. By far the most frequent are prerenal failure and acute tubular necrosis, which together account for 80 to 90% of cases of acute kidney injury seen by physicians.

Prerenal failure and acute tubular necrosis—these can best be regarded as a continuum of renal response to ischaemic injury, in much the same way that stable angina, non-ST-elevation myocardial infarction, and ST-elevation myocardial infarction are a continuum of cardiac response to ischaemia. Prerenal failure describes renal dysfunction that is entirely attributable to hypoperfusion, and where restoration of renal perfusion leads to rapid recovery. Acute tubular necrosis describes a clinical entity comprising acute kidney injury with three main characteristics: (1) it is seen in specific clinical contexts, frequently involving circulatory compromise and/or nephrotoxins; (2) urinary abnormalities usually suggest tubular dysfunction; and (3) recovery of renal function is expected within days or weeks, in most cases, if the patient survives the precipitating insult. There is no specific treatment for acute tubular necrosis, and it is a marker of severe illness with mortality around 15% in all cases, and 40 to 60% in series from intensive care units of patients receiving renal replacement therapy in the context of mechanical ventilation for respiratory failure.

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