Focused Assessment in Acute Kidney Injury
| Element | Comment |
|---|---|
| Has there been anuria, oliguria or polyuria? | Anuria is seen in severe hypotension or complete urinary tract obstruction. It is more rarely due to bilateral renal artery occlusion (e.g. with aortic dissection), renal cortical necrosis or necrotizing glomerular disease. Assume that anuria is due to bilateral urinary obstruction until proven otherwise. |
| Has the blood pressure been normal, high or low and, if low, for how long? | Hypertension and AKI: accelerated-phase hypertension, aortic dissection, pre-eclampsia, scleroderma renal crisis. |
| Is hypovolaemia likely? | Has there been haemorrhage, vomiting, diarrhoea, recent surgery or the use of diuretics? Are there signs of fluid depletion (tachycardia, low JVP with flat neck veins, hypotension or postural hypotension)? |
| Are there signs of fluid overload? | Signs include high JVP, triple cardiac rhythm, hypertension, lung crackles, pleural effusions, ascites and peripheral oedema. |
| Is systemic sepsis or urosepsis possible? | Are there predisposing factors? What are the results of recent blood, urine and other cultures? |
| Is there a past history of renal or urinary tract disease? | Are there previous biochemistry results to establish when renal function was last normal? Over how long has renal function been deteriorating? Patients with a renal transplant or pre-existing chronic kidney disease stage 4 or 5 should be discussed urgently with your renal unit. |
| Is there heart disease? | Acute heart failure (including decompensated chronic heart failure, Chapter 48) results in renal hypoperfusion or renal congestion, both of which may cause acute kidney injury. Patients with heart disease who have radiological procedures with administration of contrast are at risk of contrast nephropathy. Commonly used medications for heart disease (e.g. diuretics, ACE-inhibitors), may impair renal function, particularly in combination with other factors (e.g. concomitant administration of NSAIDs, sepsis). AKI may worsen heart function by mechanisms including hypertension, electrolyte derangements, acidosis, sodium and water retention, and the generation of cytokines. |
| Is there known arterial disease? | Peripheral arterial disease (commonly associated with atherosclerotic renal artery stenosis). Cardiac catheterization via femoral artery, with resulting cholesterolembolization. |
| Is there liver disease? | Hepatorenal syndrome, AKI from sepsis, paracentesis-induced hypovolaemia, diuretic-induced hypovolaemia, lactulose-induced hypovolaemia, cardiomyopathy, or any combination of these factors. Treatment of the trigger of deterioration and avoidance of hypovolaemia (preferably by albumin administration) can help to decrease the incidence of acute kidney injury. Terlipressin can improve glomerular filtration rate. |
| Is there diabetes or other multisystem disorder which can involve the kidneys? | Don't forget infective endocarditis and myeloma as causes of renal failure. |
| Has the patient been exposed to any nephrotoxic drugs or toxins? | Nephrotoxic drugs and toxins are summarized in Table 25.2. Consider occupational exposure to toxins. |
| Is there purpura? | AKI with purpura may be due to sepsis complicated by disseminated intravascular coagulation; meningococcal sepsis; thrombotic thrombocytopenic purpura; haemolytic-uraemic syndrome; Henoch-Schoenlein purpura and other vasculitides. |
| Is there jaundice? | AKI with jaundice may be due to hepatorenal syndrome; paracetamol poisoning; severe heart failure; severe sepsis; leptospirosis; incompatible blood transfusion; haemolytic–uraemic syndrome. |
ACE-inhibitor, angiotensin-converting-enzyme inhibitor; AKI, acute kidney injury; NSAIDs, non-steroidal anti-inflammatory drugs.