Acute kidney injury

Acute kidney injury (AKI) is a clinical syndrome which is characterised by an acute decrease kidney function (GFR) (over hours or days), as evidenced by elevated creatinine. There may also be accumulation of urinary waste products and oliguria/anuria, but not always. The cause may be prerenal, renal, or postrenal, but the most common causes are prerenal and acute tubular necrosis.

During the evaluation it’s important to determine whether it’s really acute or chronic, and to determine the underlying cause. Management includes treating the cause and correcting severe electrolyte disturbances. In some cases, renal replacement therapy may be required.

The condition is nowadays called acute kidney injury rather than acute renal failure.

Etiology

AKI is classified according to the underlying cause, whether it’s a prerenal cause, a renal cause, or a postrenal cause. However, there are usually multiple factors involved.

• Prerenal AKI
  • Hypovolaemia/hypotension
  • Decreased RBF (heart failure, renal artery stenosis)
  • Abnormal kidney haemodynamics (sepsis, hepatorenal syndrome)
• Renal AKI
  • Tubulointerstitial disorders
    • Acute ischaemic/toxic tubular necrosis
    • Acute tubulointerstitial nephritis
  • Glomerulonephritis
  • Thrombotic microangiopathies (TTP/HUS)
  • Obstruction of tubules
    • Myeloma proteins
    • Crystals
• Postrenal AKI
  • Benign prostate hyperplasia
  • Stone
  • Prostate cancer
  • Gynaecological cancer

Of these, the prerenal causes are the most common, followed by acute tubular necrosis.

Drugs which can cause AKI (by various mechanisms) are most commonly NSAIDs and RAAS inhibitors.

Chronic kidney disease is the strongest risk factor for AKI. If a person with CKD develops AKI, the condition is called acute-on-chronic AKI.

Clinical features

Oliguria is the most common symptom, but in many cases it’s asymptomatic. There may be symptoms of the underlying cause, or symptoms of uraemia.

Diagnosis and evaluation

In the evaluation of AKI, we use serum creatinine as a marker of kidney function (normal range 60 – 100 µmol/L); the estimated GFR (eGFR) can not be used, as it's estimated according to formulas which are made for chronic kidney disease. The definition of AKI requires either (1) an increase in serum creatinine by 27 µmol/L, or (2) an increase to more than 150% of baseline serum creatinine over 48 hours, or (3) a decrease in urine volume to < 3 mL/kg over 6 hours.

During the evaluation of a person with acute kidney injury, it’s important to answer these 5 questions:

• Is it really AKI, or is it CKD, or acute-on-chronic?
  • Is this really an acute loss of kidney function or is this a newly discovered CKD?
  • Did the patient already have decreased GFR and this is just a worsening?
• Is there a prerenal cause?
• Is there a postrenal cause?
• Is there a renal artery occlusion?
• Is there a renoparenchymal disease?

Patient history, physical examination, previous kidney function tests, and ultrasound can help answer these questions. An AKI kidney has normal macroscopic morphology (as seen with radiologic imaging), as opposed to a CKD kidney, which is usually shorter than normal and has a thinner cortex. A renal cause usually has abnormal urine analysis, with proteinuria, increased urinary sodium, or decreased urinary osmolality, as well as the presence of epithelial casts or brown granular casts in the urine. A postrenal cause can have a palpable bladder, or obstruction or hydronephrosis can be visible on ultrasonography. Allergic symptoms can suggest nephritis. Low BP can suggest hypovolaemia.

In case of AKI, the kidney is usually enlarged, which can be visualised on ultrasonography. Ultrasound may also reveal an underlying cause and is therefore usually the first choice imaging modality for AKI.

Previously it was suggested that the urea:creatinine ratio was useful in distinguishing between prerenal and intrinsic AKI, but a study designed to investigate this found that the ratio can not distinguish them.

If the cause remains unclear despite these investigations, a renal biopsy may be required.

Treatment

Treating the underlying cause is essential, as well as correcting any severe electrolyte disorders.

If there is hypervolaemia, a loop diuretic may be used.

If there are indications for it, renal replacement therapy may be used.

Prognosis

In many cases patients make a full recovery, but AKI can progress to chronic kidney disease as well. It might take months for kidney functions to recover completely, during which the patient may experience polyuria because the tubules need a long time to recover.