Acute Kidney Injury


Acute Kidney Injury (AKI) is the name used for a situation in which there is an acute decline in kidney function. This decline is often temporary and reversible if treated, but may become permanent if the underlying cause is not managed properly. AKI manifests as an increase in serum creatinine, retention of azotes (mostly urea) and decrease in urinary output. Electrolyte abnormalities and metabolic acidosis may also be present.

The incidence of AKI is around 2-3.000 per million per year, and around 2/3 of the ICU patients may develop AKI.

CAUSES:

Traditionally the causes of AKI can be divided in Prerenal, Renal (or Intrinsic) or Post-renal. In clinical practice, however, often patients have multiple mechanisms contributing to the AKI at the same time.

Prerenal

Hypovolemia (Bleeding, Diarrhea, Vomiting)
Heart Failure
Hepatorenal syndrome
Renal artery occlusion
Large or medium-vessel vasculitis

Intrinsic Renal

Acute Tubular Necrosis (ischemia, nephrotoxins, rhabdomyolysis, radiocontrast agents)
Glomerular disease (Lupus, Anti-GBM disease, postinfectious glomerulonephritis, infective endocarditis, cryoglobulinemia, IgA nephropathy)
Small Vessel Disease (small vessel vasculitis, renal atheroembolism, thrombotic microangiopathy)
Acute Interstitial Nephritis (drugs, infection, systemic diseases)

Postrenal

Intratubular obstruction (cast nephropathy, drugs, crystalluria)
Postrenal obstruction (tumors, renal calculi, bladder outlet obstruction, retroperitoneal fibrosis)

SIGNS & SYMPTOMS:

The patient may present with hypertension, oliguria, hematuria, edema or even completely asymptomatic.

In more severe cases, cardiovascular symptoms due to arrhythmias secondary to electrolyte disorders may occur, as well as chest pain or confusion secondary to uremia.

DIAGNOSIS:

The KDIGO criteria for AKI is any of the following:

  • Increase in serum creatinine by =0.3 mg/dL (27 micromol/L) relative to a known baseline value within 48 hours

OR

  • Increase in serum creatinine to =1.5 times the baseline value within seven days

OR

  • Decrease in urine volume to <3 mL/kg over 6 hours

History and physical examination are very important and may give clues about when and why the kidney function of the patient started to deteriorate.

CBC and CMP should be obtained. Urinalysis is also vital (may show muddy brown granular and epithelial casts on intrinsic AKI. RCB casts may indicate glomerulonephritis). Urinary sodium and creatinine may also be helpful.

Further diagnostic methods should be used to try to identify the cause when it is not obvious. Some patients may benefit from serological studies (ANA, hep. B).

If obstruction is suspected, imaging may be obtained (ultrasound, CT scan).

If an underlying disease is suspected (such as multiple myeloma) proper testing should be done.

In an oliguric patient the fractional excretion of sodium (FENa) may be useful to distinguish between pre-renal AKI and ATN.

FENa = ( [UNa x SCr]/[SNa x UCr] ) x 100

FENa lower than 1% may indicate prerenal disease, whereas FENa >2% usually indicates ATN. FENa has limited use in patients with CKD, using diuretics or with AKI due to contrast or pigments.

STAGING:

AKI can be staged as follows:

TREATMENT:

Determining the cause and the volume status is important when managing a patient with AKI. The volume status should be assessed in all patients with AKI.

Patients with hypovolemia may receive fluids (crystalloids are preferred). If there is no necessity of aggressive fluid resuscitation (e.g. shock) fluid can be administered at 75-100mL/h.

Drugs that are known to affect kidney function such as ACE inhibitors/ARBs should be put on hold.

Patients with volume overload may benefit from diuretics for symptomatic relief.

Hyperkalemia should be managed immediately. The treatment of hyperkalemia is discussed in a different article.

Patients with refractory hypervolemia, hyperkalemia, acidosis (pH <7.1) or uremia will need dialysis. Severe hyperphosphatemia (>12mg/dL) may also need dialysis.

Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057151/figure/F2/

Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057151/figure/F2/

 

SOURCES & FURTHER READING:

  1. Patschan D, Muller GA. Acute kidney injury. J Inj Violence Res. 2015 Jan; 7(1): 19–26.
  2. Hoste EAJ et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Medicine. August 2015, Volume 41, Issue 8, pp 1411–1423.
  3. Thomas ME et al. The definition of acute kidney injury and its use in practice. Kidney International. Volume 87, Issue 1, January 2015, Pages 62-73.
  4. Kellum JA, Lamiere N. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical Care 2013 17:204.