Acute Kidney Injury Explained : Causes - Stages And Prevention

In this article, we’re discussing acute kidney injury (AKI) — what it is, its causes, and how it's managed.

What is Acute Kidney Injury?

AKI is a sudden, often reversible, decline in the glomerular filtration rate (GFR), leading to elevated levels of blood urea nitrogen (BUN) and creatinine.

According to KDIGO guidelines, AKI is defined by any of the following:

1. An increase in creatinine of ≥26.5 micromoles per liter within 48 hours.
2. An increase in creatinine to ≥1.5 times the baseline within the past 7 days.
3. Reduced urine output: Less than 0.5 milliliters per kilogram per hour for over 6 hours.

In essence, AKI reflects an abrupt, reversible decline in kidney function that leads to increased BUN and creatinine levels.

Stages of AKI

AKI progresses through stages based on the severity of kidney function impairment:

• Stage 1:

  • Creatinine increase to 1.5–1.9 times baseline or ≥26.5 micromoles per liter.
  • Urine output <0.5 mL/kg/hr for 6–12 hours.

• Stage 2:

  • Creatinine increase to 2–2.9 times baseline.
  • Urine output <0.5 mL/kg/hr for >12 hours.

• Stage 3:

• Creatinine increase to ≥3 times baseline or ≥352.6 micromoles per liter.
• Urine output <0.3 mL/kg/hr for >24 hours, or dialysis is required.
• GFR reduction to <35 mL/min/1.73m².

Causes of AKI

AKI can be classified into three main categories based on the origin of the dysfunction:

1. Prerenal Causes

These involve reduced blood flow to the kidneys, often due to:

• Decreased cardiac output (e.g., myocardial infarction, pericardial tamponade).
• Shock (systolic BP <90 or diastolic BP <60 mmHg), caused by dehydration, hemorrhage, or fluid loss.
• Arterial obstruction (e.g., renal artery stenosis).
• Medications:
  • ACE inhibitors/ARBs cause efferent vasodilation.
  • NSAIDs reduce blood flow by pre-glomerular vasoconstriction.

2. Intrarenal Causes

These result from direct kidney damage, categorized by kidney structures:

• Glomerular damage: Glomerulonephritis.
• Tubular injury:
  • Ischemic or nephrotoxic acute tubular necrosis (ATN).
  • Myeloma cast nephropathy.
• Interstitial damage: Often drug-induced or caused by conditions like sarcoidosis.
• Vascular issues: Renal vein thrombosis or thrombotic microangiopathies.

3. Postrenal Causes

These occur due to urine flow obstruction, leading to kidney damage, such as:

• Kidney stones (renal calculi) anywhere along the urinary tract.
• Malignancies causing blockage.
• Benign prostatic hyperplasia (BPH) or urethral strictures, causing urinary retention and hydronephrosis.

Differentiating Prerenal, Intrarenal, and Postrenal AKI

Diagnostic clues can help identify the cause:

• Prerenal AKI:

  • BUN
    ratio >20.
  • Fractional excretion of sodium (FENa) <1%.
  • Urine osmolality >500 mOsm/kg.
  • Bland urine sediment.

• Intrarenal AKI:

  • BUN
    ratio <20.
  • FENa >2%.
  • Urine osmolality <400 mOsm/kg.
  • Granular casts in urine sediment.

• Postrenal AKI:

• Symptoms include inability to urinate or pain (renal colic).
• Imaging (e.g., ultrasound) may show hydronephrosis or dilated ureters.

Prevention and Management of AKI

Key strategies include:

1. Identifying high-risk patients (e.g., those with chronic kidney disease).
2. Avoiding nephrotoxic drugs (e.g., NSAIDs, ACE inhibitors/ARBs).
3. Ensuring adequate hydration in prerenal cases.
4. Monitoring drug levels for nephrotoxic medications (e.g., aminoglycosides, vancomycin).
5. Minimizing the use of IV contrast in at-risk patients or providing proper hydration if contrast is necessary.