Acute Kidney Injury (AKI)

Definition

Acute Kidney Injury (AKI) is a sudden decline in kidney function over hours to days, leading to an accumulation of waste products, electrolyte disturbances, and fluid imbalance.

It is defined by any of the following:

Increase in serum creatinine by ≥26.5 μmol/L within 48 hours.
Increase in serum creatinine to ≥1.5 times baseline within 7 days.
Urine output <0.5 mL/kg/hour for >6 hours.

Aetiology

1. Pre-Renal AKI (Hypoperfusion, Most Common Cause):

Hypovolaemia (e.g., dehydration, haemorrhage).
Cardiac failure (e.g., heart failure, cardiogenic shock).
Sepsis (systemic vasodilation reduces renal perfusion).
Renal artery stenosis.

2. Intrinsic (Renal) AKI:

Acute tubular necrosis (ATN) – ischemia or nephrotoxins (e.g., NSAIDs, aminoglycosides).
Glomerulonephritis (autoimmune or infectious).
Acute interstitial nephritis (e.g., due to drugs, infections).
Rhabdomyolysis (muscle breakdown releasing nephrotoxic myoglobin).

3. Post-Renal AKI (Obstructive):

Kidney stones.
Benign prostatic hyperplasia (BPH).
Bladder outlet obstruction.
Tumours (e.g., prostate, bladder).

Pathophysiology

Pre-renal AKI leads to reduced glomerular filtration rate (GFR) due to hypoperfusion.
Intrinsic AKI results from direct nephron injury (e.g., ischemia, toxins).
Post-renal AKI involves obstruction, leading to back pressure and tubular dysfunction.
If untreated, AKI can progress to chronic kidney disease (CKD) or end-stage renal failure.

Risk Factors

Age >65 years.
Chronic kidney disease (pre-existing kidney disease increases risk).
Diabetes mellitus.
Heart failure or liver disease.
Sepsis.
Use of nephrotoxic medications (e.g., NSAIDs, ACE inhibitors, diuretics, contrast agents).
Major surgery (post-operative AKI risk).
Hypovolaemia or dehydration.

Signs and Symptoms

Early Symptoms:

Reduced urine output (oliguria <400 mL/day or anuria <100 mL/day).
Fatigue, nausea, and confusion.
Signs of fluid overload (oedema, pulmonary congestion).

Severe AKI Symptoms:

Hyperkalaemia (can cause cardiac arrhythmias).
Metabolic acidosis (Kussmaul breathing).
Uraemia (causing confusion, pruritus, and asterixis).

Investigations

Serum creatinine: defines AKI based on rise from baseline.
U&Es (Urea and Electrolytes): assess sodium, potassium, and creatinine.
Urinalysis: detects blood, protein, or infection.
Urinary sodium and osmolality: differentiates pre-renal from intrinsic AKI.
Renal ultrasound: assesses obstruction (hydronephrosis suggests post-renal AKI).
ECG: check for hyperkalaemia-related arrhythmias (peaked T waves, widened QRS).

Classification

Stage	Serum Creatinine	Urine Output
AKI 1	1.5–1.9 times baseline OR ≥26.5 μmol/L rise	<0.5 mL/kg/hr for 6–12 hours
AKI 2	2.0–2.9 times baseline	<0.5 mL/kg/hr for ≥12 hours
AKI 3	≥3.0 times baseline OR ≥354 μmol/L	<0.3 mL/kg/hr for ≥24 hours OR anuria for ≥12 hours

Management

1. General Measures:

Identify and treat the underlying cause.
Monitor fluid balance: avoid overhydration in oliguric AKI.
Stop nephrotoxic drugs: NSAIDs, ACE inhibitors, aminoglycosides.
Optimise blood pressure: maintain adequate perfusion.

2. Fluid Management:

Pre renal AKI: IV fluids (e.g., 0.9% saline) if hypovolaemic.
Fluid overload: consider furosemide (loop diuretics).

3. Electrolyte Management:

Hyperkalaemia (K+ >6.0 mmol/L): treat with calcium gluconate, insulin/dextrose, and consider dialysis if severe.
Metabolic acidosis: sodium bicarbonate if severe.

4. Dialysis Indications ("AEIOU"):

A: Acidosis (pH <7.1).
E: Electrolytes (severe hyperkalaemia >6.5 mmol/L).
I: Intoxications (e.g., lithium, methanol).
O: Overload (refractory pulmonary oedema).
U: Uraemia (symptomatic, e.g., pericarditis, encephalopathy).

Renalmypanotes18 February 2025Acute Kidney Injury (AKI)