Acute Kidney Injury (AKI) – Lecture Notes
Alright students, today we’ll break down Acute Kidney Injury (AKI) – what it is, why it happens, how to spot it, and what to do about it. I’ll keep it simple and clear, just like a class discussion. Feel free to take notes or ask questions after!
1. What is AKI?
Think of AKI as a sudden “kidney trouble.” The kidneys stop working properly over hours or days. They can’t clear toxins like urea and creatinine well. Also, they lose control of fluid and electrolytes – that's why patients get swollen or have dangerous potassium levels.
Important: AKI is often reversible if caught and treated early, so don’t delay!
2. How do we know if someone has AKI? (Diagnostic criteria)
The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines say AKI happens if any of these are true:
- Serum creatinine rises by 0.3 mg/dL or more within 48 hours
- Or serum creatinine becomes 1.5 times higher than baseline within the last 7 days
- Or urine output is less than 0.5 mL/kg/hour for 6 hours (this is oliguria)
Tip: Always ask for previous kidney test results, if available, to compare creatinine!
3. What causes AKI? The big 3 categories
AKI can be divided into three main types based on what’s causing the trouble:
- Prerenal: Something happens before the kidneys — like not enough blood flow.
- Intrinsic (or renal): The kidney itself is damaged.
- Postrenal: Something after the kidneys blocks urine from leaving.
Let’s dive deeper into each.
3.1. Prerenal AKI (Hypoperfusion)
Imagine the kidneys as a waterfall powered by flowing water (blood). If water flow reduces, the waterfall slows down. Prerenal AKI happens because the kidneys aren’t getting enough blood to filter.
Common causes:
- Low blood volume from bleeding, vomiting, diarrhea, or dehydration
- Heart failure – heart can’t pump enough blood
- Liver cirrhosis – altered blood flow in body
- Drugs like NSAIDs, ACE inhibitors, and ARBs that affect kidney blood vessels
Remember: If you fix the blood flow early, the kidneys usually recover fully!
3.2. Intrinsic (Renal) AKI
Here, the problem is *inside* the kidneys. The filtering units or tubules get damaged.
Main causes:
- Acute Tubular Necrosis (ATN): The kidney tubules are injured, often because of prolonged low blood flow (ischemia) or poisons like some antibiotics, radiocontrast dye, or muscle breakdown products (rhabdomyolysis).
- Acute Interstitial Nephritis (AIN): Usually allergic reaction to drugs (penicillins, NSAIDs), leads to inflammation in kidney tissue.
- Glomerulonephritis (GN): Immune system attacks the kidney’s filters.
Tip: Intrinsic causes usually take longer to recover and need more intensive treatment.
3.3. Postrenal AKI (Obstruction)
Think of urine like water flowing through a pipe. Postrenal AKI occurs when there’s a blockage after the kidneys making urine flow back up and causing kidney damage.
Common causes:
- Prostate enlargement (benign prostatic hyperplasia)
- Urinary stones blocking ureters
- Tumors pressing on urinary tract
- Neurogenic bladder causing emptying problems
4. How does someone with AKI present?
The symptoms can range from subtle to severe. Here’s what to watch for:
- Oliguria or anuria: Reduced or no urine output
- Swelling/edema: Because kidneys can’t get rid of excess fluid
- Shortness of breath due to fluid in lungs
- Confusion, fatigue, nausea, vomiting from toxin build-up (uremia)
- Abnormal heart rhythms – watch out for hyperkalemia!
5. What tests should we order?
Here are the key investigations to understand AKI:
- Serum creatinine and urea (BUN): to check kidney function
- Electrolytes: Important to spot dangerous potassium or acid-base imbalances
- Urinalysis: to look for blood, protein, and casts (specific findings help tell cause)
- Fractional excretion of sodium (FeNa): <1% suggests prerenal; >2% suggests tubular injury
- Renal ultrasound: to exclude obstruction
- Autoimmune tests: ANA, ANCA if glomerulonephritis suspected
6. How do we treat AKI?
Treatment depends on the cause, but here are your general steps:
6.1 Fix the cause:
- Replenish fluids carefully – don’t overload! Usually isotonic saline
- Stop bad actors – nephrotoxic drugs, infections, obstruction
- Relieve urinary obstruction urgently with catheters or surgery
6.2 Supportive care:
- Manage electrolytes carefully (especially potassium!)
- Prevent fluid overload – monitor weight, input/output
- Provide nutrition, avoid excess proteins to reduce kidney burden
- Treat acid-base disturbances if severe
6.3 Dialysis – when and why?
If complications are serious, dialysis helps clear toxins and fluid until kidneys recover.
Use AEIOU to remember:
- Acidosis (severe metabolic)
- Electrolytes (dangerous hyperkalemia)
- Intoxications (poison removal)
- Overload (refractory fluid)
- Uremia (encephalopathy, pericarditis)
7. How do patients usually do?
Most recover well if treated early. But prognosis depends on:
- How bad the kidney injury is
- Underlying cause and other health problems
- How fast treatment starts
Severe AKI in critically ill patients carries high risk of death. Also, some patients progress to chronic kidney disease (CKD).
8. Summary & Tips for Exams
- Know the 3 main types: Prerenal (hypoperfusion), Intrinsic (renal parenchymal damage), Postrenal (obstruction)
- KDIGO criteria: Creatinine rise and urine output
- FeNa helps differentiate prerenal vs intrinsic causes
- AEIOU for dialysis indications
- Early recognition and fluid management save lives
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