Acute Kidney Injury Flashcards
Define AKI.
What are the RFs for developing an AKI?
What are the pre-renal causes of AKI?
What are the symptoms of a pre-renal AKI?
What are the intra-renal causes of AKI?
What are the symptoms of an intra-renal AKI?
What are the symptoms of uraemia?
What are the possible causes of a rash in the presence of a decreased urine output?
Describe the pathogenesis of glomerulonephritis including its clinical effects.
What are the two main causes of ATN?
Ischaemia and nephrotoxins.
What are key investigations for ATN?
(urine analysis) + for casts
What would you expect to see on urine analysis in ATN?
A urinalysis of Acute Tubular Necrosis (ATN) typically shows the following key findings:
Microscopic Examination:
Muddy Brown Casts: Granular casts made of degenerated tubular epithelial cells and proteins; a hallmark of ATN.
Epithelial Cell Casts: Shed tubular cells clumped together; also highly suggestive of ATN.
Tubular Epithelial Cells: Free tubular epithelial cells may also be visible in the urine.
Chemical Analysis:
Low Urine Specific Gravity (<1.015): Indicates the kidney’s inability to concentrate urine due to tubular damage.
Low Urine Osmolality (<350 mOsm/kg): Poor tubular reabsorption capacity.
High Urine Sodium (>40 mmol/L): Reflects impaired sodium reabsorption in damaged tubules.
Fractional Excretion of Sodium (FENa >2%):
Helps differentiate ATN from prerenal azotemia.
In ATN, damaged tubules cannot retain sodium efficiently.
BUN/Creatinine Ratio (<20:1):
Suggests intrinsic renal damage rather than prerenal causes of AKI.
How would you differentiate between pre-renal AKI and ATN?
What triggers AIN?
What are the types of AIN and what are the features of each?