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?
AIN type 1 = autoimmune causes => SLE, sjogrens, IgA Nephropathy, vasculitis
Type 2 = drug induced => NDAP
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?