Renal Flashcards
(14 cards)
Drugs causing pre-renal AKI
BUN : Creatinine ratio - normal and in pre-renal and post-renal AKI
Normal: 15:1
Increased: >20:1
MoA of creatinine and BUN increase in pre-renal AKI
What is Fractional Excretion of Sodium (FeNa%)?
FeNa tells us what percentage of the filtered sodium is actually excreted in urine. It’s used to distinguish between prerenal and intrinsic causes of acute kidney injury (AKI).
How does fractional excretion of sodium (FeNa) differ between prerenal and intrinsic AKI, and why?
What are the key urine findings in early vs late post-renal AKI?
What is the pathophysiologic mechanism of hemolytic uremic syndrome (HUS)?
- Trigger (usually Shiga toxin from E. coli O157:H7 after bloody diarrhea): Toxin enters circulation and damages endothelial cells, especially in the kidneys.
- Endothelial injury → exposure of subendothelial collagen and vWF: This activates platelets and the coagulation cascade.
- Platelet aggregation and microthrombi formation in small vessels: Causes mechanical destruction of red blood cells → schistocytes (fragmented RBCs). Platelets get consumed → thrombocytopenia.
- Kidney injury from thrombi in renal microvasculature → ↓ perfusion and AKI
Why is the BUN:Creatinine ratio typically < 15:1 in intrinsic (intrarenal) AKI?
- In intrarenal AKI (e.g., acute tubular necrosis), the tubules are damaged.
- This impairs urea reabsorption in the proximal tubule.
- Creatinine is not reabsorbed either, so both waste products accumulate at similar rates.
- Result: BUN:Creat ratio stays normal or low (< 15:1).
How does the BUN:Creatinine ratio differ between pre-renal, intrinsic (intrarenal), and post-renal AKI?
Why add a thiazide diuretic to a loop diuretic?
What is the pathophysiology of diabetic nephropathy?
Prolonged hyperglycemia in diabetes → Leads to non-enzymatic glycosylation of endothelial proteins → Triggers inflammation and increased production of growth factors, collagen, and fibronectin
Over time, this causes mesangial expansion, thickening of the glomerular basement membrane (GBM), glomerular sclerosis (scarring of the glomeruli)
When glomerular sclerosis becomes nodular, it is called a Kimmelstiel-Wilson (KW) lesion, which is pathognomonic for DN.
What type of renal lesion is visualized here and what is it caused by
This is a Kimmelstiel-Wilson lesion of diabetic nephropathy
What is the first clinical sign of diabetic nephropathy?
Albuminuria, which can progress to overt nephrotic syndrome (peripheral edema, heavy proteinuria, fatty casts)
Effect of nephrectomy on GFR immediately and long term
