Clinical presentations of renal disease Flashcards
Mechanism of oliguria in pre-renal acute kidney injury
Decreased RBF and GFR –> increase proximal tubule reabsorption of Na and H2O –> increased aldosterone and ADH secretion –> increased distal tubule Na and H2O reabsorption
Mechanism of oliguria in intrarenal acute kidney injury
Renal tubular injury –> cast formation –> obstruction and increased pressure –> tubular backleak –> decreased GFR
Mechanism of post-renal oliguria in acute kidney injury
Bilateral obstruction to urine flow –> increased intraluminal pressure –> release of inflammatory mediators and cells injury –> renal vasoconstriction (causes renal tubular injury) –> edema and decreased GFR
BUN/creatinine ratio in pre-renal acute kidney injury
> 20:1 –> increased
Urinary sodium levels in pre-renal acute kidney injury
<20 –> normal
Fractional excretion of sodium in pre-renal AKI
<1% –> normal
Urine osmolality in pre-renal AKI
> 500 –> normal
BUN/creatinine ratio in intra-renal AKI
10:1 –> low normal
Urinary sodium levels in intra-renal AKI
> 40 –> high
Urinary fractional excretion of sodium in intra-renal AKI
> 4% –> increased
Urine osmolality in intra-renal AKI
<350 –> low
BUN/creatinine ratio in post-renal AKI
> 10:1 –> normal
Urinary sodium levels in post-renal AKI
> 40 –> high
Fractional excretion of sodium in post-renal AKI
> 4% –> high
Urine osmolality in post-renal AKI
<350 –> low
Where are urinary casts formed?
Distal convoluted tubule or collecting duct
Type of cast believed to com from damaged and dilated tubules, and therefore seen in end-stage chronic renal disease
Broad casts
Polyuria with normal plasma glucose, low urine osmolality, and normal serum sodium. Normal urine osmolality after desmopressin.
Cranial diabetes insipidus
Polyuria with normal plasma glucose, low urine osmolality, and normal serum sodium. Low urine osmolality after desmopressin.
Nephrogenic diabetes insipidus
