Renal Flashcards
Pre-renal BUN:Cr
Increased ratio: low RBF activates RAAS, increased BUN absorption
Post-renal BUN:Cr
Early: high ratio, increased pressure “forces” BUN out
Late: low ratio, tubular damage–less absorption
Fanconi syndrome
PCT dysfunction
Bartter’s syndrome
TAL dysfunction
Gitelman’s syndrome
DCT dysfunction
Pre-renal FENa
Low FENa (RAAS activation)
Acute Tubular Necrosis FENa
High FENa: Na not reabsorbed due to tubular damage
Pyuria + WBC casts
Interstitial nephritis
“Muddy brown” granular casts, isosthenuria
Acute tubular necrosis (ATN)
Hematuria, RBC casts
Acute glomerulonephritis
Subepithelial “hump”
Post-infectious glomerulonephritis (immune complex deposition)
IF: granular mesangium
IgA nephropathy
What complement pathway is used in IgA nephropathy?
Alternative
What is Henoch-Schönlein Purpura (HSP)?
IgA nephropathy + extra-renal symptoms
Cause of Hereditary Nephritis?
Mutation in collagen type IV (Alport syndrome)
Hereditary nephritis triad
Isolated hematuria, hearing, and ocular abnormalities
RPGN Type I
Anti-basement membrane antibodies
RPGN Type II
Immune complex depositions
RPGN Type III
ANCAs cause activation of neutrophils and release of lytic enzymes
IF: linear
RPGN Type I, Goodpasture syndrome
Hematuria + Hemoptysis
RPGN Type I: antibodies against basement membrane in kidneys and lungs (Goodpasture syndrome)
“Spike and dome” on silver stain
Membranous nephropathy