EOR- GU/renal Flashcards
what defines Acute kidney injury (AKI)?
- increase in serum Cr >50% OR 2. incr blood urea nitrogen (BUN) aka “azotemia”.
what is the RIFLE criteria?
stratum of progressive AKI injury: based on increasing % GFR decrease and decreased urine output:
Risk, Injury, Failure w/ outcomes - Loss, End stage kidney dz
3 types of AKI
pre-renal (MC), intrinsic, post-renal
define pre-renal AKI, what causes it?
decreased renal perfusion. Often leads to intrinsic if not corrected. Cause- hypovolemia or afferent constriction (Nsaids, IV contrast) w/ efferent dilation (ACEs,ARBs)
define intrinsic AKI, what are the 4 subtypes? which is most common
direct structural/fxn kidney damage - nephrotoxic, cytotoxic or prolonged ischemic = cellular cast formation. Includes… ATN (MC), AIN, acute glomerulonephritis, vascular
define ATN, what are the two types?
acute destruction tubules of nephron
Ischemic: cause- prolonged prerenal, hypotension, hypovolemia, post-operative
Nephrotoxic: exogenous (i.e. aminoglycosides), endogenous (gout, myoglobinuria from rhabdo, lymphoma/leukemia.
define AIN, what is the MC cause?
inflammatory or allergic response in interstituim (spares glomeruli + vessels). Cause- drug hypersensitivity (MC), infection, autoimmune, idiopathic.
AKI: acute glomerulonephritis vs vascular
acute glomerulonephritis: immune mediated inflammation of glomeruli –> RBC + protein leakage
Vascular: TTP, DIC, aneurysm, etc.
UA: what does each result indicate?
RBCs
Muddy brown casts + epithelial cell casts
WBC casts
RBCs - glomerulonephritis (AGN)
Muddy brown casts + epithelial cell casts - ATN
WBC casts - AIN
BUN/Cr: pre-renal vs ATN
BUN/Cr: prerenal >20:1, ATN 10-15:1
txt pre-renal vs ATN
Prerenal: volume repletion - restore renal perfusion
ATN: remove offending agent, IV fluids, furosemide (if euvolemic + not urinating). Most return to baseline in 72hrs
txt AIN vs glomerulonephritis
AIN: remove offending agent
Glomerulonephritis (AGN): high-dose steroids, cytotoxic agents
pathophys of how nephrotic dz causes edema
glomerular damage → proteinuria → decrease plasma oncotic pressure → edema.
primary vs secondary causes of nephrotic syndrome
Primary - minimal change disease (MC nephrotic syndrome in kids), focal segmental glomerulosclerosis (HTN in african americans + IV heroin abuse, HIV)
Secondary - systemic dz - DM
S+S nephrotic syndrome
edema (peripheral, periorbital - kids) - from low albumin in blood = low oncotic pressure. → ascites, anscara. DVT (liver tries to make more clotting factors to incr. Oncotic pressure).
Dx nephrotic syndrome - 2 ways
24hr urine collection = >3.5 g/day. UA dipstick = protein 3+, 4+ and oval fat bodies (“maltese cross shaped). Hypoalbuminemia, hyperlipidemia
txt for nephrotic syndrome: for minimal change dz, for edema, for proteinuria reduction
Minimal change = corticosteroids
Edema- diuretics
Proteinuria reduction - ACEIs, ARBs
hallmark signs of acute glomerulonephritis
Hallmark = HTN, hematuria (RBC casts), dependent edema, azotemia.
MC cause of acute glomerulonephritis worldwide? what is the typical presenting pt?
IgA nephropathy aka berger’s dz - young males w/in days after URI or GI infection.
young boy w/ facial edema after strep + cocacola urine.
post-infectious acute glomerulonephritis (MC GABHS)
goodpastures dz: what is the basic pathophys and resultant effects?
anti-GBM antibodies vs collagen of glomerular basement membrane in kidney and lung alveoli → kidney failure and hemoptysis. = linear IgG deposits.
what are 4 causes of acute glomerulonephritis?
IgA nephropathy (berger’s), post-infectious (i.e. GABHS), goodpastures dz (IgG), vasculitis
while UA is very useful for dx glomerulonephritis, what is the GOLD std?
renal Bx
prognosis of acute glomerulonephritis?
self-limited w/ good prognosis (except if rapidly progressive glomerulonephritis- MC in good pastures and vasculitis).