Renal / Genitourinary Flashcards
Def of AKI
rapid decline in renal funciton w/ increase in Cr(relatively increase of 50% or absolute 0.5-1)
Types of AKI (2)
Prerenal - decreas in renal blood flow (6–70%)
Intrinsic - damage to renal parenchyma 925040%)
Postobstructive - outflow obst (5%)
AKI per RIFLE criteria
RISK = 1.5 fold increase in serum Cr of DFR decrease bu 25% or output<0.5 mL/kg/hr for 24 hrs or anuria 12hrs
Loss - dialysis 4 wks
ESRD - dialysis 3 months
Weight gain and edema in AKI 2/2
positive water and Na balance
Azotemia
elevated BUN and Cr
- BUN elv in catabolic drugs (steriods), GI/soft tissue bleeds and dietary protein intake
-Cr elv in muslce breakdowna nd drugs
Pre renal causes of AKI(5)
low flow -> decreased clearance
Volume loss/sequestered- dehydration, diuretics, poor PO intake, vomitting. diarrhea, hemorrhage
Low CO- CHF
Hypotension - Sepsis, HTN meds
Cirrosis, hepatorenal syndrome
NSAID and ACEi use w. low renal perfusion
Monitor w/ AKI (5)
I/Os and weight BO serum electolytes Hb and Hct for anemia infeciton
Prerenal vs intrinsic
UA
BUN/cr
FENa
Urine osm
Urine NA
Prerenal
- few Hyaline casts
- > 20:1 ratio
- 500mOSm
- Na 2/3% FENa (loss of retainment)
- 250-300 mOsm
- > 40 Na
Intrinsic renal failure(5)
kidneys can’t concentrate
Tubular disease (ATN) - ischemia and nephrotoxin
->prerenal progressing to intrinsic w/ ischemia (ATN)
Glomerular disease - acute glomerulonephtitis, Goodpastures, Wegeners, post step GN, lupus)
Vascular disease - Renal occlusion, TTP, HUS
Interstitial disease (AIN) - allergic, hypersensitivity to meds (NSAID etc)
Rhabdomyolisis and the kidneys
myoglobin released post trauma and crush injuries -> toxic to kidneys
Labs - elv Creatine phosphokinase, hyperkalemia, hypocalcemia, hyperuricemia
Tx w/ IV fluids, mannitol, bicarb (drives K into cell)
ATN causes (2)
Ischemic AKI
- severe decline in renal blood flow - shock, hemorrhage, sepsis, DIC, HF
- > death of tubular cells
Nephrotoxic AKI - direct injury 2/2 substances - Abx(aminoglycosides, vancomycin) -radiocontrast -NSAIDs in CHF - poisons myoglobinuria - chemotherapy (cisplatin) -kappa/gamma light chains
Post renal AKI
obstruction of any segment of urinary tract -> retrograde tubular pressure -> Decrease GFR
Both Kidneys for Cr to rise
Large prostate -most common nephrolithasis neoplasm retroperitoneal fibrosis uretral obstruction uncommon (need both)
Test for post renal
PE of the bladder
US of kidneys
Catheter for volume
Course of ATN(3)
insult->
oliguric phase - azotemia and uremia (10-14days), output osmotic dousers
Recovery phase
Dehydration triggers the release of what
ADH 0> water reabsorption
ATN the tubules are damaged and cannot reabsorb leading to low osmolarity urine
Tests for AKI
UA Urine Chme BMP Bladder Cath renal US
AKI and Muddy brown casts, renal tubular casinos UA
ATN
AKI and RBC casts and RBCs on UA
glomerular disease
AKI and WBC casts and WBCs on UA
Pyelonephritis
Acute interstitial nephritis
AKI and benign UA
prerenal causes,
Look at BUN/Cr, FENa and Urine OSM
-> either prerenal or intrinsic ARF
Urine Sediment
Hyaline Casts
RBC casts
WBC Casts
Fatty casts
Hyaline - prerenal, decide of contents
OBC - glomerular disease
WBC - renal parenchymal inflammation
Fatty - nephrotic syndrome
FENa calculation
UNa/PNa x UCr/PCr) x 100
2-3% ATN
Useful if oliguria (<500mL/day)
Complications of AKI(4)
K?
acid/base?
ECF volume expansion and pulm edema (Tx w. diuretic)
Metabolically
- Hyperkalemia (less exchange to retain Na -> excess K + movement from ICF -> ECF w/ cell destruction
- Metabolic Acidosis - w/ anion gap - less H excreted (w/K) (tx bicarb)
- hypocacemia - loss active Vit D
- Hyponatremia if > fluids
- hyperphosphatemia
- hyperuricemia
Uremia- toxic accum
Infection
Tx of AKI general
Avoid Drug insult (NSAIDS, contrast, aminoglycosides)
Change med doage
Correct fluids IV or duiures
Correct electrolyte disturb
Optimize BP
Dialysis if remix, academia, hyperkalemia, volume overload