AKI Flashcards
What are the hallmarks of AKI?
hallmark is inc serum BUN and sometimes reduction in urine volume
meas inc serum creatinine too
OVER SMALL PERIOD OF TIME (hrs to days)
Uremia
symptomatic azotremia
symptoms = anorexia, nausea, vomiting, muscle cramps, restless legs, anemia, electrolyte disturbances, asterixis, mental status change, pericarditis, platelet dysfunction
4 Other Causes of Azotremia (besides AKI)
protein loading
GI bleed –> endogenous protein load
Catabolic steroids
Abx that inhibit protein formation (tetracyclines)
3 Categories of AKI Causes
1- Pre-renal (hemodynamics)
- True volume depletion - Dec effective arterial blood volume - States of renal vasoconstriction
2- Intrinsic (w/in kidney itself)
- Acute tubular necrosis (ATN) - 90%
- Ischemic, nephrotoxic, sepsis
- Acute interstitial nephritis
- Acute glomerulonephritis
- Acute vascular syndromes (bilateral)
- Intra-tubular obstruction
3- Post-renal (block urine flow)
- Upper tract (ureters/renal pelvis); must be bilateral
- Intrinsic
- Extrinsic - retroperitoneal
- Lower tract (bladder outlet/urethra)
What happens in pre-renal AKI?
- normal RAAS act to maintain GFR despite dec renal flow but as dec renal perfusion persists it can no longer maintain GFR/decline in glomerular cap pressure
- In beginning as GFR is maintained, there is inc Na and urea reabsorption contributing to high BUN:creatinine ratio
High BUN: creatinine ratio, low urine volume and conc and low urine Na
Tx of pre-renal AKI
- Correct volume deficit
- STOP diuretics, NSAIDs, ACEi, ARBs
- Optimize cardiac function if CHF is cause
What happens in post-renal AKI?
- Early - inc intratubular pressure –> inc hydrostatic P of Bowmans and slight inc renal blood flow –> inc hydrostatic P of glomerular cap –> overall lower gradient –> lower GFR
- Then- renal blood flow drops –> GFR drops
- Later - intratubular pressure normalizes (dec hydrostatic P of Bowmans) but still dec renal blood flow so low GFR
Presentation of Post-Renal AKI
- Hallmark = hydronephrosis
- Present w/ urgency, nocturia, incomplete voiding, possible hematuria, etc
- Flank pain if upper obstruction
- Physical exam - distended bladder in suprapubic space
Tx of Post-renal AKI
- Relive obstruction (if > 4 wks likely permanent damage)
- Lower - cath in bladder
- Upper - stents or percutaneous nephrostomies
- Monitor vol - may get vol depleted b/c post-obstructive diuresis
ATN Pathophysiology
- 1- loss of cell polarity (apical and basolateral not diff) –> channels migrate to opp. membrane
- 2- necrosis and apoptosis of epithelial cells
- 3- debris –> obstruction + back-leak of filtrate across BM
- 4-recovery (viable epithelial cells re-differentiate)
ATN Presentation, Tx, Prognosis
- Presentation
- Hx -look for ischemic (vol), nephrotoxic (drugs, injury)
- BUN:creatinine < 10:1
- May be oligouric or not
- Normal urine Osm
- Na wasting - high Na in urine
- Urine sediment - muddy brown casts; granular casts of epithelial debris
- Tx
- Supportive
- Maybe acute dialysis
- Prognosis - inc risk chronic kidney disease later
Acute Interstitial Nephritis (pathophysiology, presentation and tx)
- Pathophysiology - drugs, infection or systemic disease, malignancy or idiopathic –> inflammation
- Presentation
- Hx - recent drug use or illness
- Triad: fever, rash, eosinophilia
- Lymphocytic infiltrate w/ eosinophils often
- Urine sediment - WBC casts
- Proteins, hematuria, pyuria (neutrophils)
- Tx - treat underlying cause
What acute vascular syndromes can cause AKI?
- thromboembolism of renal artery
- renal artery dissection
- renal vein thrombosis –> infarction
What intra-tubular obstructions can cause AKI?
- Uric acid from tumor lysis
- Calcium oxylate from ethylene glycol ingestion
- Drug crystals (sulfa, methotrexate, acyclovir)
- Mult myeloma –> proteinaceous material –> light chain casts
What can cause renal vasoconstriction that leads to pre-renal AKI?
hypercalcemia
NSAIDS during RAAS act
hepatorenal syndrome (intense renal vasoconstriction in adv liver disease - does not reverse w/ vol expansion)
