Week 3: acute kidney injury Flashcards
Define Acute Kidney Injury (AKI)
- syndrome characterized by rapid deterioration of renal function tha treads to accumulation of nitrogenous wastes in the body (azotemia).
- plasma Cr and BUN used as surrogate markers of azotemia
- bilateral process
- may or may not be associated with uremic symptoms
- may or may not be associated with drop in urine output
what is the criteria for diagnosing acute kidney injury?
One of the following occurring within 48 hrs (based on 2 creatinine elevations within 48 hrs)
- absolute increase in serum Cr concentration of greater than 0.3 mg/dL from baseline
- relative increase in serum Cr concentration of greater than 50%
- urine output < 0.5mL/kg/hr for more than 6 hours
How is acute kidney injury staged?
I. increase of Cr 1.5 x baseline, or > 0.3 mg/dL
II: increased Cr 2x baseline
III: increase Cr 3x baseline or >4 mg/dl or on dialysis
There’s also urine output criteria
What are circumstances that Cr is elevated but GRF is normal?
- medications that block tubular secretion of cr
- trimethoprim
- cimetidine
- procainamide - substances that interfere with Cr assay
- 1st gen cephalosporins
- ketotic states by acetoacetate
What are circumstances that Bun is elevated without changes in GFR?
- GI bleeding (endogenous protein load)
- high protein diet (protein metabolized to urea)
- catabolic steroids such as glucocorticoids (results in increase protein catabolism)
What are manifestations of AKI?
Main: azotemia- increase in BUN and creatinine
- hyperkalemia
- metabolic acidosis -problem with ammoniagenesis
- volume overload
- hyperphosphatemia
Distinguish between AKI and chronic kidney disease.
- chronic: kidney damage> 3 mos.
- hx: duration of symptoms of pruritus, nausea, loss of appetite, etc, usually means chronic
- renal size: small in CKD, except in DM, amyloid, polycystic kidney disease, and HIV nephropathy
- CDK: hyperparathyroidism, bone disease, anemia, half and half nails
What are causes of pre-renal AKI?
syndrome of renal hypo perfusion
- intravascular volume depletion
- diarrhea, vomiting, diuretics, hemorrhage, dehydration - Decrease effective intravascular volume
- Heart failure, cirrhosis, sepsis - renal hypoperfusion
- renovascular disease, NSAIDS, ACEI, hepatorenal syndrome
Clinical presentation of pre renal AKI.
-orthostatic symptoms
-volume loss
-intraoperative hypotension
-heart failure
-liver disease
-thirst
FINDINGS ON PE
-hypotension, orthostatic changes in bp, tachycardia, dry mucous membranes, poor skin turgor, flat neck veins
-signs of CHF or liver disease: edema, JVD, acites
laboratory findings in pre-renal AKI
- BUN: Cr ratio> 20:1
- due to depleted intravascular volume and response. BUN is first thing that goes up because kidney reabsorbs urea. - Urine indices
- oliguria: 1.020, Uosm>500mmol/L
- high renal sodium avidity: Una<20 mmol/L, Fractional excretion of Na is less than 1%
- inactive urine sediment
What are causes of post-renal AKI?
- upper tract obstruction(ureteric)
- Intrinsic: kidney stone, transitional cell CA
- Extrinsic: Retroperitoneal adenopathy, abdominal aortic aneurysm - lower tract obstruction (bladder neck)
- BPH
- prostate CA
- urethral stricture
- neurogenic bladder
Clinical presentation of post-renal AKI
- flank pain, hematuria, pelvic malignancy
- symptoms of bladder outlet obstruction: nocturne, urinary frequency, urgency, decrease urinary stream, incomplete voiding
- PE: distended bladder, enlarged prostate, abdominal/pelvic mass
What are intra-renal causes of AKI?
- vascular: atheroemboli, malignant HTN, HUS-TTP
- glomerular: glomerulonephritis
- tubular: acute tubular injury
- interstitial: acute interstitial nephritis
Distinguish between pre-renal AKI from ATN
Pre-renal -bland, hyaline casts -BUN:Cr ratio >20:1 -oliguric -improvement in renal function to volume challenge -U[Na]1% ATN -muddy brown or granular casts BUN to Cr 10:1 -may or may not be oliguric -no improvement in renal fxn to volume challenge -Uosm about 300 -U[Na}>40 -FE[Na]>2%
