Acute Kidney Injury Flashcards
Rapid (< 1 week) reduction in glomerular filtration rate (GFR)
Acute kidney injury
the inability of output to match the input (water, sodium, potassium, nitrogen, phosphorus, acid)
Failure of balance
increase 1.5-1.9 baseline Cr
Increase in Cr by 0.3 mg/dL in 48h
urine output < 0.5mL/kg/hr for 6 hours
AKI stage 1
increase of 2-2.9 baseline cr
urine output: < 0.5ml/kg for 12 hours
AKI stage 2
increase 3x baseline Cr
increase in Cr > 4.0mg/dl
intiated on renal replacement therapy
urine output < 0.3mL/Kg for 24 hours
anuric for 12 hours
AKI stage 3
accumulation of nitrogenous waste; increased BUN
Azotemia
Organ dysfunction caused by retention of uremic toxins
“symptomatic renal failure”
uremia
< 500mls in 24 hours
oliguria
< 100mls in 24 hours
anuria
decreased renal perfusion
prerenal
damage to particular parts of the kidney; ATN, AIN, GN
intrinsic
urinary obstruction
post-renal
- 10% off all patients with acute renal failure
- potentially and often easily reversible
- many times will need involvement of urology and or interventional radiology
post-renal
- Common
- reversible if treated promptly
- renal tubules are functional
- concentrate urine avidly (azotemia/elevated BUN/Cr ratio)
pre-renal
what are some etiologies of pre-renal problems?
- Hypovolemia: ex. diarrhea, vomiting, decreased po intake, diuretics, hemorrhage
- impaired cardiac function: ex. CHF (cardiorenal)
- peripheral vasodilation (ex. sepsis, liver failure (hepatorenal syndrome)
- renal vasoconstriction (ex. NSAIDs, iodinated contrast, hypercalcemia, calcineurin inhibitors
- renal vascular obstruction (ex: renal artery stenosis)
etiologies of intrinsic AKI
Glomerular nephritis
- glomerular nephritis: lupus, igA, ANCA, anti, GBM
Tubules
- ATN: Ischemic (prolonged/severe prerenal state); Toxic (exogenous meds, endogenous pigments)
Interstitium
- AIN: medications, infections, autoimmune
what are classic toxins and their clincial findings in ATN?
- radiocontrast; oliguric
- aminoglycosides: non-oliguric
- pigments (rhabdo); hemoglobinuria without RBCs
- amphotericin; hypokalemia, hypomagnesemia
- AKI in the setting of medication use
- 5-14 days
- rash
- fever
- eosinophilia
- triad 10%
- non medcation causes less common (malignancy, infectious, autoimmune, idiopathic)
Acute interstitial nephritis (AIN)
drugs assocaited with acute intersitial nephritis?
ANTIBIOTICS
others: PPIs, NSAIDs, chemotherapy
- rare but very serious
- urgernt renal referral and biopsy
- therapy varies based on underlying etiology
glomerulonephritis
- fluid losses (diuretics, burns, hemorrhage)
- symptoms of CHF and hypervolemia
- decreased PO intake
- symptoms of infections
diagnostic history of prerenal AKI
- shock
- sepsis
- surgery: anesthesia intraop reports, blood loss
- review med list
- joint pain, rashes , fever, constitutional symptoms
diagnostic history of renal AKI
- older male
- neurologic disorder (neurogenic bladder)
- hx of pelvic malignancies or radiation
- single kidney
diagnostic history of postrenal
- cylindrical structures formed in tubular lumen- shape and size of renal tubule
- matrix composed of Tamm-horsfall mucoproein (uromoduliln)- most abundant protein in normal urine
Urine sediment- casts
what casts would you expect in AIN, GN?
AIN- WBC
GN- RBC cast
Disgnosis of AKI- obstruction
- post void residual (bladder scan): false readins in obesity or ascities
- catheter insertion (straight or foley)
- renal ultrasound (most sensitive- provides structural information)
Current therapies for managment
- avoid nephrotoxins and maintain renal perfusion (NSAIDs, contrast, extremes of blood pressur)
- maintanence of metabolic and volume balance (restriction of sodium, potassium, phosphorus; more fluids is Not always the answer, if oliguric, hypervolemic—> diuretics)
when to dialyze?
- acidosis; specifically metabolic acidosis
- electrolytes: hyperkalemia, K > 6.0meq/L; rarely other electrolye abnormalities (Ca, Mg, phos)
- intoxicants: toxic alcohols, lithium, metformin
- fluid overload
- uremia: pericarditis, progressive encephalopathy, not just elevated BUN (azotemia)
- typically refractory to medical management
- RTCs do not clearly support early or late initiation
what would be seen on physical exam of prerenal AKI?
- Hypotension/orthostatic hypotension
- rales, S3, JVD, edema
- ascities/jaundice
- POCUS of lungs, heart, IVC
what would be seen on physical exam of renal AKI?
rash
findings of other systemic illness
what would be seen on physical exam of postrenal AKI?
- distended bladder
- POCUS with distended bladder or renal collecting system
management of AKI?
- avoid nephrotoxins and maintain renal perfusion
- NSAIDs, contrast, extremes of blood pressure
2 . maintanence of metabolic and volume balance
- restriction of sodium, potassium, phosphorus
- more fluids are not always the anwer
- if oliguric, hypervolemic –> diuretics
