Acute Kidney Injury

Question 1

Rapid (< 1 week) reduction in glomerular filtration rate (GFR)

Answer 1

Acute kidney injury

Question 2

the inability of output to match the input (water, sodium, potassium, nitrogen, phosphorus, acid)

Answer 2

Failure of balance

Question 3

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

Answer 3

AKI stage 1

Question 4

increase of 2-2.9 baseline cr
urine output: < 0.5ml/kg for 12 hours

Answer 4

AKI stage 2

Question 5

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

Answer 5

AKI stage 3

Question 6

accumulation of nitrogenous waste; increased BUN

Answer 6

Azotemia

Question 7

Organ dysfunction caused by retention of uremic toxins
“symptomatic renal failure”

Answer 7

uremia

Question 8

< 500mls in 24 hours

Answer 8

oliguria

Question 9

< 100mls in 24 hours

Answer 9

anuria

Question 10

decreased renal perfusion

Answer 10

prerenal

Question 11

damage to particular parts of the kidney; ATN, AIN, GN

Answer 11

intrinsic

Question 12

urinary obstruction

Answer 12

post-renal

Question 13

• 10% off all patients with acute renal failure
• potentially and often easily reversible
• many times will need involvement of urology and or interventional radiology

Answer 13

post-renal

Question 14

• Common
• reversible if treated promptly
• renal tubules are functional
• concentrate urine avidly (azotemia/elevated BUN/Cr ratio)

Answer 14

pre-renal

Question 15

what are some etiologies of pre-renal problems?

Answer 15

• 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)

Question 16

etiologies of intrinsic AKI

Answer 16

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

Question 17

what are classic toxins and their clincial findings in ATN?

Answer 17

• radiocontrast; oliguric
• aminoglycosides: non-oliguric
• pigments (rhabdo); hemoglobinuria without RBCs
• amphotericin; hypokalemia, hypomagnesemia

Question 18

• AKI in the setting of medication use
• 5-14 days
• rash
• fever
• eosinophilia
• triad 10%
• non medcation causes less common (malignancy, infectious, autoimmune, idiopathic)

Answer 18

Acute interstitial nephritis (AIN)

Question 19

drugs assocaited with acute intersitial nephritis?

Answer 19

ANTIBIOTICS

others: PPIs, NSAIDs, chemotherapy

Question 20

• rare but very serious
• urgernt renal referral and biopsy
• therapy varies based on underlying etiology

Answer 20

glomerulonephritis

Question 21

• fluid losses (diuretics, burns, hemorrhage)
• symptoms of CHF and hypervolemia
• decreased PO intake
• symptoms of infections

Answer 21

diagnostic history of prerenal AKI

Question 22

• shock
• sepsis
• surgery: anesthesia intraop reports, blood loss
• review med list
• joint pain, rashes , fever, constitutional symptoms

Answer 22

diagnostic history of renal AKI

Question 23

• older male
• neurologic disorder (neurogenic bladder)
• hx of pelvic malignancies or radiation
• single kidney

Answer 23

diagnostic history of postrenal

Question 24

• 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

Answer 24

Urine sediment- casts

Question 25

what casts would you expect in AIN, GN?

Answer 25

AIN- WBC GN- RBC cast

Question 26

Disgnosis of AKI- obstruction

Answer 26

1. post void residual (bladder scan): false readins in obesity or ascities 2. catheter insertion (straight or foley) 3. renal ultrasound (most sensitive- provides structural information)

Question 27

Current therapies for managment

Answer 27

* 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)

Question 28

when to dialyze?

Answer 28

* 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**

Question 29

what would be seen on physical exam of prerenal AKI?

Answer 29

* Hypotension/orthostatic hypotension * rales, S3, JVD, edema * ascities/jaundice * POCUS of lungs, heart, IVC

Question 30

what would be seen on physical exam of renal AKI?

Answer 30

rash findings of other systemic illness

Question 31

what would be seen on physical exam of postrenal AKI?

Answer 31

* distended bladder * POCUS with distended bladder or renal collecting system

Question 32

management of AKI?

Answer 32

1. 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