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Flashcards in Acute Kidney Injury Deck (22):
1

1. Define acute kidney injury and oliguria.

oliguria <2wk) reduction in glomerular filtration rate (GFR); RIFLE/ AKIN is a unified way to describe AKI

oliguria or hypouresis means low output of urine

2

2. Describe the three main categories of acute kidney injury and the primary causes within each category.

pre renal = decreased renal perfusion
intrarenal= disfunction of the glomeruli, tubules (ATN- ischemic and toxic)) and interstitum (AIN)
post renal: urinary obstruction

pre renal and post renal are reversible

3

3. Describe which nephron sites are involved in the pathogenesis of acute tubular necrosis and explain why the glomerular filtration rate decreases with acute tubular necrosis.

proximal and mTAL are involved in initiation and continuation of tubular necrosis, GFR decreases because of sloughing of PCT cells and infiltrate of immune cells in the mTAL

4

4. Distinguish between of ischemic and toxic causes of acute tubular necrosis and their clinical courses.

use clinical history
clinical course may be more delayed with toxic, although clinical courses are similar

5

5. Describe the clinical presentation of acute interstitial nephritis and acute glomerulonephritits.

AIN occurs while on certain classes of medication; occurs with fevers, rash or eosinophilia, WBC casts, eos in the urine and improves with removal of medication

acute glomerulonephritis presents with RBC casts

6

6. Describe how to find reversible causes of acute kidney injury using the history, and PE.

dx. 1) serial creatinines, 2) renal size, 3) hematocrit

Hx. Prerenal (fluid loss, CHF, fevers); intrarenal (hypotension, surgery , toxin); post renal (anuria, wide swings in urine output, pelvic malignancies or radiation)

PE: Prerenal: orthohypotension, dry mucus membranes, rales, S3, JVD; Postrenal: distended bladder on percussion, abnormal pelvic/rectal exam

7

7. Describe the indications for dialysis interventions.

1. hyperkalemia
2. symptomatic uremia (paricardidts, encephalopathy)
3. unresponsive acidosis
4. sodium and fluid overload

(sometimes due to uremic platelet dysfunction or BUN>100)

8

Contrast uremia and azotemia?

uremia is a clinical syndrome of multiple organ dysfunction caused by retention of uremic toxins and or lack of renal hormones due to renal failure

azotemia is the accumulation in blood of nitrogenous waste products due to decreased renal excretion

9

Describe the condition of pre renal azotemia.

caused by decreased renal perfusion ; the renal tubules function normally, but a decrease in renal perfusion causes decreased GFR

causes of hypovolemia: HYPOVOLEMIA, IMPAIRED CO, PERIPHERAL VASODILATION, renal vasoconstriction, renal vascular obstruction

10

What are causes of post renal azotemia?

bilateral ureteral obstruction (extraureteral and intraureteral)
bladder obstruction (structural and functional)
uretheral obstruction

11

Describe the process of damage in ATN- acute tubule necrosis.

proximal tubules and mTAL loose their healthy brush boarder, some cells are sloughed off, debris accumulates in the tubule

mechanism thought to be an obstructing cast or leaking of filtrate into interstitum

12

How is ATN injury initiated in the proximal tubule?

damage to the cytoskeleton which is important to the integrity of tight junctions, cellular adhesion molecules and Na/K pumps in the basement membrane--- Na begins to pump the wrong way

ischemia also causes ATP to drop and nucleotide depletion as a result causes the formation of oxygen radicals

13

Describe the extension of injury in ATN in the mTAL.

injury is continued by the infiltration of PMN and activation of immune cells in the mTAL during failure

leukocytocte infiltration due to obstruction and coagulation in microculation, increased ROS and cytotoxic cytokines; vasoactive balance is altered with increased endothelia and decreased nitric

14

List common causes of ATN caused by toxin.

radio contrast (low FEna)
amino glycosides
pigments- myoglobin
cistplatinum
amphotericin B (Severe hypokalemia, hypomagnesemia)

15

Name drugs that are commonly implicated in pre renal and ATN.

pre renal- diuretics, NSAIDs ACEI, CNI

ATN: methoxyflurane, carbamazepime, mithramycin, foscarnet, streptozocin + antivirals

Intratubular obstruction (crystals): acyclovir, gancyclovir, methotrexate, triamterene

16

Name drugs associated with acute interstitial nephritis?

antibiotics: penicillins, cephalosporins, etc
NSAIDs
PPI, analgesics, furosemide, anticonvulsants, cimetidine, allopurinol

17

AKI (ATN) mortality is hight in the surgical setting(very high) and medical setting (high) and correlates with _____ ______.

multi organ failure

18

What do patients with ATN die from?

infection
arrhythmias
GI hemorrhage

19

6. Describe how to find reversible causes of acute kidney injury using laboratory/ imaging studies with particular attention to intrarenal disease.

glomerular: RBC/RBC casts, 3-4+ protein
tubular: muddy brown casts, RTC cells/casts
interstitial: WBC/WBC casts 1-2+ protein

imaging: bladder catheter or scan (less reliable) renal ultrasound (excellent rule-out test)

use FEna to distinguish between pre renal(1%) and intrarenal (>3%), note FEurea more useful when patient is using diuretic

20

How do you calculate FEna?

FEna+ (%)= (U Na+/ P Na) / (U Cr/P Cr) x 100

21

What are the three main points of current therapies of AKI?

1) avoid nephrotoxins and hypotension
2) maintain metabolic balance (fluid, electrolytes)
3) Good nutrition - do not restrict protein

Future: need a better model/marker to study AKI, ie. cystatin C- cannot differentiate AKI

22

Discuss future kidney markers and their useful characteristics.

kidney injury molecule (KIM-1)- increases earlier, can distinguish ATN and pre renal axotemia

neutrophil gelatinase (NGAL): increase in ischemic and septic AKI, less useful with complex clinical picture

sodium/hydrogen exchanger isoform-3 (NHE3): better differentiating ATN from pre renal axotemia; assay to complicated for clinical labs