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Flashcards in Acute Kidney Injury Deck (49):

What characterizes renal failure?

Impairment of the GFR, elevation of serum BUN/creatinine, decreased GFR leads to accumulation of substances and drugs normally excreted by the kidney.


How is acute kidney injury characterized?

Rapid: hours to days but 0.5 mg/dL increase in serum creatinine or increase of 50% over baseline.


T or F. Urine output is always decreased with AKI.

F: sometimes, but not always.


What is oliguria? Anuria?

Oliguria is defined as < 400 mL urine output in 24 hours whereas anuria is defined as < 100 mL.


How does AKI manifest?

It doesn't. Usually asymptomatic and discovered on routine labs.


T or F. AKI is usually reversible if underlying disease is treated.



What are the 3 classifications of AKI? Briefly describe each.

1. Prerenal: kidney structurally intact but is not receiving enough blood flow; urine is normal.
2. Intrinsic Renal: something is damaging structures within the kidney.
3. Postrenal: urine flow obstruction.


What is seen in the urine with intrinsic renal AKI?

Granular casts.


RBC casts are indicative of what?



Eosinophiluria is indicative of what?

Allergic reaction in the kidney.


Postrenal AKI can be caused by what diseases?

Prostate disease, pelvic or retroperitoneal malignancies, neurogenic bladder.


How does a patient present with postrenal AKI?

Voiding complaints. PE may reveal distended bladder but probs not. Urinalysis will be unremarkable.


What are the 2 ways to diagnose postrenal AKI?

1. Ultrasound: reveals dilated calyxes
2. Catheter: insert catheter and if alot of urine drains then you know it is postrenal


What are the causes of prerenal AKI?

Volume depletion (GI bleed etc), CHF, shock from fluid losses, sepsis, heart failure.


What are the 3 types of prerenal AKI?

1. Hepatorenal Syndrome
2. Renal Artery Stenosis
3. Drugs that impair auto-regulation i.e. NSAIDS


What are the diagnostic clues of prerenal AKI?

1. Fractional Na excretion < 1%
2. Urine Na concentration < 25
3. Urine osmolarity > 500
Note: prerenal will activate RAAS, so Na is conserved thus all of this makes sense.


Hepatorenal syndrome occurs in what condition?

Liver cirrhosis.


What are the characteristics of hepatorenal syndrome?

1. Decreased BP despite an increased ECFV
2. Kidneys are structurally intact and urinalysis is usually normal
3. Worsening azotemia and progressive oliguria


What is the only true curative treatment for hepatorenal syndrome?

LIver transplant


Briefly describe the pathophysiology of hepatorenal syndrome.

Portal HTN. Splanchnic vasodilation. Decreased effective circulatory volume. RAAS activation. Renal Na conservation and renal vasoconstriction leads to ascites and hepatorenal syndrome.


How do you diagnose hepatorenal syndrome?

It is a diagnosis of exclusion. Must rule out other causes like NSAIDS, nephrotoxic drugs, contrast, etc. Urine sodium will be very low (< 10)- perform trial of volume infusion.


T or F. Renal artery stenosis is only seen clinically if arteries are affected bilaterally.

T: if unilateral, the other kidney can compensate.


In respect to afferent and efferent arterioles, how does the kidney maintain GFR?

Afferent arteriole vasodilated. Efferent arteriole vasoconstricted.


What causes vasodilation of afferent arteriole?



What causes vasoconstriction of efferent arteriole?

Angiotensin II


What classes of drugs can cause a form of prerenal AKI in patients with bilateral renal artery stenosis?

ACE inhibitors or Angiotensin II blockers: impairs autoregulation by effing up constriction of efferent arteriole.


What class of drugs can lead to AKI in patients with true volume depletion, CHF, or cirrhosis?

NSAIDS: they block PG synthesis thus blocking afferent arteriole vasodilation. Note, COX-2 inhibitors have similar intra-renal effects in those patients.


Intrarenal AKI can be caused by defects in which 3 parts of the nephron? List their respective diseases.

1. Glomerulus: post-strep GN, lupus, rapidly progressive GN, hepatitis related, IgA nephropathy
2. Tubular: acute tubular necrosis, acute interstitial nephritis
3. Vascular: vasculitis


What are the 2 major causes of acute tubular necrosis?

1. Ischemic injury (major)
2. Toxic injury from radiocontrast or medications


What is seen histologically with ATN?

Tubular necrosis with denuding of renal tubular epithelial cells. Most ischemic injury in proximal tubules and thick ascending limb. Occlusion of tubular lumens with cells and casts.


Why is the proximal tubule and thick ascending limb most susceptible to ischemic injury?

These segments have alot of ATP dependent transport.


What are the 3 clinical clues to diagnosing ATN?

1. Granular casts (muddy brown color)
2. Urine Na > 20
3. Fractional Na excretion > 1%


In regards to BUN:Cr ratio, urinalysis, urine Na concentration, fractional Na excretion, and urine osmolarity, how do you distinguish prerenal AKI vs. ATN?

(prerenal vs. ATN format)
1. BUN:Cr ratio: >20:1 vs. 10-15:1
2. Urinalysis: hyaline casts vs. granular casts with tubular epithelial cells
3. Urine [Na]: < 20 vs. > 25
4. Fractional Na Excretion: 1%
5. Urine Osm: > 500 vs. 300-350


What causes the increased concentration of urea, creatinine, etc. in the blood in ATN?

Tubular cells are dying and there is leaking of tubular fluid back into the peritubular capillaries.


Since there is no specific treatment for ATN, how is it managed?

1. Restore perfusion
2. Avoid nephrotoxins
3. Supportive care


What 2 classes of drugs can cause prerenal AKI?

1. NSAIDS: by blocking PG synthesis
2. ACE Inhibitors: by inhibiting formation of Angiotensin II


What 2 classes of drugs can cause ATN, an intrarenal AKI?

1. Aminoglycosides (the "mycins")
2. Amphotericin B


What 4 classes of drugs can cause acute interstitial nephritis, another intrarenal AKI?

1. Penicillins
2. Cephalosporins
3. Sulfonamides


Describe aminoglycoside toxicity.

10-20% of patients will have rise in serum creatinine. Drug accumulates in proximal tubule cells. Drug inhibits lysosomal function. Toxicity is associated with dose and duration of therapy.


How do you prevent aminoglycoside toxicity?

Once daily dosing results in high urinary concentrations which exceed the reasbsorptive capacity of the proximal tubule. Careful monitoring of drug levels and minimizing duration of therapy.


How do contrast agents/dyes used in tomography cause AKI?

They directly vasoconstrict arterioles and are toxic to tubular cells.


What are the risk factors for developing AKI with use of contrast agents?

Pre-existing renal disease, heart failure, hypovolemia, high doses, multiple closely spaced studies.


How do you prevent contrast nephropathy?

Give lower dose of contrast agent. Avoid closely spaced studies. Avoid volume depletion by giving IV fluids. Avoid other nephrotoxins i.e. NSAIDS, ACE inhibitors, etc.


Define acute interstitial nephritis.

Allergic reaction in the kidney characterized by infiltration of the interstitium by granulocytes (often eosinophils).


Which classes of drugs commonly cause acute interstitiall nephritis?

The beta-lactams (penicillins, cephalosporins, sulfa drugs) and NSAIDS.


What are the symptoms of acute interstitial nephritis?

Fever, rash, joint pain, increased eosinophils on CBC.


Urinalysis of acute interstitial nephritis will reveal what?

Pyuria (pus in the urine) and eosinophils are usually seen in the urine.


What are the 2 ways to prevent AKI?

1. Avoid nephrotoxins
2. Assure good renal perfusion prior to contrast studies and surgery


What are the 4 ways to provide supportive care to AKI patients?

1. Avoid further injury
2. Watch volume status and electrolytes
3. Dialysis (in some cases)
4. Wait for kidneys to get better