05.15 - AKI (Canada) - PP Flashcards by Ryan Lee

3 Clinical Clues to ATN

(1) Muddy brown granular casts; (2) Urine Na > 20; (3) Fractional excretion of Na > 1%

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Urinarlysis in Hepatorenal Syndrome

Usually normal

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Urine Na in HRS

Very low (Aldosterone)

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Urine in Acute Interstitial Nephritis

Pyuria +/- eosinophils

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Effect of Aminoglycosides on Kidney

Inhibits normal lysosomal function, accumulates in PT cells

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What can you do in suspected HRS to rule out simple pre-renal condition

Trial of volume (usually Albumin) infusion

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Urine [Na] and Osm in Pre-Renal AKI

Very low Na (Aldosterone overactive), Very high osmolarity (ADH overactive)

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Why is urine Na high in ATN

Necrotic tubular cells can’t reabsorb Na so excreted

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___ can cause form of pre-renal AKI in patients with Bilateral RAS

ACEi’s and ARB’s

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Main 2 Causes of ATN

Ischemic injury; Toxic injury from contrast or meds

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Symptoms of Acute Interstitial Nephritis in most patients now

Only renal dysfunction

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2 Therapeutic agents that cause Pre-Renal AKI

NSAIDs, ACEi’s

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What does survival in Hepatorenal Syndrome depend on

Liver transplant

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How to avoid Contrast Nephropathy

Avoid closely spaced studies

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Acute Kidney Injury is essentially

Impairment of GFR

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BP and ECV in Hepatorenal Syndrome

Decrease BP despite incr ECFV (decr ECV)

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Histology of ATN

Tubular necrosis with denuding of renal tubular epithelial cells; Occlusion of tubular lumens with cells/casts

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Acute Interstitial Nephritis is most commonly caused by

Beta Lactam Abx, NSAIDs

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Most common cause of Post-renal AKI

Prostate disease

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(1) Muddy brown granular casts; (2) Urine Na > 20; (3) Fractional excretion of Na > 1%

3 Clinical Clues to ATN

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Worsening renal failure in setting of cirrhosis =

Hepatorenal syndrome

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Must rule out what else to conclude HRS

NSAIDs, Nephrotoxic drugs, Contrast

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BUN/Cr in Pre-Renal vs ATN

>20:1 in Pre-Renal; 10-15:1 in ATN

Why is Uosm high in Pre-Renal and Normal in ATN

High Aldo in Pre-Renal; In ATN, necrotic cells can’t dilute or concentrate so same as blood

Most common class of AKI? Second?

55% Pre-renal, 40% intrinsic

Calyce visible on renal US means

Obstruction of outflow

2 Aminoglycosides

Gentamycin, Topomycin

How do contrast agents cause AKI

Direct vasoconstrictive effects on arterioles; Also directly toxic

Usual symptoms of AKI

Usually asymptomatic and discovered on routine labs

Why do ACEi's cause Pre-Renal AKI

Inhibit Ang2 which selectively constricts efferent arterioles

Oliguria is defined as

Less than 400mL / 24 hours

Muddy Brown Casts =

ATN

Management of Ischemic ATN

Treat underlying cause - Restore perfusion

FENa in Pre-Renal vs ATN

Less 1% in Pre-Renal; Greater than 1% in ATN

Timeframe of AKI

Rapid deterioration of kidney function \< 1 month

Hepatorenal syndrome results from what liver disease

Cirrhosis

UNa+ in Pre-Renal vs ATN

Less than 20 mEq/L in Pre-Renal; Greater than 25 mEq/L in ATN

How do you prevent Aminoglycoside toxicity

Once daily dosing; Minimize duration of tx

Impairment of GFR (AKI) leads to

Elevation of BUN/Creatinine, Accumulation of substances/drugs normally excreted by kidney

Inhibits normal lysosomal function in kidney

Aminoglycosides

3 Specific Types of Pre-Renal AKI

(1) Hepatorenal Syndrome; (2) RAS and Ang2 blockers/ACEi's; (3) Other drugs that impair autoregulation (NSAIDs)

2 causes of Post-renal AKI other than prostate

Malignancies, Neurogenic bladder

ACEi's and ARB's can cause ___ in patients with Bilateral RAS

Pre-Renal AKI

Decreased levels or inhibition of Ang2 impairs renal \_\_\_\_

Auto-Regulation (constriction of efferent arterioles in RAS)

Dx of Post-renal AKI

Foley catheter, US

Uosm in Pre-Renal vs ATN

\>500 mOsm/kg vs 300-350 mOsm/kg

As BP falls, kidneys are able to maintain BP well, unless \_\_

Ang2 blocker interferes with Efferent Arteriole vasoconstriction (impaired autoregulation)

Urine output in AKI

Sometime decr, but not always

Hyaline casts are seen in what type of kidney injury

Pre-renal AKI

Most accurate test for Pre-Renal AKI

Fractional excretion of Na - If less than 1%, suggestive of pre-renal

U/A in Pre-Renal vs ATN

Hyaline Casts vs Granular Casts

Creatinine change criteria for AKI

Greater than 0.5mg/dL incr or incr of 50% over baseline

Most important cause of Intra-renal AKI discussed

ATN

Pre-Renal AKI is due to insufficiency of

Renal perfusion

Urinalysis in Post-renal AKI

Unremarkable

How do NSAIDS cause Pre-Renal AKI

Block PG's that dilate the afferent arterioles