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Flashcards in Tubulointerstitial Disease 2 - Vo Deck (17)
1

One of what three criteria are needed to dx AKI?

a rise in serum creatinine of at least 0.3 mg/dL over a 48 hr period

A rise in serum creatinine more than 1.5X the baseline value within the 7 previous days

Urine volume less than 0.5 ml/Kg per hour for 6 hours

2

What is the one caveat of those three diagnostic criteria?

We do not diagnose AKI upon urine volume alone.

3

65 to 75% of AKI are due to what to types?

Prerenal diseae or ATN

4

What is the basical pathophysiology of all AKI?

an abrupt decrease in renal function. This can further be classified into prerenal, intrinsic or postreanl

5

What is the mechanism of prerenal AKI?

Systemic hypoperfusion. When the mean arterial pressure is reduced, activation of cardiac and arterial receptors increase sympathetic neutral tone and the release of both renin and ADH. The ensuing arteriolar and venular constriction and stimulation of cardiac function return to the systemic blood pressure and CO toward normal. Autoregulation at the glomerular level allows maintenance of GFR during mild to moderate hypoperfusion. However, with severe hypoperfusion, intense renal vasoconstriction can diminish both renal blood flow and GFR. However, glomeruli, tubules and interstitium are intact.

6

What are the causes of prerenal AKI?

True volume depletion from GI loss, Renal loss, skin or respiratory loss, or third space sequestration (crush injury)

Hypotension (from shock of post-tx of severe hypertension)

Edematous States: heart failure and cirrhosis can cause reductions of kidney perfusion.

Selective renal ischemia - from stenosis

Drugs - i.e. NSAIDs or ACEi or ARBs

7

How are prostaglandins messed up in drug use that can lead to AKI?

When you use NSAIDs, you block PG formation, which can already be reduced due to pre-existing syndromes. These vasodilate and help preserve renal reperfusion and glomerular filtration. So you don't want to inhibit their production or activity.

8

What is the mechanism of ATI/ATN?

prolonged or sever ischemia can cause it. Leads to necrosis with denuding of the epithelium and occlusion of the tubular lumen by casts and cells.

9

What other mechanism (not prolonged ischemia) can lead to ATN?

nephrotoxins

10

What are causes of ATN? 3 major ones

Renal ischemia, sepsis and nephrotoxins

11

What type of drug commonly can cause ATN?

aminoglycosides

12

WHen, after aminoglycoside use, will ATN present?

5-7 days

13

What features post aminoglycoside tx will people present with?

non-oliguria, due to a loss in renal concentrating ability
polyuria and hypomagnesemia
electrolyte abnormalities

14

How can heme pigments be introduced that can lead to ATN?

myoglobin from rhabdomyolysis and hemoglobin from hemolysis of rbcs

15

How can radiocontrast media lead to ATN?

it causes acute tubular necrosis related to vasoconstriction and cytotoxic effects from contrast.

16

What are common mechaniss of post-renal AKI?

bilateral ureteral obstruction of the bladder from malignancies

17

YOU HAVE TO KNOW HOW TO DIFFERENTIATE BETWEEN PRERENAL AND ATN AKI

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