Acute Tubular Necrosis

Question 1

Acute tubular necrosis is the most common cause of ___ ___

Answer 1

kidney failure

Question 2

pathophysiology of ATN:

ATN is the death of tubular cells. the cells of the PCT and TALOH are at high risk of getting injured, casuing cascade of __ __/__ that result in the loss of the ___ and death of tubular cell.

while these cells are dying, the blood vessels ___, causing ___ and thus further injury. this leaves the tubule denuted of healthy PCT cells.

Answer 2

TN is the death of tubular cells. the cells of the PCT and TALOH are at high risk of getting injured, casuing cascade of inflammatory mediators/cytokines that result in the loss of the microvilli and death of tubular cell.

while these cells are dying, the blood vessels constrict, causing ischemia and thus further injury. this leaves the tubule denuted of healthy PCT cells.

Question 4

Answer 4

right is aTN and left is normla

Question 5

how does GFR go down in ATN if its the PCT cells that are damaged? Shouldn’t the glomeulus still be able to filter stuff into the tubule before running into problems? 3 reasons.

Answer 5

1. in normal condiionts, the PCT are responble for major resorption of solutes. when killed off, the number of solutes and sodium rise markedly. These solutes are detected by the macular densa, which thinks that the EABV is HIGH. It then promotes the constriction of the AFFERENT ARTERIOLE, decreasing the GFR
2. another reason is due to backleak of fluid. Urine leaks out of the tubule. Normal, ultrafiltrate stays in the tubule, but when cells die, the lumen cannot contain the fluid– some leak out into the interstition.
3. Tubular obstruction by dead cells. results in a reduction of urine output.

Question 7

ATN is a diagnosis, but it can be caused by 2 broad groups of injury

Answer 7

1. ischemic– hypotension, sepsis/shock. peri-[pstiup hypotension, heart failure, drugs (causing physiological changes that reduce perfusion to kidneys or tubules)
2. toxic: exogenous (drgus including radiocontrast agents, aminoglycosides, cisplatin chemo) or endogenous toxins (hemoglobin or myoglobin, immunoglobin light chains, uric acid seen in tumor lysis syndrome).

Question 8

outline toxins that can lead to ATN

Answer 8

toxic: exogenous (drgus including radiocontrast agents, aminoglycosides, cisplatin chemo) or endogenous toxins (hemoglobin or myoglobin, immunoglobin light chains, uric acid seen in tumor lysis syndrome).

Question 9

Diagnosis of ATN is made in the lab. What signs?

Answer 9

• dropping gfr
• rising creatinine
• drop in urine output.
• main signs are in the urine and labs.
• granular “muddy brown casts” which are dead tubular cell casts.this is pathognominc for ATM.

Question 10

pathognomonic urine finding for ATN

Answer 10

• granular “muddy brown casts” which are dead tubular cell casts
• may also see epithlial cell casts– intact casts of tubular cells.
• urine microscopy is therefor diagnostic and prognostic of ATN

Question 11

Lab values (aside from urine microscopy) seen in loss of tubular clel function:

Random urine sodium > ___mmol/L

FeNa >__%

Urine osmolarity = __ osmolarity.

Answer 11

Random urine sodium > 40/L

FeNa >2%

Urine osmolarity = serum osmolarity.

Question 12

T/f the hallmark test to diagnose ATN is kidney biopsy

Answer 12

false. KB is rarely indicated. most are diagnosed in the lab.

Question 13

Question 14

pre-renal AKI and ischemic ATN look similar. Compare

Answer 14

both diseases contribute to a large fractino.

Pre-renal AKI, there is no histological damage of the tubules-. IN ATN, th etubules are dead or expressed.

Question 15

urinalysis findings in pre renal AKI vs acute tubular necrosis

Answer 15

pre renal does not have urinalysis findings.

ATN can show granular casts (tubualr death) or epithlial cell casts

Question 16

Urine sodium in pre renal AKI vs ATN

Answer 16

pre renal AKI: urine sodium will be low because reduced blood flow is sensed, and the body reabsorbs Na+ to keep water in.

ATN; urine sodium is high because there is PCT and LOH damage, so the cells responsbile for reabsorbing Na+ do not work properly.

• can be determined by FeNa or random urine sodium

Question 17

Note; even though pre renal AKI and ATN can be caused by the same thing, they manifest completely differentl

Question 18

PIMS acronym for ATN management

Answer 18

1. prevention
2. identify at risk (preexisting kidney disease and elderly)
3. monitor volume status (avoid water depletion)
4. stop nephrotoxic drugs

Question 19

What “AKI complications” are you supposed to monitor and address during the management of ATN?

Answer 19

• acidosis
• electrolyte abnomalities
• uremic symptoms

Question 20

clinical course of ATN

Answer 20

3 phases:

1. initiation phase; kidneys are getting injured
2. maintenance phase; tubular cells are dead and kidney fucntion is low. no sign of kidney recovery right now
3. recovery; kidney starts working again– either kidneys can repair or they can atrophy and die completely

Question 21

prognosis of ATN

Answer 21

• 95% of patients recover at 8 weeks
• 5-10% chronic kidney disease
• if you are on dialysis in hospital, you have a 40-60% chance of dying

Question 22

Answer 22