Pathoma Acute Renal Failure

Question 1

There are three divisions we make for acute renal failure. What are they?

Answer 1

Prerenal, postrenal, and intrarenal azotemia based on etiology

Question 2

What is azotemia?

Answer 2

Increase in nitrogenous waste products in the blood.

Question 3

What lab values indicate Azotemia

Answer 3

Elevated BUN and Cr

Question 4

Azotemia and ____ are hallmarks of acute renal failure

Answer 4

Oliguria

Question 5

Oliguria?

Answer 5

Decreased production of urine

Question 6

_______ is related to a prerenal azotemia etiology for renal failure

Answer 6

Decreased blood flow (think of this as a pre-kidney problem!)

Question 7

This would be an example of a post renal azotemia

Answer 7

Blockage in the ureter, caused backwards issues on the kindey

Question 8

Understandably, a decrease in blood flow to the kidney would also decrease this

Answer 8

GFR (less blood to glomerulus = less filtration)

Question 9

Azotemia will result in increased BUN and Cr no matter what. However, how can we distinguish between the three types?

Answer 9

The ratio.

BUN:CR>15 = prerenal, early postrenal
BUN:Cr<15 = Long standing post renal, Acute tubular necrosis

Question 10

Effect of prerenal azotemia on tubular function and how we can measure this

Answer 10

None.

FENa (Excretion) < 1%
Urine osm > 500

Question 11

Explain why in particular the ratio of BUN:Cr is >15 in a patient with prerenal acute renal failure

Answer 11

So you have your tube going to the kidney and it enters the glomerulus for filtration. BUN and Cr are both filtered. Normally, BUN is filtered by the blood, so it is taken out of the glomerulus, while the Cr will remain. This gives us a normal ration B:C of 15.

In pre-renal issues, the renin-angiotensin system will be activated, leading to aldosterone which will cause sodium to be reabsorbed, along with water, which results in further increases the BUN being taken out, causing the B:C to go > 15

Question 12

How does a post-renal obstruction cause a problem in the kidney and what do we see as a result?

Answer 12

Causes back pressure = reduced filtering = decreased GFR

Question 13

Wait…so in post renal we also have an increase in BUN:Cr…but aldosterone is not active. Why do we see this?

Answer 13

Back pressure forces more BUN out

Question 14

Early stage vs. Long-Standing Post-renal azotemia

Answer 14

Early: Exactly like prerenal with a B:Cr > 15 and a normal tubular function

Long-Standing: B:Cr < 15 along with opposite tubular values of FENa > 2% since you can’t reabsorb sodium and an inability to concentrate the urine leading to a urine osm < 500.

Question 15

Intrarenal causes of Acute Renal failure

Answer 15

1. Acute Tubular Necrosis

2. Acute interstitial Nephritis

Question 16

What is acute tubular necrosis and what does it do? How common is this?

Answer 16

Injury and necrosis of tubular epithelial cells, most common cause of ARF.

Necrotic epithelial cells then sluff off and plug tubules, obstruction decreases GFR.

Question 17

What kind of urine do we see with Acute Tubular Necrosis?

Answer 17

Brown, granular casts (meaning in the shape of the tubule since they built up first and hardened in the tubule before dislodging) in the urine because the dead sluffed off cells are coming out

Question 18

We see these tubular findings with ATN

Answer 18

Since we have a dysfunctional tube we will see a desreased reabsorption of sodium leading to an FENa > 2% as well as an inability to concentrate the urine, leading to a urine osm < 500

Question 19

Discuss the two etiologies of Acute Tubular Necrosis

Answer 19

Ischemic - Decreased blood supply leads to death of tubule epithelial

Nephrotoxic - Toxins cause the death of the cells

Question 20

In ischemic acute tubular necrosis, what portions are particularly susceptible?

Answer 20

Proximal tubule and medullary segment of thick ascending limb

Question 21

In nephrotoxic acute tubular necrosis, what portions are particularly susceptible?

Answer 21

Proximal tubule

Question 22

Causes of nephrotoxic issues

Answer 22

Aminoglycosides
Heavy metals
myoglobinuria in crush injuries
Ethylene glycol in antifreeze (we wil see oxylate crystals in the urine)
radiocontrast dye
Urate, which we see in tumor lysis syndrome

Question 23

So we know that with ATN we will see oliguria, brown granular casts and elevated BUN and Cr as expected of all of these conditions.

What is special about ATN?

Answer 23

Hyperkalemia with metabolic acidosis.

This is due to less excretion of K out of the tube as well as acid

Question 24

How do we deal with ATN?

Answer 24

Supportive dialysis to help electrolyte imbalances which can be fatal

Question 25

During ATN, we see this type of recovery pattern

Answer 25

2-3 weeks of oliguria before recovery because the tubular cells take time to reenter the cell cycle and regenerate

Question 26

What are the causes and what is the general problem with acute interstitial nephritis

Answer 26

Drug induced Hypersensitivity reaction of interstitium and tubules that results in intrarenal ARF.

Causes include NSAIDs, PCN and diuretics

Question 27

Just to clarify, when we say interstitial inflammation, what will we see on histology?

Answer 27

The space between the tubules will have inflammatory process

Question 28

Typical presentation of acute interstitial nephritis

Answer 28

Oliguria as usual, but also fever, rash days to weeks after starting the drug. Obviously will resolve when you stop taking the drug

Question 29

Acute interstitial nephritis can progress to this

Answer 29

Renal papillary necrosis

Question 30

____ are seen in the urine with acute interstitial nephritis

Answer 30

Eosinophils

Question 31

How does renal papillary necrosis present?

Answer 31

Gross hematuria and flank pain

Question 32

Causes of renal papillary necrosis

Answer 32

1. Chronic analgesic abuse
2. Diabetes Mellitus
3. SCT or SCD
4. Severe Acute pyelonephritis