Lecture 53 - 54: Acute Renal Failure + Path

Question 1

what are the three classes of causes of acute renal failure, what would be their fractional excretions ?

Answer 1

Pre Renal: FeNa < 1%
Renal: FeNa > 1%
Post Renal: Fena < 1%, then becomes greater than 1% (pathoma)

Question 2

how is kidney function measured? what is the relationship to GFR? what needs to be taken into account

Answer 2

Renal Function: measured via Cr

Cr inversely proportional to GFR

Small changes in Cr in otherwise healthy kidneys would indicate large changes in GFR

Question 3

classical laba and clinical indicators of AKI

Answer 3

Azotemia, Oliguria

Question 4

what is meant by pre-renal disease?

Answer 4

Decreased kidney perfusion, either due to true volume losses or relative volume losses (CHF, nephrotic syndrome, cirrhosis)

Question 5

classes of intrinsic renal disease that can lead to AKI

Answer 5

Acute Tubular Necrosis

Acute Interstitial nephritis

Acute GN (RPGNs) – Goodpastrures, Granulomatus Polyangitis, Post Strep GN, SLE

Microangiopathic Disease –TTP/HUS (congenital, infectious, idiopathic)

Question 6

Acute Tubular Necrosis

Causes:

Answer 6

causes:
Prolonged Ischemia –

Nephrotoxic:
1) Exogenous: radiocontrast, AmphoB, abx

2) Endogenous: Myoglobinuria, hemoglobinuria, light chain nephro

Question 7

ATN

UA:
General Pathology:
what difference might be observed between ischemic ATN and nephrotoxic ATN?
What is seen in the recovery phase?

Answer 7

UA: Muddy Brown Casts

Pathology – Luminal cell debris/necrosis; flattened epi

Nephrotoxic: more proximal tubules

Ischemic: all parts of the tubule

Recovery phase: mitotic figures, nuclear enlargement

Question 8

ATN: Treatment

Answer 8

Supportive therapy

remove the insult if nephrotoxic

Question 9

Acute Interstitial Nephritis –

types of causes:

Answer 9

Drug allergies – NSAIDs, Sulfa, Cipro, PCN, Thiazides, almost any drug

Infections – Bacterial Pyelonephritis

Allograft Rejection

Infiltrative – Sarcoid, lymphoma

Question 10

AIN - allergic
course:
Triad of sx:

Answer 10

Begins 15 days after initial drug exposure

Rash, Fever, Eos

Question 11

AIN - allergic

UA:

Bx pathology

Answer 11

UA: WBC Casts

Pathology: Parenchymal Mononuclear, eosinophilic infiltrates (not in the tubules)

Question 12

AIN: infectious 
what pathogens? 
Routes of infection? 
pathology? 
Can progress to...

Answer 12

bacterial or viral
bacterial: Gram Negative enterics (E Coli, Klebsiella, Enterobacter)

Routes: ascending

Pathology: Intratubular PMNs

Can progress to…Papillary necrosis and Perinephric Abscess

Question 13

AIN: treatment?

Answer 13

Supportive

Remove the Insult
Corticosteroids are sometimes used

Question 14

Acute GN (RPGN) –

Name 3 important causes:

what is seen on UA?

what is used to differentiate between the causes?

what serum assay is done to help make a diagnosis?

Answer 14

Goodpasture’s
Granulomatous Polyangitis (Wegener’s)
Post Strep GN

UA: RBC casts, Microhematuria

Differentiate between causes:
LM, IF, EM

Serum assay: ANCA

Question 15

Acute GN: Goodpasture’s

etiology
Presentation: 
Who get its: 
LM:
IF: 
Serum assay: 
Tx:

Answer 15

Anti GBM Antibodies; the collagen antigen is present along the entire surface of the BM and present in the alveolar BMs as well.

Presentation: Hematuria, Hemoptysis

Who: young adult males

LM: Crescentic GN

IF: Linear IgG deposits (appears smooth)

ANCA: none

Tx: plasmapheresis, pulse methylprednisone, cyclophosphamide

Question 16

Granulomatous Polyangitis (aka?)

Presenting Sx :
LM: 
IF: 
Serum assay: 
Tx:

Answer 16

sx: Pulm infiltrates, sinusitis, hemoptysis, epistaxis, renal failure

LM: Crescentic, segmental necrosis

IF: Pauci-immune; Negative IF

Serum Assay: 90% c-ANCA positive

Tx:
Corticosteroids + Cyclophosphamide

Methylpred
Rituximab
Plasmapheresis

Question 17

Post Strep GN

who:
when:
LM
IF
EM

Treatment

Answer 17

who: usually in kids
When: 2-3 weeks after GAS infection
LM: Enlarged Hypercellular Glomuerli

IF: “Lump bumpy” (granular)

EM: subepithelial “humps”

Treatment: Supportive

Question 18

Microangiopathic Disease: TTP and HUS

genetic mutation for each

other causes:

Pathologic Finding

Treatment

Answer 18

TTP: ADAMTS13 def
HUS: complement factor H def

Other causes:
Idiopathic
Infectious
Medications

Path: thrombi in small arteries

Treatment:

• Discontinue insult
• Plasma Exchange
• Supportive care
• Eculizubmab - complement blockers

Question 19

Infectious HUS:

• what is the common presentation
• possible pathogens

Answer 19

diarrhea

Shigella
Ecoli O157 H7

Question 20

Post renal disease –
what is the underlying cause?

diagnositic findings:

Answer 20

Post renal disease:
Obstruction of the tract

Dx: Enlarged palpable bladder, large Nodular prostate, Hydronephrosis on CT or US