AKI-Path

Question 1

early signs of kindey injury include _____, while later signs include?

Answer 1

increased creatinine, increased BUN, decreased GFR; oliguria and proteinuria

Question 2

causes of pre-renal acute kidney injury

Answer 2

trauma (septic shock), reduced perfusion, hypoxia

Question 3

causes of post-renal acute kidney injury

Answer 3

urinary tract obstruction (such as benign prostate hyperplasia)

Question 4

gross pathology of a “shock” kidney looks?

Answer 4

larger and lighter in color than a normal kidney (no filtration, no urine production)

Question 5

what blood nourishes the tubules?

Answer 5

from the glomerulus, which filter but do not use up oxygen (thus an injured glomerulus will result in hypoxic tubules)

Question 6

what are the four categories of intra-renal injury? (by location)

Answer 6

tubular causes, interstitial causes, vascular causes, glomerular causes

Question 7

what are the two types of tubular injury?

Answer 7

ATN, tubular obstruction

Question 8

what is the most common cause of acute kidney injury in adults?

Answer 8

ATN

Question 9

ATN is divided into what two pathogenic categories?

Answer 9

ischemic ATN and nephrogenic ATN

Question 10

causes of ischemic ATN

Answer 10

hemorrhage, shock, burns, dehydration, diarrhea, heart failure

Question 11

pathologic findings of ischemic ATN

Answer 11

dilated dysmorphic tubules and flattened or missing epithelial cells (without damage to basement membrane)

Question 12

why does the outside of the kidney turn white during ischemic ATN?

Answer 12

shunting of blood away from cortex

Question 13

causes of nephrogenic ATN

Answer 13

drugs (aminoglycosides), organic solvents (ethylene glycol, carbon tetrachloride), and poisons (paraquat)

Question 14

pathologic findings of nephrogenic ATN

Answer 14

tubule lumen filled with dead, necrotic epithelial cells that have been sloughed off (BM still intact)

Question 15

is ATN reversible?

Answer 15

YES

Question 16

tubular obstruction is also known as?

Answer 16

cast nephropathy

Question 17

causes of tubular obstruction

Answer 17

multiple myeloma, lymphoproliferative disorders

Question 18

how to detect light chain cast nephropathy

Answer 18

anti-kappa stain

Question 19

histo of a glomerulus overrun by massive influx of PMNs; can destroy architecture if not treated (fibrosis)

Answer 19

pyelonephritis

Question 20

gross pathology of pyelonephritis

Answer 20

pus bumps with darker hemorrhagic rim

Question 21

most common causes of allergic interstitial nephritis

Answer 21

NSAIDs, diuretics, ABX (beta lactams)

Question 22

histological findinds of allergic interstitial nephritis

Answer 22

lymphocytes and eosinophils in the interstitial space

Question 23

allergic interstitial nephritis is reversed by?

Answer 23

stopping the drug!

Question 24

name two major categories of vascular intra-renal injury

Answer 24

emboli (usually cholesterol) and thrombotic microangiopathy (HUS, TTP)

Question 25

this type of intra-renal injury may occur secondary to emboli or thrombi in small arteries of kidney

Answer 25

ischemic ATN

Question 26

what occurs in thrombotic microangiopathy

Answer 26

dz of small blood vessels that results in thrombosis of small arteries, thrombocytopenia, and hemolytic anemia (due to fragmentation during passage through vessel)

Question 27

a blood smear of TMA would show?

Answer 27

schistocytes and lack of platelets

Question 28

causes of TMA

Answer 28

idiopathic, infection-induced (VTEC, shigella), drug-induced, pregnancy-induced, autoimmune, hereditary

Question 29

histology of TMA artery

Answer 29

intimal expansion obliterates lumen

Question 30

what is the most common cause of acute kidney injury in children?

Answer 30

HUS; especially post-diarrheal HUS from VTEC

Question 31

pathogenesis of HUS

Answer 31

verotoxin injures endothelial cells, leading to narrowed lumen (and decreased blood flow, often with thrombi) and expanded subendothelial zone, which traps platelets and fragments RBCs

Question 32

triad of HUS

Answer 32

hemolytic anemia, thrombocytopenia, uremia (toxicity due to renal failure)

Question 33

severe ischemia may result in?

Answer 33

cortical necrosis

Question 34

signs of glomerular disease

Answer 34

asymptomatic hematuria, nephritic syndrome (blood and proteins in urine), asymptomatic proteinuria, and nephrotic syndrome (protein in urine)

Question 35

mnemonic for nephritic syndrome

Answer 35

PHAROAH

Question 36

pathology of glomerulonephritis

Answer 36

PMNs invade glomerulus, RBCs leak from broken basement membrane, resulting in RBCs and RBC casts in urine, proteinuria, and ATN from decreased flow to tubules

Question 37

causes of severe glomerulonephritis

Answer 37

post-infection (usually group A strep), immune-complex diseases (type 3 hypersensitivity)

Question 38

pathology of acute postinfectious glomerulonephritis

Answer 38

diffuse enlargement and hypercellularity of glomeruli, infiltration of PMNs and lymphocytes (usually resolves after several weeks)

Question 39

immunofluorescence of acute post-infectious glomerulonephritis will show?

Answer 39

granular peripheral reactions for IgG and C3 along BM, later only C3

Question 40

definition of crescentic glomerulonephritis

Answer 40

accumulation of epithelial cells and macrophages in Bowman’s space, resulting in a crescent-shaped structure (usually rapidly progressive)

Question 41

pathology of crescentic glomerulonephritis

Answer 41

minute ruptures of peripheral BM result in spilling of fibrin into Bowman’s space, which promotes lymphocyte and macrophage infiltration, which eventually strangle the glomerular capillaries