Histopathology - Kidney

Question 1

Answer 1

Amyloidosis

 Congo red stain for amyloid shows up mainly in mesangial matrix of glomeruli and some in interstitium walls of the peritubular vessels.

o Congo will also stain fibrin orange
o To differentiate, another method is to use polarized microscope, under which amyloid

looks apple green (metachromasia)

 With H&E, amyloid appears eosinophilic

 Amyloid ß sheet structure is insoluble

 1st place of accumulation is the small vessels, e.g. in kidney capillaries

 Macroscopically: kidneys will appear swollen, and since blood flow is obstructed, the cortex will also be paler. There will be shrinkage eventually.

 Amyloid is an inert material, so it does not promote immune response.

 Ruins basement membrane, patient will have proteinuria.

Question 2

Answer 2

Disseminated Intravascular Coagulation w/ Fibrin Staining (Phosphotungstic acid haematoxylin/Weigert’s Elastic Stain)

 Vessels with RBC stain violet/purple (not pathological)

 Darker, grape purple is a stain for fibrin

 Glomerular capillaries are filled by fibrin and RBC

o Small thrombi

 Tubules in cortex lose their nuclear and cytoplasmic differentiation

 The pattern of fibrin indicates systemc coagulation, especially in smaller vessels  acute

renal failure

Question 3

Answer 3

Fat Embolization with Oil Red O stain (Sudan Red)

 Adipocytes in pyelon are stained by oil red O (frozen section)
o Bright red fat tissue occlusions in the glomerular capillaries are the fat embolization

 Orange in vessels = fat plaque accumulation

 Glomeruli also have orange staining, delineating capillaries.

 Fat embolization obstructs capillaries, leading to glomerular dysfunction

 Splinters of bone fracture or trauma to fat can also cause fat embolization

 Systemic fat embolization is not caused by fracture; fat will not reach the kidneys because it

remains in the lungs. Fat embolus originates from the arterial system.

Question 4

Answer 4

Systemic Lupus Erythrematosus

 We should count more than 10 glomeruli to know that we have a representative sample  Subendothelial spaces filled with immune complexes

 Increased number of mesangial cells
 Note lobulated glomeruli that are widened and in wire-loop formation

 Periglomerular fibrosis

 Sclerosis

 Dilated tubules

 With PAS, glomular lobulations and thickened wall are better seen

Question 5

Answer 5

Acute Rejection

 Totally sclerotized glomerulus seen

 Tubulitis = lymphocytic infiltration of tubules with mononuclear cells (nuclei larger than normal)

 Subendothelitis

 Macrophages

 Signs of organ rejection. There is Banff categorization for grading rejection

 Hyalinosis of vessels = thickening of arteriolar walls with hyaline

Question 6

Answer 6

Wilms Tumor, Nephroblastoma

 Most common malignant kidney tumor

 <5 years old; often huge by the time the tumor is diagnosed

 Kidney is of mesodermal origin

 No normal kidney tissue

 Biphasic pattern

 3 components:

o Light area represents stroma (mesenchymal component)

o Dark part is blastema

o Epithelial component (secondary epithelium) forms tubular, glomerular structure  Hematogenous spread by renal v. to liver and lungs

Question 7

Answer 7

Arteriosclerosis

 Nephrosclerosis arteriolosclerotica

 Macroscopically, the kidneys are evenly granulated bilaterally.

 Caused by hypertension and/or diabetes

 The kidney has 3 units. Damage to one causes secondary damage in the other 2.

o Tubulo-interstitium

o Blood vessels

o Glomeruli

 Here, the glomeruli look normal. The tubuli are slightly dilated with eosinophilic cylinders,

but mostly normal.

 The arteries have thick walls, narrow lumen

 Consequences of hypertension:

o Kidney failure
o Stroke
o Cardiac hypertrophy  IHD

 In the small arteries:
o Malignant hypertension causes

fibrinoid necrosis
o Benign hypertension causes hyaline

deposition.
o Both are eosinophilic and cannot be distinguished here.

 In medium-sized arteries:
o Malignant hypertension makes vessels hyperplastic o Benign hypertension causes fibroelastosis
o Cannot be distinguished here.

 Parenchyma has diffuse scarring
o Diminishes functional reverse of kidney

Question 8

Answer 8

Nephropathia diabetica – PAS

 In kidney pathology, H&E, immunofluorescence, PAS, and trichrome, IF (IgA, IgM, IgE) are used

 Electron microscopy is still used for nephropathology

 This slide is from a biopsy

 At least 10-12 glomeruli should be seen to give an overall

impression of a kidney. Here, we have more than this

 Normal capillary: tiny wall, small capillaries

 Glomerulus is lobulated, fine structure lost

o Fibrotic, sclerotic

o Thickened Bowman membrane  PAS material clumps

o PAS stains glycosylated proteins

 Swollen epithelial cells

 Mesangium enlarged, fused, nodular

o This is Kimmelstiel-Wilson Nephropathy. It is characteristic of DM in about 30%

 Totally fibrotic, afunctional glomeruli can be seen

 Also affects tubules and interstitium

 BM thicker

 This is a sign of chronic diabetic nephropathy

 Intima of large and small vessels are thickened, PAS+

 Atrophy of tubules: flattening of tall cells, loss of cuticle

 This is a secondary change to atherosclerosis

 Glucose in urine increases the risk of pyelonephritis.

Question 9

Answer 9

Rapidly Progressing Glomerulonephritis – PAS

 Atrophic, thick BM of tubules

 Glomerulus has bigger cells at border

 Structure of glomerulus compressed

 Some leukocytes seen

 “Crescent type” glomerulus

 Patient’s kidney function is destroyed

 Occurs in post-streptococcal infection

 Also occurs in Goodpasture syndrome and immune complex

 Different etiologies, same morphology

 Main problem is rupture of BM

 Causes nephritisprotein in tubule (Tamm Horsfall protein), proteinuria, HTN, azothemia

Question 10

Answer 10

End stage kidney disease – H&E

 Totally sclerotic glomeruli

 Irreversible

 Atrophic tubules with protein

 “Thyroidization” because of proteins

 Mononuclear cells in interstitium indicate chronic inflammation

 Narrow lumen of vessels indicates decreased blood circulation

 Cause cannot be determined from here.

Question 11

Answer 11

End Stage Kidney – Picro-Sirius stain

 Picro stains collagen IV

 Glomeruli and vessels are fibrotic

 RBC stain cellow

 Azothemia, hyperK+, no uremia

Question 12

Answer 12

Adenicarcinoma renis

 Top left rim with irregularities

 Lymphocytic infiltration

 Panglomerular membrane thickening

 Generally normal structure

 Below is fibrotic capsule

 Round nuclei in empty cytoplasm forming gland-like islands

o Clear-cell renal cancer (CCRC)
o Most common adenocarcinoma of kidney
o Looks like plant cells due to dissolved glycogen. The emptiness is an artifact. In

autopsy, it would be yellow.
o Behaves like malignant tumor because fine vessels allow metastasis o Small nucleilow grade renal cancer