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RENAL > GLOMERULONEPHRITIS > Flashcards

GLOMERULONEPHRITIS Flashcards

1
Q

Normal interstitium?

A

NORMALLY, there should be VERY LITTLE visible interstitium –> in chronic kidney diseases, tubules atrophy so the interstitium becomes FAR more prevalent

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2
Q

What are trichrome stains good for?

A

Visualizing the INTERSTITIUM

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3
Q

Diffuse, focal, segmental, global

A

Diffuse = greater than 50% of ALL GLOMERULI are affected

Focal = LESS than 50% of all glomeruli affected

Segmental = only affect a PORTION of EACH glomerulus

Global = All of the glomerulus is affected

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4
Q

Four main presentations of glomerulonephritis?

A

NEPHRITIC syndrome

NEPHROTIC syndrome

Rapidly Progressive Glomerulonephritis

Asymptomatic Hematuria

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5
Q

Criteria for NEPHRITIC SYNDROME

A 
Mild-moderate proteinuria ( < 3.5 g/day)
Oliguria (output < 400 cc/day)
HEMATURIA
Hypertension
Edema

INFLAMMATION of the glomerular tuft

Due to SWELLING of the capillaries, there is DECREASED filtrate entering tubules –> oliguria

The swelling also DAMAGES VESSELS, causing blood and protein to leak into the urine –> PROTEINURIA, HEMATURIA (unique!)

Leakage of blood results in the formation of RBC CASTS

Retention of fluid results in INCREASED HYDROSTATIC PRESSURE in ALL VESSELS OF THE BODY –> EDEMA (oncotic not enough to counteract)

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6
Q

What are the main causes of NEPHRITIC?

A

DIFFUSE PROLIFERAIVE GLOMERULONEPHRITIS = POST-INFECTIOUS = POST-STREP GLOMERULO!!!!!

IgA Nephropathy (Berger’s) –> MOST COMMON WORLDWIDE

LUPUS NEPHRITIS (can present in every way though)

MEMBRANOPROLIFERATIVE (nephritic AND nephrotic)

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7
Q

Criteria for NEPHROTIC SYNDROME

A

Not really inflammatory

HALLMARK = HEAVY PROTEINURIA ( > 3.5g/day) and NO HEMATURIA

The proteinuria leads to HYPOALBUMINEMIA –> results in edema due to LACK OF ONCOTIC PRESSURE IN VASCULAR SPACE –> fluid rushes out of vessels (unopposed hydrostatic) –> SO, piss out a ton of protein, lose oncotic pressure, hydrostatic pushes fluid out –> EDEMA

HYPERLIPIDEMIA (liver compensates for low protein by cranking out more protein –> Apolipoprotein –> cholesterol increases!)

Again, HEAVY PROTEINURIA, EDEMA, HYPERLIPIDEMIA and NO HEMATURIA!

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8
Q

What are the typical causes of NEPHROTIC?

A

MM FAN (or MM FAD)

M - Membranous glomerulonephropathy
M - Miniminal Change DIsease

F = Focal Segmental GlomeruloSCLEROSIS
A = Amyloidosis
N/D = Nodular Sclerosis (via Diabetes)

And LUPUS which can cause everything

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9
Q

RAPIDLY PROGRESSING GLOMERULONEPHRITIS

A

Bad news!!! Renal function deteriorates RAPIDLY

50% of renal function will be lost within a 3 month period –> most other disorders are less progressive and take a long time to develop

HALLMARK = CRESCENT FORMATION!!!!!!! Can be named Crescentic Glomerulonephritis

Presents with RAPID destruction –> Nephritic with RED CELL CASTS

Crescent forms due to PROLIFERATION of the PARIETAL EPITHELIUM that line’s Bowman’s Capsule –> BM of the capsule prevents epithelium from growing outwards, so they have no choice but to grow towards the capillary tuft –> EVENTUALLY CAUSES THE TUFT TO SHRINK AND BECOME DAMAGED

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10
Q

What are the 3 types of Crescentic/RPGN?

A

Type 1 = GOODPASTURES SYNDROME = A disease of the LUNGS AND KIDNEYS!!!! Interstitial vessels of the lung and BM of the glomerulus are involved, causing HEMOPTYSIS (cough blood) and HEMATURIA/NEPHRITIC SYNDROME
Autoantibodies target the BM for the renal aspect –> there is a LINEAR STRING OF FLUORESCENCE (instead of granular)

Type 2 = A “hodgepodge” of all immune complex glomerulonephritities –> causes include DPGN, MPGN IgA, Lupus

Type 3 = ANCA associated –> Associated with POLYARTERITIS NODOSA, WEGENER’S –> NO IMMUNE COMPLEXES!!!!!!

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11
Q

Asymptomatic Hematuria

A

The fourth presentation –> Typically seen in YOUNG PATIENTS

Feel healthy, but RBCs end up in the urine

Prototype disease for this is IgA NEPHROPATHY –> deposition of IgA within the glomerulus

Kidney RETAINS NORMAL FUNCTION

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12
Q

What are the three cell types that swell in glomerulonephritis?

A

ENDOTHELIAL – Blood Vessels

EPITHELIAL – Podocytes (also called VISCERAL EPITHELIUM)

MESANGIAL

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13
Q

Types of DEPOSITS

A

SubEPIthelial –> Associated with LUPUS (all of them), POST-INFECTIOUS (which is DPGN and Nephritic), and MEMBRANOUS GLOMERULONEPHRITIS (nephrotic)

SubENDOthelial –> MEMBRANOUS PROLIFERATIVE (nephritic)

WIthin the MESANGIUM –> IgA NEPHROPATHY likely

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14
Q

MINIMAL CHANGE DISEASE

A

NEPHROTIC

FUSED or OBLITERATED podocyte foot processes –> NO IMMUNE DEPOSITS!

Usually a disease of CHILDREN; Associated with HODGKINS in ADULTS –> night sweats, weight loss, lymphadenopathy

Flattening of foot processes, diffuse effacement, seen on EM

STEROID SENSITIVE

May progress to FSGS

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15
Q

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

A 
Focal = < 50% of glomeruli involved
Segmental = only part of each glomerulus
Sclerosis = Fibrosis of the mesangial matrix

NO IMMUNE COMPLEXES –> but, WILL see C3 and IgM on immunofluorescence

Patients in 2nd or 3rd decade, OFTEN PROGRESSES FROM MCD

**SECONDARY TO AIDS*** or heroin abuse or Sickle Cell

LM –> Trichrome shows FIBROSIS (blue) and SEGMENTALIZATION (not all of glomerulus affected)

WORSE than MCD –> steroids less successful –> AWFUL prognosis

40%!!!! Progress to ESRD within 10 years

HIGH rate of RECURRENCE in renal transplants

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16
Q

MEMBRANOUS GLOMERULONEPHROPATHY

A

NEPHROTIC

BM involved –> thickened with small, evenly spaced SUBEPITHELIAL deposits

Middle aged, ASSOCIATED WITH MALIGNANCY

Secondaryily from LUPUS, HEP B/C, Malignancy and NSAIDs

LM –> diffusely thickened capillary loop, normal cellularity, SPIKES on the membrane(?)

FINELY GRANULAR DEPOSITS OF IgG and C3 on IMMUNOFLUORESCENCE

EM –> REMARKABLY THICKENED BM; SUBEPITHELIAL DEPOSITS; Lack of “humps” so it’s not DPGN

Prognosis –> Steroids don’t do shit and this will PROBABLY PROGRESS TO ESRD

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17
Q

MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

A

BOTH NEPHRITIC/NEPHROTIC

MESANGIAL cell PROLIFERATION
Thickened BM
“Tram Track” appearance

YOUNG and MIDDLE-AGED

Proteinuria is primary finding, but proliferative causes HEMATURIA as well!!!! (anytime we have proliferation, RBCs, RBC casts, hematuria)

Primarily idiopathic (like the others), secondarily by INFECTION, ENDOCARDITIS, AUTOIMMUNE, HEPATITIS

Two types

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18
Q

Type I MPGN

A

Similar on LM and immunofluorescence

Classical COMPLEMENT PATHWAY IMMUNE COMPLEXES

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19
Q

Type II MPGN

A

Involves C3 NEPHRITIC FACTOR (alternate complement pathway)

AUTOANTIBODY – inhibits the enzymes that stop the alternate pathway (constant activation)

SUBENDOTHELIAL DEPOSITS

20
Q

Imaging of MPGN

A

Lots of CELLULARITY (proliferative!)

TRAM TRACK APPEARANCE of BM

Effacement of FOOT PROCESSES

SUBENDOTHELIAL deposits

Type II has SAUSAGE-LINK DEPOSITS on EM, linked by a thin BM

21
Q

What leads to Asymptomatic Hematuria (usually?)

A

IgA NEPHROPATHY

22
Q

Presentation of IgA Nephropathy

A

IgA Mesangial Deposition – normal capillary walls, normal BM - ONLY mesangium affected

Presents as ASYMPTOMATIC HEMATURIA –> high serum IgA –> Chronic, progressive course

Primarily idiopathic, secondary to LUPUS, IgA disease

LOTS of IgA seen in immunofluorescence

Imaging –> INCREASE CELLULARITY in mesangium, IgA immunofluorescence, Lots of cells on EM

MOST COMMON GLOMERULONEPHRITIS WORLDWIDE!!!!!!! High recurrence in transplants

LIKELY TO PROGRESS TO ESRD!!!!!!!!!!!

23
Q

LUPUS NEPHROPATHY

A

Can present in any way we discussed –> NEPHRITIC, NEPHROTIC, HEMATURIA

Glomerular IMMUNE DEPOSITS!!!!!!!! Classic LUPUS AUTOANTIBODIES ANA, APA

Six classes from WHO

I - Minimal mesangial
II - Mesangial proliferative
III - Focal Proliferative (mesangial prolif, sclerotic deposits, less than 50% glomeruli)
IV - Diffuse Proliferative
V - Membranous - thickened GBM, may combine with other classes
VI - ADVANCED SCLEROTIC –> 90% of glomeruli globally sclerotic without fxn

24
Q

Diabetes and Nephropathy

A

NODULAR SCLEROSING!!!!!!!!

This is a NEPHROTIC syndrome (high protein)

MOST COMMON CAUSE OF ESRD

Mesangial expansion, GBM thickened, vascular intimal thickening, NODULAR GLOMERULOSCLEROSIS = KIMMESTEIL WILSON LESIONS*

NO IMMUNE DEPOSITS

PAS +

25
Q

AMYLOIDOSIS

A

Systemic disease caused by a variety of PROTEINS (Nephrotic!) capable of AGGREGATING (all share a beta-pleated sheet)

These conditions lead to PROTEIN AGGREGATION IN THE GLOMERULI and can cause PROTEINURIA

Fixing the aggregation disorder is the first line treatment

CONGO-RED POSITIVE (diagnostic)

APPLE-GREEN DEPOSITS

FIBRILLARY DEPOSITS on EM

26
Q

All of the following can be typically associated with NEPHRITIC syndrome, except:

Membranoproliferative GN
Diffuse proliferative GN
IgA nephritis
Membranous GN
Lupus nephritis
A

MEMBRANOUS GLOMERULONEPHRITIS

27
Q

SubEPIthelial deposits are characteristic of ALL of the following, except:

Lupus nephritis
Membranoproliferative GN
Diffuse Proliferative GN
Membranous GN

A

MEMBRANOPROLIFERATIVE GN (Subendo)

28
Q

SubENDOthelial deposits are a HALLMARK of which of the following?

Diffuse Proliferative
Membranoproliferative
IgA Nephritis
Membranous GN
FSGS
A

MEMBRANOPROLIFERATIVE GN

29
Q

HUMP-LIKE Deposits?

A

DIFFUSE PROLIFERATIVE GN (Subepithelial)

30
Q

Pauci Immune ANCA associated GN typically represents:

Membranoproliferative
Diffuse Proliferative
Crescentic GN
Lupus
IgA Nephritis
A

CRESCENTIC (RPGN)

31
Q

Diagnostic criteria for MCD?

Mild hypercellularity and thickened BM
Mild tubular atrophy and interstitial fibrosis
Significant foot process fusion on EM
Mild positivity on immunofluorescence
All of the above
A

SIGNIFICANT FOOD PROCESS/PODOCYTE FUSION

32
Q

Glomerular Lesions in HIV typically includes

A

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

33
Q

C3 Nephritic Factor

A

TYPE 2 MEMBRANOPROLIFERATIVE

34
Q

Tubuloreticular lesions are associated with…

SLE
HIV
Hep B
Hep C
All of the above
A

ALL OF THE ABOVE

35
Q

Kimmelstiel-Wilson Lesions are characteristic of…

Diabetic Nephropathy
Membranoproliferative GN
Amyloidosis
Focal Segmental
Lupus
A

DIABETIC NEPHROPATHY

36
Q

What are the THREE causes of SUBEPITHELIAL deposits?

A

Membranous GN

Lupus

Post-infectious GN (DPGN)

37
Q

What Nephropathies have IMMUNE COMPLEXES?

A

LUPUS
POST-INFECTIOUS GLOMERULO (DPGN)
MEMBRANOUS
^^^^these 3 are subEPIthelial^^^^

MEMBRANOUS PROLIFERATIVE (subENDOthelial)

IgA NEPHROPATHY (Mesangial)

38
Q

Which LACK immune complexes?

A

DIABETES/NODULAR SCLEROSING

MINIMAL CHANGE DISEASE

FOCAL SEGMENTAL GLOMERULOSCLEROSIS (AIDS!)

and RAPIDLY PROGRESSIVE GN

39
Q

Most common Glomerulonephritis?

A

IgA! Likely to progress to ESRD

40
Q

Most common cause of ESRD?

A

Diabetes –> Progression of Nodular Sclerosing to ESRD

41
Q

Tram Tracks?

A

MEMBRANOPROLIFERATIVE

42
Q

HUMP-like deposits?

A

DPGN/POST-INFECTIOUS GN

43
Q

What are the crescents made of for RPGN?

A

Crescent = fibrin, plasma protein,
glom parietal cells, macs and lymphos

These CRUSH the glomeruli, rapid kidney failure!

44
Q

Which nephropathies involve multiple organ systems?

A

TYPE I RPGN – GOODPASTURES (lungs and kidneys)

Type III RPGN –> Associated with WEGENERS (Lungs, Sinuses, Kidneys)

45
Q

Which has LINEAR fluorescence?

A

GOODPASTURE’S

46
Q

Which is both NEPHRITIC and NEPHROTIC?

A

MEMBRANOPROLIFERATIVE GN

Proteinuria predominates, but since it’s PROLIFERATIVE, there will be hematuria

RENAL (9 decks)

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