Renal Pathology

Front 1

Adult polycystic kidney disease

Back 1

Asymptomatic until middle age. Renal insuficiency, hematuria, hypertension. Abdominal masses and flank pain. Renal failure. Associated with liver cysts, berry aneurysms, mitral prolapse.

Front 2

Nephritic syndrome

Back 2

Hematuria, hypertension, azotemia, oliguria, proteinuria <3.5g/day

Front 3

Nephrotic syndrome

Back 3

Proteinuria >3.5g/day, hypoalbuminemia, generalized edema, hyperlipidemia

Front 4

Acute poststreptococal glomerulonephritis light microscopy

Back 4

Hypercellular glomeruli with neutrophils, red cell casts in renal tubules

Front 5

Acute poststreptococal glomerulonephritis immunofluorescence

Back 5

Granular deposits of IgG, IgM and C3 throughout the glomerulus

Front 6

Acute poststreptococoal glomerulonephritis electron microscopy

Back 6

subepithelial humps immune complex deposits

Front 7

Pathogenesis of Goodpasture syndrome

Back 7

anti-GBM antibodies damage kidneys and lungs. Antigen is collagen type IV

Front 8

Clinical presentation of Goodpasture syndrome

Back 8

nephritic syndrome with hemoptysis. Most will develop RPGN

Front 9

Goodpasture syndrome electron microscopy

Back 9

GBM disruption

Front 10

Goodpasture syndrome immunofluorescence

Back 10

Smooth and linear pattern of IgG and C3 in the GBM

Front 11

Causes of RPGN

Back 11

Goodpasture, poststreptococal, SLE, Wegner

Front 12

RPGN light microscopy

Back 12

Crescent formation in Bowman's space (macrophages, fibrin parietal endothelial cells)

Front 13

RPGN immunofluorescence

Back 13

granular or linear deposits of Ig and complement

Front 14

RPGN electron microscopy

Back 14

GBM disruption and discontinuity

Front 15

IgA nephropathy (Berger disease)

Back 15

Most common cause of GN. Nephritic syndrome with recurrent hematuria. Associated with celiac sprue and Henoch-Schonlein purpura

Front 16

IgA nephropathy light microscopy

Back 16

Mesangial proliferation

Front 17

IgA nephropathy immunofluorescence

Back 17

Mesangial deposits of IgA and C3

Front 18

IgA nephropathy electron microscopy

Back 18

Mesangial immune complex deposits

Front 19

MPGN clinical features

Back 19

Nephiritic or nephrotic. Decreased C3. C3 nephritic factor antibody activates C3 convertase with degradation of C3

Front 20

MPGN light microscopy

Back 20

Mesangial rpoliferation with BM thickening and tram tracking (splitting of basemant membrane)

Front 21

MPGN immunofluorescence

Back 21

Granular pattern of C3 often with IgG C1q and C4

Front 22

MPGN electron microscopy

Back 22

subendothelial and mesangial immune complex deposits

Front 23

Alport syndrome

Back 23

X-linked defect in type 4 collagen characterized ny nephritis, hearing loss and ocular abnormalities. EM: alternating thickening and thinning of BM

Front 24

Membranous GN etiology

Back 24

85% idiopathic, penicillamine, HBV, HCV, SLE, DM

Front 25

Membranous GN ligh microscopy

Back 25

Diffuse membrane-like thickening of capillary walls, baseman membrane projection spikes

Front 26

Membranous GN immunofluorescence

Back 26

Granular and linear pattern of IgG and C3

Front 27

Membranous GN EM

Back 27

Subepithelial deposits, effacement of podocyte foot processes

Front 28

Minimal change disease

Back 28

Nephrotic syndrome in children 2-6 years. EM: effacement of epithelial foot processes. Rx.: corticosteroids

Front 29

Focal segmental glomerulosclerosis light microscopy

Back 29

Focal segmental sclerosis and hyalinization of glomeruli

Front 30

Focal segmental glomerulosclerosis IF

Back 30

IgM and C3 deposits in sclerotic segments

Front 31

Mention all nephritic syndrome pathologies

Back 31

Poststreptococal, Goodpasture, IgA nephropathy, RPGN, MPGN, Alport

Front 32

Mention all nephrotic syndrome pathologies

Back 32

MGN, minimal changee disease, focal segmental glomerulonephritis

Front 33

Features of chronic glomerulonephritis

Back 33

Renal failure, uremia, anemia, proteinuria, hypertension, azotemia, reduction of GFR, hypocalcemia (no vitamin D), hyperphosphatemia. Hyalinization of glomeruli, fibrosis, atrophy and lymphocytes

Front 34

Features of acute tubular necrosis

Back 34

Reversible injury. Oliguria, increased BUN and creatinine, metabolic acidosis and hyperkalemia

Front 35

Causes of ischemic acute tubular necrosis

Back 35

hemorrhage, severe renal vasoconstriction, hypotension, dehydration, shock

Front 36

Causes of nephrotoxic acute tubular necrosis

Back 36

polymyxin, methicillin, gentamicin, sulfonamides

Front 37

Clinical features of acute pyelonephritis

Back 37

E. coli, proteus, kleibsiella, enterobacter. Fever, chills, dysuria, frequency, urgency, costovertebral angle tenderness, pyuria, WBC casts

Front 38

Types of renal calculi

Back 38

Calcium oxalate (75%), struvite (asoociated with urea-splitting bacteria - proteus), uric acid (gout, leukimia, acid urine)

Front 39

Clinical features of renal calculi

Back 39

Unilateral colic pain, hematuria, obstruction, infection. Calcium stones are raddiopaque.

Front 40

Clinical features of renal cell carcinoma

Back 40

Cigarette smoke is risk factor. Hematuria, palpable mass and flank pain

Front 41

Renal cell carcinoma paraneoplastic syndromes

Back 41

Polycythemia (EPO), hypertension (renin), Cushing syndrome

Front 42

Wilms tumor

Back 42

Mutations in WT-1 and WT-2 suppressor genes. WAGR syndrome - Wilm's tumor, aniridia, genital anomalies, mental retardation