Crrab 2: The Kidney

Front 1

–RBC casts/Hematuria
–Azotemia
–Oliguria

Back 1

Nephritic Syndrome

Front 2

–Hyperlipidemia
–Hypoalbuminemia
–Thromboembolism and infection risk increase

Back 2

Nephrotic Syndrome

Front 3

Edema can occur in both nephritic and nephritic syndromes due to DIFFERENT MECHANSIMS. How?

Back 3

Nephritic edema =increased Na+ retention

Nephrotic edema = hypoalbuminemia

Front 4

Beware of these false positives for proteinuria via urine dipstick.
–
–
–

Back 4

–alkaline urine
–gross hematuria
–dilute urine

Front 5

–Homogenous, diffuse, linear pattern
–Antigen of Noncollagenous domain of alpha-3 chain Type IV collagen
–In-situ deposition GBM, lung, lens

Back 5

Goodpasture Syndrome

Front 6

–Hypertension!
–PMNs do damage
–Proteinuria (<3.5g/day)

Back 6

Nephritic Syndrome

Front 7

–Cytokines do damage
–Fatty casts
–Proteinuria (>3.5g/day)

Back 7

Nephrotic Syndrome

Front 8

–Edema: Periorbital/peripheral
–LumpyBumpy Sub-EPIthelial deposits
–Low serum C3
–High ASO/antiDNAase B
–"smoky urine" (hematuria)

Back 8

Acute Post-streptococcal GLN

–Usually 2 wks post-URI
–Usually recover (kids)

Front 9

–Poor Prognosis!
–Nephritic
–Crescents w/Mø's+fibrin
– Goodpasture, Wegener, Microscopic Polyarteritis, Post-strep GLN, Berger, SLE

Back 9

Rapidly Progressive GlomeruloNephritis

RPGN = Crescentic GLN!

Front 10

Which disease can cause HYPERCOAGULABLE state? Nephritic or nephrotic, why?

Back 10

Nephrotic– hypercoaguable due to protein loss (anti-coagulative ptns III, ptn C, ptn S)

Front 11

Top Two most common causes of Nephrotic Syndrome in adults?

Back 11

1.) Focal Segmental GLN (HMS Heroin)

2.) Membranous GLN (acites, maltese crosses, cheerio capillaries, spike and dome)

Front 12

–SubEPIthelial spike & dome
–cheerio capillaries (diffuse thickening)
–due to Rxs (gold, captopril), solid tumors, HepB,HepC, SLE
–Acites, Maltese Crosses
–

Back 12

Membranous GLN

Front 13

–GBM polyanion loss; selective loss of albumin, but not Ig
–Assoc. w/ATOPY
–Diffuse foot process effacement
–NORMAL GLOMERULI
–Most common in kids

Back 13

Minimal Change Disease

(Lipoid Nephrosis)

Responds well to corticosteroids!

Front 14

–"HMS Heroin"
–Sclerosis of a portion of some gloms
–damage to visceral epithelial cells, hyalinization, foam cells
–Most COMMON adult nephrotic syndrome

Back 14

FSGS

Focal Segmental GlomeruloSclerosis

POOR PROGNOSIS! BAD NEWS BEARS!

HIV
Morbidly obese
Sickle cell trait
Heroin addiction

Front 15

–nephritic OR nephrotic
–Hep B OR Hep C
–tram track appearance (double contour)
–hypercellular gloms w/dense deposits

Back 15

Membrano-proliferative GLN

Type I = tram track
Type II = dense deposits

Front 16

There are THREE "recurrers" for nephropathy
1.)
2.)
3.)

Back 16

1.) FSGS
2.) Membrano-proliferative GLN
3.) IgA (Berger) Nephropathy

Front 17

–hematuria that occurs w/ & disappears w/ URIs
–proteinuria; worldwide commonest GLN
–Assoc w/celiac sprue, acute gastroenteritis

Back 17

IgA Nephropathy

DGX: mesangial deposition of IgA immune cmplxs gives diagnosis

Front 18

–X linked AD inheritance (M>F)
–Eye dxs, nerve Deafness, hematuria, ptnuria, Renal fail
–Defective GMB syn
–Persistance of fetal-like gloms w/ foam cells

Back 18

Alport Syndrome

Front 19

–Excellent Prognosis
–Fairly common
–Hematuria
–Thin GBM

Back 19

Thin Membrane Dx

(Benign Familial Hematuria)

Front 20

Two diseases most likely to develop CHRONIC GLN?

Back 20

1.) RPGN– "Crescentic Nephritis" or Rapidly Progressing Glomerular Nephritis
2.) FSGS– Focal Segmental Glomerular Sclerosis

Front 21

Another name of RPGN, Rapidly Progressing Glomerular Nephritis?

Back 21

Crescentic GLN

Front 22

A disease that causes loss of charge barrier or adhesion defects between epithelial cells

Back 22

Minimal Change disease

(has normal glomeruli...)

Front 23

"tram track" disease (type I) or "dense deposits" (type II; subendothelial)

Back 23

Membranoproliferative GLN

Front 24

–IgA is deposited in mesangium
–Purpuric skin lesions
–Arthralgia, Abd pain, bleeding
–Common in KIDS

Back 24

Henoch-Schonlein Purpura

Front 25

Two systemic IgA diseases that are on a continuum with each other?

Which one has worse prognosis?

Back 25

IgA Nephropathy (better) and Henoch-Schonlein Purpura (worse!)

Front 26

–initially increased GFR; glom hypertrophy
–GBM thickening
–Nodular glomerulosclerosis
–Efferent Arteriole Thickening

Back 26

Diabetic Nephropathy

Front 27

Clinical menifestations of Diabetic nephropathy? (name two)

Back 27

–microalbuminuria
–hypertension

–End Stage Renal Dx

Front 28

Most common cause of ARF?

(another three letter acronym)

Back 28

ATN- Acute Tubular Necrosis

Front 29

Name the two different flavors of ATN:
1.)
2.)

Where do they affect the nephron?

Back 29

1.) Ischemic Injury- patchy necrotic damage all over
2.) Toxic insult (drugs, dyes etc)- continuous PCT necrosis

BOTH will create casts that occlude the collecting tubule

Front 30

Disease has two forms:
•Acute form = PMNs (+/- Eos)
•Chronic form = fibrosis, atrophy

–Polyuria, Nocturia
– Metabolic acidosis results
–caused by drugs, ischemia, Pb+, severe pyelo, Multiple Myeloma

Back 30

Tubulointerstitial necrosis

(TIN)

Front 31

Only the upper and lower poles of the kidney are most commonly affected in this subset of pyelonephritis: _____________

Back 31

REFLUX PYELO (Vesicoureteral/Intrarenal)

caused by vesicoureteral and intrarenal (papillae) REFLUX!

Front 32

–Sudden CVA tenderness
–Fever, malaise
–Dysuria, polyuria
–Pregnant middle aged woman, or old man

Back 32

Acute Pyelonephritis


(OBSTRUCTION is the common denominator with the old man and pregger lady)

Front 33

–Fever, rash
–Hematuria, mild proteinuria
–Eosinophilia, few WBC in urine
–Normal gloms, interstitial LBT's

Back 33

Drug Induced AIN
–NSAIDS
–Thiazides
–Gold
–Captopril

BONUS: Is the disease dose realated?

Front 34

Two major causes of Papillary Necrosis?

Back 34

DIABETIC and ANALGESIC NEPHROPATHY

(Bonus: Sickle Cell Dx and severe Acute Pyelo can also cause papillary necrosis)

Front 35

– "flea bitten" kidney; petechial hemorrhages
–young black males, HTN
–HA, NV, Scotoma (visual dfx)
–onion-skinned arterioles

Back 35

Malignant Nephrosclerosis

75% 5yr survual rate w/anti-HTN Rx's

Front 36

–Sudden hematemesis, hematuria, MAHA, neuro dfx
–raw milk consumption
–Verocytotoxin

Back 36

Childhood HUS

(Hemolytic Uremic Syndrome)

Front 37

–Assoc with Bleomycin/Cyclosporin/Cisplatin, anti-phospolipid syndrome, typhoid, E.coli, Shigella, malignant HTN

Back 37

Adult HUS

Front 38

Form of HUS caused by "defective Factor K"

Back 38

Familial HUS (~50% lethal)

Front 39

–Protease defect that create Lg. vW factors (ADAMS-13); raises hell
–Fever, NEURO symptoms, purpura

Back 39

TTP

thrombotic thrombcytopenic purpura

Front 40

Two benign renal tumors:
1.)A__________
2.)O__________

Back 40

Angiomyolipoma

Oncocytoma

Front 41

–Autosomal dominant syn
–CNS (+retinal) hamartomas
–Cardiac/Pulm myomas
–Benign renal tumor composed of sm musc, b.v.'s, and fat

Back 41

Angiomyolipoma

Front 42

–Mahogany brown tumor
–Abundant mitos
–Always are excised even though they are benign (why?)

Back 42

Oncocytoma

BONUS: Oncocytomata are always removed because they clinically appear JUST LIKE Renal Cell Carcinoma.

Front 43

Most important risk factor for Renal Cell Carcinoma (Clear Cell Carcinoma)?

Back 43

SMOKING

Front 44

–vonHippel-Lindau gene deletion (chrom. 3)
–BRIGHT YELLOW TUMOR
–grows along renal vein, can invade IVC & heart.
–Mets to lung first then bone.
–Hematuria, flank pain, PALPABLE MASS, smokers
–Most common renal malignancy

Back 44

Renal Cell Carcinoma

AKA

Clear Cell Carcinoma

(technically CCC is a subtype of RCC, but we're only tested on CCC)