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44 Cards in this Set

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–RBC casts/Hematuria
–Azotemia
–Oliguria
Nephritic Syndrome
–Hyperlipidemia
–Hypoalbuminemia
–Thromboembolism and infection risk increase
Nephrotic Syndrome
Edema can occur in both nephritic and nephritic syndromes due to DIFFERENT MECHANSIMS. How?
Nephritic edema =increased Na+ retention

Nephrotic edema = hypoalbuminemia
Beware of these false positives for proteinuria via urine dipstick.


–alkaline urine
–gross hematuria
–dilute urine
–Homogenous, diffuse, linear pattern
–Antigen of Noncollagenous domain of alpha-3 chain Type IV collagen
–In-situ deposition GBM, lung, lens
Goodpasture Syndrome
–Hypertension!
–PMNs do damage
–Proteinuria (<3.5g/day)
Nephritic Syndrome
–Cytokines do damage
–Fatty casts
–Proteinuria (>3.5g/day)
Nephrotic Syndrome
–Edema: Periorbital/peripheral
–LumpyBumpy Sub-EPIthelial deposits
–Low serum C3
–High ASO/antiDNAase B
–"smoky urine" (hematuria)
Acute Post-streptococcal GLN

–Usually 2 wks post-URI
–Usually recover (kids)
–Poor Prognosis!
–Nephritic
–Crescents w/Mø's+fibrin
– Goodpasture, Wegener, Microscopic Polyarteritis, Post-strep GLN, Berger, SLE
Rapidly Progressive GlomeruloNephritis

RPGN = Crescentic GLN!
Which disease can cause HYPERCOAGULABLE state? Nephritic or nephrotic, why?
Nephrotic– hypercoaguable due to protein loss (anti-coagulative ptns III, ptn C, ptn S)
Top Two most common causes of Nephrotic Syndrome in adults?
1.) Focal Segmental GLN (HMS Heroin)

2.) Membranous GLN (acites, maltese crosses, cheerio capillaries, spike and dome)
–SubEPIthelial spike & dome
–cheerio capillaries (diffuse thickening)
–due to Rxs (gold, captopril), solid tumors, HepB,HepC, SLE
–Acites, Maltese Crosses
Membranous GLN
–GBM polyanion loss; selective loss of albumin, but not Ig
–Assoc. w/ATOPY
–Diffuse foot process effacement
–NORMAL GLOMERULI
–Most common in kids
Minimal Change Disease

(Lipoid Nephrosis)

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

Focal Segmental GlomeruloSclerosis

POOR PROGNOSIS! BAD NEWS BEARS!

HIV
Morbidly obese
Sickle cell trait
Heroin addiction
–nephritic OR nephrotic
–Hep B OR Hep C
–tram track appearance (double contour)
–hypercellular gloms w/dense deposits
Membrano-proliferative GLN

Type I = tram track
Type II = dense deposits
There are THREE "recurrers" for nephropathy
1.)
2.)
3.)
1.) FSGS
2.) Membrano-proliferative GLN
3.) IgA (Berger) Nephropathy
–hematuria that occurs w/ & disappears w/ URIs
–proteinuria; worldwide commonest GLN
–Assoc w/celiac sprue, acute gastroenteritis
IgA Nephropathy

DGX: mesangial deposition of IgA immune cmplxs gives diagnosis
–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
Alport Syndrome
–Excellent Prognosis
–Fairly common
–Hematuria
–Thin GBM
Thin Membrane Dx

(Benign Familial Hematuria)
Two diseases most likely to develop CHRONIC GLN?
1.) RPGN– "Crescentic Nephritis" or Rapidly Progressing Glomerular Nephritis
2.) FSGS– Focal Segmental Glomerular Sclerosis
Another name of RPGN, Rapidly Progressing Glomerular Nephritis?
Crescentic GLN
A disease that causes loss of charge barrier or adhesion defects between epithelial cells
Minimal Change disease

(has normal glomeruli...)
"tram track" disease (type I) or "dense deposits" (type II; subendothelial)
Membranoproliferative GLN
–IgA is deposited in mesangium
–Purpuric skin lesions
–Arthralgia, Abd pain, bleeding
–Common in KIDS
Henoch-Schonlein Purpura
Two systemic IgA diseases that are on a continuum with each other?

Which one has worse prognosis?
IgA Nephropathy (better) and Henoch-Schonlein Purpura (worse!)
–initially increased GFR; glom hypertrophy
–GBM thickening
–Nodular glomerulosclerosis
–Efferent Arteriole Thickening
Diabetic Nephropathy
Clinical menifestations of Diabetic nephropathy? (name two)
–microalbuminuria
–hypertension

–End Stage Renal Dx
Most common cause of ARF?

(another three letter acronym)
ATN- Acute Tubular Necrosis
Name the two different flavors of ATN:
1.)
2.)

Where do they affect the nephron?
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
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
Tubulointerstitial necrosis

(TIN)
Only the upper and lower poles of the kidney are most commonly affected in this subset of pyelonephritis: _____________
REFLUX PYELO (Vesicoureteral/Intrarenal)

caused by vesicoureteral and intrarenal (papillae) REFLUX!
–Sudden CVA tenderness
–Fever, malaise
–Dysuria, polyuria
–Pregnant middle aged woman, or old man
Acute Pyelonephritis


(OBSTRUCTION is the common denominator with the old man and pregger lady)
–Fever, rash
–Hematuria, mild proteinuria
–Eosinophilia, few WBC in urine
–Normal gloms, interstitial LBT's
Drug Induced AIN
–NSAIDS
–Thiazides
–Gold
–Captopril

BONUS: Is the disease dose realated?
Two major causes of Papillary Necrosis?
DIABETIC and ANALGESIC NEPHROPATHY

(Bonus: Sickle Cell Dx and severe Acute Pyelo can also cause papillary necrosis)
– "flea bitten" kidney; petechial hemorrhages
–young black males, HTN
–HA, NV, Scotoma (visual dfx)
–onion-skinned arterioles
Malignant Nephrosclerosis

75% 5yr survual rate w/anti-HTN Rx's
–Sudden hematemesis, hematuria, MAHA, neuro dfx
–raw milk consumption
–Verocytotoxin
Childhood HUS

(Hemolytic Uremic Syndrome)
–Assoc with Bleomycin/Cyclosporin/Cisplatin, anti-phospolipid syndrome, typhoid, E.coli, Shigella, malignant HTN
Adult HUS
Form of HUS caused by "defective Factor K"
Familial HUS (~50% lethal)
–Protease defect that create Lg. vW factors (ADAMS-13); raises hell
–Fever, NEURO symptoms, purpura
TTP

thrombotic thrombcytopenic purpura
Two benign renal tumors:
1.)A__________
2.)O__________
Angiomyolipoma

Oncocytoma
–Autosomal dominant syn
–CNS (+retinal) hamartomas
–Cardiac/Pulm myomas
–Benign renal tumor composed of sm musc, b.v.'s, and fat
Angiomyolipoma
–Mahogany brown tumor
–Abundant mitos
–Always are excised even though they are benign (why?)
Oncocytoma

BONUS: Oncocytomata are always removed because they clinically appear JUST LIKE Renal Cell Carcinoma.
Most important risk factor for Renal Cell Carcinoma (Clear Cell Carcinoma)?
SMOKING
–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
Renal Cell Carcinoma

AKA

Clear Cell Carcinoma

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