Unit 8 - 4 Pathology

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thick tubules are probbaly more proximle bc of brush border (left side of pic)

note how tubules are back to back; this is good; as you get disease they start to drop out and get farther apart

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mesangium; produce basement membrane matrix; support glomeruli;


podocytes are on the outside of the loops

notice symmetry; no fibrous deposits on one side vs the other

not cellularity, not a lot of touching between nuclei (if they were = hypercellular)

endothelial cells =inside of capillary loop
podocytes = outside of capillary loop

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mesangium = meso = middle, angium = blood vessels => supports blood vessels

endothelial cells inside vessel
podocyte cells outside vessel loops

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spikey parts = podocytes

mesangium next to capillary lumen which has blood cells in it

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two layers of basement membrane = lamina rare externa/interna

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glomerular slit diaphragm: deficiencies in nephrin or podocin = proteinuria bc these compounds are very important for holding back protein

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Non-collagenous disease

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IgG anti-NC1, which is a component of the basement membrane collagen

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azotemia

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accumulation of nitrogenous wastes

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increased BUN in GI bleeding

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rbc breakdown in gi tract

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increased BUN in increased protein intake

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protein breakdown in gi tract

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creatinine laboratory evaluation

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not much creatinine secreted into tubules (10%);

you can lose alot of kidney function 50-60% and still have normal creatinine

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BUN/Creatinine ratio

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10/1 Normal

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BUN:Cr >= 20:1

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Pre-renal azotemia likely; sluggish flow of circulation around tubules allows for more BUN resorption
Tubular secretion of creatinine persists blunting the marked rise serum creatinine (stone, clot, stenosis, low blood pressure)

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BUN: Cr = 10:1

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Something wrong in kidney because nothings working right so both BUN:Cr are not being reabsorbed preferentially

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BUN:Cr > 20:1

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early phase BUN:Cr 20:1 in early phase urea absorbed from sluggish urine flow

Later phase
BUN:Cr approximately 10:1, pressure from backup of urine can damage kidneys
This will then result in intrinsic disease

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foamy urine

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protein

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upper limit of 24 hour protein excretion in normal adults

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150mg

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which proteins are dipstick sensitive too

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only albumin; wont be sensitive to other proteins (benz-jones proteins for ex)

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dysmorphic rbc; rbc going through diseased kidneys

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Hematuria; intact rbc; indicates bleeding in kidney since it is not a rbc cast

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tubular cell cast; indicative of tubular casts

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granular cell casts; indicative of tubular diseaes

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uric acid crystals

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cystine crystals

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oxylate crystals; look like envelopes

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why cant you just look at urine volume to evaluate kidneys

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GFR-reabsorption = urine volume

BUT both could be low and thus still urinating normal volumes

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Memorize this chart

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a. global
b. segmental
c. diffuse

focal/mesangial

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poststreptococcal glomerular nephritis; big hump is pathonomonic

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Type I RPGN

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antiglomerular basement membrane antibody; linear deposition (IgG +/- C3); can go to lung and cause pulmonary hemorrhage

Goodpasture antigen = noncallagenous portion of the alpha 3 chain of type IV collagen

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Type I RPGN

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antiglomerular basement membrane antibody; linear deposition (IgG +/- C3); can go to lung and cause pulmonary hemorrhage

Goodpasture antigen = noncallagenous portion of the alpha 3 chain of type IV collagen

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Type IIII RPGN

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Pauci-immune

c-ANCA: Wegners (cytoplasmic staining)
p-ANCA: polyangitis

ANCA may direct against the MPO and PR3

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Crescents in RPGN; parietal epithelial cells proliferate and squeeze off glomerulus

fibrin proteins when spilled out into bowmans capsule promotes proliferation of parietal cells

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mc systemic causes of nephrotic syndrome

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diabetes, amyloidosis, SLE

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Spike and dome

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membranouS Spikes (membranous nephropathy)
IC deposit between podocytes; BM grows around it = spikes

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minimal change diease (lipod nephrosis)

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normal glomeruli on EM + nephrotic syndrome

effacement of foot processes

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focal segmental glomerulosclerosis

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Type I MPGN

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localization in glomerulus activates complment/alternative pathway

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Type II MPGN

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decreased levels of C3 w/ normal C4 (bc it snot involved in the classic)

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Membrano proliferative glomerulonephritis

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subendothelial IC with granular IF

basement membrane laid on top of IC deposits; IC deposition = granular

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Left: Type I: Subendothelial deposits, tram tracking

Right: Type II: Ribbon like deposits of electron dense material

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Where does IgA deposit

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Mesangium

IgA nephropathy

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Henoch-Schonlein Purpura

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vascular disease that results from immunological damage to the blood vessel walls

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differentiate henoch-schonlein purpura from IgA nephropathy

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HSP = lesions on butt + abdominal pain/vomiting, IgA affecting vessels in GI tract

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diabetic nephropathy pathogenesis

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NEG of GBM/capillary basement membrane -> increased permeability/thickening

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Kimmelstiel-Wilson Disease/DNP

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nofdulcar glomerular sclerosis; one of the ways in which diabetes will affect the kidneys; large balls of PAS positive material (christmas tree dz)

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Amyloidosis

giant tongue

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maybe add a line for how they look grossly

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autosomal dominant (adult polycystic disease

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expand out and affect entire functioning

mutation in ADPKD and PKD1/2 gene

lack of calcium signal causes abnormal growth signaling = cellular proliferation, apoptosis, interactions w ECM and secretory function of the epithelia

keep building cells around a tube

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autosomal recessive polycystic kidney disease; radial dilitation of collecting ducts

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also associated w biliary dsgenesis and portal tract fibrosis

gene mutation = PKHD1 gene -> messed up protein fibrocystin
its on chromosome 6

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nephrononphthisis; type of medullary cystic disease

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ar and ends in ESRD within the first 3 decades of life; consider this is young kids

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medullary cystic kidney disease vs nephronopthisis

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know nephronophthisis NPH1-6 gene mutations

MCKD1 and MCDK2 in medullary cystic disease

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mckd location

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hug corticomedullary region

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medullary sponge kidney

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dilated medulary and papillary collecting ducts which result in the medulla having a sponge like appearance; occur at tips of pyramids

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acquired (dialysis associated) cystic disease

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chronic renal failure (dialysis) associated with the development of renal cysts in cortex or medulla (seen anywhere)

renal cancer (seen in 7% of dialyzed pts seen for 10 yrs)

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simple cysts

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usually on cortex; translucent; smooth membrane; most asymptomatic

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urinary tract obstruction

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can occur anywhere

dysfunction in concentrating ability if you get to tubules; obstruction can eventually cause interstitial inflammation -> fibrosis, GFR may decline

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complications

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infection (stasis), stone formation, permanent renal atrophy

acute obstruction = renal colick

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urolithiasis

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increased conc. beyond soluility = precipitates = stones

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ammonium magnesium phosphate

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2nd mcc kidney stone; infection w urease-positive bugs (proteus vulgaris, staph, klebsiela); can form staghorn calculus

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cystine stones

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most often 2 to cystinuria; hexagonal shape. Rarely, may form cystine staghorn calculi

associated w genetic defects (cystinuria)

faintly radiopaque; tx w alkalnization of urine

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urolithiasis

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can lead to severe complications such as hydronephoriss and pyelonephritis; tx and prevent by encouraging fluid intake

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ureterovesciular junction stone pain radiation

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urinary uregency and frequency

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stone in lower part of ureter

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radiate to ipsilateral testicle and labium in women

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stone in upper part of ureter

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anterior radiation

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renal papillary adenoma (lots of little papilla; seen histologically as little islands)

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cortical tumors arising from the renal TUBULAR epithelium

histologically they are indistinguishable from low grade papillary renal cell adenocarcinoma

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skin manifestations of tuberous sclerosis

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shagreen patches in the lumbosacral region of patient + angiofibromas around nose + ash leaf macules (hypopigmentations) in a patient with tubule sclerosis

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oncocytoma

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mahogany brown surface

note large eosinophilic cells

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von hippel lindau syndrome association (VHL gene at 3p25)

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AD syndrome w renal cell carcinoma association

also cerebellar hemangioblastoma
retinal angiomas
pheochromocytoma
cysts in various organs

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VHL gene location

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3p25; its a tummor supressor gene

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variants of renal cell carcinoma

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clear cell carcinoma
papillary carcinoma

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clear cell carcinoma

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70-80% of RCC; many demonstrate loss of sequence on chromosome 3 (3p25); loss of VHL/tumor supressor gene

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papillary carcinoma

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Sporadic form (Trisomies 7, 16, 17)
Familia form (Trisomy 7) - chromosome 7 which encompasses the MET proto-oncogene

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chromophobe rcc prognosis

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excellent prognosis

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know this chart

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renal cell carcinoma; towards the top/pole of kidney; yellow = lots of lipids

a. clear cell type
b. papillary type
c chromophone

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note lots of blood vessels in rcc