path renal charts

8/12/2019 Path Renal Charts

1/7

Acute Nephritic

Syndrome

Nephrotic

Syndrome

Asymptomatic

Hematuria/

Protienuria

Rapidly

Progressive GN

Acute Renal

Failure

Chronic Renal

Failure

UT Nephrolithiasis

-bleeding

-classic post strep

-heavy

protienuria

-hypoalbunemia

-severe edema

-hyperlipidemia

-lipiduria

-hematuria

-RBC casts

-oliguria

-anuria

-azothemia

-

-uremia -pyelonephritis

-cystitis

-stones

-hematuria

General:

Nephrotic Syndromes

!inimal Change "isease

#$ipoid Nephrosis%

!em&ranous GN #!em&ranous

Nephropathy%

Focal Segmental Glomerular Sclerosis !em&ranoproli'erative GN

-CHILDRE !"C nephrotic

syndrome in #ids$

-$!: normal appearance o%

glomeruli

-(!: di%%use loss o% visceral

epith& %oot processes !%usion'

smeared$

-F: negative !there%ore() IC$

-mutations in nephrin

-pro*& tubule + lipids

-epithelial vacuolization

-,-cell cyto#ine

-) H,

-ELEC,I.E /R),IE0RI1

-corticosteroids(good /*

-possible ,-cell cyto#ine

protienuria

-2B" and Caps loose charge

-Bigger holes

-345 and 645s !"C nephrotic syndrome

in adults$-slo7 progressive

-subE/I,HELI1L

-di%%use thic#ening o% cap& 7all

-8ndy to LE and HE/ B' C

-resemble Heymann ephritis !2/334-

clathrin coated 9 antigen$

-"1Cscre7 cap& 7all

-$!: di%%use thic#ening o% 2B" !stu%%in the name$

-(!: subepith& depositsb7 2B"

spi#es ; domes

-F: granular !Ig2' C3$

-)-ELEC,I.E /R),IE0RI1

- don5t respond 7ell to corticosteroid r*

-longstanding%at embolism to lung

-CHILDRE

-name says all

-assc& 7 HI.

+ hematuria' H,

-)-ELEC,I.E /R),IE0RI1

-in


2/7

Nephritic Syndromes)

Acute Proli'erative Post

Strep GN

Crescentic GN #Rapidly

Progressive%

gA Nephropathy #*ergers% Hereditary Nephritis

-a#a: Di%%use /roli%erative

2

-CHILDRE !?-3$ mc-I,R1C1/

-hypocomplimentemia

-deposits o% Ig2 on 2B"

$!: +cellularity o% glom

tu%ts' crescents inside Bo7

Capsule

(!: IC in subendo and

mesangial@

subepi H0"/

F: Ig2' complement

granular

-gross hematuria

-smo#y bro7n urine

-mild edema

-%leabitten

-H, !bc dec 2ARretain

more %luids and + rennin$

-hypercell !mesangial'

endothl$

-crescents in "), o% the

glomeruli(and compression

o% glom

-,ypeI: anti-2B"

plasmapheresis bene%icial

+ in males

pulmonaryhemoptsis

-,ype II: IC-mediated

post-in%ections

LE' Ig1

granular IA

plasmaphesis don5t help

-,ype III: /auci-immune type

lac# o% IC or anti2B

1C1

$!: crescents' tu%t

hypercellularity

F: ?3 granular !IC' post

in%ectious' LE$

?3 linear !anti2B"$

?3 no deposits !=egners$

(!: IC any7here or no IC at

all !mostly subepithelial$

-proli%eration o% cells and

migration o% monos to B

!crescent$

-pronounced oligouria and

azothemia

-1l7ays have AIBRI in B

-1B to collagen I. and .

-Children and 1dults

-gross hematuria' bc o% respt

in%ection

-"), C)"") cause o%

glomerular disease ==

-deposition o% Ig1 in

mesangium

$!: normal to %ocal glom

(!: 1L=1 mesangial

deposits

F: granular(mesangial Ig1

-abnorm glycosylation o% Ig1

-+ingapore' Hong >ong

1L/)R, DR)"E

--nephritis

-nerve dea%ness' eye disorders

-hematuria 7hen young and

then 7hen olderrenal

%ailure

--lin#ed: alpha 6- ,ype I.

collagen

- 1D

-interstitial cells have %oamy

appearance

- +glomerulosclerosis

-bas#et-7eave appearance

Chronic GN

-end stage o% all other glom disease

7e discuss-scarring o% glom and B

-complete replacement or

hylanization o% glom


3/7

Tu&ules and nterstitium

Acute Pyelonephritis Chronic Pyelonephritis and

Re'lu+ Nephropathy

nterstitial Nephritis Acute Tu&ular Necrosis

-bacterial in%ection

-E&ColiFFFFF

-+common in %emales

-bc short urethra and close to

bo7el %lora

-ascending in%ection is "C

route o% in%ection

-i% there is obstruction

stasismultiplication o%

bacteria(and cant be %lushed

out 7 urineascend

-incompetent .esicourethral

ori%ice

-.0Rbact go to renal

pelvis

-#idney loo#s yello7y 7

abscesses

- result in /)E/HR)I

i% renal pelvis unable to drain

leads to ECR),IGI2

/1/ILI,I

maybe caused by analgesic

abuse

-interstitial in%lammation

-visible scarring

-8 types

,- Chronic .&structive

Pyelonephritis

-stasisin%ection

pyelonephritis

- Chronic Re'lu+0Assc-

Pyelonephritis #Re'lu+

Nephropathy%

-more common %orm-superimposion o% 0,I on

congenital vesiculoreteral

re%lu* and intrarenal re%lu*

-Hallmar#: scarring o% pelvis

or calyces(leading to

BL0,I2

1cute I

-edema?& Drug Induced:

-++ IgE 9 drug allergy

- ECR),IGI2

/1/ILI,I

maybe caused by analgesic

abuse

8& 1cute In%ection

-1cute pyelonephritis

3& "isc:

-IC in tubular basementmembranes

Chronic

-%ibrosis o% interstitium

?& Chronic /yelonephritis

-damage and scarring o%

parenchyma

-bacterial nature(same route

as acute type

8& /apillary ecrosis

-same stu%% as drug induced-%ind papilla sloughed o%% in

urine

-caused also by sic#le cell

diseases

3& Radiation ephritis

-radiationH,Chronic

I

& Bal#an ephritis

-shrun#en #idney

malignant tumors in pelvicmucosa

-caused by acute suppression

o% renal %*n&-types: ischemic' to*ic

!7orse$

-most common cause o% acute

renal %ailure

-reversible renal lesion

-lead to ischemic 1,' bc o%

trauma or septicemia

-also lead to nephroto*ic 1,

-intrarenal vasoconstriction

-tubulorrhe*is

-,amm Horse%all protein

-coagulation necrosis

-RBC' =BC casts

-) hematuria' )

protienuria

teps:

-?& nitiation: slight decline

in urine output and rise inblood B0

-8& !aintenance: 0rine op

%alls dramatically 64 to 44

mlday

-3& Recovery: increase in

urine volume(3L over %e7

days' but increase ris# o%

in%ection


4/7

1ascular Renal "iseases

*enign Nephrosclerosis !alignant HT and Nephrosclerosis Throm&otic !icroangiopathies

-bc o% benign H,

-1L=1 assc& 7 hyaline 1,H

-larger vessels(duplication o%

internal elastic lamina

and %ibrous thic#ening o% media

!%ibroelastic hyperplasia$

-%ibroid necrosis

-Hyperplastic 1,H

-++ plasma rennin-onion-s#in appearance

-includes H0 and ,//

-H0 %rom E&coli

$!: bloodless glom' narro7ing o%

gloms by amorphous material

(!: 7ide lamina rara

F: glom 7alls %illed 7 %ibrin

1ssc' 7 "al& H,' H0' Eclampsia

and /re' /ost partum renal %ailure'

1cute scleroderma

Cystic "iseases o' 2idney

Simple Cysts A" Polycystic 2idney "isease #A"U$T% AR Polycystic 2idney "isease

-%luid %illed

-con%ined to corte*

-can be prolonged-dialysis assc&

-multiple e*panding cysts o% both #idneys

-destroy parenchyma

-/>D-I genecell-matri* adhesion de%ect

-reJuires a 8ndsomatic hit

-Chrom ?Kp

-/>D-8 geneChrom

-#idney can get big

-thdecade

-%lan# pain

-heavy dragging sensation

-intermittent gross hematuria

-H,' 0,I and 0remiacause death

-r*: transplant

-Chrom K p

-present at birth

-sponge-li#e

-elongated channels at rt& 1ngles

-in%ants die %rom pulmonary or renal %ailure

-numerous cysts(in a spongy-li#e manner

-cysts have uni%orm cuboidal liningorigin %rom

collecting tubules

-cysts also in liver and lung

-proli%eration o% bile ducts

-Cirrhosis i% survive in%ancy


5/7

Urinary .ut'lo3 .&struction)

Renal Stones Hydronephrosis

-0rolithiasis

-composed o% Ca o*alate or "g 1mmonium /hosphate or 0ric acid

-all types have mucoprotien

urea splitting bacteria help cause this- by ma#ing environment more al#aline

-/roteus and taph

taghorn calculi(ta#e shape o% renal pelvis

-dilation o% renal pelvis and calices -- and atrophy o% parenchyma

?& Congenital

-atresia o% urethra

-renal art compressing urethra

-renal torsion

-#in#ing o% ureter

8& 1cJuired

-stones

-tumors

-in%lammation

-neurogenic

-normal pregnancy !mild and reversible$

Bilateral: )L 7hen obstruction is belo7 level o% ureters

-build up o% uremia(aborts the course o% the disease

-10RI1

-incomplete obstruction causes /)L0RI1

0nilateral: )L 7hen obstruction is at ureters or above


6/7

Systemic Renal Conditions)

"ia&etes !ellitus S$(

,- 1ascular Changes

-Hyaline 1,H o% B),H a%%erent and e%%erent arterioles

- Glomerular Changes

A- "i''use GlomSC

-hypercellularity

-bc mesangial proli%eration

-di%%use 2B" thic#ening

-hyalnized' scarred gloms

*- Nodular GlomSC #2immelstiel04ilson%

-+ suggestive o% D"

-Hylanized


7/7

Renal Tumors

Renal Cell Carcinoma 4ilms Tumor

-most malignant tumor

-derived %rom renal tubular epithelium

-high ris# in smo#ers and C1D"I0" handlers

-palpable mass-%ever' hematuria' %lan# pain !characteristic triad$

-hypercalcemia' H,' Cushingsbc o% tumor

,- Clear Cell Carcinoma

-"C

-assc& 7 von Hippel-Lindau !.HL$ disease

-1D

-predisposition to hemangioblastomas o%

cerebellum and retina

-Chrom 3p86l

-yello7 to orange grey

-invades renal vein

can go to I.C

R heart

- Papillary Renal Cell Carcinoma

-"E, proto-oncogene

-Chrom J3?

-"E, 9tyrosine #inase receptor(%or Heptocyte 2A

-bilateral' multiple

-necrosis' hemorrhage' cystic degeneration

5- Chromopho&e Renal Carcinoma

-stain dar#

-multiple losses o% entire chroms

-?'8'K'?4&?3'?'8?-H/)DI/L)ID

-tan-bro7n

-cell nu have clear halos o% cleared cytoplasm

-CHILDRE

-derived %rom mesoderm

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