The Kidneys

Front 1

A. 4 parts of kidneys
B. general rule about glomerular vs tubular/interstital

Back 1

A. glomeruli, tubules, interstitium, blood vessels
B. glomerular = immuno mediated
- tubular/interstitial = toxic or infectious

Front 2

Clinical manifestations of renal dz
A. Anephritic syndrome
B. rapidly progressive glomerulonephritis
C. nephrotic syn
D. asym hematuria/proteinuria
E. actue renal failure
F. chronic renal failure
G. renal tubular defects

Back 2

A. glomerular dz = acute onset, hematuria, HTN, lt protein
B. nephritic syn with rapid decline in GFR
C. gomerular: heavy proteinuria, edema, hyperlipidemia, hypoalbuminemia
D. manifestation of glomerular abnl
E. oliguria, anuria, recent onset azotemia
F. prolonged zx, uremia sx
G. polyuria, noctuira, electroly disorder (meta acidosis)

Front 3

Stages of Azotemia
A. def
B. 3 types
C. end result

Back 3

A. elevation of BUN and creatinine (due to decr GFR)
B. prerenal = hypoperfusion of kidney (hemorrhage, shock, CHF)
- postrenal: urine flow obstructed
C. failure excretion + metabolic/endocrine alteration resulting from renal damage

Front 4

Stages of renal failure

Back 4

1. dminished renal reserve: GFR 50% nl = asymptom
2. renal insuf: 20%-50% nl GFR = azotemia, anemia, HTN
3. chronic renal failure: <20-25% nl = edema, acidosis, hyperkalemia
4. endstage renal dz: GFR <5% = uremia

Front 5

Glomerular syndromes
A. nephritic syndrome
B. rapidly progressive glomerulonephritis
C. nephrotic syn
D. chronic renal failure
E. isolated urinary abnl

Back 5

A. hematuria, azotemia, oliguria, edema, variable protein
B. acute nephritis, proteinuria, actute renal failure
C. heav proteinuria, hypoalbumnemia, hyperlipidemia
D. azotemia --> uremia
E. glomerular hematuria, subnephrotic proteinemia

Front 6

Glomerulus anatomy

Back 6

- capillaries (line dby fenestrated endothelium) invested by two layers of epithelium
- viseral epi = intrinsic part of cap wall = podocyte
- parietal epi = on bowman capsule, lines urinary space
- glomerular tuft supported by mesangial cell = contractile, phagocytic

Front 7

Histologic alerations

Back 7

A. hypercellularity
B. basement membrane thickening
C. hyalinosis and sclerosis

Front 8

Hypercellularity

Back 8

- cellular proliferation: mesangila/endothelial cells
- leukocytic infiltration
- formation of crescent: accum of cells of proliferating parietla epithelium & infiltrating leukocytes

Front 9

Bamement membrane thickening

Back 9

- deposition of electron-desne material (immune complexes). use PAS (periodic acid-Schiff)
- incr syn of protein components

Front 10

Hyalinosis and sclerosis

Back 10

- hyalinosis: accum of mateiral homogenous & eosinophilic by light microscopy due to endothelial or capillary wall injury
- sclerosis: accum extracellular collagenous matrix

Front 11

A. diffse vs global
B. segmental vs focal

Back 11

A. all glomeruli vs entire glomerulus
B. proportion of glomeruli vs part of each glomerlus

Front 12

Pathogenesis of glomerular injury

Back 12

- in situ formation of immune complex: antiGBM (linear pattern) vs Heymann (granular)
- circulating immune complex glomerulonephritis: Ig not specific but trapped. subepithelial deposit rare
-

Front 13

A. def subendothelial deposits
B. def subepithelial depositis

Back 13

A. btw endothelial cells and GBM
- anionic macromolecules excluded from GBM
B. btw outer surface of GBM and odocytes
- highly cationic immunogens b/c cross GBM
C. neutral charge aacum in mesangium

Front 14

Mediators of glomerular injury

Back 14

- neutrophils, monoctes: b/c activation of complement
- platelets

Front 15

Mechanism of Progression in glomerular d
A. rule about destruction
B. major histologic characteristics of prog renal damage

Back 15

A. once GFR reduced to 30-50% of nl, progression ot EDRF CONSTANT
b. focal segmental glomerulosclerosis: initiated by adaptive change. compensatory hypertorphy of unaffect glomerli maintain renal fxn in diseased kidenys but proteinuria and segmental glomerulosclerosis develop
- tubulointersitial fibrosis:

Front 16

Nephritic syndrome
A. common sx
B. types

Back 16

A. hematuria, red cell casts, azotemia, oliguria, HTN
B. poststreptococcal glomerulonephritis
- postinfectious lgomerulonephritis

Front 17

Primary glomerulophritides

Back 17

- postinfectious glomerulonephritis: nephritic syn, immune complex mediated, subepithelial humps
- goodpasture: rapidly prog glmerulonphritis, Anti-GBM
- chornic glomerulonephritis: chornic renal failure, hyalinzed glomeruli
- membranous glomerulopathy: nephrotic, in situ immuen complex, subepithelial deposits

Front 18

Primary glomerulophritides

Back 18

- minimal change dz: nephrotic syn, loss of foot processes
- focal segmental glomerulosclerosis: nephrotic syn, loss of foot process, epithelial denudation
- membranoprolif glomerulonephrits (MPGN I: nephrotic syn, subendothelial deposits
- MPGN type II: chronic renal failure, dense depositis
- IgA nephropathy: recurrent hematuria/proteinuria, messangial dense deposits

Front 19

Poststreptococcal glomerulonephritis
A, intiator
B. morphology
C. lab findings

Back 19

A. after strp infxn of pharynx or skin (impetigo)
B. granular imune deposits in glomeruli = subepi humps
- enlarged hypercellular glomeruli: leukocyte infilrate, proliferation of endothelial and mesangial cells
C. antistrep Ig titters, decline in C3 complement
- child who develop fever, oliguria, hematuria 1-2 weeks after sore throat

Front 20

Rapidly progressive (crescentic) glomerulonephrits
A. general sx
B. type I
C. type II
D. type III
E. common denominator

Back 20

A. rapid, prog loss of renal fxn assoc w/ severe oliguria and nephritic syn
B. anti GM Ig-induced. Ig can cross-react with pulm alveolar BM = Goodpasture syn
C. immune complex deposition: grannular pattern
D. pauc-immune type: c-ANCA or p-ANCA
E. severe glomerular injury

Front 21

Rapidly progressive glomerulonephritis
A. morphology
B. clinical sx

Back 21

A. crescents obliterate Bowman space
- EM: ruptures in GBM that allows leukocytes, proteins to reach urinary space
B. hematuria, RBC casts, moderate proteinurai
- tx: plasmapheresis, steroids

Front 22

Nephrotic syndrome
A. features

Back 22

- massive proteinuria
- hypoalbuninemia
- generalize dema (Na, H20 retention aggrevates)
- hyperlipidemia, lipiduria

Front 23

Nephrotic syndrome
A. name the types

Back 23

- children: minimal change disease
- adule: membranous glomerulopathy
- all: focal segmental glomerulosclerosis

Front 24

Membranous nephropathy
A. features
B. etiology
C. pathogenesis

Back 24

A. diffuse thickening glomerular cap wall b/c accum electron-dense, Ig-containing deposits along subepithelial side of BM
B. drugs, malignant tumors, SLE, infxn
C. paucity of leukocyts but C5b-C9 damage cap wall

Front 25

Membranous nephropathy
A. morphology
B. sx

Back 25

A. thickening by irreg dense immune complexes
B. proteinuria nonselective, not respond to corticosteroid

Front 26

Minimal change disease
A. features
B. etiology

Back 26

A. diffuse effacement of foot processes (visceral epitheli)
- dramatic response to corticosteroids
B. assoc w/ resp infxn * prophylactic immunization
- atopic dz (eczema, rhinits)
- Hodgkin lymphoma

Front 27

Minimal change disease
A. morphology dx

Back 27

A. must see effacement + nl glomeruli by light microscopy
- b/c effacemetn in membranous and diabetic nephropathy
- lipoid nephrosis: proximal tbules laden with lipid, protein reabs from glomeruli

Front 28

Focal segmental glomerulosclerosis
A. explain name
B. vs minimal change dz

Back 28

A. lesion is sclerosis of some glomeruli = focal
- in affected glomeruli, portion of cap tuft = segmental
B. FSGS is proteinuria > nonselective
- poor response to corticosteroid
- prog to chronic kidney dz
- higher risk of hematuria, red GFR, HTN

Front 29

Focal segmental glomerulosclerosis
A. patho
B. morpho

Back 29

A. degen and focal disruption of visceral epithelium
- hyalinosis & sclerosis from entraping proteins
B. sclerotic seg: cap loops collapse, hyalinosis
- EM: sclerotic and non areas show diffuse effacement
- collapsing glomerulopathy: prolif and hypertrophy of glomerular visceral epithelial cells (assoc w/ HIV nephropathy), narrow cap lumen, retraction of tuft

Front 30

Membranoproliferative Glomerulonephritis
A. features
B. pathogenesis of type I MPGN
C. "" of type II MPGN

Back 30

A. alteration in GBM
- proliferation of glomerular cells & leukocyte infiltration
B. immune complexes in glomerulus & activation of calassical & alternative complement pathways
C. dense-deposit dz: ativationof alternative complement pathway (decr C3, nl Cq, C4)

Front 31

Membranoproliferative glomerulonephritis
A. morphology

Back 31

A. hypercellularity (mesangium + endocap proliferation)
- incr lobular appearance b/v proliferating mesangial
- "tram-track": duplic of BM result of subendothelial deposit
- type I: discrete subendothelial electron-dense deposit
- type II: intramembranous deposit = lamina densea of GBM into irreg ribbon-like electron-dense deposit

Front 32

Isolated urinary abnormalities

Back 32

- IgA nephropathy
- Alport syndrome
- Benign familial hematuria

Front 33

IgA nephropathy (Berger dz)
A. features
B. pathogenesis

Back 33

A. MC glomerulonephritis + freq cause of recurrent hematuraia
B. incr IgA syn in response to resp or GI exposure
- incr freq w/ gluten enteropathy
- incr freq w/ liver diz = defective hepatobiliary clearance
- HS purpura: overlapping features also cause dby IgA

Front 34

IgA nephropathy
A. morphology
B. normal course

Back 34

A. immunofluorescence: mesangial deposition of IgA
B. gross hematuria after infxn of resp or GI or urinary tract. hematuria subsides but return every few months

Front 35

Alport syndrome
A. categorize
B. features
C. morphology
D. sx

Back 35

A. hereditary nephritis (this dz is X-linked)
B. hematuria w/ prog to chronic renal failure accompanied by nerve deafness, eye disorder
C. basket-weave appearance = splitting, lamination of lamina densa
- immunohistochem: Ig to alpha3/4/5 collagen fail to stain glomerular & tubular BM
D. hematuria w/ red cell casts in ages 5-20

Front 36

Thin basement membrane lesion
A. sx
B. morphology

Back 36

A. asymptomatic hemoturia (found on urinalysis) = good prognosis
B. diffuse thinning of GBM

Front 37

Chronic glomerulonephritis
A. etiology in most likely to least
B. morphology

Back 37

A. crescentic GN, FSGS, MPGN, IgAN, membranous
B. kidneys contracted & granular cortical surfaces
- cortex thinned, incr peripelvic fat
- obliteration of glomeruli, arterial sclerosis, atrophy of tubules

Front 38

Chronic glomerulonephritis
A. dialysis changes
B. uremic complications
C. sx

Back 38

A. arterial intimal thicking
- deposition of calcium oxalate crystals in tubules
- acquired cystic dz
B. pericarditis, LV hypertrophy due to HTN
- sec hyperparathyroidism, renal osteodystrophy
- uremic pneumonitis
C. hypertensive, dominant sx cerebral/cardio

Front 39

Glomerular lesions assoc with systemic dz

Back 39

- Henoch Schonlein Purpura
- lupus nephritis
- bacterial endocarditis-assoc glomerulonephritis
- diabetic nephropathy
- amyloidosis
- fibrillary glomerulonephritis
- immunotactoid glomeruopathy
- Vascultides: goodpasture, wegener
- essential mixed cryoblobulinemia
- plasma cell dyscrasias (multiple myeloma)

Front 40

Henoch-Schonlein purpura
A. manifestation
B. morphology

Back 40

A. purpuric skin lesions on arms/egs
- abd pain, vomiting, intestinal bleeding
- nonmigratory arthralgia
- renal abnl: hematuria/nephritic/nephrotic
B. deposition of IgA in mesangial region

Front 41

Diabetic nephropathy
A. pathogenesis
B. morphology

Back 41

A. metabolic defect --> advanced glycosylation = thickened GBM & incr mesangial matrix
- hemodynamic effects due to glomerular hypertrophy
- both result in loss of podocytes
B. capillary BM thickening
- diffuse mesangial sclerosis
- nodular glomerulosclerosis
- papillary necrosis, hyalizing arteriolar sclerosis

Front 42

A. fibrillary glomerulonephritis
B. immunotactoid glomerulopathy

Back 42

A. fibrillar deposits in mesangium/glomerular cap walls that resemble amyloid fiberils but do not stain Congo red
B. deposits ar emicrotubular

Front 43

A. essential mixed cryoglobulinemia
B. multiple myeloma

Back 43

A. depostis of cryoglobulin (IgG-IgM complexes) assoc w/ MPGN type I
B. amyloidosis = light chain deposits in GBM
- distinct nodular glomerular lesion (diff from diabetic nodular glomerulosclerosis)

Front 44

Tubular and Interstitial dz

Back 44

A. ischemic/toxic tubular injury --> actue kidney injury/ failutre
B. inflamm rxn of tubutles and interstitutium (tubulointerstitial nephritis)

Front 45

Acute kidney injury (acute tubular necrosis)
A. types
B. etiology

Back 45

A. ischemic AKI: inadq blod flow --> hypotension & shock
- nephrotoxic AKI: drugs, contrast agents
B. ischemia (DIC, thrombosis, HUS, TTP, vasculitis)
- direct toxic injury to tubules (drugs)
- acute tubulointerstitial nephritis (drug hypersenstivity)
- urinary ostruction: tumors, prostatic hypertorphy

Front 46

Acute Kidney injury
A. pathogenesis

Back 46

insert picture

Front 47

Acute kidney injry
A. morphology
B. sx

Back 47

A. Ischemic AKI: tuular necrosis patchy, short lengths of tubules affected, straight segments of proximal tubules & ascending Henle's loop vulnerable
- toxic: extensive necrosis along PCT
- in both, luments of DCT and CD contain casts
- casts have Tamm--Horsfall protein (secreted by ascending thick limb & distal tubules)

Front 48

Acute Kidney Injury
A. stages

Back 48

1. initiation: slight decline in urine output, rise inBUN
2. maintenance: sustained decr in urine output
- salt & water overload, incr BUN, hyperkalemia
- metabolic acidosis, uremia
3. recovery phase: incr in ruine volume. tubules damaged so large H20, Na, K lost
- hypokalemia, incr vulnerability to infxn

Front 49

Tubulointerstitial nephritis
A. acute vs chronic
B. sx
C. types

Back 49

A. acute: rapid onset, interstitial edema w/ eosinophils & neutrophils
- chronic: interstitial fibrosis, tubular atrophy
B. absence of nephritic/nephrotic syn
- can't concen urine, polyuria, nocturia, salt wasting
- metabolic acidosis
C. peylonephritis, UTI
- REFLUX NEPHROPATHY
- analgesic nephropathy
- acute drug-induced interstitial nephritis

Front 50

Pyelonephritis
A. etiology
B. steps of ascending inxn

Back 50

A. bacteria: E.coli, proteus, Klebsiella, strep, patient's fecal flora (ascending infxn)
B. colonization of distal urethra --> urthra to bladder --> urinary tract obsturciton & stasis of urine --> vesicoureteral reflux or intrarenal reflux (urine to renal pelvis through open ducts at tips of papillae)

Front 51

Acute pyelonephritis
A. morphology
B. complications

Back 51

A. - patchy interstitial suppurative inflam (abcess)
- intratubular aggregates of neutrophils
- tubular necrosis (glomeruli resistant)
B. papillary necrosis (diabetics, urinary tract obstruction)
- pyonephrosis (obstruction --> sup exudate can't drain)
- perinephric abscess = sup inflam extend to nearby

Front 52

Acute pyelonephritis
A. sx

Back 52

- onset sudden w/ pain at CVA
- fever, malaise
- dysuria, frequency, urgency
- ppyuria (leukocyte in urine) but doesn't differentiate lower and upper urinary tract infection
- leukocyte casts (neutorphils) indicative for tubules

Front 53

Chronic pyelonephritis
A. feature
B. categories

Back 53

A. pathologic involve calyces and pelvis
B. reflux nephropathy: more common, early in childhood b/c superimposition of urinary infxn on congential VUReflux
- chornic obstructive pyelonephrits: recurrent infxn on obstructive lesion = bouts renal inflam/scarring

Front 54

Chronic pyelonephritis
A. morphology
B. sx

Back 54

A. contrast to chornic glomeruloneph, kidnesy irreg scarred
- coarse, discrete, corticomedullary scars over deformed calyces
- thyroidization: dilated tubules filled with colloid casts
- xanthogranulomatous pyelonephritis: accum of foamy macrophages w/ plasam cells, lym (assoc w/ Proteus)
B. back pain, fever, pyuria

Front 55

Tubulointerstital nephritis induced by drugs/toxins
A. Acute drug-induced interstitial nephritis
B. etiology
C. pathogenesis
D. sx

Back 55

B. sulfonamids, penicillins, rifampin, diuretics
C. IgE mediated (type I) hypersensitivity
D. fever, eosinophilia, rash, renal abnl
- rising serum creatinine
- acute renal failure w/ oliguria

Front 56

Tubulointersitital nephritis by drugs
A. analgesic nephropathy
B. patho
C. morpholgoy
D. sx

Back 56

B. papillary necoriss ---> cortical tubulinterstitial nephritis as consequence of impeded urine outflow
- acetaminophen deplete glutathione --> oxidative metabolites
- spirin inhibit vasodilatory effect of prostaglandin = papillae to ischemia
C. cotical atrophy overly necrotic papillae
- segments fo papillae sloughed and excreted
- columns of Bertin not affected
D. hyposthenuria (can't concen urine), renal stones
- gross hematouria, renal colic

Front 57

Tubulointerstitial diseases
A. name

Back 57

- urate nephropaty
- hypercalcemia & nephrocalcinosis
- acute phosphate nephropathy
- light chain cast nephropathy (myeloma kidney)
- drug -induced
- pyelonephritis

Front 58

Urate nephropathy
A. acute uric acid nephropathy
B. chronic urate nephropathy
C. nephrolithiasis

Back 58

A. in leukemias, lymphomas = precipitation of uric acid crystals
B. gouty nephropathy. urate crystal deposit of distal tubules & collecting ducts
- induce tophus = foreign-body giant cells
- renal arterial thickening common b/c HTN with gout
C. uric acid stones

Front 59

Nephrocalcinosis
A. disorders assoc with this
B. earliest feature

Back 59

A. hyperparathyroidism
- multiple myeloma
- vitamin D intoxication, metastatic cancer
B. mitochondrial distortion in tubular epithelial cell
- inability to concentrate urine

Front 60

Acute phosphate nephropathy

Back 60

A. not hypercalcemic, but excess phosphate load causes precipitation of calcium pohsphate

Front 61

Myeloma kidney
A. factors of damage

Back 61

A. bence jones proteinuria and cast nephorpathy
- Bence Jones protein directly toxic
- Bence jones combine w/ Tamm-Horsfall protein = tubular casts that obstruct tubular lumens
B. amyloidosis
C. light chain deposition dz: in GBM/mesangium = glomerulopathy, in tubular BM = tubulointerstitial
D. hypercalcemia, hyperureicemia
D.

Front 62

Myeloma Nephropathy
A. morphology
B. cx

Back 62

A. bence jones tubular casts = pink to blue amorphous masses
- casts surrounded by multinucleate giant cells
B. chronic renal failure
- Bence Jones proteinuria
- if non-light chain proteinuria = AL amyloidosis or lightchain depostiion dz

Front 63

Vascular diz
A. name

Back 63

- benign nephrosclerosis
- nephrosclerosis
- renal artery sstenosis
- thrombotic microangiopathies
- atherosclerotic ischemic renal dz
- sickle cell disease nephropathy
- atheroembolic renal dz
- renal infarcts

Front 64

Benign nephrosclerosis
A. def
B. patho
C. sx

Back 64

A. sclerosis of renal arterioles and small arteries
B. medial/intimal thickening in response to hemodyamic changes
- hyaline deposition in arterioles b/c proteins through injured endothelium
C. red in renal blood flow but GFR nl

Front 65

Benign nephrosclerosis
A. morphology

Back 65

- loss of mass due to cortical scarring
- hyaline arteriolosclerosis = narrowing of lumens
- fibroelastic hyperplasia: medial hypertrophy, redup of elastic lamina, incr myofibroblastic tissue

Front 66

Malignant hypertension/acc nephrosclerosis
A. patho
B. morphology

Back 66

A. vascular damage --> incr permeability to fibrinogen, platelet deposition = fibrinoid necrosis of arterioles
- kidney ischemic --> incr RAAS = cycle of vasoconsrict, ischemia
B. flea bitten appearance: pinpoint petechial
- fibrinoid necorsis of arterioles: acute even so no inflam = eosinophilic granular chang ein vessel wall
- onion-skinning intimal thickening due to SMC prolif

Front 67

Malignant hypertension
A. sx

Back 67

- systolic >200, diastolic > 120
- papilledema
- retinal hemorrhage
- encephalopathy
- headaches, nausea, vomiting, visual impairments

Front 68

Renal artery stenosis
A. patho
B. morpho
C. sx

Back 68

A. renin secretion by juxtaglomerular appartus
- sodium retention, endothelin, loss of nitric oxide
B. plaque concentrically placed, superimposed thrombosis
- fibromuscular dysplasia: fibromuscular thickening
C. resemble essential hypertension

Front 69

Thrombotic microangiopathies
A. features
B. vs DIC
C. two main forms

Back 69

A. microangiopathic hemolytic anemia
- thrombocytopenia, renal filure
- thrombotic lesions in capillaries
B. unlike DIC assoc w/ nl coagulation times
C. typical HUS: shiga like toxis (after Ecoli infxn) = sudden hematemesis, melena, oliguria, hematuria
- atypical HUS: acquired endothelial injury = antiphospholipid Ig, scleroderma, HTN, chemo
- TTP (thrombotic thrombocytopenic purpura): ADAMTS13 mutation that regulates vWF

Front 70

Thrombotic microangiopathies
A. pathogene
B. morphology of TTP/HUS

Back 70

A. endothelial injry --> platelet activation/aggregation
B. mesangiolysis, fibrinoid necrosis of wall
- glomeruli hypercelluar, thickening of cap walls assoc w/ splitting of BM
- onion skinning --> hypoperfusion & ischemic atrophy of parenchyma

Front 71

Sickle cell disease nephropathy
A. pathogene

Back 71

- hematuria and dim concentrating ability b/c:
- hypertonic hypoxic of renal medulla --> dhydrate red cells * incr HbS concentration = sickling

Front 72

Renal infarct
A. pathogene
B. source

Back 72

A. kidney favored sites b/c extensive blood flow and end organ nature of arterial blood supply
- limited collateral circ
B. winfarcts are white anemic type from mural thrombosis in left atriu adn ventricle

Front 73

Congenital anomalies
A. name

Back 73

- agenesis: incompatibel with life if bilateral. if unilateral, nl kidney enlarged -> progressive glomerular sclerosis
- hypoplasia: failure of kidney to nl size = no scars but red # renal lobes & pyramids
- ectopic kiney
- horseshoe kidney
- multicystic renal dysplasia: kidney enlarged, irregualr, multicystic. key = islands of undif mesenchyme (w/ cartilage) and immature collecting ducts

Front 74

Cystic disease of kidney
A. name

Back 74

- autosomal-dominant polycystic kindey
- autosomal-recessive polycystic kidney
- medullary sponge kidney
- nephronophthisis
- acquired (dialyisis-assoc) cystic dz
- simple cysts

Front 75

Atuosomal dominant polycystic kidney dz
A. def
B. pathogene

Back 75

A. AD: multiple expanding cyss of both kidneys that destroy renal parenchyma [unilateral=multicystic dysplasia]
B. insert

Front 76

ADPKD
A. morphology
B. sx

Back 76

A. enlarged kidney. functioning nephrons dispersed btw cysts
B. pts have cysts in liver too
- enlarged kidney = draggin sensation
- insidious hematuria --> prog chornic kidney dz (proteinuria, polyuria, HTN)

Front 77

Autosomal recessive polycystic kidney dz
A. morphology

Back 77

A. kidney enlarged but smooth appearance (cystic for ADPKD)
- CUT SECTION = SPONGLIKE APPEARANCE

Front 78

Cystic disease of renal medulla

Back 78

A. medullary sponge kidney: multiple cystic dilations of collecting ducts in meddula = hematuria, infxn, urinary claculi
B. nephronophthisis: cysts at corticomedullary jxn --> corical tubulointerstitial damage (glomeruli perserved)
- present w/ polyuria, polydipsia, sodium wasting

Front 79

Acquired (dialysis assoc) cystic dz

Back 79

- coritcal and medullary cysts
- cysts clear fluid --> bleed to be hematuria
- oxalate crystals

Front 80

urinary tract obsturcion
A. consequence

Back 80

A. incr risk of infxn and stone formation. unrelieved --> renal atrophy (hydronephrosis = dilation of renal pelvis/calyces)
- initial alterations tubular = impair concen ability
- later GFR fail
- obsturciton --> interstitial inflam rxn = fibrosis

Front 81

urinary tract obstruction
A. etiology

Back 81

- congential anomalies
- urinary calculi
- BPH
- tumors
- inflammation (prostatitis, urteritis, retroperitoneal fibr)
- slough papillae or blood clots
- pregnancy
- uterine prolapse, cystocele
- fxn disorders = neurogenic

Front 82

Urinary tract obstruction
A. morphology

Back 82

- if acute, GF reduced, mild dilation
- if chronic, prog dilation + interstitial inflam w/o infxn
- cortical tubular atrophy with diffuse intersitital fibrosis

Front 83

Urinary tract obstruction sx
A. acue obstruction
B. unilateral complete
C bilateral partial obstruction
Dcom. plete bilateral

Back 83

A. pain
B. asym. use ultrasonography
C. inabilit to concn urine, polyuria = pic of chornic tubulointerstitial nephritis
D. oliguira, anuria

Front 84

Urolithiasis
A. types of calculi
B. pathogen

Back 84

A. calcium oxalate: hyercalciuria, hypercalcemia, assoc w/ uric acid secretion
- triple stones/struvite stones (mg ammonium phosphate): assoc infxn proteus that convert urea to ammonia = alkaline (staghorn calculi)
- uric acid stones: gout, leukemia, acidic urine
- cystine: defects in rneal reabs of amino acids
B. urinary concn of stone constitutents exceeds solubility

Front 85

Urolithiasis
A. morphology
B. sx

Back 85

A. unilateral likely in renal calyces/pelves
- staghorn calculi: branching structures rather discrete
B. ulceration, colic
- large stones, no enter ureter = hematuria

Front 86

Tumors of kidney
A. benign
B. malignant

Back 86

A. renal papillary adenoma, angiomylipoma, oncocytoma
B. renal cell carcinoma (clear cell/papillary/chromophobe)

Front 87

Renal papillary adenoma
A. morphology

Back 87

- small tumors in cortex
- histologic no differ from low-grae papillary renal cell adenocarcinoma = use size as cut-off

Front 88

Angiomyolipoma

Back 88

- tumor made of vessels, smoth muscle, fat
- assoc w/ tuberous sclerosis (epilepsy, MR, skin abnl)
- risk of spontaneuous hemorrhage

Front 89

Oncocytoma

Back 89

- epithelial tumor of large, eosinophilic cells with numerous mitochondria
- homogeneous, well encapsulated

Front 90

Renal cell carcionoma
A. origin
B. risk factors
C. common growth feature

Back 90

A. tubular epithelium
B. tobacco, HTN, obsesity
- von hippel-lindau
- hereditary papillary carcionoma: AD, multiple bilateral tumors
C.invade renal vein & grow as solid column in vein to ICV

Front 91

Clear cell carinoma
A. stat
B. pathology
C. morphology

Back 91

A. most common type of adenocarcionoma
- cells with clear or grnaular cytoplasma and nonpapillary
B. VHL (3p) deletion -> can't target proteins for degradation
C. solitary unilateral, yellow b/c lipid accum

Front 92

Papillary carcinoma
A. features
B. pathogene

Back 92

- unlike clear cell, papillary multfocal in origin
- hemorrhagic, cystic & assoc dialysis
- cells arranged in papiillary formations
B. no assoc w/ 3p deletions but 7 trisomies = MET = proto-oncogene that is tyrosine kinase receptor for hepatocyte growth factor

Front 93

Chromophobe renal carcinoma
A. morphology

Back 93

- cells w/ prominent cell membranes & pale eosinophilic cytoplasm (halo around nucleus)
- chromosome losses * hypodiploidy but good prognosis

Front 94

Collecting duct (bellinin duct) carcinoma
A. pathogene
B. morphology

Back 94

A. from collecting duct cells in medulla
- chromosomal losses & deletions
B. nests of malignant cells within prominent fibrotic stroma

Front 95

Renal cell carcinoma
A. sx

Back 95

- classic triad: CVA, pain, palapable mass, hematuria (most reliable is hematuria)
- fever, wekaness, wt loss
- great mimics: polycythemia, hypercalcemia, HTN, hepatic dysfxn, Cushing syn, leukemoid rxn
- tendency to metastasiz widely before local signs

Front 96

Urothelial (transitional cell) carcinoma fo renal pelevis

Back 96

- multiple involving pelvis, ureters, bladder
- infiltration of pelvis wall and calyces = poor prognosis