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96 Cards in this Set

  • Front
  • Back
A. 4 parts of kidneys
B. general rule about glomerular vs tubular/interstital
A. glomeruli, tubules, interstitium, blood vessels
B. glomerular = immuno mediated
- tubular/interstitial = toxic or infectious
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
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)
Stages of Azotemia
A. def
B. 3 types
C. end result
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
Stages of renal failure
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
Glomerular syndromes
A. nephritic syndrome
B. rapidly progressive glomerulonephritis
C. nephrotic syn
D. chronic renal failure
E. isolated urinary abnl
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
Glomerulus anatomy
- 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
Histologic alerations
A. hypercellularity
B. basement membrane thickening
C. hyalinosis and sclerosis
- cellular proliferation: mesangila/endothelial cells
- leukocytic infiltration
- formation of crescent: accum of cells of proliferating parietla epithelium & infiltrating leukocytes
Bamement membrane thickening
- deposition of electron-desne material (immune complexes). use PAS (periodic acid-Schiff)
- incr syn of protein components
Hyalinosis and sclerosis
- hyalinosis: accum of mateiral homogenous & eosinophilic by light microscopy due to endothelial or capillary wall injury
- sclerosis: accum extracellular collagenous matrix
A. diffse vs global
B. segmental vs focal
A. all glomeruli vs entire glomerulus
B. proportion of glomeruli vs part of each glomerlus
Pathogenesis of glomerular injury
- in situ formation of immune complex: antiGBM (linear pattern) vs Heymann (granular)
- circulating immune complex glomerulonephritis: Ig not specific but trapped. subepithelial deposit rare
A. def subendothelial deposits
B. def subepithelial depositis
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
Mediators of glomerular injury
- neutrophils, monoctes: b/c activation of complement
- platelets
- neutrophils, monoctes: b/c activation of complement
- platelets
Mechanism of Progression in glomerular d
A. rule about destruction
B. major histologic characteristics of prog renal damage
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 glom
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:
Nephritic syndrome
A. common sx
B. types
A. hematuria, red cell casts, azotemia, oliguria, HTN
B. poststreptococcal glomerulonephritis
- postinfectious lgomerulonephritis
Primary glomerulophritides
- 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
Primary glomerulophritides
- 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
Poststreptococcal glomerulonephritis
A, intiator
B. morphology
C. lab findings
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
Rapidly progressive (crescentic) glomerulonephrits
A. general sx
B. type I
C. type II
D. type III
E. common denominator
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
Rapidly progressive glomerulonephritis
A. morphology
B. clinical sx
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
Nephrotic syndrome
A. features
- massive proteinuria
- hypoalbuninemia
- generalize dema (Na, H20 retention aggrevates)
- hyperlipidemia, lipiduria
Nephrotic syndrome
A. name the types
- children: minimal change disease
- adule: membranous glomerulopathy
- all: focal segmental glomerulosclerosis
Membranous nephropathy
A. features
B. etiology
C. pathogenesis
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
Membranous nephropathy
A. morphology
B. sx
A. thickening by irreg dense immune complexes
B. proteinuria nonselective, not respond to corticosteroid
Minimal change disease
A. features
B. etiology
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
Minimal change disease
A. morphology dx
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
Focal segmental glomerulosclerosis
A. explain name
B. vs minimal change dz
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
Focal segmental glomerulosclerosis
A. patho
B. morpho
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
Membranoproliferative Glomerulonephritis
A. features
B. pathogenesis of type I MPGN
C. "" of type II MPGN
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)
Membranoproliferative glomerulonephritis
A. morphology
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
Isolated urinary abnormalities
- IgA nephropathy
- Alport syndrome
- Benign familial hematuria
IgA nephropathy (Berger dz)
A. features
B. pathogenesis
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
IgA nephropathy
A. morphology
B. normal course
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
Alport syndrome
A. categorize
B. features
C. morphology
D. sx
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
Thin basement membrane lesion
A. sx
B. morphology
A. asymptomatic hemoturia (found on urinalysis) = good prognosis
B. diffuse thinning of GBM
Chronic glomerulonephritis
A. etiology in most likely to least
B. morphology
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
Chronic glomerulonephritis
A. dialysis changes
B. uremic complications
C. sx
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
Glomerular lesions assoc with systemic dz
- 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)
Henoch-Schonlein purpura
A. manifestation
B. morphology
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
Diabetic nephropathy
A. pathogenesis
B. morphology
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
A. fibrillary glomerulonephritis
B. immunotactoid glomerulopathy
A. fibrillar deposits in mesangium/glomerular cap walls that resemble amyloid fiberils but do not stain Congo red
B. deposits ar emicrotubular
A. essential mixed cryoglobulinemia
B. multiple myeloma
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)
Tubular and Interstitial dz
A. ischemic/toxic tubular injury --> actue kidney injury/ failutre
B. inflamm rxn of tubutles and interstitutium (tubulointerstitial nephritis)
Acute kidney injury (acute tubular necrosis)
A. types
B. etiology
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
Acute Kidney injury
A. pathogenesis
insert picture
Acute kidney injry
A. morphology
B. sx
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)
Acute Kidney Injury
A. stages
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
Tubulointerstitial nephritis
A. acute vs chronic
B. sx
C. types
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
- analgesic nephropathy
- acute drug-induced interstitial nephritis
A. etiology
B. steps of ascending inxn
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)
Acute pyelonephritis
A. morphology
B. complications
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
Acute pyelonephritis
A. sx
- 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
Chronic pyelonephritis
A. feature
B. categories
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
Chronic pyelonephritis
A. morphology
B. sx
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
Tubulointerstital nephritis induced by drugs/toxins
A. Acute drug-induced interstitial nephritis
B. etiology
C. pathogenesis
D. sx
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
Tubulointersitital nephritis by drugs
A. analgesic nephropathy
B. patho
C. morpholgoy
D. sx
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
Tubulointerstitial diseases
A. name
- urate nephropaty
- hypercalcemia & nephrocalcinosis
- acute phosphate nephropathy
- light chain cast nephropathy (myeloma kidney)
- drug -induced
- pyelonephritis
Urate nephropathy
A. acute uric acid nephropathy
B. chronic urate nephropathy
C. nephrolithiasis
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
A. disorders assoc with this
B. earliest feature
A. hyperparathyroidism
- multiple myeloma
- vitamin D intoxication, metastatic cancer
B. mitochondrial distortion in tubular epithelial cell
- inability to concentrate urine
Acute phosphate nephropathy
A. not hypercalcemic, but excess phosphate load causes precipitation of calcium pohsphate
Myeloma kidney
A. factors of damage
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
Myeloma Nephropathy
A. morphology
B. cx
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
Vascular diz
A. name
- benign nephrosclerosis
- nephrosclerosis
- renal artery sstenosis
- thrombotic microangiopathies
- atherosclerotic ischemic renal dz
- sickle cell disease nephropathy
- atheroembolic renal dz
- renal infarcts
Benign nephrosclerosis
A. def
B. patho
C. sx
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
Benign nephrosclerosis
A. morphology
- loss of mass due to cortical scarring
- hyaline arteriolosclerosis = narrowing of lumens
- fibroelastic hyperplasia: medial hypertrophy, redup of elastic lamina, incr myofibroblastic tissue
Malignant hypertension/acc nephrosclerosis
A. patho
B. morphology
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
Malignant hypertension
A. sx
- systolic >200, diastolic > 120
- papilledema
- retinal hemorrhage
- encephalopathy
- headaches, nausea, vomiting, visual impairments
Renal artery stenosis
A. patho
B. morpho
C. sx
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
Thrombotic microangiopathies
A. features
B. vs DIC
C. two main forms
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
Thrombotic microangiopathies
A. pathogene
B. morphology of TTP/HUS
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
Sickle cell disease nephropathy
A. pathogene
- hematuria and dim concentrating ability b/c:
- hypertonic hypoxic of renal medulla --> dhydrate red cells * incr HbS concentration = sickling
Renal infarct
A. pathogene
B. source
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
Congenital anomalies
A. name
- 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
Cystic disease of kidney
A. name
- autosomal-dominant polycystic kindey
- autosomal-recessive polycystic kidney
- medullary sponge kidney
- nephronophthisis
- acquired (dialyisis-assoc) cystic dz
- simple cysts
Atuosomal dominant polycystic kidney dz
A. def
B. pathogene
A. AD: multiple expanding cyss of both kidneys that destroy renal parenchyma [unilateral=multicystic dysplasia]
B. insert
A. morphology
B. sx
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)
Autosomal recessive polycystic kidney dz
A. morphology
A. kidney enlarged but smooth appearance (cystic for ADPKD)
Cystic disease of renal medulla
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
Acquired (dialysis assoc) cystic dz
- coritcal and medullary cysts
- cysts clear fluid --> bleed to be hematuria
- oxalate crystals
urinary tract obsturcion
A. consequence
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
urinary tract obstruction
A. etiology
- congential anomalies
- urinary calculi
- tumors
- inflammation (prostatitis, urteritis, retroperitoneal fibr)
- slough papillae or blood clots
- pregnancy
- uterine prolapse, cystocele
- fxn disorders = neurogenic
Urinary tract obstruction
A. morphology
- if acute, GF reduced, mild dilation
- if chronic, prog dilation + interstitial inflam w/o infxn
- cortical tubular atrophy with diffuse intersitital fibrosis
Urinary tract obstruction sx
A. acue obstruction
B. unilateral complete
C bilateral partial obstruction
Dcom. plete bilateral
A. pain
B. asym. use ultrasonography
C. inabilit to concn urine, polyuria = pic of chornic tubulointerstitial nephritis
D. oliguira, anuria
A. types of calculi
B. pathogen
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
A. morphology
B. sx
A. unilateral likely in renal calyces/pelves
- staghorn calculi: branching structures rather discrete
B. ulceration, colic
- large stones, no enter ureter = hematuria
Tumors of kidney
A. benign
B. malignant
A. renal papillary adenoma, angiomylipoma, oncocytoma
B. renal cell carcinoma (clear cell/papillary/chromophobe)
Renal papillary adenoma
A. morphology
- small tumors in cortex
- histologic no differ from low-grae papillary renal cell adenocarcinoma = use size as cut-off
- tumor made of vessels, smoth muscle, fat
- assoc w/ tuberous sclerosis (epilepsy, MR, skin abnl)
- risk of spontaneuous hemorrhage
- epithelial tumor of large, eosinophilic cells with numerous mitochondria
- homogeneous, well encapsulated
Renal cell carcionoma
A. origin
B. risk factors
C. common growth feature
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
Clear cell carinoma
A. stat
B. pathology
C. morphology
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
Papillary carcinoma
A. features
B. pathogene
- 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
Chromophobe renal carcinoma
A. morphology
- cells w/ prominent cell membranes & pale eosinophilic cytoplasm (halo around nucleus)
- chromosome losses * hypodiploidy but good prognosis
Collecting duct (bellinin duct) carcinoma
A. pathogene
B. morphology
A. from collecting duct cells in medulla
- chromosomal losses & deletions
B. nests of malignant cells within prominent fibrotic stroma
Renal cell carcinoma
A. sx
- 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
Urothelial (transitional cell) carcinoma fo renal pelevis
- multiple involving pelvis, ureters, bladder
- infiltration of pelvis wall and calyces = poor prognosis