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Renal > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Gross indications of chronic renal disease

A
  • shrunken kidney

- finely granular surface

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2
Q

gross indication of renal infarction

A

-large “geographic” scar

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3
Q

gross manifestation of pylonephritis

A

-microabesses

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4
Q

gross appearance of hydronephrosis

A

-dilation of calyceal system (can be due to tumor, stone, etc)

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5
Q

key features of normal renal histology

A
  • glomeruli: thin open capillary loops
  • cortex: back to back tubules
  • interstitium: inapparent interstitium, cellularity
  • vessels with thin, unremarkable walls
  • mesangium: not expanded. smooth contour of normal thickness (with silver stain)
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6
Q

IHC linear vs granular

A
  • linear: anti-GBM in situ
  • granular: heterogenous antigen. Can be pre-formed complexes accumulating in glomeruli or can be in-situ against podocyte antigens
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7
Q

patterns of proliferation

A
  • crescentic
  • endocapillary: segmental or diffuse
  • mesangial
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8
Q

clinical correlate of effacement of foot processes

A

-proteinuria

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9
Q

filtration of proteins by glomerulous

A
  • small > large

- cationic&raquo_space; anionic

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10
Q

Normal urine protein

A
  • quantity: <150 mg/24 hr
  • Tamm-Horsfall protein:secreted by the epithelium of the TAL. found in normal urine
  • albumin and beta2 microglobulin (mostly retained but present at such high levels in the blood that some filters through)
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11
Q

general categories of proteinuria

A
  • abnormal glomerular filter (increased albumin, transferrin, IgG)
  • PT dysfunction (decreased re-absorption of filtered protein –> < 3g/24h, normal urine dipstick (only measures albumin)
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12
Q

Nephritic syndrome

A
  • clinical presentation of INFLAMMATORY glomerulonephritis
  • microscopic hematuria, proteinuria, HTN, edema
  • Dx: urinalysis is KEY. RBCs + protein!!
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13
Q

How to distinguish RBC cast from WC cast

A

presence/absence of nuclei!

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14
Q

Nephrotic Syndrome (def, pres, complications, classification)

A
  • clinical presentation of non-inflammatory glomerulopathy/chronic renal failure
  • proteinuria (>3.5 g/24h), hypoproteinemia, edema, hyperlipidemia (liver working overdrive to replace protein lost in urine)
  • complications: edema, hypercoagulability, infection
  • classifications: primary (only kidney involved, often idiopathic), secondary (associated with known systemic disease)
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15
Q

Focal vs Diffuse renal biopsy

A

-less than or greater than 50% glomerular involvement

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16
Q

segmental vs global renal biopsy

A

-part or whole of glomerulus involved

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17
Q

Minimal change disease (histopath, etiology, natural Hx/Tx)

A
  • normal on light microscopy and IHC
  • diffuse foot process effacement on EM
  • etiology: primary unknown, secondary (NSAIDS, nesplasms)
  • Tx: Corticosteroids. High remission rate, but some pts are refractory.
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18
Q

Focal Segmental Glomerulosclerosis (histopath, etiology)

A
  • some parts (segmental) of some glomeruli (focal) have sclerosis. Segmental collapse with adhesions to Bowman’s capsule. evidence of podocyte injury and loss. Non-specific accumulation of IgM/C3 (probably just accumulating)
  • etiology: monogenetic mutx (cytoskeleton, slit diaphragm), accumulated injury to podocytes,
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19
Q

Podocyte Characteristics/response to injury

A
  • don’t renew: response to injury is death/loss –> reactive scarring (segmental sclerosis)
  • clinical correlates: proteinuria –> podocyturia –> reduced GFR
  • kinds of injury: age, toxins, free radicals, metabolic, immune complex, systemic HTN, genetic factors
  • age–> loss of podocytes –> ESKD
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20
Q

Membranous golmerulopathy (histopath, etiology, natural Hx/Tx)

A
  • normal glomerular cellularity, thickened glomerular capillary loops (silver stain shows accumulation/rattiness of basement membrane). IHC: heavy deposits of immune complexes (primary: Ig/C3; secondary: lots). EM: subepithelial electron-dense deposits. presence of additional subendothelial and/or mesangial deposits in secondary
  • etiology: secondary (infection, neoplasm, medications, rheumatologic diseases)
  • pathogenesis: subepithelial deposits. podocyte antigen, or “planted” antigen trapped in subepithelial space.
  • spontaneous remission (20%), proteinuria w/o decline in GFR (60%), progression (20%). Tx for progression: steroids, anti-B cell therapies
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21
Q

Common histopath injury pathway in inflammatory glomerulonephritis

A
  • capillary injury (wall damage)
  • Increase in cellularity in capillary tuft (“proliferation”)
  • “Acellular” crescent formation
  • “Cellular” crescent formation w/i Bowman’s space
  • Globally sclerotic glomerulus (irreversible loss of function)
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22
Q

categories of injury in inflammatory GN

A
  • antibody mediated: Ab against type IV colalgen. linear desposition of IgG on IHC. Goodpasture’s disease when lung and kidney involved.
  • immune complex: granular deposition of IgG/C3. many diseases (post-streptococcal GN,
  • mechanism X. Pauci-immune GN. Most commonly small-vessel vasculitis.
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23
Q

Rapidly progressive glomerulonephritis

A
  • clinical syndrome (not disease)
  • nephritic syndrome + subuacute rise in serum creatinine
  • need to intervene quickly! thorough Hx and biopsy.
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24
Q

DDx pulmonary-renal syndrome

A
  • Goodpasture’s (antibody mediated)
  • SLE (immune complex)
  • ANCA positive small vessel vasculitis (mechanism X)
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25
Q

Goodpasture’s

A
  • antibody mediated GN: linear IgG, no deposits on EM
  • anti-GBM serology
  • Tx: plasma exchange (if severe, immunosuppression, rituximab)
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26
Q

post-stretococcal GN

A
  • immune-complex GN: diffuse proliferative and exudative GN, granular deposits of IgG/C3. EM: large discrete sub-epithelial deposits (“humps”)
  • anti-streptolysin O serology.
  • Tx: supportive therapy
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27
Q

Lupus Nephritis

A
  • immune-complex GN: proliferative, infiltrative, necrotic. IHC: “full house”
  • clinical: RPGN
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28
Q

IgA nephropathy

A
  • clinical: slowly progressive nephritic syndrome. spontaneous waxing/waning, sometimes to ESRD
  • mesangial hypercellularity, focal crescents. IHC: IgA/C3 only, only in mesangial compartment.
29
Q

Pauci-immune glomerulonephritis

A
  • clinical: any tissue can be involved, in the kidney, RPGN.
  • acute inflamm changes in vessels. Focal crescents, segmental necrosis. IHC: negative Ig and complement, negative EM
  • ANCA positive
30
Q

Diabetic nephropathy

A
  • GN in type 1 and Type 2 DM
  • GBM thickening, mesangial expansion, glomerular sclerosis
  • clinical: albuminuria, if untreated, progressive chronic kidney disease
  • Natural History: (based on T1DM) 1. pre-nephropathy (clinically silent inc in GFR and enlarged kidney, thickened GBM) 2. incipient nephropathy (microalbuminuria, continued thickening of GBM and expansion of mesangial matrix) 3. Overt nephropathy (decline in GFR, increased albuminuria, microscopic hematuria, HTN, kidney shrinking/fibrosis, severe diffuse mesangial expansion, tubular hyelinosis/aneurysm) 4. Advanced nephropathy–nephrotic syndrome and renal failure (albuminuria/proteinuria worsens, HTN worsens, GFR declines toward end stage, increased fibrosis)
  • DDx: onset w/i 5 yrs of dx of diabetes, absence of albuminuria, active sediment, etc –> do a biopsy!
  • pathogenesis: not all hyperglycemia! Genetic risk. Environmental risk. Modifiable risk factors (hyperglycemia, hyperfiltration, HTN, obesity, smoking).
  • Tx: Don’t wait until Stage 3! Response to Tx varies. Screen with spot collection for persistent microalbuminuria (incipient nephropathy). aggressive BP control, ACEis, other risk factors.
31
Q

mediators of hyperglycemic damage in diabetic GN

A
  • Advance glycation end products (AGEs) –> fibrosis etc

- sorbitol formation by aldose reductase -> increased oxidative stress/inflammation

32
Q

hyperfiltration damage in diabetic GN

A
  • intra-golmerular HTN
  • main mech: local elevation of Angiotensin II –> constriction of efferent arteriole
  • ACE inhibitors can rescue local HTN and decrease proteinuria/scarring
  • ARBs delay progression of disease
33
Q

HTN damage in diabetic GN

A
  • vicious cycle: HTN Worsening renal function

- non-RAS HTN Tx (e.g. BBlocker) can improve kidney function/outcomes (moreso than glucose control!)

34
Q

TGF-beta and diabetic GN

A
  • hypothesized to mediate histologic features of DM GN
  • blockade in animals prevents some of the changes.
  • in humans: studies just starting.
35
Q

Acute Kidney injury (def, prognosis, classification, natural history

A
  • loss of renal fxn (declined GFR) hours-days
  • often reversible, but up to 50% mortality
  • class: prerenal causes (poor blood flow), intrinsic (tubulointerstitial or glomerulovascular), postrenal causes (obstruction). most common are prerenal or acute tubular injury.
  • Can repair –> full recovery, or –> ESRD, or somewhere in between
36
Q

Acute tubular necrosis/injury

A
  • most common form of intrinsic AKI
  • ischemic (extended prerenal failure, ACEIs, ARBS, NSAIDS or toxic
  • pathophys of ischemic ATN: paradoxical renal vasoconstriction in setting of ischemia. Impaired reabsorption of Na –> tubuloglomerular feedback. loss of polarity with reperfusion (naked basement membrane). inflammation
37
Q

urinary obstruction (result, imaging, effect on GFR, tubular effects

A
  • causes postrenal AKI.
  • generally need bilateral obstruction to see Sx
  • imaging: hydronephrosis
  • vasoconstriction –> dec GFR
  • acute: increase Na and H2O reabsorption (due to vasoconstriction. chronic: impaired Na+, impaired urinary concentration, RTA
  • if diagnosed/relieved, can have full recovery. if chronic, can lose function
38
Q

Urinalysis in AKI

A
  • prerenal: high spec gravity, generally bland sediment, few hyaline casts
  • intrinsic: ATN - granular or muddy brown casts, renal tubular epithelial cells/casts. GN - proteinuria/hematuria with dysmorphic RBCs/casts. AIN - RBCs, WBCs, casts
  • postrenal: bland sediment
39
Q

tubulointerstitial disease

A
  • diverse group of disease with multiple etiology
  • path: degenerative and reparative tubular epithelial changes, interstitial inflammation and sclerosis. spectrum/overlap between interstitial inflamm and tubular epithelium damage
40
Q

acute interstitial nephritis (path, causes

A
  • edema, lymphos, eosinophils, granulomas/syncytia, tubulitis (lymphos extravasating into tube)
  • causes: drugs! all kinds: NSAIDs, omeprazole, antibios, etc. hyperuricemia (chronic/acute), nephrocalcinosis, oxalate nephropathy, infection (pyelonephritis)
41
Q

causes of pyelonephritis

A
  • ascending infections (anatomic abnormalities)
  • analgesic abuse
  • hyperuricemia
  • sclerosis, stones, etc
42
Q

acute pyelonephritis path

A
  • intratubular and interstitial PMNs

- microabscesses if blood-born

43
Q

chronic pyelonephritis path

A
  • atrophic tubules (thyroidization)

- lymphos

44
Q

myeloma kidney path

A
  • cast with fracture line

- giant cells

45
Q

“Benign” Nephrosclerosis

A
  • clinical: longstanding mild to moderate HTN
  • gross: shrunken granular kidney w/ thinning of cortex
  • micro: chronic changes – hyaline arteriolosclerosis, patchy interstitial fibrosis and tubular atrophy, global glomerulosclerosis (hyalin changes in capillaries, sclerosis/fibrosis of Bowman’s space), intimal fibrosis in larger arteries
46
Q

malignant nephrosclerosis

A
  • clinical: malignant HTN (>130 Diastolic)
  • Gross: “flea bitten” kidney: petechiae
  • micro: fibrinoid necrosis of small vessels not hyalinosis (RBC fragments), hyperplastic arteriopathy (“onion skin”), glomerular collapse or necrosis, tubular hemorrhage,
47
Q

Scleroderma and kidney

A
  • kidney changes in 2/3 of pts
  • onionskin fibrointimal hyperplasia- similar to malignant HTN, fibrinoid necrosis of small arteries and arterioles.mucoid change (edema, first stage of fibrinoid necrosis
48
Q

Renal Artery stenosis

A
  • 2-4% of HTN pts (hyperperfusion –> RAS)
  • surgically corrected
  • gross: stenosis of main renal artery, goldblatt kidney (JG hyperplasia)
  • hist: atherosclerosis(plaque)/fibromuscular dyplasia (“string of beads”) (primary), tumors etc (secondary
49
Q

atheroemboli

A
  • plaque dislodged and embolic (surgery, cath, spontaneous)
  • renal failure acute or chronic
  • biopsy: “shadows” of cholesterol crystals + giant cells
50
Q

diffuse cortical necrosis

A
  • massive ischemic necrosis of cortex (large vessel lesion)
  • 2/2 obstetrical emergencies, sepsis, extensive surgery
  • sudden anuria; if bilateral fatal if untreated.
51
Q

sickle cell nephropathy

A
  • accelerated sickling in hypoxic renal medulla (increased viscocity, plugging of vessels)
  • hematuria, rarely proteinuria
  • path: papillary necrosis (small vessel lesion) in some cases, rare cases have MPGN
52
Q

thrombotic microangiopathies/coagulopathies

A
  • overlapping disorders with injury to endothelium/small vessels
  • -> aggregation of PLTs, damage to RBCs (schistocytes)
  • widespread PLT thrombosis of glom capillaries (fibrinoid w/ damaged RBCs)
  • HUS, TTP (fluctuating CNS abrnomalities), DIC, pre-eclampsia/eclampsia (gestational HTN and proteinuria–path: “bloodless glomeruli”)
53
Q

two main kinds of renovascular disease

A
  • athero (usually with smoking) – proximal/branch points

- fibromuscular (younger women) – more distal; “beads on a string”

54
Q

renovascular disease and HTN

A
  • HTN common
  • renovascular disease common
  • BUT HTN due to renovascular disease is a subset, and less common. ONLY present if correcting renovascular disease fixes HTN
55
Q

renovascular disease and smoking

A
  • due to widespread interaction of cigarettes and predilection to atherosclerosis, look for disease in other vascular beds
  • fixing stenosis can –> sudden vasodilation –> collapse of other diseased vasculature (e.g. carotids)
56
Q

unilateral renal vascular disease

A
  • activation of RAS by blocked kidney
  • other kidney excretes Na at first (making problem worse), then reaches steady state
  • RAS-dependent HTN. high renin activity!!
57
Q

bilateral renal vascular disease

A
  • activation of RAS –> impaired Na and water excretion
  • -> volume dependent HTN (unlike unilateral)–normal to low renin activity!!
  • if block RAS, will see no change in HTN. If give diuresis, then RAS blockade, see change.
58
Q

Tx renovascular disease

A
  • treat bp first (ACE/ARB)

- think carefully whether to do angioplasty (takes a lot of stenosis, hard to judge on 2D image).

59
Q

ischemic nephropathy

A

consequence of reduced vascular supply –> ongoing, progressive oxidative stress.

  • pulsatility of blood flow
  • determines who will/won’t benefit from angioplasty
60
Q

ADPKD (prevalence, pattern, presentation, associations, genetics and mechanism)

A
  • pretty common
  • AD pattern
  • 5-10% ESRD. 5-6th decade
  • cyst expansion –> abdominal mass, flank, back pain. Can rupture.
  • polyuria, hematuria, UTIs, nephrolithiasis.
  • not every nephron involved (normal gloms in between cysts)
  • cysts in other organs, aneurysms, MV prolapse
  • PKD1 (function unclear but involved in cilia), PKD2 (Ca Channel). “Two hits” necessary –> pres age and sparing of nephrons.
61
Q

ARPKD

A
  • “infantile”
  • oliguria and large kidneys
  • oligohydamnios, liver enlargement/fibrosis,
  • every nephron involved, dilated collecting ducts.
  • mutx PKDH1
62
Q

CNF

A
  • congenital nephrotic syndrome, Finnish type

- mutx in Nephrin –> dysfunctional slit diaphragm –> proteinuria

63
Q

Thin basement membrane nephropathy

A
  • inherited hematuria syndrome
  • AD
  • uniform thinning of GBM
  • type IV collagen mutx
64
Q

Alport’s syndrome

A
  • inherited hematuria syndrome
  • type IV collagen mutx
  • different patterns: XLD, AR, AD (rare)
  • hematuria –> proteinuria and declining GFR –> ESRD, hearing loss, ocular defects (anterior lenticonus)
  • variable thickening and thinning of GBM with “basket weave” pattern
  • with evolving disease, mesangial sclerosis, capillary thickening, FSGS, interstitial foam cells
  • Tx: supportive, transplant (problem: anti-collagen Abs –> Goodpasture’s)
65
Q

Nephroblastoma (Wilm’s tumo)

A
  • primary malignant tumor of cortex
  • pediatric
  • malignant embryonal neoplasm
  • three components (blastema, epithelium, stroma)
  • WT-1 mutation
66
Q

Renal Cell Carcinoma

A
  • primary malignant tumor of cortex
  • adult
  • risk: tobacco, heavy metal exposure, estrogen exposure
  • distinct types: clear cell, papillary, chromophobe. arise from different parts of nephron.
  • aggressive: mets quickly
  • Tx: surgery.
67
Q

urothelial carcinoma

A
  • tumor anywhere with urothelial lining: renal pelvis, ureter, bladder, urethra
  • adult: 6/7th decade 3:1 male
  • smoking
  • hist: papillary, flat. shed in urine
  • Tx: “superficial”–chemo. invasive (detruser)–cystectomy
68
Q

Von Hippel-Lindau Syndrome

A
  • AD familial cancer
  • multiple renal cysts and clear cell renal cell carcinoma
  • other tumors.
  • mutx in VHL –> increased expression of HiF –> hypoxia behavior

Renal (5 decks)

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