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medical kidney Flashcards

1
Q

Define uremia, azotemia, nephritic syndrome, nephrotic syndrome, rapidly progressive glomerulonephritis

A

Azotemia: elevation in BUN and Cr levels, due to a decreased glomerular filtration rate (can be pre-, renal, post-) i.e. failure of excretory functions

Uremia: azotemia with signs/symptoms and biochemical abnormalities. Not only failure of excretory functions but metabolic and endocrine alterations (eg. Uremic gastroenteritis, uremic fibrinous pericarditis)

Nephritic syndrome: due to glomerular disease, acute onset hematuria, mild proteinuria, HTN

Rapidly progressive glomerulonephritis: nephritic syndrome with rapid decline (hrs to days) in GFR Nephrotic syndrome: heavy proteinuria (>3.5 g/day), hypoalbuminemia, severe edema, hyperlipidemia, lipiduria

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2
Q

Name and define 5 clinical manifestations of renal disease

A

Asymptomatic hematuria/proteinuria: mild glomerular dysfunction

Acute renal failure: oliguria/anuria, recent azotemia. Can be caused by injury to any of the 4 compartments.

Chronic renal failure: prolonged uremia, end result of all kidney diseases

Renal tubular defects: polyuria, nocturia, electrolyte disorders. Inherited or acquired.

Urinary tract infection: bacteriuria/pyuria

Nephrolithiasis: pain, hematuria

Obstruction: secondary to lesion

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3
Q

Distinguish between diminished renal reserve, renal insufficiency, chronic renal failure, end-stage kidney

A

Diminshed renal reserve: GFR 50% of normal

Renal insufficiency: GFR 20-50% of normal, with azotemia. Often anemia, HTN. Illness can precipitate uremia.

Chronic renal failure: GFR less than 20-25% of normal. Kidneys cannot regulate volume/solutes and patients have edema, acidosis, hyperkalemia. Overt uremia can occur.

End-stage renal disease: GFR <5% of normal. Uremic.

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4
Q

Name 4 causes of renal papillary necrosis

A
  • Diabetes mellitus - Urinary tract obstruction - Acute pyelonephritis - Analgesic abuse
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5
Q

In SLE, what would the expected immunoglobulin deposition pattern be?

A
  • “Full house” - Granular IgA, IgG, IgM, C3 within glomeruli
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6
Q

What are histologic findings seen in cyclosporine and FK506 nephrotoxicity (transplant kidney pathology)?

A
  • Tubular isometric vacuolization - Hyaline arteriopathy - Acute thrombotic microangiopathy - Normal histology
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7
Q

What incites damage in myeloma cast nephropathy?

A
  • Immunoglobulin light chains
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8
Q

Name 4 entities that present with nephrotic syndrome:

A
  • Minimal change disease - FSGS - Membranous glomeruolpathy - Membranoproliferative glomerulonephritis
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9
Q

Hemolytic-uremic syndrome can demonstrate which finding within glomeruli?

A

-Fibrin-platelet thrombi within glomeruli

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10
Q

Describe typical clinical presentation of idiopathic membranous glomerulonephritis:

A
  • Nephrotic syndrome characterized by 3.5g protein/d, hypoalbuminemia, severe edema, hyperlipidemia, lipiduria
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11
Q

List findings for idopathic membranous glomerulonephritis on LM.

A
  • Diffuse involvement (>50% glomeruli) - Diffusely thickened capillary walls - Spikes on silver stains (BM expands around immune deposits) - Tubular epithelial cells with reabsorption droplets - Foam cells in interstitium or between tubular epithelial cells
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12
Q

Describe idiopathic membranous glomerulonephritis findings on EM and IF.

A
  • IF: granular IgG deposits along glomerular basement membrane (+/- C3) - EM: Subepithelial electron dense deposits
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13
Q

What is the typical clinical presentation of Rapidly progressive glomerulonephritis?

A
  • Rapid and progressive loss of renal function associated with severe oliguria and nephritic syndrome
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14
Q

What morphologic finding corresponds to RPGN?

A
  • Glomerular crescents in >50% glomeruli
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15
Q

What are the major immunopathological cataegories of crescentic glomerulonephritis?

A
  • Type 1: anti-GBM antibody mediated - Type 2: immune-complex mediated - Type 3: pauci-immune
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16
Q

What are the IF findings and typical disease for each of the 3 types of RPGN?

A
  • type 1: anti-GBM, linear IgG staining along glomerular basement membrane, seen in anti-GBM disease and Goodpasture’s - type 2: immune complex, granular Ig and C3 deposits along GBM and mesangium, seen in lupus, IGA and HSP - type 3: pauci-immune, absent Ig staining, seen in ANCA associated vasculitis (WEgeners), microscopic polyangiitis
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17
Q

What are IgA nephropathy findings on LM, IF, and EM?

A

LM: Range between normal, mesangioproliferative, proliferative, crescent, then sclerotic IF: dominent IgA deposition in mesangium, with C3 EM: mesangial/paramesangial electron dense deposits

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18
Q

What other diseases are considerations in the differential diagnosis of IgA nephropathy?

A
  • Lupus: can show IgA + C1q (absent in IgA nephropathy); look for subendothelial deposits - Henoch-Schonlein pupura: same kidney findings, but arthralgia, purpura, abdominal pain caused by leukocytoclastic vasculitis of dermal/bowel vessels
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19
Q

What is the clinical presentation of IgA nephropathy, and what are prognostic factors?

A
  • Presents as microscopic hematuria or intermittent gross hematuria; may also present with nephritic syndrome or renal failure - Worse prognosis with severe renal insufficiency at presentation, greater proteinuria, extensive crescent formation, extensive glomerular/tubulointerstitial scarring
20
Q

What is the classification of lupus nephritis and how does it relate to prognosis?

A

Class1: Minimal mesangial lupus nephritis-excellent prognosis Class2: mesangial proliferative lupus-Good prognosis Class 3: Focal lupus nephritis-Good Class4: diffuse segmental/global lupus-Moderate to poor Class 5: membranous lupus-Moderate Class 6: Advanced sclerosing lupus nephritis-Poor

21
Q

What are examples of active and chronic glomerular lesions?

A
  • Active: endocapillary hypercellularity, karyorrhexis, fibrinoid necrosis, rupture of GBM, crescents (cellular/fibrocellular), subendothelial deposits by LM (wire loops), intraluminal immune aggregates (hyaline thrombi) - Chronic: glomerular sclerosis, fibrous adhesions, fibrous crescents
22
Q

Renal transplant bx: What are the adequacy criteria?

A
  • At least 10 glomeruli and 2 muscular-walled small arteries for LM - one glomerulus for IF, one for EM
23
Q

How is transplant rejection classified?

A
  • Temporally: hyperacute, acute, chronic - By mechanism: cellular, humoral
24
Q

Outline the Banff classification scheme for reporting renal transplant biopsies.

A
  • Class 1: normal - Class 2: antibody-mediated rejection - Class 3: borderline changes, suspicious for acute cellular rejection - Class 4: T-cell mediated rejection - Class 5: interstitial fibrosis and tubular atrophy - Class 6: other changes not related to rejection
25
Q

What are the histologic features of acute cellular rejection?

A
  • interstitial mononuclear inflammator infiltrate - tubulitis - intimal arteritis - vasculitis with fibrinoid necrosis - glomerulitis
26
Q

What are the features of acute antibody-mediated rejection?

A
  • LM: ATN-like with minimal inflammation, capillaritis, vasculitis - IF: C4d staining in peritubular capillaries - presence of circulating anti-donor antibodies
27
Q

Name medications associated with changes to renal/urinary tract and describe change

A

Cyclosporine: - acute nephrotoxicity: acute tubular injury, isometric tubular cell vacuolization - arteriolopathy: smooth muscle cell degeneration, necrosis, loss of myocytes, hyaline deposists - thrombotic microangiopathy - chronic nephrotoxicity with patchy tubular arophy and interstitial fibrosis NSAIDS: - hemodynamically induced acute renal failure, decreased synthesis of vasodilatory prostaglandins - Acute hypersensitivity interstitial nephritis - Acute interstitial nephritis+minimal change - Membranous nephropathy phenacetin: chronic tubulointerstitial nephritis, renal papillary necrosis

28
Q

What is the typical presentation of RPGN? What morphologic finding corresponds to RPGN?

A
  • rapid and progressive loss of renal function associated with severe oliguria and nephritic syndrome - glomerular crescents in >50% of glomeruli
29
Q

List 4 lesions associated with plasma cell dyscrasias

A
  • Myeloma - Monoclonal immunoglobulin deposition disease - amyloidosis - fibrillary glomerulonephritis - immunotactoid glomerulopathy - bence-jones cast nephropathy
30
Q

Define a Bence-Jones protein

A
  • Monoclonal light chain found in urine/blood
31
Q

What are 2 mechanisms by which Bence-Jones proteins cause renal damage?

A
  • Light chains are directly toxic to epithelial cells
  • Bence jones proteins combine with urinary glycoprotein (Tamm-Horsfall) to form tubular casts that obstruct tubular lumens and induce inflammatory reaction around the casts
32
Q

List the LM, IF and EM findings for the plasma cell dyscrasia-associated kidney lesions

A
  • Myeloma cast nephropathy:
  • LM: large brittle casts w/ fracture lines, PAS neg, eosinophilic on trichrome, maybe congo red+
  • IF: monoclonal light chain in casts
  • EM: cast is deeply electron dene
  • Monoclonal Ig deposition disease:
  • LM: nodular glomerulopathy, mesangial expansion, widened tubular basement membranes
  • IF: Monoclonal Ig bound to all basement membranes
  • EM: clustered, punctate dense deposits next to tubular BM and in glomerular/vascular BM
  • Amyloidosis:
  • Amorphous, pale eosinophilic material in mesangium, capillary wll, arterioles, congo red +
  • IF: AL amyloid + for light chain Ig
  • EM: randomly arranged fibrils, 10-12 nm in arterioles, arteries, mesangium, interstitium
  • Fibrillary glomerulonephritis:
  • Increase in mesangial cellularity and irregularly thickened capillary walls, congo red -
  • IF: coares linear/confluent IgG, C3, one or both light chains
  • EM: fibrils, 10-20nm throughout mesangium/basement membrane
  • Immunotactoid glomerulopathy:
  • Membranoproliferative glomerulonephritis type 1
  • IF: granular capillary IgG, complement, one or both light chains
  • EM: corase, hollow fibrils 20-80 nm
33
Q

List the ddx of diabetic nephropathy for the glomerular changes

A
  • Mesangioproliferative glomerulonephritis
  • Monoclonal immunoglobulin deposition disease
  • IgA nephropathy
  • Lupus nephritis
34
Q

List 2 findings of diabetic nephropathy on EM

A
  • Thickened glomerular basement membrane due to protein insudation
  • Mesangial matrix expansion
35
Q

List 2 non-glomerular findings in diabetic kidney

A
  • Renal vascular lesions including renal atherosclerosis and arteriolosclerosis
  • Pyelonephritis: acute/chronic pyelonephritis common in diabetics

***papillary necrosis is more common***

36
Q

List 4 glomerular lesions seen in diabetes

A
  1. Capillary basement membrane thickening
  2. Diffuse mesangial sclerosis (PAS+)
  3. nodular glomerular sclerosis aka Kimmelstein-Wilson nodules, PAS+ in periphery surrounded by patent capillaries
  4. accumulation of hyaline material “fibrin caps” on capillary loops, and capsular drops when adherant to Bowman’s capsule
37
Q

Briefly describe how sections of kidney are prepared for EM

A
  • fixation in glutaraldehyde
  • impregnation with osmium tetroxide
  • embed tissue in epoxy resin
  • cut semi-thin 1 um section and stain with toluidine blue
  • select area for scoping; cut thin section
  • double-stain with uranyl acetate/lead citrate on copper wire
38
Q

Minimal change nephropathy

A
  • most common cause of idiopathic nephrotic syndrome in children
  • usually <6 yrs, males, caucasians
  • often preceding viral illness/vaccine/allergy/drug exposure, possibly ass. with hodgkins
  • thought to be T lymphocyte related damage to podocytes
  • presents with heavy selective proteinuria
  • complete remission after 8 weeks with steroids
  • LM: normal glomerulus, convoluted tubules are vacuolated due to lipid
  • IF: neg, albumen in tubules
  • EM: total foot process effacement, distortion of filtration slits, visceral epithelial cells wtih many organelles and cysts
39
Q

Name 10 glomerular lesions associated with nephrotic syndrome

A
  • Minimal change
  • FSGS
  • C1q nephropathy (C1q deposits in mesangium)
  • Membranous glomerulonephritis (uniform capillary wall thickening, spikes are subepithelial, IgG and C3 along capillary wall)
  • Diabetic nephropathy (nodular/diffuse mesnagial sclerosis, GBM thickening, linear IgG along capillary walls)
  • Amyloidosis
  • Light chain deposition disease
  • Heavy chain deposition disease
  • Fibrillary glomerulonephritis
  • Imuunotactoid glomerulopathy
  • COngenital neprhotic syndrome (Finnish type, diffuse mesangial sclerosis or Denys Drash)
40
Q

FSGS: list come features

A
  • presents with proteinuria, high incidence of renal failure (ESRD in 10-20 yrs)
  • sclerosis from increase in mesangial matrix obliterating glomerular capillaries
  • variants include tip lesion, perihilar lesion, cellular variant, collapsing variant and NOS
  • african americans, 10% in kids, 20-30% of nephrotic syndrome in adults, in 3-4 decade
  • segmental sclerosis involving one or more lobules of glomerular tuft near axial region, adhering to bowmans capsule
  • areas of tubular atrophy common, with interstitial fibrosis
  • EM: extensive foot process effacement, not only in sclerosed areas. Visible increase in mesangial matrix. Hyaline deposits, BM thickening/folding.

IF: IgM and C3 subendothelial in sclerosed areas

41
Q

What are some secondary causes of FSGS?

A
  • Familial (mutations in nephrin, podocin, WT1…)
  • Viral (HIV, parvovirus B19, CMV, SV40, EBV)
  • Drugs (heroin, Interferon alpha, lithium)
  • “adaptive functional response” unilateral renal agenesis, reflux nephropathy, partial cortical necrosis, surgical ablation, morbid obesity, HTN, sickle cell
42
Q

If you have collapsing glomerulopathy, what do you expect to see and what are the causes?

A
  • Distinct variant of FSGS, characterized by widespread collapse of glomerular capillary loops, poor prognosis
  • ass. with IV drug abuse, HIV, HCV and some autoimmune
  • will see segmental, global hypertrophy and hyperplasia of epithelial cells overlying sclerotic segment, cells are swollen and vacuolated with many resorption droplets. Tubulointerstiial injury is severe.
  • IF: IgM and C3
  • EM: tubuloreticular inclusions on top of podocyte effacement
43
Q

Fibrillary and immunotactoid glomerulopathies: describe

A
  • 2 rare variants of glomerolopathy defined by EM
  • Extracellular deposition of non-branching, randomly arrayed fibrils aproximately 20 nm (fibrillary) and 20-50nm in parallel/stacked arrays (immunotactoid)
  • Negative for Congo Red/Thioflavin T
  • Fibrillary is more common, middle aged African Americans, heavy proteinuria, ESRD within 2 yrs
  • LM for both: mesangial hypercellularity, thickening of glomerular capillarly walls, mesangial expansion with amorphous PAS+ material. Crescents are possible.
  • EM deposits in all compartments; foot process effacement
  • IF: IgG and C3 in all compartments
44
Q

Light-chain and Heavy-chain deposition diseases: give a few featurs

A
  • LCCDD: overproduction and extracellular deposition of monoclonal immunoglobulin light chain; can have cardiac/hepatic/neural changes
  • Much in common with AL amyloid, but granular, Congo Red negative, and usually Kappa light chain.
  • Heavy proteinuria, ESRD
  • GLomeruli enlarged, PAS+ material causing capillary wall thickening, nodular expansion of mesangium
  • EM: continuous deposition of electron-denes material in GBM, mesnagium and along tubular basement menbranes. It is finely granular!

**HCDD: ** systemic deposition of monoclonal Ig heavy chain; due to deletion in first common domain (CH1) to make it secretable by plasma cells

  • Presents with hypocomplement, otherwise similar to LCDDD
  • Looks like LCDDD on LM/EM
  • IF: gamma heavy chains+, neg for both kappa/lambda
45
Q

Fabry’s disease: list some features

A
  • uncommon x-linked disorder
  • deficiency of alpha-galactosidase A
  • accumulations of neutral lycosphingolipid Gb3 in kidneys, heart, neurons, blood vessels
  • present with many angiokeratomas, paresthesias, hypophydrosis, corneal opacities; death in 4th-5th decade
  • LM: visceral epithelial cells are enlarged and vacuolated giving honeycomb appearnace; similar change in Bowman’s epithelium, endothelial and mesangial cells. Vacuoles are PAS neg.
  • EM: massive accumulation of laminated inclusion bodies (zebra bodies) with concentric myelin-like structure; also in endothelial/tubule cells.

Kidney (2 decks)

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