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Block 2 > Kidney diseases > Flashcards

Kidney diseases Flashcards

1
Q

Nephrotic syndrome presentations

A
  • massive proteinuria (more than 3.5g/day)
  • low serum albumin
  • generalised oedema
  • Hyperlipidemia
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2
Q

Nephrotic syndrome causes

A
  • membranous nephropathy
  • membranoprolierative glomerulonephritis
  • minimal change disease
  • focal segmental glomerulosclerosis
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3
Q

Nephrotic syndrome complications

A
  • hypercoagulopathy
  • hyperlipidemia/ lipiduria
  • infection risk (due to reduction in Ig, complement and neutrophil phagocytic properties)
  • decreased serum binding protein
  • renal failure
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4
Q

Nephritic syndrome

A
  • mild to moderate proteinuria
  • gross or microscopic haematuria (red cell cast in UUTI)
  • hypertension
  • reduction in GFR
  • acute postinfectious glomerulonephritis
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5
Q

AKI

A

rapid reduce in GFR, with increase in serum creatinine and urea
maybe glomerulus, tubules, interstitium or blood vessel problem

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6
Q

Chronic kidney disease CKD

A

progressive reduction in GFR, lower than 60 from 3 months

may result from glomerulus, interstitium, tubules or blood vessel problem

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7
Q

ESRD End stage renal disease

A

less than 5% GFR, irreversible and terminal

need renal replacement therapy

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8
Q

Membranous nephropathy- pathogenesis

A
  • usually in middle aged people
  • immune complex glomerulonephritis
  • Primary: M-type phospholipase A2 receptor on podocytes (foot processes)
  • Secondary: hepatitis B or C, SLE, drug (NSAID), malignancy
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9
Q

Membranous nephropathy- pathology

A
  • silver stain: spikes formation
  • granular immune deposits (IgG)
  • subepithelial electron dense deposits (beneath the podocytes)
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10
Q

Membranous nephropathy- treatment

A

steroid

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11
Q

membranoproliferative glomerulonephritis- pathogenesis

A
  • usually in children and young adult if idiopathic
  • secondary: hepatitis B or C, lymphoid malignancy, syphilis
  • C3 glomerulonephritis
  • dense deposit disease
  • nephrotic syndrome + haematuria
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12
Q

membranoproliferative glomerulonephritis- pathology

A
  • markedly increase in number of cells, thickened capillary wall and spitting of GBM
  • immune deposits (IgG) at mesangial cells and GBM
  • splitting of GBM and subepithelial electron dense deposits
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13
Q

membranoproliferative glomerulonephritis- treatment

A
  • steroid and immunosuppressants usually not useful
  • treatment underlying cause and complement pathway
  • poor prognosis
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14
Q

Minimal change disease- pathogenesis

A
  • usually in children
  • not immune complex mediated
  • primary damage is in the podocytes -> loss of protein filtration function
  • associated factor (but not cause): recent vaccination/infection, drug (NSAID, lithium, interferon), lymphoma
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15
Q

Minimal change disease- pathology

A
  • normal in light microscopy and direct immunofluorescent studies
  • diffuse effacement of foot processes of podocytes in electron microscopy
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16
Q

Minimal change disease- treatment

A
  • steroid, use other immunosuppressant if develop steroid resistance or dependence
  • prognosis: excellent
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17
Q

Focal segmental glomerulosclerosis- pathogenesis

A
  • focal: less than 50%
  • segmental: only portion of glomerulus involved
  • glomerulosclerosis: capillary loops got replaced by acellular amorphous mass (collagen, plasma protein, basement membrane components)
  • primary/ idiopathic and secondary (HIV, obesity, hypertension)
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18
Q

Focal segmental glomeruolosclerosis- pathology

A
  • if primary, very similar to minimal change
  • but do not respond/ very little response to steroid therapy
  • progress to CKD and may recur after transplant
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19
Q

Acute postinfectious glomerulonephritis- pathogenesis

A
  • nephritis syndrome
  • immune complex glomerulonephritis
  • usually 1-4 weeks after pharyngitis or skin infection by group A beta hemolytic strep
  • may also be caused by staphylococcal, pneumococcal, viral or parasitic infection
  • usually in children
20
Q

Acute postinfectious glomerulonephritis- pathology

A
  • hypercellular glomeruli with neutrophils
  • spotty immune deposits
  • subepithelial humps (electron dense deposits)
21
Q

Acute postinfectious glomerulonephritis- treatment

A
  • conservative therapy

- 1% progress to rapidly progressive glomerulonephritis

22
Q

AKI- rapidly progressive (cresentic) glomerulonephritis- types

A 
Type I (anti-GBM Ab)- goodpasture syndrome
Type II (immune complex)- IgA nephropathy, post infectious glpomerulonephritis, lupuc nephritis
Type III (pauci-immune)- ANCA-associated
23
Q

Goodpasture syndrome- pathogenesis

A
  • usually in older age patients
  • autoantibodies against NC1 domain of alpha 3 chain of type 4 collagen in GBM
  • can cross-react with alveolar basement membrane, causing pulmonary haemorrhage and death
  • preceded by flu-like illness, hydrocarbon or solvent exposure
24
Q

Goodpasture syndrome- pathology

A
  • GBM breaks
  • cellular crescent formation (epithelial proliferation in response to GBM in the bowman’s space)
  • fibrin deposits
  • linear staining pattern for IgG
  • no findings on electron microscope because too small
25
Q

Goodpasture syndrome- treatment

A

plasmapheresis/ plasma exchange to wash away the autoAb
high dose steroid and cyclophosphamide
poor prognosis, needs renal replacement therapy

26
Q

IgA nephropathy- pathogenesis

A
  • wide age presentation, most common cause of glomerulonephritis
  • immune complex glomerulonephritis
  • nephritic syndrome
27
Q

IgA nephropathy- pathology

A
  • mesangial proliferation, increase in the size and matrix (normally 3 cells in one segment, now maybe 5)
  • IgA immune deposits in the mesangium
  • mesangial electron dense deposits
28
Q

IgA nephropathy- treatment

A
  • depends, if serious can give corticosteroid

- can recur even after transplant

29
Q

Acute tubular injury/necrosis- cause

A
  • usually ischemia
  • direct toxic injury
  • tubulointerstitial nephritis
  • urinary obstruction by prostatic hypertrophy or tumour or blood clot
30
Q

Acute tubular injury/necrosis- pathology

A
  • necrotic tubular epithelial cells in the tubules

- dilated tubules

31
Q

Acute tubular injury/necrosis- phases

A
  • initiation phase: raised blood urea, creatinine, slight decrease in urine production
  • maintenance phase: oliguria (40-400mL), raised urea and creatinine, water and salt retention, hyperkalemia and metabolic acidosis
  • recovery phase: raised urine output up to 3L, decreased sodium and water and potassium

present as AKI

32
Q

Tubulointerstitial nephritis- definition

A

inflammation of the tubules and interstitium

- present as acute or subacute worsening of kidney function

33
Q

Tubulointerstitial nephritis- cause

A
  • DRUGS: nsaid, radiology contrast, diuretics, antibiotics = hypersensitivity
  • infections (acute and chronic pyelonephritis)
  • light chain cast nephropathy
  • immunological: sarcoidosis
  • chronic urinary tract obstruction
  • metabolic diseases: urate/oxalate nephropathy
34
Q

Tubulointerstitial nephritis- pathology

A
  • interstitial inflammation (if eosinophils present, hypersensitity to drugs)
  • tubulitis (infiltration of inflammatory cells to tubules)
  • interstitial edema (acute) or fibrosis (chronic)
35
Q

Acute pyelonephritis- pathology

A
  • a lot of inflammatory cells in the interstitium and tubules
  • pus formation in gross anatomy
36
Q

Acute pyelonephritis- presentations

A

failure to thrive in children

shaking chills

37
Q

Acute pyelonephritis- complications

A
  • perinephric abscess: perinephric tissue spread of the pus (out of the renal capsule)
  • pyelonephrosis: the accumulation of pus in calyces, pelvis and the ureters (need surgical removal)
  • scattered (minimal scar) formation
38
Q

Chronic pyelonephritis- pathogenesis

A
  • usually due to recurrent bacterial infections

- associated with vesicoureteral reflux/ urinary tract obstruction

39
Q

Chronic pyelonephritis- pathology

A

very similar to other tubulointerstitial nephritis
may involve the glomerulus and cause glomerular damage in the long run
scar formation and thinning of the cortex/ medulla in gross

40
Q

Chronic pyelonephritis- presentations

A
  • commonly the recurrent acute pyelonephritis symptoms
  • may be mild or none in the beginning: nocturia, polyuria due to loss of capacity to reabsorb
  • may lead to CKD and ESRD- uremia
41
Q

Light chain cast nephropathy

A
  • usually in more than 50 yo
  • neoplasm of plasma cells
  • presentation: AKI and proteinuria
42
Q

hypertensive nephrosclerosis

A
  • associated with hypertension
  • sclerosis of the small arteries and arterioles: intimal fibrosis and medial thickening (smooth muscle hypertrophy), hyalinization of arterioles (extravasation of plasma protein due to endothelial injury)
  • due to wall thickening and lumen narrowing -> ischaemia -> glomerulosclerosis and chronic TI injury -> CKD/ESRD
43
Q

Malignant nephrosclerosis

A
  • associated with malignant nephrosclerosis (200/120)
  • other symptoms: papilloedema, retinal haemorrhage, encephalopathy, CVS abnormality
  • pathology: hyperplastic arteriolitis (onion-skin lesion), fibrinoid necrosis
  • need aggressive and prompt anti-hypertensives
44
Q

Diabetic nephropathy

A
  • arteriolosclerosis (renal vascular lesion)
  • affect the glomerulus (thickened GBM- normal 350nm, increased mesangial matrix, Kimmelstiel Wilson nodules)
  • ischaemia -> glomerulosclerosis, chronic TI injury -> CKD and ESRD
45
Q

ANCA-associated vasculitis- pathogenesis

A
  • one of the cause of rapidly progressive glomerulonephritis
  • pauci-immune because no immune complexes and anti-GBM Ab is detected in electron/ immunofluorescent
  • antineutrophil cytoplasmic antibodies circulating in blood: c-ANCA, p-ANCA (perinuclear)
46
Q

ANCA-associated vasculitis- disease entities

A
  • wegener granulomatosis (granulomatosis with polyangiitis)

- microscopic polyangiitis

47
Q

ANCA-associated vasculitis- pathology

A
  • fibrin deposits in blood vessels (vasculitis)

- same as crescentic glomerulonephritis

Block 2 (25 decks)

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