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Renal Exam > Hematuria & Nephritis > Flashcards

Hematuria & Nephritis Flashcards

1
Q

nephritic syndrome - defined

A

*clinical syndrome resulting from inflammatory lesions in the glomerulus

*hallmarks:
-hematuria
-hypertension
-decreased GFR with azotemia (AKI)
-oliguria

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2
Q

hematuria - defined

A

*blood in the urine
*macroscopic (gross) - visible as a red or brown discoloration to the urine
*microscopic: red blood cells visible only under the microscope (3+ RBCs per high powered field)

*evaluation: goal is to determine:
-transient vs. persistent
-glomerular vs. non-glomerular

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3
Q

macroscopic hematuria

A

*visible as a red or brown discoloration to the urine
*after centrifugation:
-if supernatant is clear + sediment is red/brown, color change is due to hematuria
-if supernatant is red/brown: color change is due to pigment in the urine (hemoglobin, myoglobin, drugs/foods)

*urine dipstick detects reducing substances + positive for either RBCs or pigment

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4
Q

common causes of TRANSIENT hematuria

A

*contamination from menses
*vigorous exercise
*sexual activity
*fever
*infection (cystitis, prostatitis)
*trauma
*instrumentation (foley)

approach: repeat urinalysis; transient hematuria is typically benign

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5
Q

risk factors that warrant further workup for transient hematuria

A

*females > 50 yo / males > 40 yo
*smoking history (> 10 pack-years)
*other

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6
Q

glomerular vs. non-glomerular hematuria

A

*findings suggestive of glomerular source:
-dysmorphic RBCs
-cellular casts
-proteinuria
-other signs/symptoms of glomerular disease

*blood clots are suggestive of NON-glomerular disease

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7
Q

diseases that cause nephritic syndrome

A
  1. post-infectious glomerulonephritis
  2. membranoproliferative glomerulonephritis
  3. IgA nephropathy
  4. Alport Syndrome
  5. thin basement membrane

note - these can all be primary/idiopathic or secondary to another source

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8
Q

post-infectious glomerulonephritis (PIGN) - light microscopy findings

A

*diffuse, exudative proliferative glomerulonephritis, endocapillary hypercellularity with numerous neutrophils
*enlarged and hypercellular glomeruli

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9
Q

post-infectious glomerulonephritis (PIGN) - immunofluorescence findings

A

*subendothelial deposits with prominent IgG and C3 along the GBM, as well as mesangium deposits
*granular (“starry sky”) appearance (“lumpy-bumpy”) due to IgG, IgM, and C3 deposition along GBM and mesangium

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10
Q

post-infectious glomerulonephritis (PIGN) - electron microscopy findings

A

*scattered subepithelial hump shaped deposits without BM reaction, occasional mesangial and subendothelial deposits

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11
Q

post-infectious glomerulonephritis (PIGN) - etiology / mechanism

A

*immune complex deposition (type III hypersensitivity reaction) causing exudative hypercellularity; with consumptive hypocomplementemia
*nephritogenic infectious antigens thought to be the cause of immune complex formation (ex. erythrogenic toxin type B from streptococci)

*most common cause is STREPTOCOCCAL INFECTION

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12
Q

post-infectious glomerulonephritis (PIGN) - epidemiology

A

*more common in children and in developing countries

*children: seen 2-4 weeks after group A streptococcal pharyngitis or skin infection
*adults: Staph is an additional causative agent

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13
Q

post-infectious glomerulonephritis (PIGN) - clinical presentation

A

*sudden onset edema, hematuria, HTN, and azotemia 2-3 weeks after strep pharyngitis or cellulitis
*streptozyme test looks for extracellular strep products
*LOW COMPLEMENT (SERUM C3)

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14
Q

post-infectious glomerulonephritis (PIGN) - treatment

A

*supportive care

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15
Q

post-infectious glomerulonephritis (PIGN) - prognosis

A

*good - most have rapid, full recovery in 1-4 weeks
*may have increased risk for proteinuria, CKD, and HTN later

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16
Q

membranoproliferative glomerulonephritis (MPGN) - light microscopy findings

A

*endocapillary hypercellularity, “tram-track” appearance due to GBM splitting from mesangial infiltration, mesangial expansion/hypercellularity
*mesangial ingrowth → GBM splitting →”tram track” on H&E and PAS stains

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17
Q

membranoproliferative glomerulonephritis (MPGN) - immunofluorescence findings

A

*immune complex deposition with GRANULAR staining in GBM and mesangium IgG, C3, C1q/C4

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18
Q

membranoproliferative glomerulonephritis (MPGN) - electron microscopy findings

A

*subendothelial immune complexes

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19
Q

membranoproliferative glomerulonephritis (MPGN) - pathogenesis

A

*hallmark: immune complex deposition in the subendothelial and mesangial compartments
*results in GBM alterations, endocapillary proliferation, leukocyte infiltration, mesangial proliferation → new inner basement membrane laid down as a reaction to subendothelial deposits, resulting in double contour
*circulating antigens likely result in immune complex formation

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20
Q

membranoproliferative glomerulonephritis (MPGN) - PRIMARY etiology

A

*inciting antigens unknown

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21
Q

membranoproliferative glomerulonephritis (MPGN) - SECONDARY etiology

A

*infection: HEP C (usually with cryoglobulinemia) > hep B; endocarditis; other
*alpha 1 antitrypsin deficiency
*lupus nephritis
*malignancy: CLL, lymphoma, dysproteinemias

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22
Q

membranoproliferative glomerulonephritis (MPGN) - epidemiology

A

*rare
*children or young adults
*older adults with chronic infections

23
Q

membranoproliferative glomerulonephritis (MPGN) - clinical presentation

A

*MIXED nephrotic/nephritic syndrome
*low complement: low C3 and LOW C4 (classic)

24
Q

membranoproliferative glomerulonephritis (MPGN) - treatment

A

*secondary: treatment of underlying disease
*primary: corticosteroids and immunosuppresive agents

25
Q

membranoproliferative glomerulonephritis (MPGN) - prognosis

A

*more than 50% progress to ESRD by 10 years

26
Q

C3 glomerulopathies - defined

A

*glomerular diseases caused by abnormalities in complement regulation

  1. glomerulonephritis with dominant C3 (C3GN)
    -MPGN-like appearance
    -C3 deposition dominant on immunofluorescence
  2. dense deposit disease (DDD)
    -MPGN-like appearance
    -irregular, RIBBON-LIKE electron dense deposit in GBM
27
Q

dense deposit disease (DDD) - etiology/pathogenesis

A

*disorder of complement activation
*alternate pathway is being constantly activated due to pathologic stabilization of the C3 convertase by two ways;
1. C3 nephritic factor (C3NeF): circulating autoantibody which binds and stabilizes C3 convertase
2. genetic defect in factor H, factor I, MCP: usually degrades C3/C5 convertase
*glomerular damage occurs due to recruitment of inflammatory cells similarly to MPGN type 1

28
Q

dense deposit disease (DDD) - epidemiology

A

*rare
*usually seen in young adults

29
Q

dense deposit disease (DDD) - clinical presentation

A

*variable, mixed nephrotic/nephritic syndrome
*low C3 levels and normal C4 (not always)

30
Q

dense deposit disease (DDD) - treatment

A

*eculizumab (binds and inhibits C5)
*plasma exchange
*immunosuppression

31
Q

dense deposit disease (DDD) - prognosis

A

*high rate of recurrence in kidney transplant

32
Q

IgA nephropathy (IGAN) - light microscopy findings

A

*varies; minimal mesangial expansion to diffuse proliferative lesions
*mesangial proliferation

33
Q

IgA nephropathy (IGAN) - immunofluorescence findings

A

*diffuse global IgA deposits in the mesangium
*lambda > kappa light chains + C3

34
Q

IgA nephropathy (IGAN) - electron microscopy findings

A

*electron dense deposits in mesangium
*subendothelial deposits with endocapillary hypercellularity
*occasional subepithelial with intramembranous

35
Q

IgA nephropathy (IGAN) - pathogenesis

A

*generation of abnormally glycosalated IgA (galactose-deficient IgA1)
*impaired clearance of these defective IgA from circulation
*IgA1 immune complexes form in circulation and favor deposition in the mesangium → inflammatory mesangial cell reaction to immune complexes
*occurs CONCURRENTLY with respiratory or GI tract infections

36
Q

IgA nephropathy (IGAN) - epidemiology

A

*most common cause of glomerulonephritis worldwide
*patient ancestry: asians > caucasion > african

37
Q

IgA nephropathy (IGAN) - clinical presentation

A

*present with GROSS HEMATURIA concurrently with MUCOSAL INFECTION (syn-pharyngitic)
*asymptomatic hematuria, proteinuria, HTN
*can cause RPGN
*isolated kidney involvement or part of a syndrome:
-Henoch-Schonlein Purpura (HSP): IgA Vasculitis (systemic form) - abdominal pain, GI bleeding, palpable purpura, and hematuria

38
Q

IgA nephropathy (IGAN) - treatment

A

*supportive: ACEi/ARB, SGLT2
*for higher creatinine, more proteinuria: immnuosuppression + corticosteroids

39
Q

IgA nephropathy (IGAN) - prognosis

A

*worst for: elevated creatinine, HTN, proteinuria > 1 g/day

39
Q

Alport Syndrome - overview

A

*genetic defect in type IV collagen (mostly X-linked)

*hallmarks:
-hematuria
-low level proteinuria
-progressive loss of GFR with progression to ESRD

*other sx: eye problems, hearing problems

40
Q

Alport Syndrome - light microscopy findings

A

*for the most part unremarkable
*can have early periglomerular fibrosis and tubulointerstitial fluid
*irregular thinning and thickening and splitting of glomerular basement membrane

41
Q

Alport Syndrome - immunofluorescence findings

A

*negative, but staining to demonstrate ABSENCE of alpha 5 type IV collagen can help make the diagnosis

42
Q

Alport Syndrome - electron microscopy findings

A

*thickening of GBM
*mottled “basket-weave” appearance of GBM due to irregular thickening and longitudinal splitting of GBM

43
Q

Alport Syndrome - etiology

A

*inherited mutation of type IV collagen
*classical Alport Syndrome: X-linked dominant mutation of alpha 5 subunit of type IV collagen
*other types: autosomal recessive mutation of alpha 3 subunit; autosomal dominant mutation of alpha 4 subunit

*result: abnormal incorporation of alpha 3, 4, 5 subunits of type IV collagen into the GBM causing compromise of GBM integrity

44
Q

Alport Syndrome - clinical presentation

A

*males (X-linked) with hematuria in childhood with progression to ESRD
*HEARING LOSS AND OCULAR DEFECTS IN ADULTHOOD
*female carriers may have hematuria without progressive renal disease

45
Q

Alport Syndrome - treatment

A

*supportive care
*BP control
*RAAS blocking drugs

46
Q

Alport Syndrome - prognosis

A

*chronic hematuria & scarring with 905 of X-linked cases are ESRD by age 30
*depends on the type of mutation in the gene
*TRANSPLANT KIDNEYS can develop de-novo anti-glomerular basement membrane antibodies (anti-GBM disease) with glomerulonephritis because normal GBM is recognized as foreign

47
Q

thin basement membrane (TBM) - light microscopy findings

A

*no specific lesion

48
Q

thin basement membrane (TBM) - immunofluorescence findings

A

*negative

49
Q

thin basement membrane (TBM) - electron microscopy findings

A

*thinning of the lamina densa of the GBM

50
Q

thin basement membrane (TBM) - etiology

A

*on a continuum of the Alport Syndrome
*familial inheritance pattern: AD and AR both seen

51
Q

thin basement membrane (TBM) - clinical presentation

A

*hematuria, either microscopic or macroscopic, intermittent or persistent

52
Q

thin basement membrane (TBM) - treatment and prognosis

A

*tx: monitor
*prognosis: good; aka benign familial hematuria

Renal Exam (44 decks)

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