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Nephrology > Glomerulonephropathies > Flashcards

Glomerulonephropathies Flashcards

1
Q

Nephritic vs. nephrotic?

A
  • nephritic:
    + RBCs, - WBCs
    red cell or mixed cellular casts
    variable degrees of proteinuria
  • nephrotic:
    proteinuria greater tahn 3.5 g/day (sig amount)
    lipiduria, fatty casts
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2
Q

What are nephritic causes of glomerulonephritis?

A
  • postinfectious glomerulonephritis
  • IgA nephropathy
  • HSP aka IgA vasculitis
  • mesangial proliferative glomerulonephritis
  • lupus nephritis
  • thin basement membrane disease
  • hereditary nephritis
  • membranoproliferative glomerulonephritis
  • rapidly progressive (crescentic) glomerulonephritis
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3
Q

nephrotic causes of glomerulonephritis?

A
  • systemic: diabetic nephropathy, amyloidosis, systemic lupus
  • minimal change disease (kids)
  • FSGS (focal segmental glomerulosclerosis)
  • membranous nephropathy
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4
Q

Focal nephritic disease characteristics?

A
  • inflammatory lesions in less than 1/2 glomeruli
  • UA shows RBCs, occasional RBC casts, mild proteinuria
  • example: IgA nephropathy
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5
Q

Diffuse nephritic disease characteristics?

A
  • affects more than 1/2 of the glomeruli
  • UA similar to focal but will have more proteinuria, also edema, HTN and/or renal insufficiency
  • ex: PSGN
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6
Q

Patterns of nephrotic disease?

A
  • affects MANY of the glomeruli
  • w/o obvious inflammation or immune complex deposition
  • edema, hyperlipidemia, hypoalbuminemia
  • ex: diabetic nephropathy
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7
Q

Epidemiology of PSGN?

A
  • most common cause of acute nephritis worldwide
  • it primarily occurs in developing world
  • risk is greater in kids b/t 5-12 years of age
  • annual incidence: 20/100000
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8
Q

When does PSGN present itself?

A
  • usually occurs 1-3 weeks post strep throat
  • 3-6 weeks post skin infection with GABS
  • abx doesn’t always prevent glomerular disease
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9
Q

Pathophys of PSGN?

A
  • caused by glomerular immune complex disease induced by specific nephritogenic strains of GABS
  • can also be assoc with various viral illnesses and parasitic infections (rare)
  • resulting glom. immune complex disease triggers complement activation and inflammation
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10
Q

Clinical signs and sxs of PSGN?

A
  • often asx
  • microscopic hematuria - lead to gross hematuria
  • proteiniuria (can reach nephrotic range)
  • edema
  • HTN
  • increased serum creatinine
  • variable decline in GFR
  • hypocomplementemia (C3, C4)
  • acute renal failure and need for dialysis is uncommon
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11
Q

Dx tests for PSGN? Signs that rule out PSGN?

A
  • look for elevated titers of Abs to extracellular strep (evidence of recent GABS)
  • streptozyme test measure 5 strep abs, 95% positive in pharyngitis and 80% positive in skin infections
  • Most common ab: ASO (anti-streptolysin)
  • renal bx: NOT performed in most pts to confirm dx of PSGN but it can be performed if:
    other glomerular disorders are being considered because they deviate from the natural course of PSGN
    -or it presents late w/o clear hx of prior strep infection
  • Persistently low C3 levels beyond 6 weeks are suggestive of a dx membranoproliferative glomerulonephritis
  • recurrent episodes of hematuria: **suggest IgA nephropathy, rare in PSGN
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12
Q

Tx of PSGN?

A
  • management is supportive and focused upon tx the volume overload and HTN
  • Na and water restriction
  • Diuretic: lasix tx HTN and volume overload
  • Dialysis may be reqd in acute renal failure
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13
Q

Prognosis of PSGN?

A
  • most pts, esp kids, have complete recovery, and resolution of their disease process - within the first 2 weeks
  • small subset: have late renal complications (HTN, increasing proteinuria, and renal insufficiency)
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14
Q

Epidemiology of IgA nephropathy (Berger’s disease)?

A
  • most common lesion to cuase primary GN in developed world
  • higher frequency in Asians and caucasians (rare in blacks)
  • Male to female 2:1
  • age: 80% b/t 15-35 yo at dx
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15
Q

Pathophys of Berger’s disease?

A
  • unknown
  • initiating event: mesangial deposition of IgA
  • dysregulated synthesis and metabolism of IgA results in immune complexes that lead to mesangial depositon and accumulation
  • enviro factors: dietary Ags and mucosal infections may drive the generation of pathogenic IgA
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16
Q

Presentation of Berger’s disease?

A

can present in 1 of 3 ways:

  • 50% present with gross hematuria (may be recurrent, usually after URI), flank pain, fever
  • 30% present with microscopic hematuria (eventually will lead to gross hematuria), mild proteinuria
  • 10% present with: nephrotic syndrome (proteinuria, lipiduria, fatty casts), edema, renal insufficiency, HTN: rare malignant HTN, hematuria
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17
Q

Dx of Berger’s disease?

A
  • suspicion based on clinical hx and UA
  • confirmation: prominent IgA deposits in mesangium and along glomerular capillary walls, C3 and IgG are also deposited
  • Mesangial IgA deposition also occurs in cirrhosis, celiac disease, and HIV
  • IgA nephropathy may rarely be seen with other glomerular diseases - minimal change disease and granulomatosis with polyangiitis (wegeners)
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18
Q

Tx of IgA nephropathy?

A
  • BP control
  • ACEIs/ARBs: pts with persistent proteinuria, slightly reduced GFR, and mild/mod changes in bx
  • look for reduction in protein excretion
  • pt with severe or progressive disease: corticosteroids and/or immunosuppressants
19
Q

IgA nephropathy (bergers) prognosis?

A
  • most pts enter sustained clinical remission
  • some have persisten low-grade hematuria and or proteinuria
  • slow progression to ESRD occurs in 50%
  • predictors of progression: elevated serum Cr, HTN, and persistent protein excretion above 1000 mg/day
  • patients who have recurrent episodes of gross hematuria w/o proteinuria are at low risk for progressive kidney disease
20
Q

What is HSP/IgA vasculitis? Who does it usually effect?

A
  • systemic vasculitis characterized by tissue deposition of IgA containing immune complexes
  • most common cause of vasculitis in children (90%)
  • HSP: usually occurs b/t 3-15
  • underlying cuase of HSP unknown main theory: immune mediated vasculitis, may be triggered by variety of Ags
21
Q

What is the tetrad of clinical manifestations of HSP?

A
  • palpable purpura w/o thrombocytopenia or coagulopathy
  • arthritis/arthralgias
  • abdominal pain
  • renal disease (GN)
  • this can develop over days to weeks and manifestations can vary in order of presentation
22
Q

Pathogenesis of HSP nephritis?

A
  • similar to IgA nephropathy ( deposition of IgA immune complexes)
  • can have mild (asx hematuria) to varying degrees of proteinuria to severe presentation with nephrotic syndrome and even renal failure
  • generally mild in children, moderate to severe in adults
23
Q

Dx of HSP nephritis?

A
  • confirmed by kidney bx
  • reserved for when dx is uncertain or severe renal involvement: marked proteinuria and or impaired renal fxn during the acute episode
24
Q

Prognosis of HSP nephritis? Tx?

A
  • Renal disease is favorable in most, recurrence is common
  • minority will develop persistent renal manifestations or ESRD

Tx:

  • pts with cresentic GN: pulse IV methylprednisolone, followed by oral prednisone
  • dialysis and renal transplantation cna be performed for those that progress to ESRD
25
Q

What is RPGN (rapidly progressive GN)? Characterized by?

A
  • acute GN marked by rapid progression to ESRF
  • features of glomerular disease in urine
  • progressive loss of renal fxn over short period (days, weeks, months)
  • characterized morphologically by extensive CRESCENT formation and clinically progression to ESRD
26
Q

Pathophys of RPGN?

A
  • crescentic GN: crescent formation nonspecific response to severe injury to glomerular cap wall
  • initially begins as active inflammation of cap wall, results in movement of plasma products, including fibrinogen, into Bowman’s space with subsequent fibrin formation, the influx of macrophages and T cells, and the release of proinflamm cytokines
  • followed by the development of fibrocellular and fibrous crescents, which represent a stage of disease that isn’t likely to respond to immunosuppressive therapy
27
Q

Types of RPGN?

A
  • anti-glomerular basement membrane (GBM/goodpastures): Ab disease of LUNGS and glomerulus caused by anti-GBM ABs
  • Immune complex RPGN: deposition of immune complexes in the glomeruli: IgA nephropathy, PSGN, lupus nephritis
  • Pauci-immune RPGN: necrotizing GN and vasculitis: ANCA positive, systemic sxs of vasculitis
28
Q

Presentation of RPGN? What if it is GBM?

A
  • insidious onset: fatigue and edema
  • more acute onset: macroscopic hematuria, oliguria, edema, renal insufficiency
  • If GBM:
    pulmonary hemorrhage, hemoptysis, pulmonary infiltrates, dyspnea
29
Q

RPGN eval?

A
  • UA: hematuria, RBC casts and other casts, proteinuria
  • high BUN, and creatinine
  • Renal bx
  • serologic assays to determin type and cause:
    ANCA, anti-GBM abs, ANAs
30
Q

Tx of RPGN?

A
  • early dx with renal bx and serologic testing and early tx is essential to min. degree of irreversible renal injury
  • empiric therapy with severe disease while awaiting bx results:
    pulse methylprednisolone
    oral or IV cyclophosphamide
    sometimes: plasmapharesis
  • tx after bx results: specific
31
Q

What is acute interstitial nephritis?

A
  • AIN: renal lesion that causes decline in creatinine clearance and is characterized by an inflammatory infiltrate in the kidney interstitium
  • accounts fo 10-15 of cases of intrinsic renal failure
  • pathologically: interstitial inflammatory response with edema and possible tubular cell damage
32
Q

Etiologies of AIN?

A
  • drugs account for 70% of cases: PCN, cephalosporins, sulfanamides, sulfanamide containing diuretics, NSAIDs, rifampin, dilantin, allopurinol
  • ID: strep, leptospirosis, CMV, histoplasmosis, rocky mountain spotted fever
  • immunologic entities: lupus, sjogren’s syndrome, sacroidosis, cryoglobulinemia (abnorm protein formation in response to cold temp - impaired circulation - lead to color changes, hives, damage to extremities, purpura)
33
Q

Presentation of AIN?

A

fever: greater than 80%
rash: 25-50%
arthalgias
peripheral blood eosinophilia (80%)
red cells in urine (95%)
white cells and white cell casts in urine
oliguria
azotemia

34
Q

Eval of AIN?

A
  • UA:
    RBCs in urine (95%)
    white cells and WBC casts
    proteinuria commonly found in NSAID related interstitial nephritis
35
Q

Tx of AIN?

A
  • supportive measure
  • removal of inciting agent
  • if renal failure persists: short course of corticosteroids, high dose methylprednisolone or prednisone for 1-2 weeks, then taper
  • carries good prognosis
  • rarely progresses to ESRD
  • recovery usually over weeks to months
36
Q

Case study:
12 y/o has orange urine with sediment for 4 days, elevated BP, wt gain
- what will you see on UA?

A

+ hematuria, + proteinuria, and + red cell casts, (RBC dysmorphology implies glomerular damage - 95% sensitive and 90% specific)

  • combo of hematuria and proteinuria increase risk of renal disease
  • HTN: sx of fluid overload
37
Q

What is the total work up you want on this pt?

A
  • UA
  • CMP
  • CBC
  • C3, C4
  • ASO, RST
38
Q

Difference b/t nephrotic syndrome and glomerulonephritis?

A
  • nephrotic: edema, proteinuria, hypoproteinemia, elevated LDL, hypercoag: elevated fibrinogen, and factor V
- GN: ROPE 
R = red urine 
O = oliguria
P = proteinuria
E = elevated BP, BUN
low C3: post strep, membranoproliferative, SLE
39
Q

Case study:
pt has hematuria, proteinuria, numerous RBC, and granular casts, low Hbg, and low C3,
ASO is 2130, and + rapid strep, Dx?

A
  • PSGN
  • most common type of acute GN
  • common in 5-15 yo
  • 50% asx
  • dx by evidence of GAS (ASO detectable 2-4 weeks s/p pharyngitis)
40
Q

Tx of acute GN?

A
  • admit if HTN, edema, or signs of renal failure
  • monitor/correct electrolyte anomalies
  • tx HTN to avoid sequelae: diuresis: loop diuretics like lassie, fluid and Na+ restriction, anti HTN meds
41
Q

Tx for PSGN?

A
  • abx to target GABS
  • cultures often + even if no sxs
  • tx may result in milder course of PSGN
  • epidemics of GABS may warrant prophylaxis to prevent PSGN, especially in underdeveloped societies
42
Q

Prognosis and sequelae of PSGN?

A
  • good prognosis in kids
  • close F/U:
    HTN resolves 1-2 weeks
    C3 levels normal in 6 w
    gross hematuria in 6 w
    micro hematuria in 1 year
    proteinuria resolves in 6 months
    progression to renal dysfxn is RARE!!!
43
Q

What is the key test to work up discolored urine? What findings in a UA points to GN?

A
  • UA

- UA with casts/dysmorphic RBCs = GN

44
Q

32 yo male presents with R flank pain for 2-3 weeks, urine is brownish red. Had recent cold. Once before had similar episode of dark urine, UA: 2+ for blood, and 1+ for protein. Dx? Tx?

A
  • Dx: IgA nephopathy (Berger’s)
    want a CMP, CBC, confirm with bx
  • mesangial staining for IgA

tx: HTN (ACEI), if rapid progressionL corticosteroids, immunosuprressants

** recurrent episodes with proteinuria: higher risk of CKD

Nephrology (15 decks)

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