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Renal > Glomerular disease > Flashcards

Glomerular disease Flashcards

1
Q

Clinical Px of glomerular disease in general

A

• glomerular disease has diverse clinical presentations including hematuria, proteinuria,hypertension, edema and decreased GFR
• each glomerulopathy presents as one of four major glomerular syndromes (these are NOTdiagnoses):
○ acute nephritis
○ rapidly progressive glomerulonephritis
○ nephrotic
○ asymptomatic urinary abnormalities
• glomerulopathies can be caused by a primary disease OR can occur secondary to a systemic disease
• some glomerulopathy can present as more than one syndrome at different times

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2
Q

What is Protein-creatinine ratio

A

relates to concentration of urine sample. Has good correlation (1g=100)
Albumin makes about 1/3 of protein that’s being leaked.

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3
Q

How is urine albumin-to-creatinine ratio (ACR) helpful?

A

to early diagnose kidney problems especially diabetic nephropathy (they selectively have albuminuria instead of general proteinuria)

used to screen for diabetic nephropathy

- microalbuminuria
- defined as ACR ≥2.8 mg/mmol (female) or ≥2.0 mg/mmol (male)
- marker of vascular endothelial function
- an important prognostic marker for kidney disease in diabetes and hypertension (see Diabetes, NP28)
- an elevated ACR ≥2.0 or 2.8 mg/mmol is the earliest sign of diabetic nephropathy
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4
Q

What amount of protein excretion is ‘abnormal’ and hence proteinuria?

A

3500mg total protein/1.73m^2 per day = nephrotic range proteinuria

  • upper limit of normal daily excretion of total protein is 150 mg/d
    • upper limit of normal daily excretion of albumin is 30 mg/d

the other normally excreted proteins are either filtered low molecular weight proteins (such as immunoglobulin, light chains or β-2 microglobulin) or proteins secreted by the tubular epithelial cells (e.g. Tamm-Horsfall mucoprotein)

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5
Q

Ix for proteinuria

A

• urine R&M, C&S, urea, Cr
• further workup (if degree of proteinuria >0.5 g/d, casts and/or hematuria)
- CBC, glucose, electrolytes, 24-h urine protein and Cr
- urine and serum immunoelectrophoresis, abdominal/pelvic ultrasound
- serology: ANA, RF, p-ANCA (MPO), c-ANCA, (PR3) Hep B, Hep C, HIV, Antisteptolysin-O (ASOT)
• indications for nephrology referral
- generally, if there is “heavy” proteinuria, should refer to nephrologist
- heavy proteinuria is ACR >30 mg/mmol
• definitely if there is nephrotic syndrome: marked proteinuria >3.5g/1.73m2/d with hypoalbuminemia (

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6
Q

Definen haematuria

A

• hallmark of nephritic syndromes
• presence of blood or RBCs in urine
- gross hematuria: pink, red, or tea-coloured urine
- in gross hematuria, the urine should be centrifuged:
○ if the sediment is red, true hematuria.
○ if the supernatant is red, test for heme with a dipstick
○ if supernatant +ve for heme: myoglobinuria or hemoglobinuria
○ if –ve for heme: pseudohematuria. Consider medications (e.g. rifampin), food dyes (e.g. beets) or metabolites (e.g. porphyria)
• microscopic hematuria: normal coloured urine, >2-3 RBCs/HPF on microscopy

Normally there should be no RBC

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7
Q

Ix of haematuria

A
  • Hx and Px: family history of nephrolithiasis, hearing loss (Alport’s), cerebral aneurysm (PCKD), diet, recent URTI, irritative and obstructive urinary symptoms (UTI)
  • urine R&M, C&S, urea, Cr
  • renal ultrasound
  • 24-h urine stone workup if there is a history of stone formation or if there is a stone noted on imaging: calcium, oxalate, citrate, magnesium, uric acid, cysteine
  • further workup (if casts and/or proteinuria): CBC, electrolytes, 24-h urine protein and Cr, serology (ANA, RF, C3, C4, p-ANCA, c-ANCA, ASOT)
  • consider urology consult and possible cystoscopy if not clearly a nephrologic source for hematuria or if >50 yr of age
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8
Q

Causes of isolated proteinuria in asymptomatic urinary abnormalities

A
  • can be postural

- occasionally can signal beginning of more serious GN (e.g. FSGS, IgA nephropathy, amyloid, diabetic nephropathy)

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9
Q

Causes of hematuria with or without proteinuria in asymptomatic urinary abnormalities

A
  • IgA nephropathy (Berger’s disease): most common type of primary glomerular disease worldwide, usually presents after viral URTI
  • hereditary nephritis (Alport’s disease): X-linked nephritis often associated with sensorineural hearing loss; proteinuria
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10
Q

What is a Bence-Jones protein?

A

a monoclonal globulin protein or immunoglobulin light chain found in the urine

Detection of Bence Jones protein may be suggestive of multiple myeloma or Waldenström’s macroglobulinemia

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11
Q

Describe amyloidosis as a secondary cause of glomerular disease

A
  • nodular deposits of amyloid in mesangium, usually related to amyloid light chain (AL)
  • presents as nephrotic range proteinuria with progressive renal insufficiency
  • can be primary or secondary
  • secondary causes: multiple myeloma, TB, rheumatoid arthritis, malignancy
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12
Q

Describe Lupus as a secondary cause of glomerular disease

A
  • lupus nephritis can present as any of the glomerular syndromes
  • nephrotic syndrome with an active sediment is most common presentation
  • glomerulonephritis caused by immune complex deposition in capillary loops and mesangium with resulting renal injury
  • serum complement levels are usually low during periods of active renal disease
  • children and males with SLE are more likely to develop nephritis
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13
Q

Describe Henoch-Schonlein purpura as a secondary cause of glomerular disease

A

HSP is a systemic vasculitis (inflammation of blood vessels) and is characterized by deposition of immune complexes containing the antibody IgA; the exact cause for this phenomenon is unknown. It usually resolves within several weeks and requires no treatment apart from symptom control, but may relapse in a third of the cases and cause irreversible kidney damage in about one in a hundred cases

  • seen more commonly in children
  • purpura on buttocks and legs, abdominal pain, arthralgia and fever
  • glomeruli show varying degrees of mesangial hypercellularity
  • IgA and C3 staining of mesangium
  • usually benign, self-limiting course, 10% progress to CKD
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14
Q

Describe Goodpasture’s disease as a secondary cause of glomerular disease

A
  • antibodies against type IV collagen present in lungs and GBM
  • more common in 3rd and 6th decades of life, men slightly more affected than females
  • present with RPGN type I and hemoptysis/dyspnea
  • pulmonary hemorrhage more common in smokers and males
  • treat with plasma exchange, cyclophosphamide, prednisone
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15
Q

Describe ANCA associated vasculitis as a secondary cause of glomerular disease

A
  • pr3-ANCA (c-ANCA) most commonly associated with the clinical picture of granulomatosis with polyangiitis (previously called Wegener’s granulomatosis)
  • mpo-ANCA (p-ANCA) most commonly associated with the clinical picture of microscopic polyangiitis
  • renal involvement very common
  • focal segmental necrotizing RPGN with no immune staining (pauci-immune)
  • may be indolent or fulminant in progression
  • vasculitis and granulomas rarely seen on renal biopsy
  • treating typically involves cyclophosphamide and prednisone
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16
Q

Describe cryoglobulinemia as a secondary cause of glomerular disease

A
  • cryoglobulins: monoclonal IgM and polyclonal IgG
  • presents as purpura, fever, Raynaud’s phenomenon and arthralgias
  • at least 50% of patients have hepatitis C
  • renal disease seen in 40% of patients (isolated proteinuria/hematuria progressing to nephritic syndrome)
  • most patients have decreased serum complement (C4 initially)
  • treat hepatitis C, plasmapheresis
  • overall prognosis: 75% renal recovery
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17
Q

Describe shunt nephritis as a secondary cause of glomerular disease

A
  • immune-complex mediated nephritis associated with chronically infected ventriculoatrial shunts inserted for treatment of hydrocephalus
  • presents as acute nephritic syndrome with decreased serum complement
  • nephrotic range proteinuria in 25% of patients
18
Q

Describe HIV as a secondary cause of glomerular disease

A
  1. direct nephrotoxic effect of HIV infection, antiretroviral drugs (e.g. tenofovir, indinavir) and other drugs used to treat HIV-associated infections
  2. HIV-associated nephropathy (HIVAN)
    • histology: focal and segmental glomerular collapse with mesangial sclerosis, “collapsing FSGS”
    • tubular cystic dilation and tubulo-reticular inclusions
    • clinical features: predominant in black men, heavy proteinuria, progressive renal insufficiency
    • prognosis: kidney failure within 1 yr without treatment
    • therapy: short-term, high dose steroids, ACEI, HAART
19
Q

Describe infective endocarditis as a secondary cause of glomerular disease

A
  • manifests as mild form of acute nephritic syndrome with decreased serum complement
  • S. aureus is most common infecting agent
  • treatment with appropriate antibiotics usually resolves GN
20
Q

Describe Hep B & C as a secondary cause of glomerular disease

A

Hep B: can result in membranous nephropathy, polyarteritis nodosa, membranoproliferative GN

Hep C: can result in membranoproliferative GN, cryoglobulinemia and membranous nephropathy

21
Q

Describe syphilis as a secondary cause of glomerular disease

A

can result in membranous GN

22
Q

Px of nephrotic syndrome (4)

A

HELP

Hypoalbuminemia
Edema
Lipid abnormalities
Proteinuria

23
Q

Px of nephritic syndrome (6)

A

PHAROH

Proteinuria
Hematuria
Azotemia
RBC casts
Oliguria
Hypertension
24
Q

(2) types of GN that is nephritic

A

IgA GN

Post infectious GN - although rare now

25
Q

(3) types of GN that is nephrotic

A

Membranous glomerulonephropathy

Minimal change disease

Focal segmental glomerulosclerosis (FGGS)

26
Q

Describe IgA GN

A
  • (huge spectrum of people who have benign IgA and 15-20% have ESKD)
    • Mesangial proliferative glomerulonephritis with segmental lesions and crescents and mild tubular atrophy/interstitial fibrosis
    • Usually due to recent illness; synpharyngitic.
    • Demographics: 20-40yo, male, Asian
    • Proliferation of mesangial cells

Seen on IgA immunofluorescence

27
Q

Describe post infectious GN

A
  • Rare
    • Autoimmune
    • Complex depositions deposit in the kidneys
    • Hypertension
    • A few weeks post infection.
    • Mechanism is unknown.
    • Immune complex deposit in the kidney. Some become chronic. ?underlying renal impairment
    • Third world country residents in First world countries e.g. Aborigines (higher detection rate)
28
Q

Describe membranous glomerulonephropathy

A
  • 1/3 people spontaneously resolve
    • a slowly progressive disease of the kidney affecting mostly patients between ages of 30 and 50 years, usually Caucasian.
    • It is the second most common cause of nephrotic syndrome in adults, with focal segmental glomerulosclerosis (FSGS) being the most common
    • Membranoproliferative glomerulonephritis involves the basement membrane and mesangium, while membranous glomerulonephritis involves the basement membrane but not the mesangium
    • 85% of MGN cases are classified as primary membranous
    • MGN is caused by immune complex formation in the glomerulus. The immune complexes are formed by binding of antibodies to antigens in the glomerular basement membrane.
29
Q

Describe minimal change disease

A
  • 4-12yo (kids)
    • No need for biopsy. Nephrotic syndrome in young: typically minimal change disease
    • Easily treatable with steroids
    • Does not cause kidney problems/impairment. Only causes proteinuria and features of nephortic syndrome
    • But it can relapse and remit.

Often kids grow out of it (like asthma) but some have recurrent relapses to the point to need cyclosporin

30
Q

Describe focal segmental glomerulosclerosis (FSGS)

A
  • Scarring disorder
    • Nasty
    • Idiopathic
    • Difficult to treat
    • Many progress to ESKD
    • Treat it like membranous. Give immunosuppression (cyclosporin/steroids)
    • likely to recur after transplant
    • In adults
    • Secondary causes: obesity, HIV
    • End result of any kidney disease that ends up sclerosing
31
Q

What GN is intermediate between nephrotic and nephritic?

A

Membranoproliferative GN

* Mesangial proliferation like IgA
* Capillary thickening like in membranous 
* Secondary: Hep C
* Idiopathic mostly 
* Immunosuppression but not as successful

Rare

32
Q

What pathological changes do you see in minimal change disease?

A

no changes when viewing specimens under light microscopy; hence the name minimal change disease.

With the advent of electron microscopy, the changes now known as the hallmarks for the disease were discovered. These are diffuse loss of visceral epithelial cells foot processes (podocyte effacement), vacuolation, and growth of microvilli on the visceral epithelial cells

33
Q

SE of cyclophosphamide (immunosuppressant/cytotoxic)

A

infections, infertility, cystitis (if IV and large amount used for breast cancer), TCC, nausea

34
Q

Rx of IgA nephropathy

A

IgA usually it is benign.

Treat with ACEI/ARB, spironolactone to lower BP. Monitor only

35
Q

What 3 features are indicators for poor prognosis in renal conditions in general?

A
  1. Poor renal function
  2. Hypertension
  3. Proteinuria
36
Q

What are the 4 types of glomerulonephritis with nephritic features?

A

RPGN type I: Anti-GBM mediated (GPD, anti-GBM disease)

RPGN type 2: immune complex mediated (IgA nephropathy, SLE, membranoproliferative GN, post-infectious GN)

RPGN type 3: non-immune mediated (Churg-Strauss, microscopic polyangiitis for p-ANCA, granulomatosis with polyangiitis for c-ANCA)

RPGN type 4: double antibody positive disease. Has features of type I & III

37
Q

What do you see in renal histopathology in RPGN (rapidly progressive GN)?

A

FIBROUS CRESCENTS typically present on renal histopathology

• RBC casts and/or dysmorphic RBCs in urine

*Red blood cell casts mean there is a microscopic amount of bleeding from the kidney. They are seen in many kidney diseases. Renal tubular epithelial cell casts reflect damage to tubule cells in the kidney.

38
Q

In nephrotic syndrome, is pt in a hypercoagulable state or hypocoagulable state?

A

hypercoagulable state

(due to antithrombin III, Protein C and Protein S/anticoagulant urinary losses) -> arterial thrombose can occur

39
Q

What renal pathology do you see in nephrotic syndrome?

A

abnormality of podocytes on pathology: fusion, effacement, abliteration etc.

Need EM to see anything in minimal change disease (very heavy proteinuria) -> abnormalities in podocytes (not very visible in LM)

Membranous: little spikes on silver staining.

40
Q

Which nephrotic GN is easier to treat than what?

A

Minimal change disease - responds to steroids better than FSGS.

Renal (11 decks)

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