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Renal - Glomerulonephritis Flashcards

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1
Q

Features of nephritic syndrome

A

Haematuria means blood in the urine. This can be microscopic (not visible) or macroscopic (visible).
Oliguria means there is a significantly reduced urine output.
Proteinuria is protein in the urine. In nephritic syndrome, there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.
Fluid retention

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2
Q

Criteria for nephrotic syndrome diagnosis

A

Peripheral oedema
Proteinuria more than 3g / 24 hours
Serum albumin less than 25g / L
Hypercholesterolaemia

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3
Q

What does glomerulonephritis refer to

A

Glomerulonephritis is an umbrella term applied to conditions that cause inflammation of or around the glomerulus and nephron

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4
Q

What is interstitial nephritis

A

Interstitial nephritis is a term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney

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5
Q

What is glomerulosclerosis

A

Glomerulosclerosis is a term to describe the pathological process of scarring of the tissue in the glomerulus. It is not a diagnosis in itself and is more a term used to describe the damage and scarring done by other diagnoses

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6
Q

What can cause glomerulosclerosis

A

Glomerulosclerosis can be caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a specific disease called focal segmental glomerulosclerosis.

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7
Q

What are most types of glomerulonephritis treated with

A

Immunosuppression (e.g. steroids)
Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)

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8
Q

Most common cause of nephrotic syndrome in children

A

Minimal change disease

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9
Q

Most common cause of nephrotic syndrome in adults

A

Focal segmental glomerulosclerosis

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10
Q

Aetiology of minimal change disease

A

Majority are idiopathic
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

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11
Q

Features of minimal change disease

A

nephrotic syndrome
normotension - hypertension is rare
highly selective proteinuria
only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus

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12
Q

What might a renal biopsy show in minimal change disease

A

normal glomeruli on light microscopy

electron microscopy shows fusion of podocytes and effacement of foot processes

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13
Q

Mx of minimal change disease

A

majority of cases (80%) are steroid-responsive

cyclophosphamide is the next step for steroid-resistant cases

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14
Q

What is focal segmental glomerulosclerosis(FSGS)

A

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.

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15
Q

Causes of FSGS

A 
idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport's syndrome
sickle-cell
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16
Q

In which patients is FSGS likely to recur

A

Patients with renal transplants

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17
Q

What might a renal biopsy show in FSGS

A

focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy

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18
Q

Mx of FSGS

A

steroids +/- immunosuppressants

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19
Q

What does nephrotic syndrome predispose patients to

A

Nephrotic syndrome predisposes patients to thrombosis, hypertension and high cholesterol.

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20
Q

Most common cause of primary glomerulonephritis

A

IgA nephropathy(Berger’s disease)

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21
Q

How does IgA nephropathy classically present

A

It classically presents as macroscopic haematuria in young people following an upper respiratory tract infection.

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22
Q

Conditions associated with IgA nephropathy

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A

alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

23
Q

Histology in IgA nephropathy

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A

Mesangial hypercellularity

Positive immunofluorescence for IgA and C3

24
Q

IgA nephropathy presentation

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A

young male, recurrent episodes of macroscopic haematuria
typically associated with a recent respiratory tract infection(1-2 days after URTI)
nephrotic range proteinuria is rare
renal failure is unusual and seen in a minority of patients

25
Differentiation of IgA nephropathy and post-strep glomerulonephritis
post-streptococcal glomerulonephritis is associated with low complement levels main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur) there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis(Posy-strep glomerulonephritis develops 1-2 weeks after URTI)
26
Mx of IgA nephropathy if isolated hematuria with no/minimal proteinuria
no treatment needed, other than follow-up to check renal function
27
Mx of IgA nephropathy if persistent proteinuria, a normal or only slightly reduced GFR
initial treatment is with ACE inhibitors if there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors immunosuppression with corticosteroids
28
What is the most common type of glomerulonephritis overall
Membranous glomerulonephritis
29
How does membranous glomerulonephritis usually present
Nephrotic syndrome or proteinuria
30
What might a renal biopsy demonstrate in membranous glomerulonephritis
electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a 'spike and dome' appearance
31
Causes of membranous glomerulonephritis
diopathic: due to anti-phospholipase A2 antibodies infections: hepatitis B, malaria, syphilis malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia drugs: gold, penicillamine, NSAIDs autoimmune diseases: systemic lupus, thyroiditis, rheumatoid
32
Mx of membranous glomerulonephritis
all patients should receive an ACE inhibitor or an angiotensin II receptor blocker (ARB) A combination of corticosteroid + another agent such as cyclophosphamide is often used
33
What is post strep glomerulonephritis
Post-streptococcal glomerulonephritis typically occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (usually Streptococcus pyogenes). It is caused by immune complex (IgG, IgM and C3) deposition in the glomeruli. Young children are most commonly affected.
34
Features of post strep glomerulonephritis
``` headache malaise visible haematuria proteinuria this may result in oedema hypertension oliguria ```
35
Renal biopsy features of post strep glomerulonephritis
endothelial proliferation with neutrophils electron microscopy: subepithelial 'humps' caused by lumpy immune complex deposits immunofluorescence: granular or 'starry sky' appearance
36
What is Anti-GBM/goodpasture's syndrome
Is a rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis. It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen.
37
Features of Anti-GBM disease
pulmonary haemorrhage rapidly progressive glomerulonephritis this typically results in a rapid onset acute kidney injury nephritis → proteinuria + haematuria
38
IX for Anti-GBM disease
renal biopsy: linear IgG deposits along the basement membrane raised transfer factor secondary to pulmonary haemorrhages
39
Mx of Anti-GBM disease
plasma exchange (plasmapheresis) steroids cyclophosphamide
40
Factors that increase likelihood of anti-gbm disease
``` smoking lower respiratory tract infection pulmonary oedema inhalation of hydrocarbons young males ```
41
What does rapidly progressive glomerulonephritis refer to
Rapidly progressive glomerulonephritis is a term used to describe a rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli.
42
Causes of rapidly progressive glomerulonephritis
Goodpasture's syndrome Wegener's granulomatosis others: SLE, microscopic polyarteritis
43
Features of rapidly progressive glomerulonephritis
nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria features specific to underlying cause (e.g. haemoptysis with Goodpasture's, vasculitic rash or sinusitis with Wegener's)
44
Gene associated with Anti-GBM disease
HLA DR2
45
What is granulomatosis with polyangiitis (Wegener's granulomatosis)
It is an autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting both the upper and lower respiratory tract as well as the kidneys.
46
Features of wegener's granulomatosis
upper respiratory tract: epistaxis, sinusitis, nasal crusting lower respiratory tract: dyspnoea, haemoptysis rapidly progressive glomerulonephritis ('pauci-immune', 80% of patients) saddle-shape nose deformity also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
47
Wegener's granulomatosis vs Churg-Strauss syndrome
Wegener's granulomatosis - Renal failure, epistaxis/haemoptysis, cANCA Churg-Strauss syndrome - Asthma, pANCA, eosinophilia
48
IX for wegner's disease
cANCA positive in > 90%, pANCA positive in 25% chest x-ray: wide variety of presentations, including cavitating lesions renal biopsy: epithelial crescents in Bowman's capsule
49
Causes of transient or spurious non-visible haematuria
urinary tract infection menstruation vigorous exercise (this normally settles after around 3 days) sexual intercourse
50
Causes of persistent non-visible haematuria
``` cancer (bladder, renal, prostate) stones benign prostatic hyperplasia prostatitis urethritis e.g. Chlamydia renal causes: IgA nephropathy, thin basement membrane disease ```
51
Spurious causes of haematuria where blood is not present on dipstick
foods: beetroot, rhubarb drugs: rifampicin, doxorubicin
52
When should urgent referral be made for haematuria
Aged >= 45 years AND: unexplained visible haematuria without urinary tract infection, or visible haematuria that persists or recurs after successful treatment of urinary tract infection Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test
53
What might bloods show in post strep glomerulonephritis
bloods: low C3 raised ASO titre

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