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Urinary > Glomerular pathology > Flashcards

Glomerular pathology Flashcards

1
Q

What is nephrotic syndrome?

A

loss of protein through the glomerulus into urine

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2
Q

What is nephritic syndrome?

A

loss of blood into urine w/ renal failure and hypertension, you usually get protein loss with it

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3
Q

What is the site of injury in nephrotic syndromes?

A

the podocytes/ subepithelium or basement membrane

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4
Q

What is the site of injury in nephritic syndromes?

A

the endothelium of the glomerulus

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5
Q

Why can lupus cause either nephritic or nephrotic syndrome?

A

because the autoantibodies can attack the endothelium, GBM or podocytes, and the location of damage determines the type

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6
Q

Give the 4 commonest primary causes of nephrotic syndrome

A
  • minimal change nephritis
  • focal segmental glomerular sclerosis (FSGS)
  • Membranous glomerular nephritis
  • lupus
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7
Q

Give two secondary causes of nephrotic syndrome

A
  • diabetes
  • hypertension
  • amyloidosis
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8
Q

What are the signs and symptoms of a nephrotic syndrome?

A
  • odema, particularly in the face in children and legs in adults
  • frothiness of urine due to prescence of protein
  • infections, lethargy, fatigue
  • hypercoagulabilty (may present as DVT)
  • Xanthelasma
  • breathlessness (due to pleural effusion)
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9
Q

Why do ppl with nephrotic syndrome get hyper-coagulability and xanthelasma?

A

Albumin levels drop as its being excreted in urine, so liver works harder to replace it, a side effect of this however is increased lipid production (xanthelasma) and increased clotting factor production

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10
Q

What is the commonest cause is nephrotic syndrome in children?

A

Minimal change nephritis

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11
Q

What causes minimal change nephritis?

A

they dont know, there is no evidence of immune complex deposition of anything

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12
Q

How is minimal change nephritis managed?

A
  • biopsy + need TEM to see podocyte damage (no pathology can be seen under a light microscope)
  • give steroids to put them into remission
  • doesnt often progress to renal failure
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13
Q

What is the pathophysiology to focal segmental glomerular sclerosis?

A

Something (they dont know what) causes scarring of sections of glomerulus

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14
Q

Do transplants or steroids work to treat FSGS?

A

Steroids have some benefit.
The transplants also get FSGS so dont really help.
Most progress to renal failure as scarring eventually leads to drop in GFR

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15
Q

What is the classic triad of findings seen in nephrotic syndrome

A
  • Protein urea of >3.5 g/day
  • Low blood albumin
  • Odema and high lipids
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16
Q

What is the pathophyiology do membranous glomerularnephritis

A

Damage to the basement membrane as a result of IgG forming immune complexes with an antigen on the basement membrane/ podocytes (autoimmune).
It may be secondary to other diseases for example its been associated with lymphoma

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17
Q

Describe how diebetes starts to cause nephropathy and why the early signs are kidney hypertrophy and increased GFR

A
  • Glycation damages the microvascular structures such as the afferent arteriole to thicken (hyaline sclerosis). This increases glomerular pressure and increases GFR.
  • More glucose in nephron means more Na+ reabsorbtion in PCT, so less goes to DCT and this activates RAAS leading to hypertension
  • The mesangeal cells secrete more matrix and so cause more hypertrophy
  • The increased GFR which leads to kidney hypertrophy
18
Q

What are kimmelsteil wilson nodules?

A

Nodules made by mesangeal cells secreteing more matrix as a result of diabetic nephropathy

19
Q

Why do microalbuminurea start to occur after latent diabetic nephropathy?

A

The mesangeal cells secreting more matrix thickens the basement membrane and leads to podocytes being more spaced out, so the glomerulus is more permeable and so albumin starts to be filtered. At this stage GFR is still normal but small quantities of albumin can be detected by albustix (extrasensitive dipsticks)

20
Q

What happens to GFR when macroalbuminurea sets in?

A

Eventually mesangeal expansion will impinge on filtration, until GFR drops and lots of albumin is filtered out.

21
Q

What are the risk factors for someone with diabetes to develop end stage renal disease?

A
  • poor control of blood glucose and blood pressure
  • genetics
  • increasing age
  • duration of diabetes (takes yrs to set in)
  • smoking
22
Q

How can diabetic nephropathy be treated?

A
  • can be slowed but not stopped
  • tight control of diabetes to try make sure youre not hypeglycaemic for too long
  • tight control of blood pressure particularly with ACEi and angiotensin blockers because this stops vasoconstriction of the afferent arteriole
23
Q

What are the 6 major primary causes of nephritic syndrome

A
  • IgA nephropathy
  • anti GBM
  • ANCA vasculitis
  • lupus
  • thin GBM (may be secondary to alport syndrome)
  • post infections
24
Q

What are the signs and symptoms of nephritic syndrome?

A 
haemtauria 
hypertension 
low GFR (causes hypertension)
fatigue 
frothy urine
25
Q

What classical finding is seen on microscopy of a kidney with nephritic syndrome?

A

red cell clasts (they form in nephrons due to glomerular damage)

26
Q

What age does IgA nephropathy most commonly present?

A

any age

27
Q

Describe the pathogenesis of IgA nephropathy

A

IgA- antigen complexes travel from blood and desposit in the mesangium, this damages the endothelium and causes blood to leak out and filter into the nephron. It is often precipitated by mucosal infections which would increase circulating IgA levels.

28
Q

What is the outcome for IgA nephropathy?

A

some progress to renal failure but some run a benign course

29
Q

What is benign familial nephropathy?

A

Same as thin GBM nephropathy, basically just that you have a gentically thin GBM, so blood and protein can leak into urine. It is often never noticed unless they get a urine dipstick as its almost always invisible haematuria.

30
Q

What is the defect in alport syndrome? why does this cause nephropathy?

A

X linked recessive defect in T4 collagen.

Means thin GBM, often progresses to renal failure due to mesangeal expansion, hypertrophy and the resulting drop in GFR

31
Q

What is goodpasture syndrome?

A

A rare autoimmune attack of the T4 collagen in the GBM, it will rapidly progress to renal failure. It is also called anti GBM

32
Q

How is goodpasture syndrome/ anti GBM treated?

A

Need urgent referral and immunosurpressants as it can be reversed if caught early but if not it will rapidly progress to renal failure

33
Q

What is ANCA vasculitis and how does it causes nephropathy?

A

A systemic disorder causing inflammation of the blood vessels, thought to be due to anti neutrophil cytoplasmic antibody (ANCA) release, which causes neutrophils to attack blood vessels of the glomerulus, leading to segmental necrosis of some glomeruli.

34
Q

What other location in the body is commonly affected and systemic symptoms are seen in ANCA vasculitis?

A

Arterioles in the lungs are also affected.

Systemic symptoms inc: fatigue, arthralgia, myalgia and weight loss

35
Q

How are nephritic and nephrotic syndromes treated generally? (5)

A
  • Treat any odema w/ diuretics and fluid restriction
  • ACEi to drop BP
  • Treat underlying conditions- generally by immunosurpression
  • Statins to lower cholesterol in nephrotic
  • Manage CVD risks in nephritic
36
Q

Describe how hypertension can cause glomerular nephropathy

A
  1. fibroelastic intima thickens and so the lumen narrows
  2. hylanosis of afferent arteriole walls-> drop in GFR
  3. these vascular changes lead to ischaemia of glomerulus-> causes glomerular sclerosis
  4. sclerosis will cause protein to leak into the nephron
  5. when GFR drops, raas is activated, BP increases and hypertension gets worse, leading to a negative cycle
37
Q

State 4 features of hypertensive glomerular sclerosis

A
  • History of poorly controlled hypertension
  • Recent drop in GFR, proteinuria, heamaturia if very bad
  • slowly progressive
  • tiredness, headache, nausia and vomiting may be present if GFR very low
  • Theyll tend to get hypertensive eye disease and LV hypertrophy before it affects the kidneys
38
Q

How can renal artery stenosis be differentiated from hypertensive renal disease causing GN?

A
  • Hypertension is acute (caused by the renal artery stenosis)
  • Decline in GFR is more rapid
  • Often evidence of atherosclerosis elsewhere
  • Treatment with ACEi will make renal function worse as less compensatory EA constriction so GFR decreases
39
Q

How is hypertensive renal disease managed?

A

Good control of BP- this will slow progression of the disease

40
Q

How can acute hypertension cause AKI?

A

An acute large increase in BP can damage kidney vessel endothelium, which can cause ischaemia and necrosis, leading to haematuria and proteinurea as well as a drop in GFR.

Urinary (9 decks)

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