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SA urinary > S8) Diabetes and Other Systemic Conditions Affecting the Kidney > Flashcards

S8) Diabetes and Other Systemic Conditions Affecting the Kidney Flashcards

1
Q

Describe the structure of the glomerular capillary wall

A
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2
Q

What is the commonest cause of ESRD (end stage renal disease)?

A

Diabetic nephropathy

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3
Q

Identify 5 pathological processes which occur in diabetic nephropathy

A
  • Hyperfiltration / capillary hypertension (occurs first)
  • GBM thickening (increases pore size)
  • Mesangial expansion
  • Podocyte injury
  • Glomerular sclerosis / arteriolosclerosis
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4
Q

What causes afferent vasodilation in Diabetes?

A
  • Hyperglycaemia
  • Low NaCl delivery to macula densa
  • High blood amino acid levels
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5
Q

What causes the arteriolosclerosis observed in diabetic nephropathy and what impact does this have?

A

Hyalinosis of arterioles which causes tissue ischaemia

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6
Q

The clinical signs and symptoms observed in diabetic nephropathy can be arranged into 5 stages.

Identify them

A
  1. Hyperfiltration & hypertrophy
  2. Latent stage
  3. Microalbuminuria (moderately increased albuminuria)
  4. Overt proteinuria (severely increased albuminuria)
  5. ESRD - end stage renal disease
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7
Q

What is observed in the latent stage of diabetic nephropathy?

A
  • Normal albuminuria
  • GBM thickening
  • Mesangial expansion
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8
Q

What is observed in the third stage of diabetic nephropathy (microalbuminuria)?

A
  • Variable mesangial expansion / sclerosis
  • Increased GBM thickening
  • Podocyte changes
  • GFR normal
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9
Q

What is observed in the fourth stage of diabetic nephropathy (overt proteinuria)?

A
  • Diffuse glomerular histopathological changes
  • Worsening systemic hypertension
  • Falling GFR
  • Microvascular changes (hyalinosis of arterioles)
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10
Q

What is the first clinical sign of diabetic nephropathy?

A

Microalbuminuria (assuming isotope GFR not measured)

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11
Q

Overt proteinuria in the third stage of diabetes is detectable on conventional dipstick.

What is the expected value in a woman?

A

Proteinuria > 30 mg/mmol Cr (0–3.5mg/mmol Cr)

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12
Q

Overt proteinuria in the third stage of diabetes is detectable on conventional dipstick.

What is the expected value in a man?

A

Proteinuria > 30 mg/mmol Cr (0–2.5mg/mmol Cr)

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13
Q

What is the clinical significance of overt proteinuria?

A
  • Average decline in GFR 12mls / min/ year (2 – 20 mls)
  • Most patients reach end-stage kidney disease in 3-7 years
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14
Q

Identify 5 risk factors for diabetic nephropathy

A
  • Genetic susceptibility
  • Race
  • Hypertension
  • Hyperglycaemia
  • Increasing age
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15
Q

Describe the primary prevention of diabetic nephropathy

A
  • Tight blood glucose control < 48 mmol/mol (<6.5%)
  • Tight blood pressure control
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16
Q

Tight glycaemic control involves multiple injections or insulin pump to achieve a near normal blood glucose.

Describe 4 effects of this

A
  • Can reverse initial hyperfiltration
  • Can delay microalbuminuria
  • Can reduce microalbuminuria over 2 years treatment period
  • Doesn’t slow GFR loss once overt proteinuria develops
17
Q

Referring to 5 options, describe the managment of microalbuminuria and proteinuria

A
  • Inhibition of RAAS
  • Tight blood pressure control < 130/75 mmHg
  • Statin therapy

- CV risk management (exercise, diet, stop smoking)

  • Moderate protein intake
18
Q

Angiotensin II is released following renin release.

Identify 4 effects of this substance on the kidney

A
  • Increases glomerular permeability to proteins
  • Mesangial cell proliferation
  • Increases mesangial matrix
  • Constricts efferent glomerular arteriole
  • Increases glomerular pressure
19
Q

State 2 effects of RAAS inhibition in the management of diabetic nephropahty

A
  • Reduces glomerular hyperfiltration (efferent > afferent arterioles)
  • Reduces proteinuria & slows progression at stages 2 - 4 of diabetic nephropathy
20
Q

What is the first renal sign of hypertensive renal disease / nephrosclerosis?

A

Microalbuminuria

21
Q

Describe the general diagnosis of hypertensive nephrosclerosis

A
  • Hypertension precedes proteinuria
  • Long-term decline in GFR
  • Often, left ventricular hypertrophy and hypertensive eye disease before developing kidney disease
22
Q

How does the clinical presentation of renal artery stenosis differ from hypertensive nephrosclerosis?

A
  • More acute hypertension
  • More rapid decline in GFR
  • Evidence of atherosclerosis elsewhere
  • Acute worsening with RAAS-blockade
23
Q

Describe the vascular changes of hypertensive nephrosclerosis

A

Vascular changes to renal arteries & arterioles:

  • Fibroelastic intimal thickening → narrowing of lumen
  • Hyalinosis of afferent arteriolar walls
24
Q

Describe the glomerular changes of hypertensive nephrosclerosis

A

Glomerular changes secondary to ischaemia from vascular changes:

  • Wrinkling of glomerular tuft
  • Glomerulosclerosis (patchy)
25
Q

Briefly, describe how hypertensive disease in young black patients is probably different than that in older Caucasian patients

A
26
Q

The managment of hypertension in hypertensive nephrosclerosis slows the overall progression of the disease.

Describe the management

A

Good BP control:

  • ACE-Inhibitors
  • Angiotensin-receptor blockers (if there is albuminuria)
27
Q

Hypertensive emergency involves an acute large increase in BP with target organ damage.

Describe how this presents

A
  • Damage to endothelium (haematuria)
  • Fibrinoid necrosis of arterioles (ischaemia – activation of RAAS)
  • Shearing of blood cells (haemolytic anaemia)
  • AKI
28
Q

Identify the 3 characteristic features of Nephrotic Syndrome

A
  • Proteinuria > 350 mg/mmol
  • Hypoalbuminaemia / hyperalbuminuria
  • Oedema
29
Q

Identify 3 other serum measurements which often accompany Nephrotic Syndrome

A
  • High cholesterol
  • Normal BP often (can be low or high)
  • Creatinine may be normal
30
Q

Identify 3 primary and secondary causes of Nephrotic Syndrome

A
  • Primary: minimal change disease, FSGS, membranous nephropathy
  • Secondary: diabetes, amyloidosis, SLE
31
Q

Describe the management of Nephrotic Syndrome

A
  • Diuretics (large doses) – oedema
  • ACE-Inhibitor – proteinuria
  • Atherogenic – hypercholesterolaemia (if long-term nephrotic)
  • Treat underlying condition
32
Q

Identify 4 clinical features of Nephritic Syndrome

A
  • Haematuria
  • Reduction in GFR (renal impairment / oliguria)
  • Hypertension
  • Non-nephrotic proteinuria
33
Q

What is occurring in Nephritic Syndrome?

A

In Nephritic syndrome, the disruption of the endothelium results in inflammatory response and damage to the glomerulus

34
Q

Onset of Nephritic Syndrome may be insidious or rapidly progressive.

What is Rapidly Progressive / Crescentic GN?

A

Rapidly Progressive / Crescentic GN is a fulminant form of nephritic syndrome caused by crescent formation

35
Q

Identify 5 common causes of Nephritic Syndrome

A
  • Goodpastures Syndrome
  • ANCA-associated vasculitis
  • IgA / Henoch-Schönlein purpura*
  • Post-infectious*
  • SLE*

*can also present as nephrotic

36
Q

Describe the management of Nephritic Syndrome

A
  • Proteinuria – blood pressure control (ACE-I/AIIR)
  • Oedema – diuretics (large doses)
  • Disease specific treatments – generally immunosuppressants
  • CV risk management – stop smoking, statin, etc.
37
Q

What is Systemic Lupus Erythematosus?

A
  • SLE is an auto-immune systemic disease which can affect multiple systems and has many different patterns of renal disease
  • It can cause nephritic or nephrotic syndrome
38
Q

What is ANCA vasculitis?

A

- ANCA vasculitis is a type of autoimmune swelling caused by autoantibodies which affects small arterioles often in the kidneys and lungs

  • It offten presents with systemic symptoms: fatigue, arthralgia, myalgia, weight loss

SA urinary (25 decks)

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