15 - Diabetes and the Kidney Flashcards

1
Q

What are the different pathological processes that can lead to glomerulonephritis?

A

Inflammation of the capillary loops in the glomeruli

  • Increased number of mesangial cells
  • Invasion of leukocytes
  • Immune complexes
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2
Q

What are the different ways of classifying glomerulonephritis?

A
  • Clinical presentation e.g nephritic or nephrotic
  • Histological appearnce
  • Diagnosis
  • Primary or Secondary
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3
Q

What are some clinical presentations of glomerulonephritis?

A
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4
Q

How can we manage nephrotic syndrome?

A
  • Diuretics/salt and fluid restriction for oedema
  • ACE-inhibitor: anti-proteinuric but only if not volume depleted
  • Statins for hypercholesterolaemia as atherogenic
  • Treat underlying condition, e.g steroids
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5
Q

What are some diseases that can present both nephritically and nephrotically?

A
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6
Q

How can we manage nephritic syndrome?

A
  • ACEi or AngIIRB/salt restrict for blood pressure and proteinuria
  • Diuretics for little oedema
  • Treat underlying condition e.g immunosuppressants
  • CVS risk management, e.g stop smoking
  • Short term dialysis
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7
Q

What is ANCA associated vasculitis?

A
  • Systemic vasculitis like microscopic polyangitis and Wegener’s affect small arterioles of the glomerulus and lead to nephritic issue
  • Systemic symptoms like fatigue, weight loss, arthralgia
  • Endothelial damage not by immune deposits but by antiodies to WBC
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8
Q

How does Anti-GBM (Goodpasture’s) disease lead to GN?

A
  • GN but not a vasculitis
  • Production of antibodies to type 4 collagen in the GBM
  • Leads to rapidly progressive GN and 90% mortality if not treated

Any fast destruction of glomerulus leads to crescent on biopsy and with antibodies

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9
Q

How does systemic lupus nephritis lead to glomerulonephritis?

A
  • Type of vasculitis
  • Has lots of different patterns of nephritis and can cause nephrotic and nephritic
  • Autoimmune
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10
Q

What are some symptoms of SLE and how is it treated?

A

Autoimmune condition treated with steroids. Immune complexes formed between antibodies and nuclei of organ cells leading to damage

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11
Q

What are some changes to the structure of the glomerulus in diabetic nephropathy?

A
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12
Q

How does diabetes lead to changes in the glomerulus?

A
  • Commonest cause of ESRD, not a GN

1. Hyperfiltration/Capillary hypertension due to hyperglycaemia in urine

2. GBM thickens

3. Mesangial expansion

  1. Podocyte injury and then glomerular sclerosis
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13
Q

Why do you get an increased GFR with diabetic nephropathy when the basement membrane is thickening?

A

All damage done is due to capillary hypertension as less Na getting to the macula densa

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14
Q

What would diabetic nephropathy look like histologically?

A

Initial: Glomerulosclerosis so thicker GBM and mesangial expansion

Overt: Kimmelsteil-Wilson nodule (diffuse nodular glomerulosclerosis) and hyaline in arterioles

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15
Q

What is the first signs and progression of diabetic nephropathy?

A

- Increased GFR due to hypertrophy and hyperfiltration

- Latent where everything is normal as GBM thickens and mesangial expands

- Microalbuminuria 1st sign so thickened GBM and podocyte damage but GFR normal (treatment can intervene at this point)

- Overt proteinuria wwhere there is a falling GFR and diffuse changes

- ESRD

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16
Q

How can you tell what stage a diabetic is in in their nephropathy journey?

A
  • Albustix for microalbuminuria as can’t be seen on normal dipstick. Mesangial expansion and GBM thickening at this point and is first clinical sign. Still reversible
  • Dipstick for protein >30mmol/mg. Not now reversible but progression to ESRD can be slowed
17
Q

How long does it take for most kidney patients to reach ESRD?

A

- 3-7 years after 1st sign, decline of 12mls/min GFR a year

  • However overt diabetic nephropathy doesn’t develop until around 8-15 years after diabetes diagnosis
18
Q

What are risk factors for diabetic nephropathy?

19
Q

How can we prevent diabetic nephropathy?

A

- Tight glycaemic control <6.5% HbA1C can reverse hyperfiltration and delay microalbuminuria

  • Tight blood pressure control with RAAS (also helps proteinuria)
  • Statins
  • CVS risk management
  • ?SGLT2 inbitors

Only before overt proteinuria can this help

20
Q

What damage can angiotensin II do to the kidney?

A
  • Increase glomerular permeability to proteins
  • Mesangial proliferation
  • Efferent glomerular constriction so increased glomerular pressure
21
Q

In simple terms what causes haematuria and proteinuria?

A

- Haematuria = damage to endothelium

- Protienuria = damage to podocyte, GBM thickening and glomerulosclerosis

22
Q

Why would a paediatrician not see a child with diabetes about their nephropathy?

A

Nephropathy takes 8-15 years to develop so won’t be a child anymore

23
Q

Does this patient have diabetic nephropathy?

A
  • Evidence of hyperfiltraion, first warning
  • Start ACE-I
  • Tight glycaemic control
  • Use albumin stick
24
Q

What is acute polycystic kidney disease?

A

Inherited disorder where benign small cysts accumulate on the kidney and lower its function

25
What renal condition is somebody post MI who is struggling to maintain adequate blood pressure, at risk of?
Acute tubular injury
26
What is the prevalence of kidney stones?
- 2-3% of people will have at some point and once they do there is a high recurrence rate - 12,000 a year in UK - Usually made of calcium and supersaturation