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?

A
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
Q

What renal condition is somebody post MI who is struggling to maintain adequate blood pressure, at risk of?

A

Acute tubular injury

26
Q

What is the prevalence of kidney stones?

A
  • 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