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MBChB > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Give some secondary causes of glomerulonephritis

A 
Haematological: myeloma, CLL
Gastro: ALD, IBD, coeliac disease
Resp: bronchiectasis, lung cancer, TB 
Infectious disease: hepatitis, HIV, malaria, Abx
Rheum: SLE, RA, amyloid
Drugs: bisphosphonates, NSAIDs, heroin
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2
Q

What is key to the clinical diagnosis of GN?

A

Kidney biopsy (need 10-12 glomeruli)

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3
Q

Describe Rapidly Progressing Glomerulonephritis (RPGN)

A

Crescenteric damage
Rapid increase in sCr over days
Aggressive - progresses to ESRF in 80-90% without treatment

Causes:
ANCA vasculitis
Goodpastures Syndrome (anti-GBM)
Lupus nephritis
Infection associated (strept/staph) - happens weeks after infection
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4
Q

Describe nephritic syndrome

A

Haematuria and proteinuria
High BP, raising sCR
Associated with IgA, SLE, post-infective

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5
Q

Describe nephrotic syndrome

A

Proteinuria (PCR >300 or >3.5g/d of protein)
Low serum albumin (<30)
Oedema
(+hyperlipidaemia)

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6
Q

What is the most common primary glomerular disease?

A

IgA nephropathy

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7
Q

Describe IgA nephropathy

A

Most common primary glomerular disease
May be secondary due to coeliac disease/cirrhosis
May be precipitated by an infection - synpharyngitic (strept. infection + blood in urine at same time)
Abnormal/overproduction of IgA –> proliferation of mesangial cells

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8
Q

What are the effects of IgA nephropathy?

A

Haematuria
HTN
Proteinuria (varies with prognosis)

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9
Q

How is IgA nephropathy managed?

A

ACEi (reduce permeability of GBM)

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10
Q

How many people with IgA nephropathy will develop ESRF?

A

1/3

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11
Q

Describe Membranous Glomerulonephritis

A

A disease of adults - effects podocytes
Presents with nephrotic syndrome
10% secondary to malignancy, drugs

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12
Q

What Auto-Ab is associated with membranous glomerulonephritis?

A

Anti-phospholipase A2 receptor Ab (70%)

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13
Q

What is the history of membranous glomerulonephritis like?

A

1/3 will spontaneously remit in 12-18 months
1/3 will progress onto ESRF in 1-2 years
1/3 will have persistent proteinuria with maintained eGFR

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14
Q

Describe the management of membranous glomerulonephritis

A

Treat underlying condition
ACEi, statins, diuretics, salt restriction
Cyclosporin, ritixumab, alkylating agents (cyclosphosphamide), steroids

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15
Q

Describe minimal change disease

A

The commonest GN in children (90% <10y)
Generally idiopathic but may be due to malignancy ie lymphoma
Presents with nephrotic syndrome

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16
Q

What changes are seen on:
A) light microscopy
B) electron microscopy
in minimal change disease?

A

A) no changes on light microscopy

B) foot process fusion on electron microscopy

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17
Q

How is minimal change disease treated?

A

High dose steroids

50% will relapse

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18
Q

Give some functions of the kidney

A 
Metabolic waste excretion - urea, creatinine
Endocrine functions - Vit D, EPO, PTH
Drug metabolism/excretion
Control of solutes/fluid balance
BP control
Acid/base balance
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19
Q

Describe the Glomerular Filtration Barrier

A

Negatively charged - no protein in filtrate

Large molecules are maintained within capillaries

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20
Q

What is the normal amount of protein in the urine?

A

<150mg/24 hours

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21
Q

What type of protein is detected by urine dipsticks?

A

Albumin

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22
Q

Define renal clearance

A

(Urine concentration of substance x urine volume) / plasma concentration of substance

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23
Q

How else can renal clearance be known as?

A

Glomerular Filtration Rate

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24
Q

When calculating eGFR, what parameters are taken into context?

A

Age
Gender
Race
Plasma creatinine

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25
Q

What is the unit for eGFR?

A

ml/min/1.73m^3

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26
Q

What things need to be taken into consideration when assessing a patient’s eGFR?

A

Assumes stable renal function - not useful for AKI
Can lose up to 50% renal function because eGFR starts to deteriorate
Useful for drug dosing

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27
Q

How does eGFR correspond to staging of CKD?

A 
>/= 90% + abnormality = stage 1 
60-89 + abnormality = stage 2
30-59 = stage 3 (moderate impairment)
15-29 = stage 4 (severe impairment)
<15 = stage 5 (advanced renal failure)
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28
Q

What is the mechanism of inheritance for adult polycystic kidney disease?

A

Autosomal dominant

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29
Q

What gene mutations are involved in adult polycystic kidney disease?

A 
PKD 1 (chromosome 16) - 85%
PKD 2 (chromosome 4) - 15%
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30
Q

What do PDK 1 and 2 genes encode?

A

Polycystin 1 & 2
Membrane protein involved in calcium regulation

Present in renal tubular epithelia (+ liver and pancreas)
Overexprssed in cyst cells

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31
Q

What is the natural history of adult polycystic kidney disease?

A

Cysts enlarge
Kidney volume increases
Some compensation initially
eGFR starts to fall –> ~10y later kidneys fail

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32
Q

If a person has a FHx of adult polycystic kidney disease, how should they be investigated to see if they also have it?

A

Renal US at 21
Repeat at 30 if normal

Age 15-30: 2 unilateral/bilateral cysts
Age 30-59: 2 cysts in each kidney
Age >60: 4 cysts in each kidney

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33
Q

If a person doesn’t have a FHx of adult polycystic kidney disease, what is diagnostic for the condition?

A

> 10 cysts in each kidney
Renal enlargement
Liver cyst

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34
Q

What are some of the clinical consequences associated with adult polycystic kidney disease?

A

50% risk of ESRD by 50
Cyst accidents - rupture, bleeding, infection

Other:
HTN
Intracranial aneurysm 
Aortic incompetence
Mitral valve prolapse 
Colonic diverticular disease
Liver/pancreatic cysts
Hernia
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35
Q

Describe the management of adult polycystic kidney disease

A 
Supportive
Early detection and management of HTN
Treat complications
Manage extra-renal associations
Renal replacement therapy
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36
Q

Describe Von Hippel Lindau Syndrome

A

Autosomal dominant

Multiple benign and malignant tumours

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37
Q

Describe Autosomal Recessive PKD

A

Affects children

Results in hepatic fibrosis

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38
Q

Describe Tuberous Sclerosis

A

Autosomal dominant
Multiple benign tumours - brain, heart, eyes, kidney, skin
Epilepsy and learning difficulties

39
Q

Describe Medullary Cystic Disease

A

Autosomal dominant
Cysts in medulla
Small to normal sized kidneys
Gout

40
Q

Describe Alpert’s Syndrome

A

Usually X-linked
Second most common cause of inherited kidney disease
Collagen 4 abnormality (Alpha 3/4/5 gene mutation)
Deafness and renal failure (deafness first)

Microscopic haematuria, proteinuria, ESRF

41
Q

Describe Fabry’s Disease

A

X-linked storage disorder
Alpha galactosidase A deficiency resulting in accumulation of Gb3 in the glomeruli (podocytes)

Proteinuria + ESRF (+neuropathy + cardiac and skin features)

42
Q

Describe the diagnosis of Fabry’s Disease

A

Alpha-Gal A activity in leucocytes

Renal biopsy - inclusion bodies of G3b

43
Q

How is Fabry’s Disease managed?

A

Enzyme replacement therapy

44
Q

Describe the pathophysiology of diabetic nephropathy

A 
Hyperglycaemia
Volume expansion
Intraglomerular hypertension
Hyperfiltration (initially serum Cr decreases, so eGFR looks to improve) 
Proteinuria
HTN + renal failure
45
Q

How long does it take for diabetic nephropathy to occur following the development of diabetes?

A

Approximately 20 years

46
Q

How should diabetic nephropathy be managed?

A

Tight glycemic control
Good BP control - ACEi/ARB
SGLT2 inhibitors

47
Q

Describe renal artery stenosis

A

Stenosis of renal artery –> not enough blood supply to kidney –> kidney becomes fibrotic and shrinks down

48
Q

What can cause progressive narrowing of the renal artery?

A

Atheroma

49
Q

What happens if the renal perfusion has fallen to >20%?

A

GFR falls

Tissue oxygenation of cortex and medulla is maintained

50
Q

What happens if the renal perfusion has fallen to >70%?

A

Cortical hypoxia –> microvascular damage and activation of inflammatory and oxidative pathways

Parenchymal inflammation and fibrosis –> becomes irreversible

Restoration of blood flow does not provide any benefit

51
Q

Describe the management of renal artery stenosis

A

Good BP control (not with ACEi/ARB)
Statin
Good glycemic control if diabetic

Smoking cessation, increased exercise, reduce NaCl intake

Angioplasty

52
Q

What are the indications for angioplasty in renal artery stenosis?

A

Rapidly deteriorating renal function
Uncontrolled HTN on multiple agents
Flash pulmonary oedema

53
Q

Describe amyloidosis

A

Deposition of highly stable insoluble proteinous material in the extracellular space

54
Q

What stain can be used to identify amyloid, and what will it stain?

A

Congo Red Stain

Apple green birefringence

55
Q

What are the two types of amyloid?

A

AA amyloid: inflammation/infection

AL amyloid: immunoglobulin fragments - myeloma

56
Q

How should amyloidosis be treated?

A

AA amyloid: treat underlying inflammatory/infection

AL amyloid: treat underlying haematological malignancy

57
Q

In SLE, what can autoantibodies be directed against?

A

DNA
Histones
snRNPs
Transcriptional/translational machinery

58
Q

Describe lupus nephritis

A

Auto-antibodies against dsDNA or nucleosomes
Form intravascular immune complexes or attach to GBM
Activates complement
Renal damage

59
Q

How should lupus nephritis be managed?

A

Renal biopsy to confirm diagnosis + stage

Immunosuppression - steroids, retuximab, cyclophosphamide

60
Q

Define Acute Kidney Injury

A

Decline of renal excretory function over hours/days which is recognised by an increase in serum urea and creatinine

61
Q

What are the three classifications of AKI?

A

Pre-renal: circulatory failure
Renal: the cells of the kidney
Post-renal: obstruction

62
Q

Give some pre-renal causes of AKI

A 
Hypotension
Hypovolaemia
Hypoxic
Hypoperfusion
Sepsis
Drugs/toxins
63
Q

Give some causes of post-renal AKI

A 
Obstruction:
Calculi
Tumours
Lymph nodes
Prostate
64
Q

Give some causes of renal AKI

A

Acute tubular necrosis
GN
Rhabdomyolysis
Gentamicin

65
Q

Describe acute tubular necrosis

A 
Usually reversible
Under-perfusion of tubules and/or direct toxicity
Hypotension
Sepsis
Toxins
66
Q

Give some endogenous toxins that can cause acute tubular necrosis

A 
Myoglobin
Haemoglobin
Immunoglobin
Calcium
Urate
67
Q

Give some exogenous toxins that can cause acute tubular necrosis

A

Drugs: ACEi, NSAIDs, gentamicin
Contrast
Poisons: metals, antifreeze

68
Q

How does ACEi exacerbate AKI?

A

Inhibits production of ACE

Don’t get efferent arteriole constriction

69
Q

How do NSAIDs exacerbate AKI?

A

Inhibits production of prostaglandins

Don’t get afferent arteriole dilation

70
Q

What two drugs should always be stopped in a patient with AKI?

A

ACEi

NSAIDs

71
Q

Describe the investigations required in a patient with suspected AKI

A

Bloods: urea, creatinine, potassium
Urine output
Clinical assessment: BP, JVP, oedema, heart sounds

72
Q

Describe the initial treatment of a patient with AKI

A

Treat hyperkalaemia
Treat pulmonary oedema
Remove cause - NSAIDs, ACEi, sepsis
Exclude obstruction (renal US), and consider renal causes

73
Q

What are some components of a GN screen?

A

ANCA
ANA
Immunoglobulins
Bence-Jones proteins

74
Q

How should hyperkalaemia be managed?

A

Reduce reabsorption of K from gut - calcium resonium
Calcium gluconate - stabilises cardiac membrane
Insulin+dextrose - moves K into cells

75
Q

What are the absolute indications of RRT in a patient with AKI?

A

Refractory K >/= 6.5mmol/L

Refractory pulmonary oedema

76
Q

What are the relative indications of RRT in a patient with AKI?

A

Acidosis pH<7.1
Uraemia esp if urea >40
Pericarditis, endocarditis
Toxins (lithium)

77
Q

Define CKD

A

Kidney damage or GFR >60ml/min/1.73m^3 for >3 months

78
Q

Describe stable CKD

A

eGFR is not changing

79
Q

Describe unstable CKD

A

eGFR is changing

80
Q

What can cause a protein result of +1 on dipstick?

A

Fever, exercise, normal

81
Q

How can proteinuria be quantified?

A

Comparing [protein] to [creatinine]

82
Q

What is a normal ACR result?

A

<2.5

83
Q

What is a normal PCR result?

A

<20

84
Q

How does ACR relate to PCR?

A

ACR is around 2/3 of PCR result

85
Q

Give some symptoms of CKD

A 
Pruritis
Nausea, anorexia, weight loss
Fatigue
Leg swelling
Breathlessness
Nocturia
Joint/bone pain
Confusion
86
Q

Give some signs of CKD

A 
Peripheral and pulmonary oedema 
Pericardial rub 
Rash/excoriation
HTN
Tachypnoea
Cachexia
Pallor/lemon yellow tinge
87
Q

How can the progression of CKD be slowed down?

A 
Aggressive BP control with ACEi and ARB
Good glycemic control 
Diet
Smoking cessation 
Lowering cholesterol - statins
Treating acidosis
88
Q

When is anaemia common in CKD?

A

When eGFR <30ml/min/1.73m^3

89
Q

What should be replaced first if a patient with CKD has anaemia?

A

Folate, B12, iron

90
Q

What is the target Hb in a patient with CKD?

A

100-120g/l

91
Q

What phosphate binders can be used in secondary hyperparathyroidism?

A

Calcium: calcium carbonate/acetate

Non-calcium: aluminium

92
Q

What is the target phosphate concentration in a patient with secondary hyperparathyroidism?

A

0.9-1.5mmol/L

93
Q

If a patient has hyperparathyroidism secondary to CKD, what vitamin D replacement should they be given?

A

Alfacalcidol

MBChB (14 decks)

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