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Renal and Uro > renal > Flashcards

renal Flashcards

1
Q

NICE criteria for AKI

A
  • rise in creatinine of >25micromol/L in 48hrs
  • rise in creatinine of >50% in 7 days
  • urine output of <0.5ml/kg/hour for >6hrs
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2
Q

8 risk factors for AKI

A
  1. CKD
  2. HF
  3. DM
  4. liver disease
  5. older age (>65)
  6. cognitive impairment
  7. nephrotoxic medications - NSAIDs, ACE-i
  8. use of contrast medium i.e. CT
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3
Q

categories for causes of AKI

A

pre-renal
renal
post-renal

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4
Q

3 pre-renal causes of AKI

A

inadequate blood supply:

  • dehydration
  • hypotension
  • heart failure
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5
Q

3 renal causes of AKI

A

intrinsic disease:

  • glomerulonephritis
  • interstitial nephritis
  • acute tubular necrosis
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6
Q

4 post-renal causes of AKI

A

obstruction to urine outflow:

  • kidney stones
  • masses (cancers)
  • ureter/urethral strictures
  • enlarged prostate, prostate cancer
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7
Q

investigations in AKI

A

urinalysis

US KUB

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8
Q

urinalysis results and what they suggest

A
  • leucocytes and nitrites suggest infection
  • protein and blood suggest acute nephritis (or infection)
  • glucose suggests diabetes
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9
Q

treatment of AKI

A

treat underlying cause:

  • fluid rehydration (pre-renal)
  • stop nephrotoxic meds
  • relieve obstruction (post-renal) e.g. insert catheter
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10
Q

4 complications of AKI

A
  1. hyperkalaemia
  2. fluid overload, heart failure and pulmonary oedema
  3. metabolic acidosis
  4. uraemia -> encephalopathy, pericarditis
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11
Q

6 causes of CKD

A
  1. diabetes
  2. hypertension
  3. age-related decline
  4. glomerulonephritis
  5. polycystic kidney disease
  6. medications: NSAIDs, PPIs, lithium
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12
Q

5 risk factors for CKD

A
  1. older age
  2. hypertension
  3. diabetes
  4. smoking
  5. use of medicines which affect kidneys
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13
Q

8 signs/symptoms of CKD

A

can be asymptomatic

  1. pruritis
  2. loss of appetite
  3. nausea
  4. oedema
  5. muscle cramps
  6. peripheral neuropathy
  7. pallor
  8. hypertension
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14
Q

investigations to diagnose CKD

A

U&E - eGFR

measured twice, 3 months apart

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15
Q

investigations for CKD

A
  • eGFR (U&E)
  • urine albumin:creatinine ratio >3mg/mmol
  • haematuria (urine dip) 1+
  • renal USS
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16
Q

staging of CKD

A

G and A scores:

  • G score based on eGFR
  • A score based on Albumin:creatinine ration
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17
Q

G score for CKD

A 
G1 - eGFR >90
G2 - eGFR 60-89
G3a - eGFR 45-59
G3b - eGFR 30-44
G4 - eGFR 15-29
G5 - eGFR <15 (end-stage renal failure)
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18
Q

A score for CKD

A

A1 - ACR <3mg/mmol
A2 - ACR 3-30mg/mmol
A3 - ACR >30mg/mmol

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19
Q

diagnostic criteria for CKD

A

eGFR <60 or proteinuria

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20
Q

5 complications of CKD

A
  1. anaemia
  2. renal bone disease
  3. cardiovascular disease
  4. peripheral neuropathy
  5. dialysis related problems
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21
Q

4 criteria for specialist referral in CKD

A
  1. eGFR <30
  2. ACR >70mg/mmol
  3. accelerated progression: decrease in eGFR of 15 or 25% or 15ml/min in 1 year
  4. uncontrolled HTN despite 4+ antihypertensives
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22
Q

4 main aims of CKD management

A
  1. slow progression
  2. reduce risk of CVD
  3. reduce risk of complications
  4. treat complications
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23
Q

3 management approaches to slow progression of CKD

A
  1. optimise diabetic control
  2. optimise HTN control
  3. treat glomerulonephritis
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24
Q

lifestyle modifications to reduce risk of complications from CKD

A
  1. exercise
  2. maintain healthy weight
  3. stop smoking
  4. dietary advice regarding: phosphate, sodium, potassium and water
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25
Q

which medication should be prescribed in CKD to prevent CVD

A

atorvastatin 20mg

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26
Q

4 complications of CKD and associated treatments

A
  1. metabolic acidosis - oral sodium bicarbonate
  2. anaemia - iron supplementation and erythropoietin
  3. renal bone disease - vitamin D
  4. end stage - dialysis or renal transplant
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27
Q

HTN treatment in CKD and when given

A

ACE-i (renoprotective)

  • diabetes + ACR >3
  • HTN + ACR >30
  • anyone with ACR >70
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28
Q

aims of HTN tx in CKD

A

maintain BP <140/90 or <130/80 if ACR >70

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29
Q

monitoring necessary in HTN management in CKD

A

serum potassium

ACE-i and CKD cause hyperkalaemia

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30
Q

pathophysiology of anaemia in CKD

A

healthy kidney cells produce erythropoietin which stimulates production of RBC
CKD = decreased kidney function = less RBC produced

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31
Q

why are blood transfusions not recommended for management of anaemia in CKD

A

can sensitise immune system (allosensitisation) so transplanted organs are more likely to be rejected

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32
Q

management of anaemia in CKD

A

‘anaemia of chronic disease;

  1. treat iron deficiency first (IV iron or oral iron)
  2. exogenous erythropoietin
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33
Q

3 features of renal bone disease

A
  1. osteomalacia (softening of bones)
  2. osteoporosis (brittle bones)
  3. osteosclerosis (hardening of bones)
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34
Q

x-ray changes in renal bone disease

A
  • osteosclerosis (hardening) of both ends of vertebra = denser white appearance
  • osteomalacia (softening) in centre of vertebra = less white appearance
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35
Q

pathophysiology of renal bone disease

A
  • reduced phosphate excretion => high serum phosphate
  • low active vit D => reduced calcium absorption from intestines and kidneys
  • secondary hyperparathyroidism (PT glands react to low calcium and high phosphate by excreting more PTH) => increased osteoclast activity
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36
Q

why does osteomalacia occur in renal bone disease

A

increased turnover of bones without adequate calcium supply

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37
Q

why does osteosclerosis occur in renal bone disease

A

osteoblasts respond by increasing activity to match osteoclasts (due to secondary hyperparathyroidism)
new tissue is not properly mineralized due to low calcium

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38
Q

management of renal bone disease

A
  • active forms of vitamin D (alfacalcidol, calcitriol)
  • low phosphate diet
  • bisphosphonates to treat osteoporosis
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39
Q

5 indications for acute dialysis and mnemonic

A

AEIOU

  • Acidosis (severe, not responding to tx)
  • Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
  • Intoxication (overdose of certain meds)
  • Oedema (severe and unresponsive pulmonary oedema)
  • Uraemia symptoms (seizure, reduced consciousness)
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40
Q

indications for long term dialysis

A
  • end stage renal failure (CKD stage 5)

- acute indications continuing long term

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41
Q

3 main options for long-term dialysis

A
  1. continuous ambulatory peritoneal dialysis
  2. automated peritoneal dialysis
  3. haemodialysis
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42
Q

what is peritoneal dialysis

A

special dialysis solution added to the peritoneal cavity. ultrafiltration from blood to dialysis solution occurs through the peritoneal membrane (natural filtration membrane). leftover fluid with waste products filtered from blood then removed and clean dialysis fluid replaced and process repeats.

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43
Q

types of peritoneal dialysis

A
  1. continuous ambulatory peritoneal dialysis
    - dialysis solution in peritoneum at all times
    - different regimes e.g. 2L fluid inserted and changed 4x day
  2. automated dialysis
    - dialysis occurs overnight
    - machine continuously replaces fluid overnight, takes 8-10hrs
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44
Q

5 complications of peritoneal dialysis

A
  1. bacterial peritonitis - infusion of glucose solution predisposes to bacterial growth
  2. peritoneal sclerosis
  3. ultrafiltration failure - starts to absorb dextrose in solution making filtration gradient less effective
  4. weight gain - absorb carbohydrates in solution
  5. psychosocial effect
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45
Q

what is haemodialysis

A

patients have blood filtered by haemodialysis machine e.g. 4hrs a day 3x week
need good access to blood supply

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46
Q

types of vascular access for haemodialysis

A
  1. tunnelled cuffed catheter

2. AV fistula

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47
Q

what is a tunnelled cuffed catheter for dialysis

A
  • tube inserted into subclavian or jugular vein with tip sitting in SVA or RA
  • 2 lumens (enter/exit)
  • Dacron cuff ring surrounding catheter promotes healing and adhesion to make more permanent and protect against infection
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48
Q

what is an AV fistula

A
  • artificial connection between an artery and a vein
  • bypasses capillary system allowing high pressure blood from artery into vein
  • permanent, large, easy access to blood supply
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49
Q

3 typical sites for AV fistula (vessels)

A
  • radio-cephalic
  • brachio-cephalic
  • brachio-basilic
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50
Q

complications of tunnelled cuffed catheter in haemodialysis

A

infection

blood clots

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51
Q

time-frame for AV fistulas from formation to usage

A

requires surgical operation

4 week - 4 month maturation (needs to be made in advance of when dialysis is required)

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52
Q

signs to look for with AV fistula on examination

A
  • skin integrity
  • aneurysms
  • palpable thrill
  • stereotypical ‘machinery murmur’ on auscultation
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53
Q

6 complications of AV fistula

A
  1. aneurysm
  2. infection
  3. thrombosis
  4. stenosis
  5. STEAL syndrome
  6. high output heart failure
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54
Q

what is STEAL syndrome

A

inadequate blood supply to limb distal of AV fistula - fistula ‘STEALs’ blood from distal limb causing distal ischaemia

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55
Q

how does AV fistula cause high output cardiac failure

A

blood flows very quickly from arterial to venous system
rapid return of blood to the heart which increases pre-load to the heart which leads to hypertrophy of heart muscle and heart failure

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56
Q

how are patients and donors matched for kidney transplant

A

based on human leucocyte antigen (HLA) type A, B and C on chromosome 6

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57
Q

kidney transplant procedure

A

patients own kidneys left in place
donor kidneys blood vessels connected with patients pelvic vessels (external iliac)
donor ureter anastomosed directly with patients bladder
donor kidney placed anterior in abdomen and can be palpated in iliac fossa

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58
Q

typical scar for kidney transplant

A

‘hockey stick scar’

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59
Q

immunosuppressant regime after kidney transplant

A

tacrolimus
mycophenolate
prednisolone
can also use: cyclosporine, sirolimus, azathioprine

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60
Q

transplant-related complications from kidney transplant

A
  • transplant rejection
  • transplant failure
  • electrolyte imbalance
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61
Q

immunosuppressant-related complications from kidney transplant

A
  • ischaemic heart disease
  • T2DM
  • infection risk
  • unusual infections: PCP, PJP, CMV, TB
  • non-Hodgkin lymphoma
  • skin cancer (SCC)
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62
Q

definition of nephritis

A

generic term: inflammation of the kidneys

not a diagnosis

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63
Q

what is nephritic syndrome

A

group of symptoms not a diagnosis
fit a clinical picture of having kidney inflammation
does not give diagnosis or underlying cause

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64
Q

features of nephritic syndrome

A
  • haematuria (microscopic or macroscopic)
  • oliguria (reduced UO)
  • proteinuria (<3g in 24hrs)
  • fluid retention
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65
Q

criteria for nephrotic syndrome

A
  1. peripheral oedema
  2. proteinuria >3g in 24hrs
  3. serum albumin <25g/L
  4. hypercholesterolaemia
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66
Q

what is glomerulonephritis

A

umbrella term for conditions which cause inflammation of or around glomerulus and nephron
many conditions described as glomerulonephritis

67
Q

definition of interstitial nephritis

A

inflammation of the space between cells and tubules (interstitium) within the kidney

68
Q

specific diagnoses within interstitial nephritis

A
  1. acute interstitial nephritis

2. chronic tubulointerstitial nephritis

69
Q

definition of glomerulosclerosis

A

pathological process of scarring of tissue in glomerulus

not a diagnosis itself

70
Q

causes of glomerulosclerosis

A
  • any type of glomerulonephritis
  • obstructive uropathy (blockage of urine outflow)
  • focal segmental glomerulosclerosis
71
Q

8 types of glomerulonephritis

A
  1. minimal change disease
  2. focal segmental glomerulosclerosis
  3. membranous glomerulonephritis
  4. IgA nephropathy (mesangioproliferative glomerulonephritis, Berger’s disease)
  5. post-strep glomerulonephritis
  6. mesangiocapillary glomerulonephritis
  7. rapidly progressive glomerulonephritis
  8. Goodpasture syndrome
72
Q

basic treatment approach for most types of glomerulonephritis

A

immunosuppression (steroids)

blood pressure control by inhibiting RAS: ACE-i or ARBs

73
Q

common presentation of nephrotic syndrome

A

oedema

may notice frothy urine (proteinuria)

74
Q

most common cause of nephrotic syndrome in children vs adults

A 
children = minimal change disease
adults = focal segmental glomerulosclerosis
75
Q

complications of nephrotic syndrome

A

predisposes you to:

  • thrombosis
  • HTN
  • high cholesterol
76
Q

histology of IgA nephropathy (Berger’s)

A

IgA deposits and glomerular mesangial proliferation

77
Q

what is meant by primary glomerulonephritis and what i the most common cause

A 
not caused by another disease
IgA nephropathy (Berger's)
78
Q

peak age of presentation of IgA nephropathy (Berger’s)

A

20s

79
Q

which is the overall most common cause of glomerulonephritis

A

membranous glomerulonephritis

80
Q

peak age of presentation of membranous glomerulonephritis

A

20s and 60s (2 peaks)

81
Q

histology of membranous glomerulonephritis

A

IgG and complement deposits on basement membrane

82
Q

aetiology of membranous glomerulonephritis

A 
70% idiopathic
secondary to:
- malignancy
- rheumatoid disorders
- drugs e.g. NSAIDs
83
Q

presentation of post-strep glomerulonephritis

A

<30yo

  • presents 1-3 weeks after strep infection e.g. tonsillitis, impetigo
  • nephritic syndrome (haematuria, oliguria)
84
Q

pathophysiology of Goodpasture syndrome

A

anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes
causes glomerulonephritis and pulmonary haemorrhage

85
Q

example presentation of Goodpasture syndrome

A

patient presenting with acute kidney failure and haemoptysis
(antibodies attack glomerular and pulmonary basement membranes)

86
Q

histology of rapidly progressive glomerulonephritis

A

crescentic glomerulonephritis

87
Q

presentation of rapidly progressive glomerulonephritis

A

very acute illness and sick patients but responds well to tx (immunosuppression)

88
Q

aetiology of rapidly progressive glomerulonephritis

A

often secondary to Goodpasture syndrome

89
Q

6 medications which are usually safe to continue in AKI

A
  1. paracetamol
  2. warfarin
  3. statins
  4. aspirin (75mg OD)
  5. clopidogrel
  6. beta-blockers
90
Q

5 medications which should be stopped in AKI

A
  1. NSAIDs (except aspirin if 75mg OD)
  2. aminoglycosides
  3. ACE-i
  4. ARBs
  5. diuretics
91
Q

3 medications which may need to be stopped in AKI as increased risk of toxicity

A
  1. metformin
  2. lithium
  3. digoxin
92
Q

what is the most common cause of glomerular pathology and CKD in the UK

A

diabetic nephropathy

93
Q

pathophysiology of diabetic nephropathy

A

chronic high glucose levels passing through glomerulus causes scarring = glomerulosclerosis

94
Q

features of diabetic nephropathy

A
  • glomerulosclerosis

- proteinuria (damage to glomerulus allowing protein to be filtered)

95
Q

management of diabetic nephropathy

A

optimizing blood sugar and blood pressure

ACE-i tx of choice - should be started in diabetic nephropathy even with normal BP

96
Q

presentation of acute interstitial nephritis

A
  • AKI
  • HTN
  • hypersensitivity features: rash, fever, eosinophilia
97
Q

aetiology of acute interstitial nephritis

A

hypersensitivity reaction to drugs (NSAIDs, abx) or infection
presents with hypersensitivity features: rash, fever, eosinophilia

98
Q

treatment of acute interstitial nephritis

A

treat underlying cause i.e. infection, stop medications

steroids to reduce inflammation and improve recovery

99
Q

aetiology of chronic tubulointerstitial nephritis

A

chronic inflammation of the tubules and interstitium

underlying disease: autoimmune, infectious, iatrogenic, granulomatous

100
Q

presentation of chronic tubulointerstitial nephritis

A

presents with CKD

101
Q

management of chronic tubulointerstitial nephritis

A

treat underlying cause

steroids

102
Q

definition of acute tubular necrosis

A

damage and death of the epithelial cells of the renal tubules
most common cause of AKI

103
Q

causes of acute tubular necrosis

A 
ischaemia:
- shock
- sepsis
- dehydration
direct toxin damage:
- radiology contrast dye
- gentamycin
- NSAIDs
104
Q

prognosis of acute tubular necrosis

A

epithelial cells have the ability to regenerate therefore ATN is reversible
takes 7-21 days to recover

105
Q

urinalysis findings in acute tubular necrosis

A

‘muddy brown casts’

renal tubular epithelial cells

106
Q

treatment of acute tubular necrosis

A

same as mx of AKI:

  • supportive
  • IV fluids
  • stop nephrotoxic meds
  • treat complications
107
Q

definition of renal tubular acidosis

A

metabolic acidosis due to pathology in the tubules of the kidney

108
Q

pathophysiology of renal tubular acidosis

A

tubules are responsible for balancing hydrogen and bicarb ions between blood and urine and maintaining normal pH therefore disruption to tubular function can cause disturbance to pH

109
Q

4 types of renal tubular acidosis and key facts

A
  • type 1 = distal tubule pathology meaning DCT is unable to excrete hydrogen ions
  • type 2 = proximal tubule pathology meaning PCT is unable to resorb bicarb
  • type 3 = combination of type 1 and 2 (rare)
  • type 4 = MOST COMMON, reduced aldosterone
110
Q

7 causes of type 1 renal tubular acidosis

A
  1. genetic (autosomal dominant and recessive forms)
  2. SLE
  3. Sjogren’s
  4. primary biliary cirrhosis
  5. hyperthyroidism
  6. sickle cell anaemia
  7. Marfan’s
111
Q

presentation of type 1 renal tubular acidosis

A
  • failure to thrive in children
  • hyperventilation (respiratory compensation)
  • CKD
  • bone disease (osteomalacia)
112
Q

biochemistry results in type 1 renal tubular acidosis

A
  • hypokalaemia
  • metabolic acidosis
  • high urine pH (>6)
113
Q

treatment of type 1 renal tubular acidosis

A

oral bicarb

114
Q

main cause of type 2 renal tubular acidosis

A

Fanconi’s syndrome

115
Q

biochemistry results in type 2 renal tubular acidosis

A
  • hypokalaemia
  • metabolic acidosis
  • high urinary pH (>6)
116
Q

treatment for type 2 renal tubular acidosis

A

oral bicarb

117
Q

3 causes of type 4 renal tubular acidosis

A

reduced aldosterone due to:

  • adrenal insufficiency
  • drugs: ACE-i, spironolactone
  • systemic conditions: SLE, DM, HIV
118
Q

biochemistry results in type 4 renal tubular acidosis

A
  • hyperkalaemia
  • high chloride
  • metabolic acidosis
  • low urinary pH
119
Q

management of type 4 renal tubular acidosis

A

fludrocortisone

sodium bicarb + tx of hyperkalaemia may be required

120
Q

exchange of substances in the PCT

A

secreted:
- creatinine
- drugs
- H+

reabsorbed:

  • sodium, chloride, potassium
  • glucose
  • amino acids
  • urea
  • bicarb
  • water
121
Q

exchange of substances in the descending limb of the LOH

A

water is reabsorbed

122
Q

exchange of substances in the ascending limb of the LOH

A

reabsorption of sodium, chloride and potassium

123
Q

exchange of substances in the DCT

A

secreted:

  • H+
  • potassium

reabsorbed:

  • sodium, chloride, calcium, magnesium
  • bicarb
124
Q

exchange of substances in the CD

A

reabsorption of sodium, chloride, urea and water

125
Q

definition of haemolytic uraemic syndrome

A

thrombosis in the small blood vessels throughout the body usually triggered by bacterial toxin called shiga toxin

126
Q

triad of biochemical signs in haemolytic uraemic syndrome

A
  1. haemolytic anaemia
  2. AKI
  3. low platelet count (thrombocytopaenia)
127
Q

pathophysiology of haemolytic uraemic syndrome

A
  • formation of clots consumes platelets = thrombocytopaenia
  • clots within small vessels chop up RBCs as they pass through = haemolytic anaemia
  • blood flow through kidney affected by clots = AKI
128
Q

aetiology of haemolytic uraemic syndrome

A

toxin called the shiga toxin which is produced by:

  • e. coli 0157
  • shigella
129
Q

which medicines increase the risk of haemolytic uraemic syndrome

A
  • antibiotics

- antimotility meds such as loperamide (tx gastroenteritis)

130
Q

presentation/disease course of haemolytic uraemic syndrome

A

e. coli causes brief gastroenteritis with blood diarrhoea then 5 days after display symptoms of HUS

131
Q

symptoms of HUS

A
  • reduced urine output
  • haematuria or dark brown urine
  • abdo pain
  • lethargy, irritability
  • confusion
  • HTN
  • bruising
132
Q

management of HUS

A

self-limiting with supportive management

  • antihypertensives
  • blood transfusions
  • dialysis
133
Q

definition of rhabdomyolysis

A

skeletal muscle breaks down and releases breakdown products into the blood
usually triggered by events causing muscles to break down such as extreme under- or over- use or trauma

134
Q

pathophysiology of rhabdomyolysis

A

myocytes undergo apoptosis (cell death) resulting in the release of:

  • myoglobin (myoglobinaemia)
  • potassium (hyperkalaemia)
  • phosphate
  • creatine kinase
135
Q

complications of rhabdomyolysis

A
  • potassium = cardiac arrhythmias e.g. VF => cardiac arrest
  • myoglobin is nephrotoxic => AKI
  • AKI causes breakdown products to further accumulate in the blood
136
Q

4 causes of rhabdomyolysis

A
  1. prolonged immobility
  2. extreme rigorous exercise
  3. crush injuries
  4. seizures
137
Q

5 signs/symptoms of rhabdomyolysis

A
  1. muscle aches and pains
  2. oedema
  3. fatigue
  4. confusion (especially in the elderly)
  5. red-brown urine
138
Q

investigations in rhabdomyolysis

A
  • creatine kinase (CK) in 100,000s
  • urine dipstick positive for blood (myoglobinuria which gives red-brown appearance)
  • U&E for AKI and hyperkalaemia
  • ECG to assess for effects of hyperkalaemia
139
Q

management of rhabdomyolysis

A
  • IV fluids to encourage filtration of breakdown products
  • consider IV sodium bicarb
  • consider IV mannitol to increase GFR and reduce oedema
  • treat complications especially hyperkalaemia
140
Q

main complications of hyperkalaemia

A

cardiac arrhythmias such as ventricular fibrillation which can lead to cardiac arrest

141
Q

5 causes of hyperkalaemia (not medications)

A
  1. AKI
  2. CKD
  3. rhabdomyolysis
  4. adrenal insufficiency
  5. tumour lysis syndrome
142
Q

5 medications that can cause hyperkalaemia

A
  1. aldosterone antagonists (spironolactone and eplerenone)
  2. ACE-i
  3. ARBs
  4. NSAIDs
  5. potassium supplements
143
Q

what to consider with hyperkalaemia found on U&E

A

could be falsely elevated due to haemolysis during blood sampling

144
Q

ECG changes in hyperkalaemia

A
  1. tall peaked T waves
  2. flattening or absence of P waves
  3. broad QRS
    VF
145
Q

levels of hyperkalaemia and associated management approach

A
  • potassium <6mmol/L and otherwise stable renal function = no urgent tx required, change in diet and meds
  • potassium >6mmol/L and ECG changes = urgent tx
  • potassium >6.5mmol/L regardless of ECG = urgent tx
146
Q

mainstay of treatment for hyperkalaemia

A
  1. insulin and dextrose infusion - drives carbohydrates into cells and takes potassium with it, reducing blood potassium
  2. IV calcium gluconate - stabilises cardiac myocytes reducing risk of arrhythmias
147
Q

5 other options for tx of hyperkalaemia

A
  1. nebulised salbutamol - drives K into cells
  2. IV fluids - increase urine output
  3. oral calcium resonium - draws K into stool
  4. sodium bicarb - drives K into cells as acidosis corrected
  5. dialysis if severe/persistent
148
Q

definition of polycystic kidney disease

A

genetic condition where kidneys develop multiple fluid-filled cysts
kidney function significantly impaired

149
Q

extra-renal findings associated with polycystic kidney disease

A
  • hepatic, splenic, pancreatic, ovarian and prostatic cysts
  • berry (cerebral) aneurysms
  • cardiac valve disease (MR)
  • colonic diverticula
  • aortic root dilation
150
Q

genetics of polycystic kidney disease

A 
autosomal dominant and autosomal recessive types 
(AD > AR)
autosomal dominant genes:
- PKD-1 on chromosome 16
- PKD-2 on chromosome 4
151
Q

6 complications of polycystic kidney disease

A
  1. chronic loin pain
  2. hypertension
  3. CVD
  4. gross haematuria
  5. renal stones
  6. end-stage renal failure
152
Q

common presentation of autosomal recessive polycystic kidney disease

A

often presents during pregnancy with oligohydramnios as foetus doesn’t produce enough urine
leads to underdevelopment of lungs => respiratory failure shortly after birth

153
Q

features of children with AR polycystic kidney disease

A

dysmorphic features such as underdeveloped ear cartilage, low set ears, flat nasal bridge
may require dialysis within first few days of life
usually have end-stage renal failure before reaching adulthood

154
Q

management of autosomal dominant polycystic kidney disease

A

tolvaptan (vasopressin receptor antagonist) to slow development of cysts and progression of renal failure

155
Q

management of complications of PKD

A
  • antihypertensives
  • analgesia for renal colic (stones or cysts)
  • abx for infections, drainage of infected cysts
  • dialysis or transplant for end-stage RF
156
Q

general management approaches and lifestyle modifications for PKD

A
  • genetic counselling
  • no contact sports (rupture)
  • no anti-inflammatory meds or anticoagulants
  • regular US, U&E, BP
  • MR angiogram to diagnose intracranial aneurysms in symptomatic/FHx
157
Q

definition of renal papillary necrosis

A

coagulative necrosis of the renal papillae

158
Q

5 causes of renal papillary necrosis

A
  • severe acute pyelonephritis
  • diabetic nephropathy
  • obstructive nephropathy
  • analgesic nephropathy e.g. NSAIDs
  • sickle cell anaemia
159
Q

features of renal papillary necrosis

A
  • visible haematuria
  • loin pain
  • proteinuria
160
Q

genetics of Alport syndrome

A

x-linked dominant condition

defect in gene coding for type IV collagen

161
Q

definition of Alport syndrome

A

genetic condition leading to defects in glomerular-basement membrane

162
Q

features of Alport syndrome

A
  • microscopic haematuria
  • progressive renal failure
  • bilateral sensorineural hearing loss
  • retinitis pigmentosa
163
Q

renal biopsy findings in Alport syndrome

A

splitting of lamina densa seen on electron microscopy giving ‘basket-weave’ appearance

Renal and Uro (2 decks)

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