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Medicine Finals > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Presentation: patient presenting with diarrhoea illness alongside reduced urine output - most likely cause?

A

Haemolytic uraemic syndrome caused by Shiga toxin (either due to E.coli or Shigella)

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2
Q

Presentation: headache in a patient with Autosomal Dominant Polycystic kidney disease?

A

Ruptured berry aneurysm (SAH)

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3
Q

What are the two features of AKI?

A

Raised creatinine

Reduced urine output

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4
Q

How is AKI staged?

A

AKI 1 -creatinine raised to 1.5-1.9x baseline, urine output <0.5ml/kg/hr for 6 hours

AKI 2 - creatinine raised to 2-2.9x baseline, urine output <0.5ml/kg/hr for 12 hours

AKI 3 - creatinine raised to over 3x baseline, urine output <0.3ml/kg/hr for 24 hours

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5
Q

What are pre-renal causes of AKI?

A

Pre-renal AKI = due to lack of perfusion to the kidneys

Dehydration

Hypotension

Renal artery stenosis

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6
Q

What are causes of renal AKI?

A

Acute tubular necrosis

Acute interstitial nephritis

Glomerulonephritis

Rhabdomyolysis

Tumour lysis syndrome

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7
Q

What are causes of post-renal AKI?

A

Renal calculi

Stricture

Prostate enlargement

Mass

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8
Q

How can you determine the cause of AKI from urine results?

A

Pre-renal = low urine sodium (high urine osmolality)

Renal = high urine sodium (low urine osmolality)

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9
Q

What drugs are directly nephrotoxic?

A

NSAIDs

Gentamicin

ACEi/ARBs

Diuretics

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10
Q

Which drugs are not directly nephrotoxic but are renally excreted and should be stopped in AKI?

A

Lithium

Metformin

Digoxin

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11
Q

What is acute tubular necrosis and what are the main causes?

A

Damage/necrosis of the renal tubules (renal cause of AKI)

Mainly due to

  1. Ischaemia (due to sepsis/dehydration)
  2. Toxins - contrast dye, NSAIDs, Gentamicin
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12
Q

What is seen on urinalysis in acute tubular necrosis?

A

Muddy brown casts

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13
Q

How is acute tubular necrosis managed?

A

Stop any nephrotoxic drugs

IV fluids

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14
Q

How can you prevent acute tubular necrosis due to contrast media in patients at risk? Who is at risk?

A

At risk = known renal impairment, age >70, dehydration, cardiac failure, use of nephrotoxic drugs

Prevention = IV 0.9% NaCl 1ml/kg/hr for 12 hours pre and post contrast

Nephrotoxic drugs should be stopped for 48 hours prior to procedure

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15
Q

How does acute interstitial nephritis present?

A

AKI and Hypertension

As well as - rash, fever, raised eosinophils

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16
Q

What can cause acute interstitial nephritis?

A

NSAIDs

Penicillin antibiotics

Rifampicin

Ciprofloxacin

PPIs

Allopurinol

Furosemide

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17
Q

How is acute interstitial nephritis managed?

A

Stop offending drug

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18
Q

What is Rhabdomyolysis?

A

Breakdown of muscle which releases breakdown products into the blood

Myoglobin (nephrotoxic)

Potassium

Phosphate

Creatinine kinase (markedly elevated)

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19
Q

What is the most immediately dangerous breakdown product in Rhabdomyolysis?

A

Potassium - hyperkalaemia can cause cardiac arrhythmias and cardiac arrest

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20
Q

Why does Rhabdomyolysis cause an AKI?

A

Releases myoglobin into blood

Myoglobin is nephrotoxic

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21
Q

What are causes of Rhabdomyolysis?

A

Prolonged immobility (e.g. elderly patient falls and spends time on the floor before being found)

Extremely rigorous exercise

Crush injuries

Seizures

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22
Q

How does Rhabdomyolysis present?

A

Myalgia

Oedema

Fatigue

Confusion

Tea coloured (red brown) urine

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23
Q

What investigations should be done in suspected Rhabdomyolysis?

A

Creatine kinase will be markedly elevated

Myoglobinurea

U+Es - look for AKI

ECG - look for cardiac arrhythmia caused by hyperkalaemia (widened flattened P wave, tall tented T waves, broad QRS complex)

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24
Q

How is Rhabdomyolysis treated?

A

Mainstay = IV fluids - 0.9% sodium chloride

Treat hyperkalaemia - insulin + glucose, calcium gluconate (stabilisation of cardiac membranes), potassium

Can give IV Bicarbonate to neutralise the acidity of urine

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25
Q

What ECG changes are seen in hyperkalaemia?

A

Tall tented T waves

Flattened P waves

Broad QRS complex

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26
Q

What level of potassium warrants urgent treatment?

A

> 6.5

Or >6 with ECG changes (check ECG first if in between 6 and 6.5)

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27
Q

What warrants dialysis in hyperkalaemia?

A

If severe hyperkalaemia associated with AKI

Non-responsive to treatment

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28
Q

What is the difference between nephritic syndrome and nephrotic syndrome?

A

Nephritic syndrome: haematuria, oliguria, Proteinuria, fluid retention

Nephrotic syndrome: peripheral oedema, massive Proteinuria, low albumin <25, hypercholesterolaemia

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29
Q

What is the main complication of nephrotic syndrome?

What are other complications?

A

Increased risk of VTE due to loss of Antithrombin III

AKI, CKD, end stage renal disease

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30
Q

What is the most common cause of nephrotic syndrome in children? What is seen on renal biopsy? How is it managed?

A

Minimal change disease

Renal biopsy shows fusion of podocytes and effacement of foot processes (on electron microscopy only - light microscopy is normal)

Treated with oral prednisolone

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31
Q

What might you want to let someone know who has had minimal change disease?

A

Majority of people have at least one more episode

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32
Q

What is the most common cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

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33
Q

What is the difference between IgA Nephropathy and post-strep glomerulonephritis?

A

IgA nephropathy - usually within 1-2 of infection, mainly macroscopic haematuria (but can also be proteinuria)

Post-strep glomerulonephritis - 1-2 weeks post-infection, can be both haematuria + proteinuria, low complement C3 levels
Anti-streptolysin O

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34
Q

How does membranous glomerulonephitis present and how is it seen on renal biopsy?

A

Nephrotic syndrome

Renal biopsy - thickened basement membrane, igG and complement deposits on basement membrane –> “Spike and dome appearance”

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35
Q

Which antigen is associated with membranous glomerulonephritis?

A

PLA2

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36
Q

How is membranous glomerulonephritis treated?

A

ACEi/ARB

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37
Q

What is rapidly progressive glomerulonephritis?

A

Presents with very acute illness - rapid loss of renal function

Histology - epithelial crescents

Often secondary to Anti-GBM (Goodpasture’s) or GPA Granulomatosis with Polyangiitis (Wegener’s)

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38
Q

What is Anti-GBM disease (Goodpasture’s)? How does it present?

A

A rare type of small vessel vasculitis

Pulmonary haemorrhage (presents with Haemoptysis)

Rapidly progressive glomerulonephritis (Proteinuria, haematuria)

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39
Q

What is seen on renal biopsy in anti-GBM disease?

A

Linear IgG deposits on basement membrane

Epithelial crescents

(Same as what is seen in rapidly progressive glomerulonephritis)

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40
Q

How can you differentiate between Anti-GBM and GPA?

A

Anti-GBM = Haemoptysis, rapidly progressive glomerulonephritis, Anti-GBM antibodies

GPA = glomerulonephritis, Haemoptysis, epistaxis, sinusitis, saddle shaped nose deformity, associated with cANCA

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41
Q

What is Henoch Schonlein Purpura? How is it managed?

A

IgA mediated small vessel vasculitis

Usually seen in children following an URTI

Palpable purpuric rash on the buttocks and limbs

Abdominal pain

Polyarthritis

Features of IgA nephropaty - haematuria, Proteinuria

Management is supportive

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42
Q

What are complications of chronic kidney disease?

A

Anaemia (normocytic) - due to decreased erythropoietin production

Bone disease - kidney does not convert vitamin D to active form (decreased calcium absorption), and stops excreting phosphate

Low calcium and high phosphate leads to increased PTH production (secondary hyperparathyroidism)

Increased PTH causes bone disease - osteomalacia

Hypertension

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43
Q

How is anaemia in CKD treated?

A

Erythropoietin

Treat iron deficiency prior to giving erythropoietin

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44
Q

How is renal bone disease treated?

A

Reduced dietary phosphate

Active forms of vit D

Phosphate binder e.g. Sevelamar/Calcium acetate/Calcium carbonate

Bisphosphonates

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45
Q

What Spinal X-ray changes can be seen in chronic kidney disease?

A

Spinal x-ray =

sclerosis of both ends of vertebra (denser white)

Osteomalacia in centre of vertebra (less white)

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46
Q

How is hypertension in chronic kidney disease treated?

A

ACE inhibitors

Monitor serum potassium - CKD with ACEi can cause hyperkalaemia

A decrease in eGFR of up to 25% and an increase in creatinine of 30% after starting ACEi = acceptable

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47
Q

How is CKD staged?

A

1 - >90 (plus evidence of renal disease - Proteinuria, albumin:creatinine ratio >30)

2 - 60-89

3a - 45-59

3b - 30-44

4 - 15-29

5 - <15

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48
Q

What is the most common cause of CKD in the UK?

What are other causes?

A

Diabetic nephropathy

Hypertension
PKD
Glomerulonephritis
Pyelonephritis

49
Q

How is diabetic nephropathy diagnosed?

A

Monitor early morning albumin:creatinine ratio

If abnormal - conduct 1st pass urine for Proteinuria

50
Q

How are kidneys seen on X-ray in CKD?

A

Small and scarred

In diabetic nephropathy- can be large

51
Q

What is the string of beads sign?

A

Seen in fibromuscular dysplasia

String of beads appearance to renal artery on angiogram

Fibromuscular dysplasia = cause of renal artery stenosis

52
Q

What are the two types of ADPKD?

A

PKD1 - chromosome 4

PKD2 - chromosome 16

53
Q

What is the diagnostic criteria for Polycystic kidney disease?

A

Age below 30 - two cysts (can be in one kidney or two)

Age 30-60 - two cysts in both kidneys

Age over 60 - four cysts in both kidneys

54
Q

How does Polycystic kidney disease present?

A

Abdominal pain

Early satiety

Hypertension

CKD

Hepatomegaly

Diverticulitis

Ovarian cysts

55
Q

How is Polycystic kidney disease managed?

A

Tolvaptan

Only needed if patient has reached CKD 2/3

56
Q

What are extra-renal manifestations of Polycystic kidney disease?

A

Liver cysts (Hepatomegaly)

Berry aneurysms (can present as SAH if rupture)

57
Q

How is Polycystic kidney disease screened for in family members?

A

Abdominal ultrasound

58
Q

What is haemolytic uraemic syndrome?

A

Triad of AKI, Haemolytic anaemia and low platelets

Haemolytic anaemia will cause raised bilirubin due to breakdown

Firstly a diarrhoea illness

Then around 5 days later - reduced urine output, abdominal pain, confusion, oedema, hypertension, bruising, vomiting

Treatment is supportive

59
Q

What is the most common type of renal cell carcinoma?

A

Adenocarcinoma (Clear cell)

60
Q

What is the classic triad of symptoms seen in renal cell carcinoma?

A

Haematuria

Flank pain

Palpable mass

61
Q

What is the 2WW criteria for suspected renal cancer?

A

> 45 plus visible unexplained haematuria

62
Q

What is the most common place for renal cell carcinoma to metastasise?

A

Lung (seen as cannonball metastases)

63
Q

What are causes of metabolic alkalosis?

A

Vomiting

Diuretics

Hypokalaemia

Primary hyperaldosteronism

Cushing’s

64
Q

What are causes of metabolic acidosis? (raised anion gap vs. normal anion gap)

A

Raised anion gap = sepsis, shock, DKA, alcohol, aspirin, methanol

Normal anion gap = diarrhoea, renal tubular acidosis, Addison’s

65
Q

How is the anion gap calculated? What is a normal anion gap?

A

(Sodium+potassium) - (bicarbonate+chloride)

Normal anion gap = 8-14

66
Q

What is Alport’s syndrome?

A

X-linked recessive condition

Microscopic haematuria

Progressive renal failure

Bilateral sensorineural deafness

Protrusion of lens surface

Retinitis pigmentosa

67
Q

Presentation: renal failure + deafness +/- vision problems?

A

Alports syndrome

68
Q

What is seen on renal biopsy in Alport’s syndrome?

A

Longitudinal splitting of the lamina densa

Basket-weave appearance

69
Q

What is the NICE criteria for AKI?

A

Rise in creatinine of ≥ 25 micromol/L in 48 hours

Rise in creatinine of ≥ 50% in 7 days

Urine output of < 0.5ml/kg/hour for > 6 hours

70
Q

What is renal tubular acidosis? What is the normal function of the renal tubules?

A

Metabolic acidosis due to a pathology of the renal tubules

Renal tubules maintain hydrogen and bicarbonate ion balance to maintain normal pH

71
Q

What is type 1 and type 2 renal tubular acidosis? What lab results are seen?

A

Type 1 = distal tubule fails to excrete hydrogen ions

Type 2 = proximal tubule fails to reabsorb bicarbonate ions

Lab results = HYPOkalaema, metabolic acidosis, low urinary pH

72
Q

What are causes of type 1 renal tubular acidosis?

A

Genetic

SLE

Sjorgen’s syndrome

Hyperthyroidism

Sickle cell anaemia

Marfan’s

73
Q

How does type 1 renal tubular acidosis present?

A

In children - failure to thrive

Hyperventilation (compensation for metabolic acidosis)

CKD

Osteomalacia

74
Q

What is the treatment for type 1 and type 2 renal tubular acidosis?

A

Oral bicarbonate

Hypokalaemia does not need to be treated - oral bicarbonate will fix it

75
Q

Which type of renal tubular acidosis is associated with Fanconi syndrome?

A

Type 2 renal tubular acidosis

76
Q

What is the most common type of renal tubular acidosis?

A

Type 4

77
Q

What is type 4 renal tubular acidosis? What are causes/?

A

Reduced aldosterone which leads to reduced ammonium excretion by the proximal tubule

Due to…

Adrenal insufficiency

ACEi

Spironolactone

SLE

HIV

78
Q

What lab results are seen in type 4 renal tubular acidosis?

A

HYPERkalaemia

Metabolic acidosis

High chloride

Low urinary pH

79
Q

How is type 4 renal tubular acidosis managed?

A

Fludrocortisone

Oral bicarbonate

Hyperkalaemia management

80
Q

What tests do you want to do in ?Rhabdomyolysis

A

Blood tests- FBC, U+E, Myoglobin, CK

ECG - due to potential raised potassium

81
Q

What is seen on urinalysis in acute interstitial nephritis?

A

Sterile pyuria

White cell casts

82
Q

What is sterile pyuria and what are causes?

A

Raised white cells in urine but Negative urine culture

Renal tuberculosis

Partially treated UTI

Acute interstitial nephritis

Urinary tract stones

83
Q

How can you differentiate heart failure from nephrotic syndrome?

A

Both will have oedema

Nephrotic syndrome will have massive proteinuria

Heart failure will have little/no proteinuria

84
Q

What are indications for acute dialysis?

A

AEIOU

Acidosis (severe metabolic acidosis with pH of less than 7.20)

Electrolyte imbalance (persistent hyperkalaemia with ECG changes)

Intoxication (poisoning)

Oedema (refractory pulmonary oedema not responding to medication)

Uraemia (symptomatic uraemia - encephalopathy or pericarditis)

85
Q

Which autoantibodies are raised in Anti-GBM disease?

A

Type IV Collagen autoantibodies

86
Q

What are physical signs of haemolytic uraemic syndrome?

A

Jaundice (due to haemolysis)

Bruising(due to low platelets)

Abdominal tenderness

87
Q

Who is at risk of AKI?

A

Chronic kidney disease

Diabetes with chronic kidney disease

Heart failure

Renal transplant

Aged 75 or over

Hypovolaemia (dehydration)

Contrast agent

88
Q

What autoantibodies are raised in post-strep glomerulonephritis?

A

Anti-streptolysin O antibodies

89
Q

What is seen on electron microscopy in IgA Nephropathy?

A

IgA deposition in the mesangium

90
Q

What is seen on electron microscopy in Post-strep Glomerulonephritis?

A

IgG and C3 sub epithelial deposition

91
Q

What is seen on electron microscopy in Membranous nephropathy?

A

Spike and dome appearance

92
Q

What is seen on electron microscopy in minimal change disease?

A

Effacement of foot processes

Fusion of podocytes

93
Q

If AKI is associated with proteinuria, what is the most likely cause? (Renal, pre-renal or post-renal)

A

Renal AKI

94
Q

Urinary sodium - pre renal vs renal AKI

A

Pre-renal = Low urinary sodium

Renal = High urinary sodium

95
Q

Urine osmolality - pre renal vs renal AKI

A

Pre-renal = high urine osmolality

Renal = Low urine osmolality

96
Q

Serum urea:creatinine ratio - pre renal vs renal AKI

A

Pre-renal = Raised urea:creatinine ratio

Renal = Normal urea:creatinine ratio

97
Q

How can you treat steroid resistant nephrotic syndrome?

A

Tacrolimus/Ciclosporin/Cyclophosphamide

98
Q

What are risks of oral corticosteroids in children?

A

Poor growth

Obesity

Osteoporosis

DM

Behavioural disturbances

99
Q

What are the two main causes of renal artery stenosis?

A

Atherosclerosis

Fibromuscular dysplasia

100
Q

What does worsening renal function after starting an ACEi suggest?

A

Bilateral renal artery stenosis

101
Q

What is the gold standard diagnostic investigation for renal artery stenosis?

A

Renal angiography

Also renal ultrasound (first line)

102
Q

How is renal artery stenosis managed?

A

Transluminal angiography +/- stenting

103
Q

What is an acceptable rise in creatinine after starting an ACEi?

A

<30% rise

104
Q

Which type of renal replacement therapy is used in AKI?

A

Haemofiltration

105
Q

What are complications of haemodialysis?

A 
Site infection
Endocarditis
Cardiac arrhythmia
Air embolus
Anaphylactic reaction
Amyloidosis
Hypertension
Disequilibration syndrome (Acute cerebral oedema - headache+drowsy)
106
Q

What are complications of peritoneal dialysis?

A 
Peritonitis
Catheter infection
Catheter blockage
Constipation
Fluid retention
Hyperglycaemia
Hernia
Back pain
Malnutrition
107
Q

What is the most common organism which causes peritonitis due to peritoneal dialysis?

A

Staph epidermis

108
Q

What are complications of renal transplant?

A 
DVT/PE
Opportunistic infection
Malignanies - lymphoma/skin cancer
Bone marrow suppression
Urinary tract obstruction
CVD
Graft rejection
109
Q

What are the different types of renal transplant rejection?

A

Hyperacute rejection = minutes to hours
Due to antibodies
Graft must be removed

Acute rejection = less than 6 months
Mismatched HLA
May be reversible with immunosuppressants

Chronic graft rejection = more than 6 months
Due to fibrosis

110
Q

Which autoantibody is raised in post-strep glomerulonephritis?

A

Anti streptolysin O

111
Q

What are causes of focal segmental glomerulonephritis?

A

HIV
Heroin
Alport’s syndrome
Sickle cell disease

112
Q

Which valvular abnormality is associated with polycystic kidney disease?

A

Mitral valve prolapse

113
Q

What is the definitive diagnosis of acute interstitial nephritis?

A

Kidney biopsy - will show eosinophils, lymphocytes and plasma cells

urinalysis will show sterile pyuria

114
Q

What is a risk of giving someone too much sodium chloride?

A

Hypercholeraemic metabolic acidosis

115
Q

How do you screen for diabetic nephropathy?

A

Measure albumin:creatinine ratio - microalbumnaemia is the first sign of diabetic nephropathy

If abnormal - do a first pass morning urine sample for proteinuria

116
Q

How is diabetic nephropathy managed?

A

ACEi/ARB

117
Q

When to give calcium gluconate for hyperkalaemia?

A

> 6.5 or ECG changes

118
Q

What factor in U+Es points towards dehydration being a cause of AKI?

A

Urea proportionately higher than the creatinine

Hypernatraemia

119
Q

What is Fanconi syndrome?

A

Generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule resulting in:

type 2 (proximal) renal tubular acidosis
polyuria
aminoaciduria
glycosuria
phosphaturia
osteomalacia

Medicine Finals (32 decks)

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