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MRCP part 1 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Normal anion gap ( = hyperchloraemic metabolic acidosis)

A 
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison's disease
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2
Q

Raised anion gap

A

actate: shock, sepsis, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol

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3
Q

Metabolic acidosis secondary to high lactate levels may be subdivided into two types:

A

lactic acidosis type A: sepsis, shock, hypoxia, burns

lactic acidosis type B: metformin

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4
Q

IgA Nephropathy

what is it?

A

(also known as Berger’s disease) is the commonest cause of glomerulonephritis worldwide. It classically presents as macroscopic haematuria in young people following an upper respiratory tract infection.

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5
Q

IgA Nephropathy

associated diseases

A

alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

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6
Q

Pathophysiology of IgA Nephropathy

A

thought to be caused by mesangial deposition of IgA immune complexes
there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)
histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3

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7
Q

IgA Nephropathy presentations

A

young male, recurrent episodes of macroscopic haematuria
typically associated with a recent respiratory tract infection
nephrotic range proteinuria is rare
renal failure is unusual and seen in a minority of patients

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8
Q

Differentiation between igA nephropathy and post-streptococcal

A

glomerulonephritis
post-streptococcal glomerulonephritis is associated with low complement levels
main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis

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9
Q

Management of IgA Nephropathy

A

Isolated hematuria, no or minimal proteinuria (less than 500 to 1000 mg/day), and a normal glomerular filtration rate (GFR)
no treatment needed, other than follow-up to check renal function
persistent proteinuria (above 500 to 1000 mg/day), a normal or only slightly reduced GFR
initial treatment is with ACE inhibitors
if there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors
immunosuppression with corticosteroids

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10
Q

Prognosis of IgA Nephropathy

A

25% of patients develop ESRF
markers of good prognosis: frank haematuria
markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD

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11
Q

Post streptococcous glomerulonephritis

A

typically occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (usually Streptococcus pyogenes). It is caused by immune complex (IgG, IgM and C3) deposition in the glomeruli. Young children are most commonly affected.

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12
Q

Post streptococcous glomerulonephritis

features

A 
general
headache
malaise
visible haematuria
proteinuria
this may result in oedema
hypertension
oliguria
bloods:
low C3
raised ASO titre
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13
Q

Post streptococcous glomerulonephritis

Renal biopsy features

A

post-streptococcal glomerulonephritis causes acute, diffuse proliferative glomerulonephritis
endothelial proliferation with neutrophils
electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
immunofluorescence: granular or ‘starry sky’ appearance

Carries a good prognosis

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14
Q

histology of IgA nephropathy

A

histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3

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15
Q 
membranoproliferative glomerulonephritis (type I)
histology
A

Subendothelial immune complex deposits with ‘tram-track’ appearance on electron microscopy

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16
Q

membranous glomerulonephritis histology

A

Thickened basement membrane with subepithelial electron dense deposits creating a ‘spike and dome’ appearance

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17
Q

Mechanism of action: Spironolactone

A

aldosterone antagonist which acts in the cortical collecting duct.

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18
Q

Indications for Spironolactone

A

ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
hypertension: used in some patients as a NICE ‘step 4’ treatment
heart failure (see RALES study below)
nephrotic syndrome
Conn’s syndrome

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19
Q

adverse effects of spironolactone

A

hyperkalaemia

gynaecomastia

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20
Q

Aetiology of Faconi’s syndrome

A

Generalised disorder of renal tubular transport in the proximal convoluted tubule

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21
Q

Features of Anti-Glomerular Basement Membrane Disease

A

pulmonary haemorrhage
rapidly progressive glomerulonephritis
this typically results in a rapid onset acute kidney injury
nephritis → proteinuria + haematuria

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22
Q

Investigation findings in Anti-glomerular basement membrane disease (Goodpasteurs)

A

renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages

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23
Q

Management of Anti-glomerular basement membrane disease

A

plasmaphoresis
steroids
cyclophosphamide

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24
Q

Risk factors for pulmonary haemorrhage in anti-glomerular basement membrane disease

A 
smoking
lower respiratory tract infection
pulmonary oedema
inhalation of hydrocarbons
young males
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25
Q

urine sodium in acute tubular necrosis

A

> 40mmol

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26
Q

metabolic abnormalities caused by ammonium chloride injection

A

normal anion gap metabolic acidosis

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27
Q

normal anion gap metabolic acidosis causes

A 
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison's disease
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28
Q

raised anion gap metabolic acidosis

A

lactate: shock, sepsis, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol

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29
Q

raised anion gap metabolic acidosis

A

lactate: shock, sepsis, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol

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30
Q

typical history: minimal change disease

A

a 15-year-old presents with nephrotic syndrome. Their blood pressure and renal blood tests are normal

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31
Q

typical history IgA nephropathy

A

a 25-year-old man presents with visible haematuria. He also complains of having a bad sore throat at the current time

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32
Q

Features of Henoch-Schonlein purpura

A

palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure

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33
Q

what is Henoch-Schonlein purpura

A

An IgA mediated small vessel vasculitis. There is a degree of overlap with IgA nephropathy (Berger’s disease). HSP is usually seen in children following an infection.

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34
Q

treatment of Henoch-Schonlein purpura

A

analgesia for arthralgia
treatment of nephropathy is generally supportive. There is inconsistent evidence for the use of steroids and immunosuppressants

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35
Q

typical histories of streptococcus pyogenes

A

a 10-year-old boy boy presents after passing ‘brown’ urine. Two weeks ago he had a severe sore throat. On examination his blood pressure is high for his age and there is periorbital oedema
a 10-year-old presents with fever. They complain of fleeting large joint pain and ‘jerking’ movements of the hand and face. On examination a murmur is noted and subcutaneous nodules on the wrists
a 10-year-old presents with fever and a sore throat. Today they have a developed a fine, erythematous, ‘sand-paper’ rash which is more prominent in flexural areas.

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36
Q

Type 1 Membranoproliferative glomerulonephritis

A

accounts for 90% of cases
cause: cryoglobulinaemia, hepatitis C
renal biopsy
electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

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37
Q

Type 2 Membranoproliferative glomerulonephritis

A
  • ‘dense deposit disease’
    causes: partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face), factor H deficiency
    caused by persistent activation of the alternative complement pathway
    low circulating levels of C3
    C3b nephritic factor is found in 70%
    an antibody to alternative-pathway C3 convertase (C3bBb)
    stabilizes C3 convertase
    renal biopsy
    electron microscopy: intramembranous immune complex deposits with ‘dense deposits’
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38
Q

Type 3 Membranoproliferative glomerulonephritis

A

causes: hep B and C

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39
Q

What is Alport’s syndrome

A

Alport’s syndrome is usually inherited in an X-linked dominant pattern*. It is due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM). The disease is more severe in males with females rarely developing renal failure.

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40
Q

typical question around Alport’s syndrome

A

an Alport’s patient with a failing renal transplant. This may be caused by the presence of anti-GBM antibodies leading to a Goodpasture’s syndrome like picture

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41
Q

Features of Alport’s syndrome

A

microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy

42
Q

minimal change histology:

A

Effacement of foot processes on electron microscopy

43
Q

CKD bone disease- basic problems

A

low vitamin D (1-alpha hydroxylation normally occurs in the kidneys)
high phosphate
low calcium: due to lack of vitamin D, high phosphate- due to reduced excretion
secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

44
Q

CKD bone disease - clinical manifestations

A 
Osteitis fibrosa cystica
aka hyperparathyroid bone disease 
Adynamic
reduction in cellular activity (both osteoblasts and osteoclasts) in bone
may be due to over treatment with vitamin D
Osteomalacia
due to low vitamin D
Osteosclerosis
Osteoporosis
45
Q

Atypical haemolytic uraemic syndrome

A

encompasses many diseases with microangiopathic haemolytic anaemia with schistocytes and thrombocytopenia
No DIARRHOEAL syndromes

46
Q

Haemolytic uraemic syndrome triad

A

Acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia

47
Q

Secondary causes of HUS

A

classically Shiga toxin-producing Escherichia coli (STEC) 0157:H7 (‘verotoxigenic’, ‘enterohaemorrhagic’). This is the most common cause in children, accounting for over 90% of cases
pneumococcal infection
HIV
rare: systemic lupus erythematosus, drugs, cancer

48
Q

Investigations of HUS

A 
full blood count: anaemia, thrombocytopaenia, fragmented blood film
U&E: acute kidney injury
stool culture
looking for evidence of STEC infection
PCR for Shiga toxins
49
Q

Management of HUS

A

Largely supportive

eculizumab (a C5 inhibitor monoclonal antibody) may be more beneficial than plasma exchange

50
Q

Alports syndrome

A

hereditary nephritis due to a basement membrane disorder resulting in haematuria as a renal manifestation. Microscopic hematuria is persistent and invariable in males affected by Alport’s disease. Haematuria may present with/without bilateral anterior lenticonus and sensorineural hearing loss.

51
Q

Genetics of Alports syndrome

A

X-linked dominant inheritance

Type IV collagen defect that leads to abnormal basement membrane

52
Q

Features of Alport syndrome

A

microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy

53
Q

Diagnosis of Alport syndrome

A

molecular genetic testing
renal biopsy
electron microscopy: characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance

54
Q

mechanism of action: Calcium resonium

A

Calcium and sodium cations are exchanged for hydrogen ions in the stomach. These hydrogen ions are then exchanged for potassium ions in the large intestine and the potassium ions are excreted from the bowel as part of the resin comple

55
Q

What is cystinuria

A

Cystinuria is an autosomal recessive disorder characterised by the formation of recurrent renal stones. It is due to a defect in the membrane transport of cystine, ornithine, lysine, arginine (mnemonic = COLA)

56
Q

Features of cystinuria

A

recurrent renal stones

are classically yellow and crystalline, appearing semi-opaque on x-ray

57
Q

Diagnosis of cystinuria

A

cyanide-nitroprusside test

58
Q

Management of cystinuria

A

hydration
D-penicillamine
urinary alkalinization

59
Q

Glomerulonephritis and low complement

A

post-streptococcal glomerulonephritis
subacute bacterial endocarditis
systemic lupus erythematosus
mesangiocapillary glomerulonephritis

60
Q

Glomerulonephritis with normal complement

levels

A

Goodpastures syndrome
rare condition associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis. It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen

61
Q

Complications of nephrotic syndrome

A

Anti-thrombin III deficiency (and plasminogen)- lost through glomerular basement membrane –> DVT/PE/renal vein thrombosis
Hyperlipidaemia
CKD
Increased infection risk - loss of urinary immunoglobulin loss
hypocalcaemia

62
Q

Rapidly progressive glomerulonephritis

A

Rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli.

Causes
Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritisR

63
Q

Urine dip - protein positive

A

intra-renal AKI

64
Q

Bacterial infections in Peritoneal dialysis

A

Coagulase-negative Staphylococcus species e.g. Staphylococcus epidermidis and Staphylococcus capitis peritonitis remains a common complication of peritoneal dialysis. Empiric antibiotic therapy usually aims to cover both gram-positive and gram-negative organisms.

65
Q

Goodpastures accronyms

A

IgG deposits on renal biopsy

anti-GBM antibodies

66
Q

Features of Goodpastures/anti-glomerular basement membrane disease

A

pulmonary haemorrhage
rapidly progressive glomerulonephritis
this typically results in a rapid onset acute kidney injury
nephritis → proteinuria + haematuria

67
Q

Investigations in Goodpastures/ anti-glomerular membrane basement disease

A

renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages

68
Q

Management of Goodpastures

A

plasma exchange (plasmapheresis)
steroids
cyclophosphamide

69
Q

Risk factors for pulmonary haemorrhage in Goodpastures disease

A 
smoking
lower respiratory tract infection
pulmonary oedema
inhalation of hydrocarbons
young males
70
Q

Poor prognostic factors in IgA Nephropathy

A

male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD

71
Q

Management of IgA nephropathy

A

isolated hematuria, no or minimal proteinuria (less than 500 to 1000 mg/day), and a normal glomerular filtration rate (GFR)
no treatment needed, other than follow-up to check renal function
persistent proteinuria (above 500 to 1000 mg/day), a normal or only slightly reduced GFR
initial treatment is with ACE inhibitors
if there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors
immunosuppression with corticosteroids

72
Q

Differentiating between IgA Nephropathy and post streptococcous glomerulonephritis

A

post-streptococcal glomerulonephritis is associated with low complement levels
main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis

73
Q

Pathophysiology of IgA Nephropathy

A

thought to be caused by mesangial deposition of IgA immune complexes
there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)
histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3

74
Q

What is diabetes insipidus

A

a condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI)

75
Q

Causes of cranial diabetes insipidus

A 
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
histiocytosis X
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome)
haemochromatosis
76
Q

Causes of nephrogenic diabetes insipidus

A

genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes: hypercalcaemia, hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

77
Q

Features of HSP

A

palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure

78
Q

Pre-renal or ATN - AKI

A

In prerenal uraemia think of the kidneys holding on to sodium to preserve volume
Pre-renal = urinary sodium excretion = 20%

79
Q

Mechanism of action: Spironalactone

A

aldosterone antagonist which acts in the cortical collecting duct.

80
Q

Indications for spironolactone

A

ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
hypertension: used in some patients as a NICE ‘step 4’ treatment
heart failure (see RALES study below)
nephrotic syndrome
Conn’s syndrome

81
Q

Adverse effects of spironolactone

A

hyperkalaemia

gynaecomastia: less common with eplerenone

82
Q

Prevention of calcium renal stones

A 
high fluid intake
low animal protein, low salt diet (a low calcium diet has not been shown to be superior to a normocalcaemic diet)
thiazides diuretics (increase distal tubular calcium resorption)
83
Q

prevention of oxalate renal stones

A

cholestyramine reduces urinary oxalate secretion

pyridoxine reduces urinary oxalate secretion

84
Q

prevention of uric acid renal stones

A

allopurinol

urinary alkalinization e.g. oral bicarbonate

85
Q

Genetic changes that cause nephrogenic diatbetes insipidus

A

the more common form affects the vasopression (ADH) receptor

the less common form results from a mutation in the gene that encodes the aquaporin 2 channel

86
Q

Fibromuscular dysplasia

A

Young female, hypertension and asymmetric kidneys

87
Q

Features of fibromuscular dysplasia

A

hypertension
chronic kidney disease or more acute renal failure e.g. secondary to ACE-inhibitor initiation
‘flash’ pulmonary oedema

88
Q

Electron microscopy in minimal change disease

A

normal glomeruli on light microscopy

electron microscopy shows fusion of podocytes and effacement of foot processes

89
Q

Membranoproliferative glomerulonephritis type 1

A

accounts for 90% of cases
cause: cryoglobulinaemia, hepatitis C
renal biopsy
electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

90
Q

Membranoproliferative glomerulonephritis type 2

A

causes: partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face), factor H deficiency
caused by persistent activation of the alternative complement pathway
low circulating levels of C3
C3b nephritic factor is found in 70%
an antibody to alternative-pathway C3 convertase (C3bBb)
stabilizes C3 convertase
renal biopsy
electron microscopy: intramembranous immune complex deposits with ‘dense deposits’

91
Q

AL amyloidosis

A

the most common form of amyloidosis
L for immunoglobulin Light chain fragment
due to myeloma, Waldenstrom’s, MGUS
features include: nephrotic syndrome, cardiac and neurological involvement, macroglossia, periorbital eccymoses

92
Q

AA amyloidosis

A

A for precursor serum amyloid A protein, an acute phase reactant
seen in chronic infection/inflammation
e.g. TB, bronchiectasis, rheumatoid arthritis
features: renal involvement most common feature

93
Q

Beta-2 microglobulin amyloidosis

A

precursor protein is beta-2 microglobulin, part of the major histocompatibility complex
associated with patients on renal dialysis

94
Q

Magnesium ammonium phosphate, (also known as struvite) renal stones

A

caused by urea splitting bacteria e.g. proteus.

can cause staghorn calculi

95
Q

Causes of papillary necrosis

A 
chronic analgesia use
sickle cell disease
TB
acute pyelonephritis
diabetes mellitus
96
Q

Features of papillary necrosis

A

fever, loin pain, haematuria

IVU - papillary necrosis with renal scarring - ‘cup & spill’

97
Q

Nephrogenic diabetes insipidus

A

presents with polyuria and polydipsia. The kidneys are not responding to antidiuretic hormone (ADH) and so osmolality remains low post-water deprivation, as they fail to concentrate urine. Osmolality remains low after administering desmopressin, as the kidneys cannot res

98
Q

Tolvaptan mechanism of action

A

action of vasopressin at the V2 receptor. This receptor is found on the basolateral membrane of the principal cells in the collecting ducts of the kidney. This reduces water absorption (through decreased aquaporin 2) and increases aquaresis without sodium loss. Desmopressin is a synthetic analogue of vasopressin that exerts agonism at the V2 receptor.

99
Q

V1 receptors

A

found on vascular smooth muscle and when activated cause vasoconstriction. V3 receptors are expressed in the pituitary gland and modulate ACTH secretion.

100
Q

Mechanism of action Abiraterone acetate

A

selective androgen synthesis inhibitor that works by blocking cytochrome P450 17 alpha-hydroxylase. It blocks androgen production in the testes and adrenal glands, and in prostatic tumour tissue. Abiraterone is administered orally in combination with prednisolone

101
Q

paraneoplastic hepatic dysfunction syndrome

A

Also known as Stauffer syndrome. Typically presents as cholestasis/hepatosplenomegaly. It is thought to be secondary to increased levels of IL-6

MRCP part 1 (15 decks)

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