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MRCP > Nephrology > Flashcards

Nephrology Flashcards

1
Q

what kind of anaemia do you usually get in CKD

A

normocytic anaemia

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2
Q

what does anaemia in CKD lead to?

A

left ventricular hypertrophy

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3
Q

what are the causes of anaemia in CKD?

A

reduced EPO levels which leads to diminished red blood cell production

reduced absorption of iron

reduced erythropoesis due to toxic effects of uraemia on bone marrow

reduced red cell survival especially in haemodyalysis

blood loss due to capillary fragility and poor lately function

stress ulceration leading to chronic blood loss

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4
Q

how does CKD cause reduced absorption of iron?

A

epcidin is an acute-phase reactant
in CKD, hepcidin levels are often increased due to inflammation and reduced renal clearance
elevated hepcidin levels lead to decreased iron absorption from the gut and impaired release of stored iron from macrophages and hepatocytes, reducing the iron available for erythropoiesis
additionally, metabolic acidosis, a common condition in CKD, can inhibit the conversion of ferric iron (Fe³º) to its absorbable form, ferrous iron (Fe²º), in the duodenum → reduced iron absorption.

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5
Q

how is anaemia in CKD managed?

A

aim for Hb 100 - 120
oral iron should be offered for patients not erythropoiesis agents
if target Hb levels not reached in 3 months patients should be on IV iron

ESAs such as EPO or darbepoetin should be used in those who are likely to benefit in terms of quality of life and physical function
those on ESAs generally require IV iron

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6
Q

what are the complications of nephrotic syndrome?

A

Increased risk of VTE related to loss of antithrombin III and plasminogen in the urine
DVT, PE , renal vein thrombosis, resulting in a sudden deterioration in renal function

hyperlipidaemia- increasing risk of acute coronary syndrome, stroke etc

chronic kidney disease

increased risk of infection due to urinary immunoglobulin loss

hypocalcaemia (vitamin D and binding protein lost in urine)

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7
Q

what is minimal change disease?

A

a form of nephrotic syndrome
accounts of 75% of cases in children and 25% of cases in adults

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8
Q

what is the pathophysiology of minimal change disease?

A

T-cell and cytokine mediated damage to the glomerular basement membrane –> polyanion loss
the resultant reduction of the electrostatic charge - increase glomerular permeability to serum albumin

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9
Q

what are the features of minimal change disease and what is seen on renal biopsy?

A

nephrotic syndrome

Normotension, hypertension is rare

highly selective proteinuria - only intermediate sized proteins such as albumin and transferrin leak through the glomerulus

renal biopsy - normal glomeruli on light microscopy
electron microsocopy shows fusion of podocytes and effacement of foot processes

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10
Q

how is minimal change disease managed?

A

oral corticosteroids - majority of cases are steroid responsive - 1mg/kg daily
cyclophosphamide is the next step

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11
Q

what is the prognosis in minimal change disease ?

A

1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood

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12
Q

what is nephrotic syndrome characterised by?

A
  1. Proteinuria (> 3g/24hr) causing
  2. Hypoalbuminaemia (< 30g/L) and
  3. Oedema
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13
Q

what are the causes of nephrotic syndrome?

A

Primary causes: Minimal change disease, focal segmental glomerulosclerosis (FSGS), membranous nephropathy.

Secondary causes: Diabetes mellitus, systemic lupus erythematosus (SLE), amyloidosis, infections (HIV, hepatitis B and C), drugs (NSAIDs, gold therapy).

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14
Q

why is there an increased risk of thrombosis in nephrotic syndrome>

A

Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis

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15
Q

what are the characteristics and symptoms of nephritic syndromes?

A

haematuria
hypertension
mild proteinuria <3.5g/day
mild oedema
oliguria and uraemia

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16
Q

what are types of nephritic syndromes?

A

IgA nephropathy
post strep glomerular nephritis

rapid progressive glomerular nephritis -
anti GBM glomerularnephritis
ANCA vasculitis

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17
Q

what are the types of autosomal dominant polycystic kidney disease?

A

Type 1 - 85% of cases, chromosome 16, presents with renal failure earlier

Types 2 - 15% of cases - chromosome 4

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18
Q

what is the USS diagnostic criteria for patient with a positive family history?

A

two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years

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19
Q

how is PKD managed?

A

tolvaptan (vasopressin receptor 2 antagnost
Nice recommends the use of it if:
they have chronic kidney disease stage 2 or 3 at the start of treatment
there is evidence of rapidly progressing disease and
the company provides it with the discount agreed in the patient access scheme.

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20
Q

what is the classification of CKD?

A

1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a 45-59 ml/min, a moderate reduction in kidney function
3b 30-44 ml/min, a moderate reduction in kidney function
4 15-29 ml/min, a severe reduction in kidney function
5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

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21
Q

When does post step glomerulonephritis develop compared to IgA nephropathy?

A

PSGN - develops 1-2 weeks after URTI

IgA nephropathy develops 1-2 days after URTI

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22
Q

what is post-streptococcal glomerulonephritis?

A

Post-streptococcal glomerulonephritis 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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23
Q

what are the features of post streptococcal glomerulonephritis?

A

general - headache, malaise
visible haematuria
proteinuria - this may result in oedema
hypertension
oliguria

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24
Q

what would bloods show in post-steptococcal glomerulopnephririts ?

A

raised anti-streptolysin O titre are used to confirm the diagnosis of a recent streptococcal infection
low C3

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25
Q

what would renal biopsy show in post streptococcal glomerulonephritis?

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

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26
Q

what is Fanconi syndrome?

A

Fanconi syndrome - describes a generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule

resulting in the excretion of most amino acids, glucose, and phosphate

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27
Q

what does fanconi syndrome result in?

A

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

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28
Q

what are the causes of Fanconi syndrome?

A

cystinosis (most common cause in children)
Sjogren’s syndrome
multiple myeloma
nephrotic syndrome
Wilson’s disease

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29
Q

what are the features of autosomal dominant polycystic kidney disease?

A

hypertension
recurrent UTIs
flank pain
haematuria
palpable kidneys
renal impairment
renal stones

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30
Q

what are the extra renal manifestations of autosomal dominant polycystic kidney disease?

A

liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly

berry aneurysms (8%): rupture can cause subarachnoid haemorrhage

cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection

cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary

diverticulosis

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31
Q

when is plasma exchange indicated?

A

aka plasmapheresis

Guillain-Barre syndrome
myasthenia gravis
Goodpasture’s syndrome
ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage
TTP/HUS
cryoglobulinaemia
hyperviscosity syndrome e.g. secondary to myeloma

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32
Q

what are the complications of plasma exchange?

A

hypocalcaemia: due to the presence of citrate used as an anticoagulant for the extracorporeal system
metabolic alkalosis
removal of systemic medications
coagulation factor depletion
immunoglobulin depletion

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33
Q

what kind of murmur is heard in mitral valve prolapse?

A

late systolic murmur accompanied by a mid-systolic click, best auscultated at the cardiac apex. The mid-systolic click is attributable to the abrupt tensioning of the mitral valve leaflets as they prolapse into the atrium during systole.

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34
Q

what are the different types of testicular cancer?

A

germ cell tumours account for 95% of tumours - can be divided into seminomas and non seminomas (including embryonal, yolk sac, teratoma, and choriocarcinoma)

Non germ cell tumour include leading cell tumours and sarcomas.

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35
Q

what are the risk factors for testicular cancer?

A

infertility (increases risk by a factor of 3)
cryptorchidism
family history
Klinefelter’s syndrome
mumps orchitis

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36
Q

what are the features of testicular cancer?

A

a painless lump is the most common presenting symptom
pain may also be present in a minority of men
hydrocele
gynaecomastia

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37
Q

why does gynaecomastia occur in testicular cancer?

A

this occurs due to an increased oestrogen:androgen ratio
germ-cell tumours → hCG → Leydig cell dysfunction → increases in both oestradiol and testosterone production, but rise in oestradiol is relatively greater than testosterone
leydig cell tumours → directly secrete more oestradiol and convert additional androgen precursors to oestrogens

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38
Q

what ate the tumour markers in testical cancer?

A

seminomas: seminomas: hCG may be elevated in around 20%
non-seminomas: AFP and/or beta-hCG are elevated in 80-85%
LDH is elevated in around 40% of germ cell tumours

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39
Q

how is prostate cancer managed?

A

localised T1/T2 - conservative - active monitoring and watchful waiting, radical prostatectomy, radiotherapy - external beam and brachytherapy

Localised advanced T3/T4 - hormonal therapy, radical prostatectomy, radiotherapy - external beam brachytherapy

metastatic prostate cancer - one of the key aims of treating advanced prostate cancer is reducing the androgen levels with hormone treatment

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40
Q

what is a complication of radiotherapy in prostate cancer?

A

patients may develop proctitis and are also at increased risk of bladder, colon, and rectal cancer following radiotherapy for prostate cancer

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41
Q

what hormone treatment is used in prostate cancer?

A

anti- androgen therapy

GnRH agonists (Goserelin - Zoladex) or antagonist (degaarelix)
Bicalutamide - non-steroidal anti-androgen, blocks the androgen receptor
Cyproterone acetate - steroidal anti-androgen - prevents DHT binding from intracytoplasmic protein complexes
Abiraterone - androgen synthesis inhibitor - used in hormone relapsed metastatic prostate cancer in patients who have no or mild symptoms after androgen deprivation therapy has failed

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42
Q

how do GnRH agonists work ?

A

paradoxically result in lower LH levels longer term by causing overstimulation, resulting in disruption of endogenous hormonal feedback systems. The testosterone level will therefore rise initially for around 2-3 weeks before falling to castration leves
initially therapy is often covered with an anti-androgen to prevent a rise in testosterone - ‘tumour flare’. The resultant stimulation of prostate cancer growth may result in bone pain, bladder obstruction and other symptoms

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43
Q

what chemotherapy is used in prostate cancer?

A

docetaxel

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44
Q

how do you calculate anion gap?

A

(sodium + potassium) - (bicarbonate + chloride)

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45
Q

what is a normal anion gap?

A

8-14 mmol/L

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46
Q

what can cause a normal anion gap metabolic acidosis?

A

Causes of a normal anion gap or hyperchloraemic metabolic acidosis

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

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47
Q

what can causes a raised anion gap metabolic acidosis?

A

lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use

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48
Q

what Is vesicoureteric reflux?

A

Vesicoureteric reflux (VUR) is the abnormal backflow of urine from the bladder into the ureter and kidney. It is a relatively common abnormality of the urinary tract in children and predisposes to urinary tract infection (UTI), being found in around 30% of children who present with a UTI.

** As around 35% of children develop renal scarring it is important to investigate for VUR in children following a UTI

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49
Q

what is the pathophysiology of vesicoureteric reflux?

A

ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle
therefore shortened intramural course of the ureter
vesicoureteric junction cannot, therefore, function adequately

50
Q

how does vesicoureteric reflux present?

A

antenatal period: hydronephrosis on ultrasound
recurrent childhood urinary tract infections
reflux nephropathy
term used to describe chronic pyelonephritis secondary to VUR
commonest cause of chronic pyelonephritis
renal scar may produce increased quantities of renin causing hypertension

51
Q

What investigations are performed for vesicoureteric reflux?

A

VUR is normally diagnosed following a micturating cystourethrogram
a DMSA scan may also be performed to look for renal scarring

52
Q

what are the grades of vesicourteric reflux?

A

I Reflux into the ureter only, no dilatation
II Reflux into the renal pelvis on micturition, no dilatation
III Mild/moderate dilatation of the ureter, renal pelvis and calyces
IV Dilation of the renal pelvis and calyces with moderate ureteral tortuosity
V Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity

53
Q

How are Voiding LUTs managed?

A

Voiding symptoms
conservative management - pelvic floor training, bladder training etc
moderate or severe symptoms - alpha blocker

if prostate is enlarged - 5-alpha reductase inhibitor

if prostate enlarged and moderate or severe symptoms - alpha blocker and 5-alpha reductase inhibitor

if there are mixed symptoms of voiding and storage not responding to an alpha blocker then a antimuscarinic (anticholinergic) drug may be added

54
Q

How are symptoms of an overactive bladder managed?

A

conservative measures include moderating fluid intake
bladder retraining should be offered
antimuscarinic drugs should be offered if symptoms persist. NICE recommend oxybutynin (immediate release), tolterodine (immediate release), or darifenacin (once daily preparation)
mirabegron may be considered if first-line drugs fail

55
Q

How can nocturne be managed?

A

advise about moderating fluid intake at night
furosemide 40mg in late afternoon may be considered
desmopressin may also be helpful

56
Q

What conditions are associated with hypokalaemia due to raised serum aldosterone?

how would you differentiate these conditions

A

Primary hyperaldosteronism, bilateral renal artery stenosis and Bartter syndrome

Aldosterone is elevated in bilateral renal artery stenosis and Bartter syndrome due to reduced renal perfusion. Aldosterone is high in primary hyperaldosteronism due to (most commonly) an aldosterone producing adenoma.

Serum renin is usually low primary hyperaldosteronism due to the hypertension causing excessive renal perfusion.
High renin levels are seen in renal artery stenosis and Bartter syndrome as a mechanism to improve renal perfusion.

renal artery stenosis associated with HTN and may have abdominal bruits caused by turbulent flow within the stenosed arteries

Barrets syndrome is associated with normotension

57
Q

what can lead to non-atherosclerotic renal artery stenosis?

A

Fibromuscular dysplasia
common in young woman
characteristically a string of beads appearance on angiography

58
Q

how would you investigate renal vascular disease?

A

MR angiography is now the investigation of choice
CT angiography
conventional renal angiography is less commonly performed used nowadays, but may still have a role when planning surgery

59
Q

why does alcohol binge lead to polyuria?

A

Alcohol causes polyuria via anti-diuretic hormone (ADH) inhibition. This leads to reduced aquaporin insertion in the collecting tubules of the nephron. This reduces water reabsorption, leading to polyuria.

60
Q

what are causes of polyuria ?

A

Common (>1 in 10)
diuretics, caffeine & alcohol
diabetes mellitus
lithium
heart failure

Infrequent (1 in 100)
hypercalcaemia
hyperthyroidism

Rare (1 in 1000)
chronic renal failure
primary polydipsia
hypokalaemia

Very rare (<1 in 10 000)
diabetes insipidus

61
Q

what may cause a false negative PSA result?

A

finasteride can decrease the level of serum PSA

62
Q

what levels of PSA is normal ?

A

< 40 Use clinical judgement
40–49 > 2.5
50–59 > 3.5
60–69 > 4.5
70–79 > 6.5
> 79 Use clinical judgement

63
Q

what may cause PSA levels to be high ?

A

benign prostatic hyperplasia (BPH)
prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 6 weeks after treatment)
ejaculation (ideally not in the previous 48 hours)
vigorous exercise (ideally not in the previous 48 hours)
urinary retention
instrumentation of the urinary tract

64
Q

how would you differentiate between pre renal uraemia and acute tubular necrosis?

A

In prerenal uraemia think of the kidneys holding on to sodium to preserve volume
a low urine sodium points towards prerenal acute kidney injury

In acute tubular necrosis the urinary sodium will be high, they will respond poorly to a fluid challenge

65
Q

what is acute tubular necrosis?

A

Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) seen in clinical practice. Necrosis of renal tubular epithelial cells severely affects the functioning of the kidney.

66
Q

what are the causes of acute tubular necrosis?

A

There are two main causes of ATN; ischaemia and nephrotoxins:

ischaemia
shock
sepsis

nephrotoxins
aminoglycosides
myoglobin secondary to rhabdomyolysis
radiocontrast agents
lead

67
Q

what are the features of acute tubular necrosis?

A

features of AKI: raised urea, creatinine, potassium
muddy brown casts in the urine

68
Q

what are the histopathological features of acute tubular necrosis?

A

tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
dilatation of the tubules may occur
necrotic cells obstruct the tubule lumen

69
Q

what are the phases of acute tubular necrosis?

A

oliguric phase
polyuric phase
recovery phase

70
Q

what is the action of calcium resonium?

A

Calcium resonium is a polystyrene cation exchange resin, acting to increase potassium excretion from the body through cation ion exchange. It exchanges potassium for the Ca++ in the resin.

It increases potassium excretion by preventing enteral absorption’

71
Q

what are the ECG changes seen in hyperkalaemia?

A

peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern

72
Q

What medications can be given to remove potassium from the body?

A

calcium resonium (orally or enema)
enemas are more effective than oral as potassium is secreted by the rectum
loop diuretics
dialysis
haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia

73
Q

what length of time is needed for an AV fistula to develop to be used?

A

6 to 8 weeks

74
Q

What are the potential complications associated with AV fistula?

A

infection
thrombosis
may be detected by the absence of a bruit
stenosis
may present with acute limb pain
steal syndrome

75
Q

Is Albumin-creatinine ration or protein creatinine ratio more sensitive?

A

CR has been found to be a more sensitive measure of small amounts of albuminuria, which can be an early sign of kidney damage in conditions such as diabetes and hypertension

An ACR of 30 mg/mmol is approximately equal to a PCR of 50 mg/mmo

76
Q

what is considered as clinically important proteinuria?

A

3mg/mmol or more

77
Q

when should you refer to a nephrologist in terms of urinary ACR?

A

a urinary albumin:creatinine ratio (ACR) of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated

a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection

consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease

78
Q

How is proteinuria in CKD managed?

A

ACEi or ARB are key in management
they should be used first line in patients with co-existent hypertension and CKD if ACR > 30. If the ACR > 70 then they are indicated regardless of the patients blood pressure

SGLT-2 inhibitors - patients who have proteinuric CKD (with or without diabetes) may benefit from treatment with SGLT2 inhibitors

79
Q

how do SGLT-2 inhibitors work?

A

they primarily act by blocking reabsorption of glucose in the proximal tubule → lowers the renal glucose threshold → glycosuria
by blocking the cotransporter, they also reduce sodium reabsorption → natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa → normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure

80
Q

what are causes of pre-renal AKI

A

hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis

81
Q

what causes intrinsic AKI?

A

relate to intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves.

glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome

82
Q

what causes post-renal AKI?

A

kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter

83
Q

what is considered oliguria?

A

oliguria (urine output less than 0.5 ml/kg/hour)

84
Q

How is AKI defined?

A

a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than

85
Q

what medications should be stopped in AKI?

A
  • NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
  • Aminoglycosides
  • ACE inhibitors
  • Angiotensin II receptor antagonists
  • Diuretics
86
Q

which causes of glomerularnephritis have a low complement level?

A

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

87
Q

what are the side effects of EPO?

A

accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
bone aches
flu-like symptoms
skin rashes, urticaria
pure red cell aplasia* (due to antibodies against erythropoietin)
raised PCV increases risk of thrombosis (e.g. Fistula)
iron deficiency 2nd to increased erythropoiesis

88
Q

why may patients not respond to EPO?

A

iron deficiency
inadequate dose
concurrent infection/inflammation
hyperparathyroid bone disease
aluminium toxicity

89
Q

what is focal segmental glomerulosclerosis\?

A

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.

90
Q

what are the causes of focal segmental glomerulosclerosis?

A

idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell

91
Q

what investigations would you do for focal segmental glomerulosclerosis ?
what would it show?

A

renal biopsy
focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy

92
Q

what are the features of HIV associated nephropathy?

A

massive proteinuria resulting in nephrotic syndrome
normal or large kidneys
focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
elevated urea and creatinine
normotension

93
Q

what is diabetes insipidus?

A

Diabetes insipidus (DI) is 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).

94
Q

what are the causes of cranial diabetes Insipidus?

A

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

95
Q

what are the causes of nephrogenic diabetes insipidus?

A

genetic:
more common form affects the vasopression (ADH) receptor
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

96
Q

what are the features of diabetes insipidus?

A

polyuria
polydipsia

97
Q

what are the investigations for diabetes insipidus?

A

high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test

98
Q

how do you manage diabetes insipidus?

A

nephrogenic diabetes insipidus
thiazides
low salt/protein diet

central diabetes insipidus can be treated with desmopressin

99
Q

what is membranous glomerulonephritis?

A

Membranous glomerulonephritis is the commonest type of glomerulonephritis in adults and is the third most common cause of end-stage renal failure (ESRF). It usually presents with nephrotic syndrome or proteinuria.

100
Q

what would be seen on renal biopsy on membranous glomerulonephritis?

A

electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

101
Q

what are the causes of membranous glomerulonephritis?

A

idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

102
Q

what is the management of membranous glomerulonephritis?

A

ACEi or ARB

Immunosuppression - if there is severe or progressive disease
steroids alone are not effective
A combination of corticosteroid + another agent such as cyclophosphamide is often used
consider anticoagulation for high-risk patients

103
Q

what are causes of rapidly protective glomerulonephritis?

A

Goodpasture’s, ANCA positive vasculitis
Usually rapid onset, often presents as an AKI
will present with nephritic syndrome (haematuria and hypertension)

104
Q

Who is IgA nephropathy commonly seen in?

A

typically young adult with haematuria following an URTI
there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)

105
Q

what may present with a mixed nephrotic/nephritic pattern?

A

Diffuse proliferative glomerulonephritis
classical post-streptococcal glomerulonephritis in child
presents as nephritic syndrome / acute kidney injury
most common form of renal disease in SLE

Membranoproliferative glomerulonephritis (mesangiocapillary)
type 1: cryoglobulinaemia, hepatitis C
type 2: partial lipodystrophy

106
Q

what causes papillary necrosis and what are the features?

A

Causes
chronic analgesia use
sickle cell disease
TB
acute pyelonephritis
diabetes mellitus

Features
fever, loin pain, haematuria
IVU - papillary necrosis with renal scarring - ‘cup & spill’

107
Q

what glomerulonephritides will present with nephrotic syndrome?

A

Minimal change disease
typically a child with nephrotic syndrome (accounts for 80%)
causes: Hodgkin’s, NSAIDs
good response to steroids

Membranous glomerulonephritis
presentation: proteinuria / nephrotic syndrome / chronic kidney disease
cause: infections, rheumatoid drugs, malignancy
1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop chronic kidney disease

Focal segmental glomerulosclerosis
may be idiopathic or secondary to HIV, heroin
presentation: proteinuria / nephrotic syndrome / chronic kidney disease

108
Q

what is IgA nephropathy?

A

IgA nephropathy (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.

109
Q

what are the associated conditions with IgA nephropathy?

A

alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

110
Q

what is the 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

111
Q

how does IgA nephropathy present?

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

112
Q

how to differentiate between IgA nephropathy and post streptococcal 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

113
Q

how is IgA nephropathy managed?

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

114
Q

what are markers of good vs poor prognosis in 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

115
Q

what is the tired of symptoms in haemolytic uraemia syndrome?

A

acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia

116
Q

what causes primary HUS?

A

Primary HUS (‘atypical’) is due to complement dysregulation.

117
Q

what are the causes of secondary 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

118
Q

what are the investigations for HUS?

A

full blood count
anaemia: microangiopathic hemolytic anaemia characterised by a haemoglobin level less than 8 g/dL with a negative Coomb’s test
thrombocytopenia
fragmented blood film: schistocytes and helmet cells
U&E: acute kidney injury
stool culture
looking for evidence of STEC infection
PCR for Shiga toxins

119
Q

how is HUS managed?

A

treatment is supportive e.g. Fluids, blood transfusion and dialysis if required
there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients
the indications for plasma exchange in HUS are complicated
as a general rule plasma exchange is reserved for severe cases of HUS not associated with diarrhoea
eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS

120
Q

what is the most likely cause of death in patients on dialysis ?

A

ischaemic heart disease

MRCP (18 decks)

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