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Nephrology Flashcards

1
Q

Causes of transient non-visible haematuria

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

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2
Q

Causes of persistent non-visible haematuria

A

cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease

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3
Q

Management of haematuria

A

urine dipstick is the test of choice for detecting haematuria

renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked

urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected

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4
Q

definition of persistent non-visible haematuria

A

blood being present in 2 out of 3 samples tested 2-3 weeks apart

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5
Q

when should haematuria be referred on to secondary care?

A

urgent:
Aged >= 45 years AND:
unexplained visible haematuria without UTI, or
visible haematuria that persists or recurs after successful treatment of UTI

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test

non-urgent:
Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection

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6
Q

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

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7
Q

causes of normal anion gap metabolic acidosis

A

Normal anion gap ( = 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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8
Q

causes of raised anion gap metabolic acidosis

A

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

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9
Q

causes of metabolic alkalosis

A

Metabolic alkalosis may be caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of the kidney or gastrointestinal tract

Causes
vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction)
diuretics
liquorice, carbenoxolone
hypokalaemia
primary hyperaldosteronism
Cushing’s syndrome
Bartter’s syndrome
congenital adrenal hyperplasia

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10
Q

causes of respiratory acidosis

A

Respiratory acidosis may be caused by a number of conditions
COPD
decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema
sedative drugs: benzodiazepines, opiate overdose

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11
Q

causes of respiratory alkalosis

A

Common causes
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy

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12
Q

causes of nephrotic syndrome

A

minimal change disease

membranous glomerulonephropathy

focal segmental glomerulosclerosis

amyloidosis

diabetic nephropathy

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13
Q

definition of nephrotic syndrome

A

Triad of:
1. Proteinuria (> 3g/24hr) causing
2. Hypoalbuminaemia (< 30g/L) and
3. Oedema

Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis. Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.

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14
Q

definition of nephritic syndrome

A

haematuria, hypertension

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15
Q

causes of nephritic syndrome

A

rapidly progressive glomerulonephrosis

IgA nephropathy

Alport syndrome

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16
Q

what is acute interstitial nephritis

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

Pathophysiology
histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

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17
Q

causes of acute interstitial nephritis

A

drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjögren’s syndrome
infection: Hanta virus , staphylococci

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18
Q

common findings in acute interstitial nephritis

A

Investigations
sterile pyuria
white cell casts

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19
Q

main differences between AKI and CKD

A

renal ultrasound - most patients with CKD have bilateral small kidneys.

Exceptions to this rule include:
autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy

Other features suggesting CKD rather than AKI
hypocalcaemia (due to lack of vitamin D)

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20
Q

definition of AKI

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 8 hours in children

> = 25% fall in eGFR in children / young adults in 7 days.

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21
Q

causes of AKI

A

prerenal
hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis

intrinsic
The second group of causes relate to intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves. This may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.

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

postrenal
obstruction to the urine coming from the kidneys resulting in things ‘backing-up’ and affecting the normal renal function
kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter

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22
Q

signs of AKI

A

Many patients with early AKI may experience no symptoms. However, as renal failure progresses the following may be seen:
reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (for example, pericarditis or encephalopathy)

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23
Q

findings in AKI

A

Urinalysis
all patients with suspected AKI should have urinalysis

Imaging
if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound within 24 hours of assessment.

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24
Q

drugs to stop in AKI

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

may need to stop:
* Metformin
* Lithium
* Digoxin

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25
Q

treating AKI

A

supportive management - careful fluid balance to ensure that the kidneys are properly perfused but not excessively to avoid fluid overload

review a patient’s medication list

treating hyperkalaemia

All patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist.

Renal replacement therapy (e.g. haemodialysis) is used when a patient is not responding to medical treatment of complications, for example hyperkalaemia, pulmonary oedema, acidosis or uraemia (e.g. pericarditis, encephalopathy).

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26
Q

treatments for hyperkalaemia

A

treating hyperkalaemia
IV calcium gluconate - stabilisation of cardiac membrane

short term EC to IC shift
* Combined insulin/dextrose infusion
* Nebulised salbutamol

removal of K+ from body
* Calcium resonium (orally or enema)
* Loop diuretics
* Dialysis

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27
Q

stages of AKI

A

Stage 1 Increase in creatinine to 1.5-1.9 times baseline, or
Increase in creatinine by ≥26.5 µmol/L, or
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours

Stage 2 Increase in creatinine to 2.0 to 2.9 times baseline, or
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours

Stage 3 Increase in creatinine to ≥ 3.0 times baseline, or
Increase in creatinine to ≥353.6 µmol/L or
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2

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28
Q

diagnostic criteria for ADPKD

A

The screening investigation for relatives is abdominal ultrasound:

Ultrasound diagnostic criteria (in patients with positive family history)
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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29
Q

managing ADPKD

A

tolvaptan (vasopressin receptor 2 antagonist) may be an option. NICE recommended it as an option for treating ADPKD in adults to slow the progression of cyst development and renal insufficiency only 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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30
Q

what is ADPKD

A

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of kidney disease, affecting 1 in 1,000 Caucasians. Two disease loci have been identified, PKD1 and PKD2, which code for polycystin-1 and polycystin-2 respectively

ADPKD type 1 - 85% cases, chr16, presents with renal failure earlier

ADPKD type 2 - 15% cases, chr4

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31
Q

what are the features (and extra-renal features) of ADPKD

A

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

Extra-renal manifestations
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

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32
Q

what is Alport’s syndrome

A

X-linked dominant pattern
defect in gene coding for type IV collagen - causes abnormal glomerular basement membrane
more severe in males

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33
Q

how is Alport syndrome diagnosed

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

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34
Q

what are the features of Alport syndrome

A

Alport’s syndrome usually presents in childhood. The following features may be seen:
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

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35
Q

what is amyloidosis

A

extracellular deposition of an insoluble fibrillar protein termed amyloid
the accumulation of amyloid fibrils leads to tissue/organ dysfunction

can be systemic or localized
further characterised by precursor protein (e.g. AL in myeloma - A for Amyloid, L for immunoglobulin Light chain fragments)

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36
Q

how is amyloidosis diagnosed

A

Congo red staining: apple-green birefringence
serum amyloid precursor (SAP) scan
biopsy of skin, rectal mucosa, or abdominal fat

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37
Q

what is the anion gap

A

The anion gap is calculated by:

(sodium + potassium) - (bicarbonate + chloride)

A normal anion gap is 8-14 mmol/L

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38
Q

what 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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39
Q

what causes a normal anion gap 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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40
Q

what is anti-glomerular basement membrane (GBM) disease

A

Rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis

caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen

more common in men (sex ratio 2:1) and has a bimodal age distribution (peaks in 20-30 and 60-70 age bracket)

associated with HLA DR2

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41
Q

what are some features of anti-glomerular basement membrane (GBM) disease

A

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

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42
Q

what are the investigation findings for anti-glomerular basement membrane (GBM) disease

A

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

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43
Q

how is anti-glomerular basement membrane (GBM) disease managed

A

plasma exchange (plasmapheresis)
steroids
cyclophosphamide

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44
Q

what is an arteriovenous fistula

A

direct connections between arteries and veins. They may occur pathologically but are generally formed surgically to allow access for haemodialysis.

preferred method of access for haemodialysis due to the lower rates of complications.

The time taken for an arteriovenous fistula to develop is 6 to 8 weeks

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45
Q

what are some complications of arteriovenous fistulas

A

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

46
Q

how does CKD cause anaemia

A

usually a normochromic normocytic anaemia and becomes apparent when the GFR is less than 35 ml/min

reduced erythropoietin levels → diminished red blood cell production

reduced absorption of iron (due to high hepcidin, leading to reduced iron absorption)

reduced erythropoiesis due to toxic effects of uraemia on bone marrow

anorexia/nausea due to uraemia

reduced red cell survival (especially in haemodialysis)

blood loss due to capillary fragility and poor platelet function

stress ulceration leading to chronic blood loss

47
Q

how is anaemia in CKD managed

A

target haemoglobin of 10 - 12 g/dl

determination and optimisation of iron status should be carried out prior to the administration of erythropoiesis-stimulating agents (ESA).

oral iron should be offered for patients who are not on ESAs or haemodialysis. If target Hb levels are not reached within 3 months then patients should be switched to IV iron

48
Q

what are the bone issues in CKD

A

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

Osteitis fibrosa cystica
aka hyperparathyroid bone disease
Osteomalacia
due to low vitamin D
Osteosclerosis
Osteoporosis

49
Q

causes of CKD

A

diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease

50
Q

how to stage CKD

A

CKD may be classified according to GFR:

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

51
Q

features of CKD

A

Chronic kidney disease is usually asymptomatic and is generally diagnosed following abnormal urea and electrolyte results. However, some patients with undetected late-stage disease may become symptomatic.

Possible features include:
oedema: e.g. ankle swelling, weight gain
polyuria
lethargy
pruritus (secondary to uraemia)
anorexia, which may result in weight loss
insomnia
nausea and vomiting
hypertension

52
Q

treating HTN in CKD

A

ACEi - first line, help in proteinuric renal disease
reduces filtration pressure therefore causes a lower GFT and high creatinine

Furosemide - useful when the GFR falls to below 45 ml/min*. It has the added benefit of lowering serum potassium

53
Q

mineral bone disease in CKD

A

1-alpha hydroxylation normally occurs in the kidneys → CKD leads to low vitamin D

the kidneys normally excrete phosphate → CKD leads to high phosphate

the high phosphate level ‘drags’ calcium from the bones, resulting in osteomalacia

low calcium: due to lack of vitamin D, high phosphate

secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

54
Q

how to manage mineral bone disease in CKD

A

reduced dietary intake of phosphate is the first-line management
phosphate binders
vitamin D: alfacalcidol, calcitriol
parathyroidectomy may be needed in some cases

55
Q

what is diabetes insipidus

A

decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI)

causes polyuria and polydipsia

56
Q

causes of cranial DI

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

57
Q

causes of nephrogrenic DI

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

58
Q

how to test for diabetes insipidus

A

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

59
Q

how to manage diabetes insipidus

A

nephrogenic diabetes insipidus
thiazides
low salt/protein diet

central diabetes insipidus can be treated with desmopressin

60
Q

how to manage diabetic nephropathy

A

dietary protein restriction
tight glycaemic control
BP control: aim for < 130/80 mmHg
ACE inhibitor or angiotensin-II receptor antagonist
should be start if urinary ACR of 3 mg/mmol or more
dual therapy with ACE inhibitors and angiotensin-II receptor antagonist should not be started
control dyslipidaemia e.g. Statins

61
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

62
Q

causes of fanconi syndrome

A

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

63
Q

what is fibromuscular dysplasia

A

renal artery stenosis secondary to artherosclerosis causes 90% of renal vascular disease
fibromuscular dysplasia - causes the other 10%

usually affects females

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

64
Q

fluid prescribing requirements in adults

A

25-30 ml/kg/day of water and
approximately 1 mmol/kg/day of potassium, sodium and chloride and
approximately 50-100 g/day of glucose to limit starvation ketosis

0.9% saline
if large volumes are used there is an increased risk of hyperchloraemic metabolic acidosis

Hartmann’s
contains potassium and therefore should not be used in patients with hyperkalaemia

65
Q

what is focal segmental glomerulosclerosis

A

FSGS - causes nephrotic syndrome and CKD in young adults

66
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

67
Q

how is focal segmental glomerulosclerosis diagnosed and managed

A

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

managed by steroids +/- immunosuppressants

high recurrence rate in renal transplants

68
Q

what are the features of haemolytic uraemic syndrome

A

acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia

69
Q

what are the causes of haemolytic uraemic syndrome

A

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

secondary HUS
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

70
Q

how is haemolytic uraemic syndrome investigated and diagnosed

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

71
Q

how is haemolytic uraemic syndrome managed

A

supportive - fluids, blood transfusion and dialysis if required

plasma exchange is reserved for severe cases of HUS not associated with diarrhoea

eculizumab (a C5 inhibitor monoclonal antibody)

72
Q

what is henoch-schonlein purpura

A

an IgA mediated small vessel vasculitis causing 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

seen in children following infection

self limiting especially in children without renal involvement

73
Q

what is HIV associated nephropathy

A

features:
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

treat with ART

74
Q

classification of hyperkalaemia

A

mild: 5.5 - 5.9 mmol/L
moderate: 6.0 - 6.4 mmol/L
severe: ≥ 6.5 mmol/L

75
Q

what are the features of hypokalaemia

A

Features
muscle weakness, hypotonia
hypokalaemia predisposes patients to digoxin toxicity - care should be taken if patients are also on diuretics

76
Q

what are the ECG features of hypokalaemia

A

U waves
small or absent T waves
prolonged PR interval
ST depression

77
Q

what are the ECG changes of hyperkalaemia

A

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

78
Q

what is IgA nephropathy

A

commonest cause of glomerulonephritis worldwide causing macroscopic haematuria in young males 1-2 days following an URTI

caused by mesangial deposition of IgA immune complexes

histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3

assx with
alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

79
Q

what are the features of post-streprococcal glomerulonephritis

A

caused by immune complex (IgG, IgM and C3) deposition in the glomeruli
develops 1-2 weeks after URT

headache
malaise
visible haematuria
proteinuria (may result in oedema)
hypertension
oliguria
bloods:
raised anti-streptolysin O titre are used to confirm the diagnosis of a recent streptococcal infection
low C3

80
Q

what is type 1, 2 and 3 membranoproliferative glomerulonephritis

A

type 1
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

Type 2 - ‘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’

Type 3
causes: hepatitis B and C

81
Q

how does membranoproliferative glomerulonephritis present

A

nephrotic syndrome
haematuria/proteinuria
poor prognosis

82
Q

what is minimal change disease and how does it present

A

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

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 microscopy shows fusion of podocytes and effacement of foot processes

83
Q

causes of minimal change disease

A

drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

84
Q

management of minimal change disease and prognosis

A

oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases

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

85
Q

complications of nephrotic syndrome

A

increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
deep vein thrombosis, pulmonary embolism
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)

86
Q

what is peritoneal dialysis

A

Peritoneal dialysis (PD) is a form of renal replacement therapy. It is sometimes used as a stop-gap to haemodialysis or for younger patients who do not want to have to visit hospital three times a week.

Continuous Ambulatory Peritoneal Dialysis -
involves four 2-litre exchanges/day.

87
Q

complications of peritoneal dialysis

A

peritonitis
coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause. Staphylococcus aureus is another common cause
antibiotics should cover both Gram positive and Gram negative organisms
the BNF recommends vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth

sclerosing peritonitis

88
Q

what are the features of rapidly progressive glomerulonephritis

A

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

nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria
features specific to underlying cause (e.g. haemoptysis with Goodpasture’s, vasculitic rash or sinusitis with Wegener’s)

89
Q

causes of rapidly progressive glomerulonephritis

A

Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritis

90
Q

what is renal papillary necrosis

A

visible haematuria, loin pain and proteinuria

results from coagulative necrosis of the renal papillae due to a variety of causes:
severe acute pyelonephritis
diabetic nephropathy
obstructive nephropathy
analgesic nephropathy
phenacetin was the classic cause but this has now been withdrawn
NSAIDs
sickle cell anaemia

91
Q

what are the types of renal replacement therapy

A

haemodialysis
peritoneal dialysis
renal transplant

92
Q

what is haemodialysis

A

most common form of renal replacement therapy
regular filtration of the blood through a dialysis machine in hospital
3 times per week, with each session lasting 3-5 hours
8 weeks before the commencement of treatment, the patient must undergo surgery to create an arteriovenous fistula, which provides the site for haemodialysis

93
Q

what is peritoneal dialysis

A

Dialysis solution is injected into the abdominal cavity through a permanent catheter. The high dextrose concentration of the solution draws waste products from the blood into the abdominal cavity across the peritoneum. After several hours of dwell time, the dialysis solution is then drained, removing the waste products from the body, and exchanged for new dialysis solution

Continuous ambulatory peritoneal dialysis (CAPD) - as described above, with each exchange lasting 30-40 minutes and each dwell time lasting 4-8 hours. The patient may go about their normal activities with the dialysis solution inside their abdomen

Automated peritoneal dialysis (APD) - a dialysis machine fills and drains the abdomen while the patient is sleeping, performing 3-5 exchanges over 8-10 hours each night

94
Q

what is renal transplantation

A

receipt of a kidney from either a live or deceased donor. The average wait for a kidney in the UK is 3 years, though patients may also receive kidneys donated by cross-matched friends or family. The donor kidney is transplanted into the groin, with the renal vessels connected to the external iliac vessels. The failing kidneys are not removed. Following transplantation, the patient must take life-long immunosuppressants to prevent rejection of the new kidney. The average lifespan of a donor kidney is 10-12 years from deceased donors and 12-15 years from living donors.

95
Q

describe hyperacute rejection

A

Hyperacute rejection (minutes to hours) - due to pre-existing antibodies against ABO or HLA antigens (type II hypersensitivity reaction)
widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
no treatment is possible and the graft must be removed

96
Q

describe acute graft failure

A

acute graft failure (<6 months)
usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
other causes include cytomegalovirus infection
may be reversible with steroids and immunosuppressants

97
Q

describe chronic graft failure

A

chronic graft failure (> 6 months)
both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)

98
Q

what are some immunosuppressants used in renal transplantation

A

Example regime
initial: ciclosporin/tacrolimus with a monoclonal antibody
maintenance: ciclosporin/tacrolimus with MMF or sirolimus
add steroids if more than one steroid responsive acute rejection episode

99
Q

what are the side effects of immunosuppression for renal transplant

A

Hypertension and hyperglycaemia. Tacrolimus can also cause hyperlipidaemia. Patients must be monitored for accelerated cardiovascular disease.

Renal failure - due to nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease in transplanted kidney

Malignancy - patients should be educated about minimising sun exposure to reduce the risk of squamous cell carcinomas and basal cell carcinomas

100
Q

what are the causes of rhabdomyolysis

A

seizure
collapse/coma (e.g. elderly patient collapses at home, found 8 hours later)
ecstasy
crush injury
McArdle’s syndrome
drugs: statins (especially if co-prescribed with clarithromycin)

101
Q

what are the features of rhabdomyolysis

A

acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK)
the CK is significantly elevated, at least 5 times the upper limit of normal
elevations of CK that are ‘only’ 2-4 times that of normal are not supportive of a diagnosis and suggest another underlying pathophysiology

myoglobinuria: dark or reddish-brown colour
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis

102
Q

how is rhabdomyolysis managed

A

IV fluids to maintain good urine output
urinary alkalinization is sometimes used

103
Q

when would you use 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

104
Q

what are some renal side effects of systemic lupus erythematosus

A

WHO classification
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis

105
Q

how to treat the renal side effects of systemic lupus erythematosus

A

treat hypertension
initial therapy for focal (class III) or diffuse (class IV) lupus nephritis
glucocorticoids with either mycophenolate or cyclophosphamide
subsequent therapy
mycophenolate is generally preferred to azathioprine to decrease the risk of developing end-stage renal disease

106
Q

what are some findings in urine?

A

Hyaline casts
consist of Tamm-Horsfall protein (secreted by distal convoluted tubule)
seen in normal urine, after exercise, during fever or with loop diuretics

Acute tubular necrosis
brown granular casts in urine

Prerenal uraemia
‘bland’ urinary sediment

Red cell casts
nephritic syndrome

107
Q

features of type 1 renal tubular acidosis (distal)

A

inability to secrete H+ in DCT

causes hypokalaemia, nephrocalcinosis, renal stones

causes include idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy

108
Q

features of type 2 renal tubular acidosis (proximal)

A

reduced HCO3- resorption in PCT

causes hypokalaemia, osteomalacia

causes include idiopathic, as part of Fanconi syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors (acetazolamide, topiramate)

109
Q

features of type 4 renal tubular acidosis

A

reduction in aldosterone leads in turn to a reduction in PCT ammonium excretion

causes hyperkalaemia

causes include hypoaldosteronism, diabetes

110
Q
A

Finals (27 decks)

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