Renal stones: imaging
The table below summarises the appearance of different types of renal stone on x-ray
Type
|
Frequency
|
Radiograph appearance
|
Calcium oxalate
|
40%
|
Opaque
|
Mixed calcium oxalate/phosphate stones
|
25%
|
Opaque
|
Triple phosphate stones
|
10%
|
Opaque
|
Calcium phosphate
|
10%
|
Opaque
|
Urate stones
|
5-10%
|
Radio-lucent
|
Cystine stones
|
1%
|
Semi-opaque, 'ground- glass' appearance
|
Xanthine stones
|
<1%
|
Radio-lucent
|
61-year-old man with a history of hypertension presents with central chest pain. Acute coronary syndrome is diagnosed and conventional management is given. A few days later a diagnostic coronary angiogram is performed. The following week a deteriorating of renal function is noted associated with a purpuric rash on his legs. What is the most likely diagnosis?
|
A.
|
Aspirin-induced interstitial nephritis
|
|
B.
|
Heparin-induced thrombocytopaenia
|
|
C.
|
Renal artery stenosis
|
|
D.
|
Cholesterol embolisation
|
|
|
E.
|
Antiphospholipid syndrome
|
|
Cholesterol embolisation is a well-documented complication of coronary angiography
Cholesterol embolisation
Overview
cholesterol emboli may break off causing renal disease
seen more commonly in arteriopaths, abdominal aortic aneurysms
Features
eosinophilia
purpura
renal failure
livedo reticularis
5 2-Which one of the following statements is true regarding autosomal recessive polycystic kidney disease?
|
A.
|
Onset is typically in the third decade
|
|
B.
|
Liver involvement is rare
|
|
C.
|
Is due to a defect on chromosome 16
|
|
D.
|
More common than autosomal dominant polycystic kidney disease
|
|
E.
|
May be diagnosed on prenatal ultrasound
|
ARPKD
Autosomal recessive polycystic kidney disease (ARPKD) is much less common than autosomal dominant disease (ADPKD). It is due to a defect in a gene located on chromosome 6
Diagnosis may be made on prenatal ultrasound or in early infancy with abdominal masses and renal failure. End-stage renal failure develops in childhood. Patients also typically have liver involvement, for example portal and interlobular fibrosis
5 3-Alport's syndrome is associated with each one of the following, except:
|
A.
|
Chronic renal failure
|
|
B.
|
Presentation in childhood
|
|
C.
|
Microscopic haematuria
|
|
D.
|
Lenticonus
|
|
E.
|
Anosmia
|
Alport's syndrome
Alport's syndrome is a hereditary condition, usually X-linked dominant but may be autosomal recessive or dominant. 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
A favourite question in the MRCP is 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
Alport's syndrome usually presents in childhood. The following features may be seen:
microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
retinitis pigmentosa
lenticonus: protrusion of the lens surface into the anterior chamber
5 4-Each one of the following is a recognised complication of nephrotic syndrome, except:
|
A.
|
Hyperlipidaemia
|
|
B.
|
Acute renal failure
|
|
C.
|
Increased risk of infection
|
|
D.
|
Hypercalcaemia
|
|
E.
|
Increased risk of thromboembolism
|
5 5-You are asked to review a 75-year-old female on the surgical wards due to hyperkalaemia. Results are as follows:
-
|
Plasma
|
Urine
|
Na+ (mmol/l)
|
129
|
5
|
K+ (mmol/l)
|
6.8
|
|
Urea (mmol/l)
|
26
|
350
|
Creatinine (µmol/l)
|
262
|
|
Osmolality (mosmol/kg)
|
296
|
470
|
What is the most likely diagnosis?
-
|
A.
|
Acute tubular necrosis
|
|
B.
|
Hyperosmolar non-ketotic coma
|
|
C.
|
Hydronephrosis
|
|
D.
|
Prerenal uraemia
|
|
E.
|
Pyelonephritis
|
ATN or prerenal uraemia? In prerenal uraemia think of the kidneys holding on to sodium to preserve volume
The low urine sodium points towards prerenal uraemia, as does the urine:plasma osmolality and urea ratio
ARF: ATN vs. prerenal uraemia
Prerenal uraemia - kidneys hold on to sodium to preserve volume
|
Pre-renal uraemia
|
Acute tubular necrosis
|
Urine sodium
|
< 20 mmol/L
|
> 30 mmol/L
|
Fractional sodium excretion*
|
< 1%
|
> 1%
|
Fractional urea excretion**
|
< 35%
|
>35%
|
Urine:plasma osmolality
|
> 1.5
|
< 1.1
|
Urine:plasma urea
|
> 10:1
|
< 8:1
|
Specific gravity
|
> 1020
|
< 1010
|
Urine
|
'bland' sediment
|
brown granular casts
|
Response to fluid
challenge
|
Yes
|
No
|
|
*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100
**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100
5 6-A patient with type 1 diabetes mellitus is reviewed in the nephrology outpatient clinic. He is known to have stage 3 diabetic nephropathy. Which of the following best describes his degree of renal involvement?
|
A.
|
Overt nephropathy
|
|
B.
|
Microalbuminuria
|
|
C.
|
Latent phase
|
|
D.
|
End-stage renal failure
|
|
E.
|
Hyperfiltration
|
Diabetic nephropathy: stages
Diabetic nephropathy may be classified as occurring in five stages*: Stage 1
hyperfiltration: increase in GFR
may be reversible
Stage 2 (silent or latent phase)
most patients do not develop microalbuminuria for 10 years
GFR remains elevated
Stage 3 (incipient nephropathy)
microalbuminuria (albumin excretion of 30 - 300 mg/day, dipstick negative)
Stage 4 (overt nephropathy)
persistent proteinuria (albumin excretion > 300 mg/day, dipstick positive)
hypertension is present in most patients
histology shows diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)
Stage 5
end-stage renal disease, GFR typically < 10ml/min
renal replacement therapy needed
The timeline given here is for type 1 diabetics. Patients with type 2 diabetes mellitus (T2DM) progress through similar stages but in a different timescale - some T2DM patients may progress quickly to the later stages
5 7-A two-year old boy presents with an abdominal mass. Which of the following is associated with Wilm's tumour (nephroblastoma)?
|
A.
|
Deletion on short arm of chromosome 12
|
|
B.
|
Tuberose sclerosis
|
|
C.
|
Beckwith-Wiedemann syndrome
|
|
D.
|
Autosomal dominant polycystic kidney disease
|
|
E.
|
Autosomal recessive polycystic kidney disease
|
Beckwith-Wiedemann syndrome is a inherited condition associated with organomegaly, macroglossia, abdominal wall defects, Wilm's tumour and neonatal hypoglycemia.
Wilm's tumour
Wilm's nephroblastoma
occurs mostly < 3 years (80% < 5 years); 20% of all childhood malignancies
Features
abdo mass in otherwise well child
also: painless haematuria, abdo pain, anorexia, BP, fever
Associations
Beckwith-Wiedemann syndrome
AGR triad of Aniridia, Genitourinary, Retardation
deletion on short arm of chromosome 11
Management
USS --> nephrectomy, chemo
prognosis: good, 80% cure rate
5 8-A 45-year-old presents to A&E with chest pain. An ECG shows anterior ST elevation and he is thrombolysed with alteplase. His chest pain settles and he is started on aspirin, atorvastatin, bisoprolol and ramipril. Three days later his blood results are as
follows:
-
Urea
|
16 mmol/l
|
Creatinine
|
277 µmol/l
|
What is the most likely cause for the deterioration in renal function?
|
A.
|
Renal artery stenosis
|
|
B.
|
NSAID related nephropathy
|
|
C.
|
Statin nephropathy
|
|
D.
|
Dressler's syndrome
|
|
E.
|
Haemorrhage into renal cyst
|
Flash pulmonary oedema, U&Es worse on ACE inhibitor, asymmetrical kidneys --> renal artery stenosis - do MR angiography
|
There is likely underlying renal artery stenosis revealed by the addition of an ACE inhibitor
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