MRCP2 Flashcards

1
Q

Drugs causes of acute interstitial nephritis?

A

penicillin
rifampicin
NSAIDs
allopurinol
furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Connective tissue causes of acute interstitial nephritis?

A

SLE
sarcoidosis
Sjögren’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Infective causes of acute interstitial nephritis?

A

Hanta virus
staphylococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathophysiology of acute interstitial nephritis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Presentation of acute interstitial nephritis?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Investigation findings of acute interstitial nephritis ?

A

sterile pyuria
white cell casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Differentiate between pre-renal and acute tubulonephritis?

A

Pre-renal AKI - kidneys hold on to sodium to preserve volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diagnostic criteria of AKI?

A

Rise in creatinine of 26µmol/L or more in 48 hours

or

> = 50% rise in creatinine over 7 days

or
Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is stage 1 AKI?

A

Increase in creatinine to 1.5-1.9 times baseline,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is stage 2 AKI?

A

Increase in creatinine to 2.0 to 2.9 times baseline,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is stage 3 AKI?

A

Increase in creatinine to ≥ 3.0 times baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Chromosome mutation in ADPKD type 1?

A

Chromosome 16

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chromosome mutation in ADPKD type 2?

A

Chromosome 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ultrasound diagnostic criteria (in patients with positive family history) for ADPKD?

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Management of ADPKD

A

tolvaptan (vasopressin receptor 2 antagonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Criteria for ADPKD tolvaptan?

A

chronic kidney disease stage 2 or 3 at the start of treatment

rapidly progressing disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Features of ADPKD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Extra renal manifestations of ADPKD?

A

liver cysts
berry aneurysms

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Inheritance of alports syndrome?

A

X linked dominant

type IV collagen resulting in an abnormal glomerular-basement membrane (GBM).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Alports + lung involvement?

A

Anti-GBM antibodies
Leads to a goodpasteurs type syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Renal biopsy: splitting of lamina densa seen on electron microscopy

A

Alport syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Characteristic electronic microscopic of alport syndrome ?

A

characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Types of amyloid?

A

AL in myeloma - A for Amyloid, L for immunoglobulin Light chain fragments

AA amyloid - serum amyloid A protein, an acute phase reactant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Diagnosis of amyloid?
biopsy of skin rectal mucosa abdominal fat
26
Causes of AL amyloid?
most common form of amyloidosis L for immunoglobulin Light chain fragment - Myeloma - Waldenstroms - MGUS
27
Causes of AA amyloid?
- TB - bronchiectasis - rheumatoid arthritis
28
Presentation of AL amyloid?
nephrotic syndrome cardiac and neurological involvement macroglossia periorbital eccymoses
29
Presentation of AA amyloid?
renal involvement most common feature
30
What is normal anion gap?
8-14
31
Causes of 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
32
Causes of raised anion gap + metabolic acidosis?
lactate: shock, hypoxia ketones: diabetic ketoacidosis, alcohol urate: renal failure acid poisoning: salicylates, methanol 5-oxoproline: chronic paracetamol use# Methanol Uraemia (renal failure) Diabetic ketoacidosis Paracetamol use (chronic) Isoniazid Lactate Ethanol or propylene glycol Salicylates
33
How to calculate anion gap?
(sodium + potassium) - (bicarbonate + chloride)
34
Features of goodpasteurs disease?
pulmonary haemorrhage rapidly progressive glomerulonephritis this typically results in a rapid onset acute kidney injury nephritis → proteinuria + haematuria
35
Renal biopsy in goodpasteurs disease ?
renal biopsy: linear IgG deposits along the basement membrane raised transfer factor secondary to pulmonary haemorrhages
36
Management of goodpasteur disease?
plasma exchange (plasmapheresis) steroids cyclophosphamide
37
Defect in autosomal recessive ARPKD?
Chromosome 6 - fibrocystin
38
Renal biopsy: Multiple cylindrical lesions at right angles to the cortical surface?
ARPKD
39
When does ARPKD present ?
In utero - in babies or in early infancy with abdominal masses Typically has liver involvement, for example portal and interlobular fibrosis.
40
Complications of arteriovenous fistulas?
infection thrombosis may be detected by the absence of a bruit stenosis may present with acute limb pain steal syndrome
41
Ateriovenous fistula + absence of bruit ?
fistula thrombosis
42
How does calciphylaxis occur?
hypercalcaemia, hyperphophataemia and hyperparathyroidism
43
what can provoke or exacerbate calciphylaxis?
Warfarin
44
How should calciphylaxis be managed ?
focuses on reducing calcium and phosphate levels, controlling hyperparathyroidism and avoiding contributing drugs such as warfarin and calcium containing compounds.
45
Causes for anaemia in renal failure?
reduced erythropoiesis due to toxic effects of uraemia on bone marrow reduced absorption of iron 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
46
What is the target haemoglobin in renal failure ?
10-12
47
Problems with CKD electrolytes?
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
48
CDK stage 1?
Greater than 90 ml/min, with some sign of kidney damage on other tests I.e. No proteinaemia or U&E(if all the kidney tests* are normal, there is no CKD)
49
CDK stage 2?
60-90 ml/min with some sign of kidney damage However if kidney tests* are normal, there is no CKD
50
CDK stage 3a?
45-59 ml/min, a moderate reduction in kidney function
51
CKD stage 3b?
30-44 ml/min, a moderate reduction in kidney function
52
CKD stage 4 ?
15-29 ml/min, a severe reduction in kidney function
53
CKD stage 5 ?
Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
54
Management of chronic prostatitis?
A prolonged course of a quinolone
55
What is cysinuria?
formation of recurrent renal stones. It is due to a defect in the membrane transport of cystine, ornithine, lysine, arginine (mnemonic = COLA)
56
What is the genetics in cystinuria?
chromosome 2: SLC3A1 gene chromosome 19: SLC7A9
57
Diagnostic test for cystinuria?
cyanide-nitroprusside test
58
Management of cystinura?
hydration D-penicillamine urinary alkalinization
59
Causes of cranial diabetes insidious ?
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
60
Causes of nephrogenic DI?
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
61
Investigation findings for diabetic insidious?
high plasma osmolality, low urine osmolality a urine osmolality of >700 mOsm/kg excludes diabetes insipidus water deprivation test
62
management of diabetic insipidous?
nephrogenic diabetes insipidus - thiazides central diabetes insipidus can be treated with desmopressin
63
How to assess diabetic nephropathy?
ACR > 2.5 = microalbuminuria
64
Management of diabetic nephropathy?
BP control: aim for < 130/80 mmHg ACE inhibitor or angiotensin-II receptor antagonist control dyslipidaemia e.g. Statins
65
What type of renal tubule acidosis is Fanconi
Type 2 renal tubule acidosis
66
Features of Fanconi syndrome?
type 2 (proximal) renal tubular acidosis polyuria aminoaciduria glycosuria phosphaturia osteomalacia
67
Causes of cystinosis?
cystinosis (most common cause in children) Sjogren's syndrome multiple myeloma nephrotic syndrome Wilson's disease
68
Causes of focal segmental glomerulosclerosis?
idiopathic secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy HIV heroin Alport's syndrome sickle-cell
69
Renal biopsy of FSGS?
Light microscopy: focal and segmental sclerosis and hyalinosis Electron microscope: effacement of foot processes
70
Treatment of FSGS?
steroids +/- immunosuppressants untreated FSGS has a < 10% chance of spontaneous remission
71
Glomeulonephritis that presents with nephritis?
Rapidly progressive glomerulonephritis - aka crescentic glomerulonephritis IgA nephropathy - aka Berger's disease (mesangioproliferative GN)
72
Causes of rapid glomerulonephritis?
Goodpasture's ANCA positive vasculitis
73
Presentation of IgA nephropathy or mesangioproliferative GN?
typically young adult with haematuria following an URTI
74
Glomeulonephritis that presents as a nephritis and nephrotic syndrome?
Diffuse proliferative glomerulonephritis Membranoproliferative glomerulonephritis (mesangiocapillary)
75
What type of glomerulonephritis occurs in post strep glomerulonephritis?
Diffuse proliferative glomerulonephritis
76
Presentation of Diffuse proliferative glomerulonephritis?
classical post-streptococcal glomerulonephritis in child presents as nephritic syndrome / acute kidney injury most common form of renal disease in SLE
77
Causes of membranoproliferazive glomerulonephritis?
type 1: cryoglobulinaemia, hepatitis C type 2: partial lipodystrophy
78
Glomerulonephritis that presents as nephrotic syndrome?
Minimal change disease Membranous glomerulonephritis Focal segmental glomerulosclerosis
79
Presentation of minimal change disease?
typically a child with nephrotic syndrome (accounts for 80%) causes: Hodgkin's, NSAIDs good response to steroids
80
What is the treatment of minimal change disease?
Steroids
81
Causes of membraneous glomerulonephritis?
presentation: proteinuria / nephrotic syndrome / chronic kidney disease cause: infections, rheumatoid drugs, malignancy
82
Management of membraneous glomerulonephritis?
1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop chronic kidney disease
83
Causes of FSGS?
may be idiopathic or secondary to HIV, heroin
84
Frank haematuria and > 45 - how should they be referred?
Aged >= 45 years AND: unexplained visible haematuria without urinary tract infection, or visible haematuria that persists or recurs after successful treatment of urinary tract infection
85
Frank haematuria and > 60 - how should they be referred?
Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test
86
What is triad of haemolytic uraemia syndrome?
acute kidney injury microangiopathic haemolytic anaemia thrombocytopenia
87
In HUS, there is no role for what?
No role for antibiotics?
88
Management of HUS?
1. Plasma exchange eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS
89
Investigations in HUS
Blood film - fragments Stool culture - PCR for toxin
90
What is HSP?
Small vessel IgA vasculitis
91
Features of HSP?
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 failur
92
Management of HSP?
Purely supportive
93
Kidney disease in HIV?
1. HIV virus itself 2. indinavir can precipitate intratubular crystal obstruction.
94
Features of HIV associated nephropathy?
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
95
Causes of unilateral hydronephrosis ?
Pelvic-ureteric obstruction (congenital or acquired) Aberrant renal vessels Calculi Tumours of renal pelvis PACT
96
Causes of bilateral hydronephrosis?
Stenosis of the urethra Urethral valve Prostatic enlargement Extensive bladder tumour Retro-peritoneal fibrosis SUPER
97
Management of hyperkalaemia?
1. Stabilise with calcium gluconate 2. combined insulin/dextrose infusion +nebulised salbutamol 3. Calcium resonium / Loop diuretic / dialysis
98
ECG features of hypokalaemia?
ECG features U waves small or absent T waves prolonged PR interval ST depression
99
What is the presentation of IgA nephropathy?
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
100
Associated conditions of IgA nephropathy?
alcoholic cirrhosis coeliac disease/dermatitis herpetiformis Henoch-Schonlein purpura
101
What is the pathophysiology of IgA nephropathy?
mesangial deposition of IgA immune complexes there is considerable pathological overlap with Henoch-Schonlein purpura (HSP) histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3
102
How to differentiate between Post strep and IgA nephropathy?
Low complement --> post strep proteinurea --> post strep Interval between infection --> Post strep No interval --> IgA
103
Markers of good prognosis in IgA?
Frank haematuria
104
Poor prognosis IgA?
Male gender proteinurea >2g hypertension, smoking, hyperlipidaemia, ACE genotype DD
105
What is the effect of constriction of the afferent arteriol?
Decrease in glomerular filtration rate Decreases renal plasma flow
106
What is the affect of vasodilation of afferent arteriol?
Increases glomerular filtration rate Increases renal plasma flow
107
What causes vasodilation of the afferent arteriole?
Prostaglandin
108
What is the affect of constriction of the efferent arteriol?
Increases glomerular filtration rate Reduces renal plasma rate
109
What is the affect of vasodilation of the efferent arteriol?
Decreases glomerular filtration Increase renal plasma fow
110
What causes constrriction of afferent arteriol?
sympathetic nerve stimulation, NSAIDs
111
What causes constriction of the efferent arteriol?
angiotensin II
112
What causes dilation of the efferent arteriol?
ACE Inhibitor
113
What is membranoproliferative glomerulonephritis also known as?
mesangiocapillary glomerulonephritis
114
Causes of type 1 membraneoproflierative glomerulonephritis?
Cryglobulinaemia Hepatitis C
115
What is the electron microscope finding for type 1 membranoproliferative glomerulonephritis/
electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a 'tram-track' appearance
116
Causes of type 2 membranoproliferative glomerulonephritis?
partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face) factor H deficiency
117
What is the electron microscope finding for type 2 membranoproliferative glomerulonephritis/
electron microscopy: intramembranous immune complex deposits with 'dense deposits'
118
Causes of type 3 membranoproliferative glomerulonephritis ?
Hepatitis B Hepatitis C
119
How to differentiate between type 1 and type 2 membranoproliferative glomerulonephritis?
Type 2: --> alternative pathway complement activation Type 2 --> low circulating levels of C3
120
Management of membranoproliferative glomerulonephritis?
Steroids
121
Difference between membranoproliferative and membraneous glomerulonephritis?
Membraneous: Nephrotic Membranoproliferative: Nephrotic / Nephritic
122
Renal biopsy of membranous glomerulonephritis?
basement membrane is thickened with subepithelial electron dense deposits. This creates a 'spike and dome' appearance
123
Causes of membranous glomerulonephritis?
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
124
Management of membranous glomerulonephritis?
1. ACEi 2. Immunosuppression 3. Anticoagulation
125
Causes of normal anion gap metabolic acidosis?
gastrointestinal bicarbonate loss: prolonged diarrhoea: may also result in hypokalaemia ureterosigmoidostomy fistula renal tubular acidosis drugs: e.g. acetazolamide ammonium chloride injection Addison's disease
126
Causes of raise anion gap metabolic acidosis?
lactate: shock sepsis hypoxia ketones: diabetic ketoacidosis alcohol urate: renal failure acid poisoning: salicylates, methanol
127
Difference between type A and type B metabolic acidosis?
lactic acidosis type A: sepsis, shock, hypoxia, burns lactic acidosis type B: metformin
128
Presentation of minimal change disease?
Nephrotic syndrome
129
Causes of minimal change disease?
drugs: NSAIDs, rifampicin Hodgkin's lymphoma, thymoma infectious mononucleosis
130
Features of minimal change disease?
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
131
fusion of podocytes and effacement of foot processes
Minimal change disease
132
Treatment of minimal change disease?
oral corticosteroids: majority of cases (80%) are steroid-responsive cyclophosphamide is the next step for steroid-resistant cases
133
Complications of nephrotic syndrome?
increased risk of thromboembolism - renal vein thrombosis, resulting in a sudden deterioration in renal function hyperlipidaemia chronic kidney disease immunoglobulin loss hypocalcaemia (vitamin D and binding protein lost in urine)
134
When is the onset of contrast induced nephropathy?
2-5 days post
135
Definitation of contast induced nephropathy?
ephrotoxicity may be defined as a 25% increase in creatinine occurring within 3 days of the intravascular administration of contrast medi
136
Preventation of contrast induced nephropathy?
intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure
137
Causes of papillary necrosis?
chronic analgesia use sickle cell disease TB acute pyelonephritis diabetes mellitus
138
Features of papillary necrosis?
fever, loin pain, haematuria
139
Complications of peritoneal dialysis?
Peritonitis Sclerosing peritonitis
140
Most common cause of infection from peritoneal dialysis?
Coagulase negative staph - staph epidermis
141
Management of peritoneal dialysis?
vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid
142
Indications for plasma exchange?
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
143
Complications for plasma exchnage?
Hypocalcaemia metabolic alkalosis removal of systemic medications coagulation factor depletion immunoglobulin depletion
144
What is the onset of post streptococcal glomerulonephritis?
6-14 days
145
Mechanism of post streptococcal glomerulonephritis?
Immune complex deposition IgG, IgM and C3
146
Investiations for poster streptococcal glomerulonephritis?
raised anti-streptolysin O titre are used to confirm the diagnosis of a recent streptococcal infection low C3
147
Renal biopsy findings for post streptoccal glomerulonephritis?
electron microscopy: subepithelial 'humps' caused by lumpy immune complex deposits immunofluorescence: granular or 'starry sky' appearance
148
Causes of rapidly progressive glomerulonephritis ? And its presentation?
Goodpasture's syndrome Wegener's granulomatosis others: SLE, microscopic polyarteritis
149
Presentation of renal cellcarcinoma?
haematuria loin pain abdominal mass varicocele majority are left-sided caused by the tumour compressing veins
150
Paraneoplasic effect of renal cell carcinoma?
may secrete erythropoietin (polycythaemia) parathyroid hormone-related protein (hypercalcaemia), renin ACTH
151
T1 Renal cell carcinoma?
Tumour ≤ 7 cm and confined to the kidney
152
T2 Renal cell carcinoma?
Tumour > 7 cm and confined to the kidney
153
T3 Renal cell carcinoma?
Tumour extends into major veins or perinephric tissues, but not into the ipsilateral adrenal gland and not beyond Gerota's fascia
154
T4 Renal cell carcinoma?
Tumor invades beyond Gerota's fascia (including contiguous extension into the ipsilateral adrenal gland)
155
Most common to least renal stones?
Calcium oxolate ( most common) Cystine Uric acid calcuim phosphate Struvite
156
Radiodense stone + contains sulphur?
cystine
157
Radio-opaque stone ?
Clacium oxalte calcium phosphate
158
Radiolucent stone + in born error of metabolism?
Uric acid stone
159
Normal / alkaline urine + radio opaque?
calcium phosphate
160
Radio-lucent stone + Acidic urine
Urate stones
161
radio-opaque + alkaline ?
struvite
162
Investigations for renal stones?
urine dipstick and culture serum creatinine and electrolytes: check renal function FBC / CRP: look for associated infection calcium/urate: look for underlying causes also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis
163
Size of stone to pass spontaneously?
< 5mm
164
Management of complex calculi?
Percutaneous nephrolithotomy
165
Stone burden of less than 2cm in pregnant females
Ureteroscopy
166
Stone burden of less than 2cm in aggregate
Lithotripsy
167
What are class 1 antigens of HLA?
class 1 antigens include A, B and C.
168
What are class 2 antigens of HLA?
Class 2 antigens include DP,DQ and DR
169
Mechanism of hyperacute rejection?
OCCURS IN MINUTES due to pre-existing antibodies against ABO or HLA antigens an example of a type II hypersensitivity reaction leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ no treatment is possible and the graft must be removed
170
Mechanism of 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
171
Mechanism of chronic graft failure?
both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy) recurrence of original renal disease (MCGN > IgA > FSGS)
172
Investigation of choice for renal-vascular disease?
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
173
Associations of retroperitoneal fibrosis?
Riedel's thyroiditis previous radiotherapy sarcoidosis inflammatory abdominal aortic aneurysm drugs: methysergide
174
Indications for starting renal replacement therapy?
Indicated by the impact of symptoms of uraemia on daily living biochemical measures uncontrollable fluid overload estimated glomerular filtration rate (eGFR) of around 5 to 7 ml/min/1.73 m2 if there are no symptoms'
175
What ferritin is required to start EPO?
100
176
What must be done before starting EPO?
Complete iron studies
177
pH > 7.2 - renal stone?
Struvite
178
Back pain and crap renal function?
Think amylidosis If previous condition: AA If new AL
179
Gold standard management: Poorly controlled T1DM + Renal failure ?
Combined pancreas + kidney transplant
180
Scan for prostate cancer?
Tecnitium - 99
181
Clubbed calyxes and ring signs?
Analgesia nephropathy
182
When should diabetic patients get ACEi?
ACR > 3
183
Initial management of CKD-mineral bone disease:
Correct hyperphosphataemia first; start with dietary changes before starting a phosphate binder
184
Tumour markers in trsticular cancer?
germ cell tumours 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
185
CMV in transplant patients?
here is often a leukopaenia, atypical lymphocytosis with a mild rise in transaminases and graft dysfunction. Specific organ involvement can lead to hepatitis, pancreatitis, gastrointestinal ulceration and bleeding, pneumonitis, colitis and meningoencephalitis. The diagnosis is confirmed with CMV polymerase chain reaction (PCR). Treatment for patients with invasive disease is initially IV ganciclovir.
186
What can increase risk of post biopsy bleed?
Plasma exchange Remove clotting factors
187
Chronic prostatits treatment?
4 weeks of ciprofloxacin
188
What type of glomerulonephritis is post strep?
Diffuse proliferative glomerulonephritis
189
Atypical HUS vs HUS?
Atypical HUS caused by genetic component Mimics TTP However no diarrhoeal illness, and has normal ADAMST13
190
Tubulointerstitial nephritis with uveitis (TINU) ?
Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.
191
What is eculizumab and what is it used for?
Eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS
192
Iron replacement in CKD?
Give oral iron before IV
193
Treating hypertension in CKD?
If eGFR <30 do not use hypertension algorithm Use loop diruetic
194
Indications for ACNA positive vasculitis dialysis?
Severe active renal disease (serum creatinine above 354 micromol/L or who require dialysis), Pulmonary haemorrhage, Concurrent anti-GBM autoantibody disease.
195
What is dialysis disequalibrium syndrome?
cerebral oedema which can present as focal neurological deficits, papilloedema and a decreased level of consciousness. It can be treated with mannitol or hypertonic saline
196
How do you treat dialysis disequalibrium syndrome?
mannitol or hypertonic saline
197
Cancer + nephrotic syndrome?
Membranous glomerulonephritis
198
Hepatitis B + Nephrotic syndrome?
Membranous glomerulonephritis
199
Antibody implicated in idiopathy membranous glomerulonephritis?
anti-phospholipase A2 antibodies
200
Lupus nephritis, choice of immunosuppresion?
Mycophenolate
201
At extremes of body mass, what should be done to give a more accurate picture of renal function?
Cystatin C measurement
202
Amyloidosis: Nephrotic or nephritic?
Nephrotic
203
High plasma osmolality + Low urine osmolalty?
diabetes insipidus
204
Initial test for testicular ultrasound?
Ultrasound Not tumour markers
205
Transplanted alports patient: Decline renal function?
New anti GBM anitbodies
206
WHat should be done before kidney biospy?
Ultrasound renal tract
207
Mutation in alports?
COL4A5 gene
208
What type of antibody is ant-GBM?
IgG
209
What type of antibody is ANCA
IgG
210
WHat kidney issue is associated with neurofibromatosis?
Renal artery stenosis
211
Fistula thrombosis is a complication is a contraindication to RRT
Fistula thrombosis is a complication is a contraindication to RRT
212
Elevated PSA, testosterone?
Testosterone is contraindicated in elevated PSA
213
HAART renal complications? :
Indinavir can cause renal stones
214
High renin + High aldosterone
Renal artery stenosis
215
Whait is chlorthalidone?
Thiazide like diuretic
216
Treatment of peritoneal sepsis from peritoneal dialysis?
Peritoneal dialysis peritonitis: treat with intraperitoneal vancomycin + ceftazidime
217
When do you supplement clacium and vitmain D in secondary hyperparathyroidism?
When PTH twice normal
218
String bead appearance?
Fibromuscular dystrophy a non-atherosclerotic, non-inflammatory condition producing segmental stenoses in all vascular beds. FMD patients have carotid artery involvement1, hence the frequent presentation of cerebral ischaemia such as transient ischaemic attacks, strokes, headache and tinnitus2.
219
ADPKD management of blood pressure?
blood pressure target of < 110 / 75 mmHg
220
Is FSGS as diagnosis?
No
221
Clarithromycin + Statin
Rhabdomyolysis
222
What CK reading is supportive of rhabdomyolysis?
the CK is significantly elevated, at least 5 times the upper limit of normal
223
Granular casts + high urine osmolality?
Acute tubular necrosis
224
Spironolactone gynaecomastia management?
Eplerenone can be used in patients with troublesome gynaecomastia on spironolactone
225
Features of post transplant lymphoproliferative disorder?
weight loss anaemia lymphadenopathy
226
Mechanism of post transplant lymphoproliferative disorder?
EBV
227
Management of berger's disease?
IgA nephropathy management no proteinuria, normal GFR: observe proteinuria: ACE inhibitor signifcant fall in GFR/not responding to ACE inhibitor: corticosteroid
228
What condition causes brown lesions?
Secondary hyperparathyroidism
229
Indication for dialysis in urea?
Complications of it e.g. seizure
230
What is the most common damaghe done by SLE to kidney?
Class IV (diffuse proliferative glomerulonephritis)
231
Management of SLE nephritis?
1. Treat hypertension 2. initial therapy for focal (class III) or diffuse (class IV) lupus nephritis glucocorticoids with either mycophenolate or cyclophosphamide 3. subsequent: mycophenolate
232
Is plasma exchange used in HUS?
Rarely - only severe cases
233
Management of membrane glomerulonephritis?
ACE inhibitors and immunosuppression with either cyclophosphamide, chlorambucil, ciclosporin or mycophenolate mofetil along with prednisolone. Rituximab has also been shown to have a benefit in the short term.
234
Sickle cell disease can cause what?
Membranous glomerulonephritis
235
US kidney: rings seen in medulla?
Papillary necrosis
236
spikes' on the surface of the capillary loops.
Membranous glomerulonephritis
237
In HUS how do you confirm Ecoli?
Stool culture looking for Shiga toxin-producing Escherichia coli should be sent in patients with suspected haemolytic uraemic syndrome
238
Apparently cycling > 3 hours per day can cause rile dysfunction
who knew