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Renal 7.5 Flashcards

1
Q

Options of renal replacement therapy

A

Tx: living/deceased; always has better outcomes than any dialysis, and more effective when pre-emptive

Haemodialysis
Haemofilltration
Haemodiafiltration (in a Rx centre more effective than HD in a Rx centre)

PD - continuous ambulatory, & automated PD

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2
Q

Indications for considering starting RRT?

A
  • Sx of uraemia on ADLs
  • biochemical measures
  • uncontrollable fluid overload
  • eGFR 5-7 if no Sx
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3
Q

When to start assessment for RRT/conservative Rx?

A

At least 1yr before therapy e.g. Tx/HD is likely to be needed, inc for those with a failing Tx

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4
Q

What are AV fistulas?

A

= Direct connections between arteries & veins, may occur pathologically but gene formed surgically to allow access for HD - now regarded as preferred method of access due to lower rates of complications

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5
Q

What are the potential complications of AV fistulas?

A
  • infection
  • thrombosis
  • stenosis
  • steal syndrome
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6
Q

How to calculate anion gap?

A

(Na + K) - (HCO3 + Cl)

normal 8-14

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7
Q

Causes of a normal anion gap or hyperchloraemic metabolic acidosis?

A
  • GI bicarbonate loss: diarrhoea, fistula, ureterosigmoidostomy
  • renal tubular acidosis
  • drugs e.g. Acetazolamide
  • Ammonium chloride injection
  • Addison’s disease
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8
Q

Causes of a raised anion gap metabolic acidosis?

A
  • lactate: shock, hypoxia, burns, metformin (type B)
  • ketones: DKA, etoh
  • urate: renal failure
  • acid poisoning: salicylates, methanol
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9
Q

What is Alport’s syndrome? what is the inheritance?

A

X-linked dominant

  • defect in the gene which codes for type IV collagen -> abnormal glomerular-basement membrane
  • more severe in males (females rarely develop renal failure)
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10
Q

Pt with Alport’s syndrome has a renal Tx that starts to fail - what is the cause?

A

presence of anti-GBM antibodies, leading to a Goodpasture’s syndrome like picture

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11
Q 
When does Alport's syndrome present?
what are the features?
renal
ear
eye
A
  • microscopic haematuria
  • progressive renal failure
  • BL SNHL
  • lenticonus: protrusion of the lens surface into the anterior chamber
  • retinitis pigmentosa
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12
Q

What is on renal biopsy in Alport’s syndrome?

A

Splitting of lamina densa on electron microscopy

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13
Q

What is amyloidosis?

A

Extracellular deposition of an insoluble fibrillar protein amyloid
- accumulation of amyloid fibrils leads to tissue/organ dysfunction

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14
Q

What are the component of amyloid?

A
  • many different precursor proteins
  • fibrillar component, insoluble amyloid
  • non-fibrillary components inc: amyloid-P (derived from acute phase protein serum amyloid P), apolipoprotein E & heparan sulphate proteoglycans
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15
Q

How to classify amyloidosis?

A

systemic vs localised

- further characterised by precursor protein e.g. AL in myeloma - A amyloid, L Light chain Ig fragments

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16
Q

3 ways to Dx amyloidosis?

A
  • Congo red staining of tissue: apple-green birefringence
  • SAP: serum amyloid precursor scan
  • Biopsy of rectal tissue
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17
Q

What are the 3 main types of amyloidosis?

A
  1. AL amyloid (Light chain Ig fragment)
  2. AA amyloid (precursor serum amyloid A protein, acute phase reactant)
  3. Beta-2 microglobulin amyloidosis (precursor protein, part of the major histocompatibility complex)
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18
Q

AL amyloid

  • what are the causes?
  • what are the features?
A
  • myeloma, MGUS, Waldenstom’s

- cardiac & neuro involvement, macroglossia, periorbital eccymoses

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19
Q

AA amyloid

  • when is it seen?
  • what are the features?
A
  • chronic infection/inflammation eg TB, RA, bronchiectasis

- fenal involvement is most common feature

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20
Q

Beta-2 microglobulin amyloidosis (precursor that is a part of the MHC) - what is it associated with?

A

pts on renal dialysis

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21
Q

ARPKD: what is the genetic defect?

A
  • defect in gene on chr 6 which encodes fibrocystin (protein important for normal renal tubular development)
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22
Q

How to Dx ARPKD?

What are the features?

A
  • prenatal US or in early inference with abdo masses & renal failure
  • newborns may have features consistent with Potter’s syndrome 2ry to oligohydramnios
  • ESRF develops in childhood
  • pts also typically have liver involvement e.g. portal & interlobular fibrosis
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23
Q

What is on renal biopsy in ARPKD?

A

multiple cylindrical lesions at right angles to the cortical surface

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24
Q

What is the genetics of ADPKD type 1?

A

PKD1 loci, which codes for polycystin-1
chr 16
85% of cases, presents with renal failure earlier

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25
Q

What is the genetics of ADPKD type 2?

A

PKD2 loci, which codes for polycystin-2
chr 4
15% of cases

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26
Q

What is the screening Ix for relatives of ADPKD?

A

Abdo US/S

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27
Q

ADPKD: what is the Ultrasound Dx criteria (in pts with +ve FHx)?

A

Age<30: 2 cysts UL/BL
Age 30-59: 2 cysts in both kidneys
Age>50: 4 cysts in both kidneys

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28
Q

What are the features of ADPKD?

A
  • hypertension
  • recurrent UTIs
  • abdo pain
  • haematuria
  • renal stones
  • CKD
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29
Q

What are the extra-renal manifestations of ADPKD?

A
  • liver cysts 70%
  • berry aneurysms 8%
  • CVS: MVP, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
  • cysts in other organs: pancreas, spleen (v rarely thyroid, oesophagus, ovary)
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30
Q

Prerenal causes of AKI?

A

think ischaemia

  • hypovolaemia 2ry to diarrhoea/vomiting etc
  • renal artery stenosis
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31
Q

Intrinsic causes of AKI?

A

think damage to glomeruli, renal tubules or interstitium, immune-mediated or dye to toxins/drugs/contrast

  • glomerulonephritis
  • acute tubular necrosis
  • acute interstitial nephritis
  • rhabdomyolysis
  • tumour lysis syndrome
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32
Q

Postrenal causes of AKI?

A

think obstructive uropathy e.g. UL ureteric stone/BL hydronephrosis 2ry to acute urinary retention caused by BPH

  • stone in ureter/bladder
  • BPH
  • external compression of ureter
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33
Q

RFs for AKI?

A
  • age>65
  • Hx of AKI
  • CKD
  • other organ failure.chronic disease e.g. heart failure, liver disease, diabetes
  • nephrotoxics inc contrast within past wk
  • emergency surgery
  • intraperitoneal surgery
  • oliguria of urine output <0.5ml/kg/h
  • neuro or cognitive impairment or disability that may mean limited access to fluids due to reliance on someone else
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34
Q

Sx & signs of AKI?

A
  • reduced urine output
  • fluid overload eg peripheral, pulmonary
  • rise in K, urea, Cr, change in acid-base balance which can lead to
  • arrhythmias
  • uraemic complications eg pericarditis, encephalopathy
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35
Q

Criteria for Dx of AKI?

A
  • rise in Cr of >25 within 48h
  • 50%+ rise in Cr within 7 days
  • fall in urine output to <0.5ml/kg/h for >6hours
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36
Q

What drugs should be stopped in AKI as it may worsen renal function?

A 
NSAIDs
aminoglycosides
ACE-I
A2RBs
diuretics
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37
Q

What drugs may have to be stopped in AKI as there is increased risk of toxicity (but don’t usually worsen AKI itself)

A

metformin
lithium
digoxin

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38
Q

What Ix to consider when you suspect AKI?

A
  • bloods (U&Es)
  • urinalysis
  • ecg (hyperkalaemic change/arrhythmias)
  • renal US with 24h if at risk/obstructive cause is suspect - +/- urology r/v
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39
Q

Rx of hyperkalaemia to stabilise the cardiac membrane?

A

IV calcium gluconate

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40
Q

Rx of hyperkalaemia for a short-term shift in K from extra to intracellular fluid compartment?

A
  • combined insulin/dextrose infusion

- nebulised salbutamol

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41
Q

Rx of hyperkalaemia to remove K from the body?

A

Calcium resonium - oral/enema
loop diuretics
dialysis

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42
Q

In AKI NICE guidelines - when to refer to a nephrologist?

A
  • renal Tx
  • ITU pt with unknown cause of AKI
  • vasculitis/glomerulonephritis/tubulointerstitial nephritis/myeloma
  • AKI with no known cause
  • inadequate response to Rx
  • complications of AKI
  • stage 3 AKI
  • CKD stage 4/5
  • any indication for renal replacement therapy e.g. refractory hyperkalaemia, metabolic acidosis, uraemic complications, refractory fluid overload
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43
Q 
Prerenal Uraemia - kidneys hold onto sodium to preserve volume - what happens to:
urine sodium?
fractional Na excretion?
fractional urea excretion?
urine:plasma osmolality?
urine:plasma urea?
specific gravity?
urine?
response to fluid challenge?
A 
urine sodium <20
fractional Na excretion <1%
fractional urea excretion <35%
urine:plasma osmolality >1.5
urine:plasma urea >10.1
specific gravity >1020
urine: bland sediment
response to fluid challenge - Yes
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44
Q 
Acute tubular necrosis - what happens to:
urine sodium?
fractional Na excretion?
fractional urea excretion?
urine:plasma osmolality?
urine:plasma urea?
specific gravity?
urine?
response to fluid challenge?
A 
urine sodium >30
fractional Na excretion >1%
fractional urea excretion >35%
urine:plasma osmolality <1.1
urine:plasma urea <8.1
specific gravity <1010
urine: brown granular casts
response to fluid challenge - No
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45
Q

BPH - what are the RFs?

what are the typical LUTS?

A
  • ethnicity black >white >Asian
  • age; 50% of 50y.o. men will have evidence of BPH, 30% will have Sx; 80% of 80y.o. men have evidence of BPH
  • obstructive voiding Sx - weak/poor flow, straining, hesitancy, terminal dribbling, incomplete emptying
  • storage irritative Sx - urgency, frequency, urgency incontinence, nocturia
  • post-micturition Sx - dribbling
  • complications - UTI, retention, obstructive uropathy
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46
Q

Rx options for BPH?

A
  • watchful waiting
  • medications: alpha-1 blockers, 5 alpha-reductase inhibitors
  • surgery: TURP
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47
Q

How do alpha-1 blockers work in BPH?
what are examples?
what are the adverse effects?

A
  • decrease smooth muscle tone (prostate & bladder)
  • 1st line, improve Sx in 70% men
  • tamsulosin, alfuzosin
  • dry mouth, dizziness, depression, postural hypotension
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48
Q

How do 5 alpha-reductase inhibitors work in BPH?
how long does it take?
what are the adverse effects?

A
  • e.g. finasteride
  • block conversion of testosterone to DHT, which is known to induce BPH
  • causes a reduction in rotate volume (unlike alpha blockers) and hence may slow disease progression
  • may take 6months to improve Sx
  • decreases PSA conc by unto 50%, erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia
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49
Q

RFs for transitional cell carcinoma of the bladder?

A
  • smoking
  • aniline dyes eg 2-naphthylamine, benzidine
  • rubber manufacture
  • cyclophosphamide
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50
Q

RFs for squamous cell carcinoma of the bladder?

A
  • schistosomiasis
  • BCG Rx
  • smoking
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51
Q

What is Cystinuria?

what is the genetic defect?

A
  • autosomal recessive disorder characterised by recurrent renal stones formation
  • defect in the membrane transport of cystine, ornithine, lysine & arginine (COLA)
  • chr 2: SLC3A1 gene
  • chr 19: SLC7A9 gene
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52
Q

Dx of Cystinuria?

A

cyanide-nitroprusside test

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53
Q

Features of cystinuria?

A
  • recurrent renal stones

- classically yellow & crystalline, appearing semi-opaque on X-ray

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54
Q

Rx of cystinuria?

A
  • hydration
  • D-penicillamine
  • urinary alkalinisation
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55
Q

What is diabetes insipidus?

A
  • ADH deficiency or insensitivity
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56
Q

Causes of cranial diabetes insipidus?

A
  • idiopathic
  • posy-head injury
  • pituitary surgery
  • craniopharyngiomas
  • histiocytosis X
  • DIDMOAD: ass of cranial DI, DM, Optic Atrophy & Deafness = Wolframs syndrome
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57
Q

Causes of nephrogenic diabetes insipidus?

A
  • genetic: vasopressin/ADH receptor (commoner) gene mutation, aquaporin 2 channel gene mutation
  • electrolytes: hypercalcaemia, hypokalaemia
  • drugs: demeclocycline, lithium
  • tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
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58
Q

Features of diabetes insipidus?

A
  • polyuria, polydipsia
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59
Q

Ix of diabetes insipidus:
plasma & urine osmolality?
test?

A
  • water deprivation test
  • plasma osmolality high
  • urine osmolality low (>700 excludes DI)
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60
Q

tubulo-interstitial disease causes of nephrogenic DI?

A
  • obstruction
  • sickle cell
  • pyelonephritis
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61
Q

electrolyte causes of nephrogenic DI?

A
  • hypercalcaemia

- hypokalaemia

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62
Q

drug causes of nephrogenic DI?

A
  • lithium

- demeclocycline

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63
Q

What is stage 1 of T1 diabetic nephropathy?

A
  • hyperfiltration: increase in GFR

- may be reversible

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64
Q

What is stage 2 of T1 diabetic nephropathy?

A
  • (silent/latent phase)
  • most pts don’t develop microalbuminuria for 10yrs
  • GFR remains elevated
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65
Q

What is stage 3 of T1 diabetic nephropathy?

A
  • incipient nephropathy

- microalbuminuria (albumin excretion of 30-300mg/day, dipstick negative)

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66
Q

What is stage 4 of T1 diabetic nephropathy?

A
  • overt nephropathy
  • persistent proteinuria (albumin excretion >300mg/day, dipstick positive)
  • histology shows diffuse glomerulosclerosis & focal glomerulosclerosis (Kimmelstiel-Wilson nodules)
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67
Q

What is stage 5 of T1 diabetic nephropathy?

A
  • ESRF, typically GFR<10

- RRT needed

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68
Q

What is epididymo-orchitis?
cause?
most important DDx?

A

Infection of the epididymis +/- testes, resulting in pain & swelling
- most commonly caused by local spread of infections from genital tract e.g. Chlamydia, gonorrhoea, Or the bladder

  • ?Testicular torsion***
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69
Q

Features of epididymo-orchitis?

A
  • UL testicular pain & swelling
  • urethral discharge may be present, but urethritis is often aSx
  • factors suggesting testicular torsion inc pts<20yrs, severe pain & acute onset
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70
Q

Rx of epididymo-orchitis?

A
  • IM Ceftriaxone 500mg stat + Doxycycline 100mg BD PO for 10-14days if organism unknown
  • further Ix after Rx to exclude any underlying structural abnormalities
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71
Q

What is erythropoietin?

what are the main uses?

A
  • haematopoietic growth factor that stimulates the production of erythrocytes
  • Rx anaemia ass with CKD or cytotoxic therapy
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72
Q

Why may pts fail to respond to EPO therapy?

A
  • iron deficiency
  • inadequate dose
  • concurrent infection/inflammation
  • hyperparathyroid bone disease
  • aluminium toxicity
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73
Q

Side-effects of EPO?

A
  • accelerated hypertension, potentially leading to encephalopathy & seizures (BP increases in 25%)
  • bone aches
  • flu-like Sx
  • skin rashes, urticaria
  • pure red cell aplasia due to Abs against EPO (risk reduced with darbepoetin)
  • raised PCV increases risk of thromboses e.g. of fistula
  • iron deficiency 2ry to increased erythropoiesis
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74
Q

What is Fanconi syndrome?

What are the features?

A

Generalised disorder of renal tubular transport in the proximal convoluted tubule, resulting in:

  • type 2 proximal renal tubular acidosis
  • polyuria
  • aminoaciduria
  • glycosuria
  • phosphaturia
  • osteomalacia
  • lots of urine with AA, sugar & phosphate
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75
Q

Causes of Fanconi syndrome?

A
  • cystinosis (commonest cause in children)
  • Sjogren’s syndrome
  • multiple myeloma
  • nephrotic syndrome
  • Wilson’s disease
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76
Q

What are the maintenance fluid requirements for adults?

A
  • 25-30ml/kg/day water
  • 1mmol/kg/day of K, Na, Cl
  • 50-100g/day of glucose to limit starvation ketosis
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77
Q

How many mmol of Na & Cl in 0.9% NaCl?

A

Na 154

Cl 154

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78
Q

How many mmol of Na & Cl in 0.18% saline with 4% glucose?

A

Na 30
Cl 30
glucose 40g

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79
Q

How much Na, Cl, K HCO3 in Hartmanns?

A

Na 131
Cl 111
K 5
HCO3 29

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80
Q

What type of renal impairment does focal segmental glomerulosclerosis lead to?
what happens with renal Tx?

A

NEPHROTIC syndrome

  • CKD
  • generally presents in young adults
  • has a high recurrence rate in renal Tx
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81
Q

Causes of focal segmental glomerulosclerosis?

A
  • idiopathic
  • 2ry to other renal pathology e.g. IgA nephropathy, reflux nephropathy
  • HIV
  • heroin
  • Alport’s syndrome
  • sickle cell
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82
Q

What variables does th MDRD equation use to calculate eGFR?

What factors may affect the result?

A
  • serum Cr
  • age
  • gender
  • ethnicity
  • pregnancy
  • muscle mass
  • eating red meat within 12h prior
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83
Q

CKD stages?

A
  1. GFR>90 with sign of kidney damage on other tests
  2. 60-90 with sign of kidney damage on other tests
    3a. 45-59
    3b. 30-44
  3. 15-29 (severe reduction)
  4. <15, established kidney failure - RRT may be needed
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84
Q

Common causes of CKD?

A
  • HTN
  • diabetic nephropathy
  • chronic glomerulonephritis
  • chronic pyelonephritis
  • ADPKD
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85
Q

What type of anaemia is seen in CKD?

What does it predispose pts to - increasing mortality 3x in renal pts?

A
  • normochromic, normocytic - becomes apparent when GFR <35
  • mainly due to reduced EPO
  • LV hypertrophy
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86
Q

Causes of anaemia in renal failure?

A
  • reduced EPO levels (most significant)
  • reduced erythropoiesis due to toxic effects of uraemia on bone marrow
  • reduced iron absorption
  • anorexia/nausea due to uraemia
  • reduced red cell survival (esp in haemodialysis)
  • blood loss due to capillary fragility & poor platelet function
  • stress ulceration leading to chronic blood loss
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87
Q

Rx of anaemia in CKD?

- what is target Hb?

A
  • target Hb 10-12
  • optimise iron status before starting ESAs: erythropoiesis-stimulating agents - many pts esp on HD need IV iron
  • ESAs eg EPO & darbepoetin should be used in those who are likely to benefit in terms of QoL & physical function
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88
Q

How is proteinuria identified in CKD?

A

ACR: albumin:creatinine ratio (more sensitive than PCR)

- proteinuria is an esp important marker of CKD for diabetic nephropathy

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89
Q

How is an ACR albumin:creatinine ration sample collected?

A
  • spot sample (avoids 24h collection)
  • 1st pass morning
  • if initial ACR is 3-70, this should be confirmed by a subsequent early morning sample
  • if initial ACR>70, repeat sample not needed
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90
Q

What level of urine ACR: albumin creatinine ratio is clinical significant for proteinuria?

A

3mg/mmol +

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91
Q

When to refer to a nephrologist with regards to urine ACR?

A
  • urine ACR 70+ (unless known to be diabetes & appropriately treated)
  • urine ACR 30+ with persistent haematuria, after excluding UTI
  • consider referral to nephrologist if urine ACR 3029 with persistent haematuria and other RFs e.g. declining eGFR or CVD
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92
Q

1st line anti-hypertensive in proteinuria renal disease?

A

ACE-I

  • tend to reduce filtration pressure and a small fall in GFR & rise in Cr can be expected
  • decrease in eGFR upto 25% or rise in Cr upto 30% is acceptable
  • if more than this, may suggest underlying renovascular disease
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93
Q

Furosemide for hypertension in CKD?

A
  • useful if GFR<45
  • also lowers potassium
  • high doses usually required
  • may need withholding during periods of risk of dehydration
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94
Q

What basic problems lead to bone disease 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
  • 2ry hyperparathyroidism: due to low calcium, high phosphate, low it D
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95
Q

What clinical manifestations of bone disease occur in CKD?

A
  • osteitis fibrosa cystica = hyperparathyroid bone disease
  • osteosclerosis
  • osteoporosis
  • osteomalacia = low vit D
  • adynamic = reduction in cellular activity (both blasts & clasts) - may be due to over Rx with it D
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96
Q

What are the aims of bone disease Rx in CKD?

what are the options?

A
  • reduce high phosphate
  • reduce PTH level
  • phosphate binders
  • vitamin D i.e. alfacalcidol (doesn’t require activation in kidneys)
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97
Q

what are the phosphate binders used in CKD?

what is the main problem with them?

A
  • calcium-based binders

- vascular calcification

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98
Q

Causes of transient or spurious non-visible haematuria?

A
  • UTI
  • menses
  • vigorous exercise
  • sex
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99
Q

Causes of persistent non-visible haematuria?

A
  • cancer: bladder, kidney, prostate
  • stones
  • BPH
  • prostatitis
  • urethritis eg Chlamydia
  • renal causes: IgA nephropathy, thin basement membrane disease
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100
Q

Spurious causes of ?haematuria of red/orange urine where blood isn’t present on dipstick?

A
  • foods: beetroot, rhubarb

- drug: rifampicin, doxorubicin

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101
Q

When to do an urgent 2WW referral for haematuria?

A

Age 45+ with:
- unexplained persistent visible haematuria after ruling out or treating a UTI

Age 60+ with:
- unexplained non-visible haematuria with dysuria/raised WCC

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102
Q

When to do a non-urgent referral for haematuria?

A

Age 60+ with:

- recurrent/persistent unexplained UTI

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103
Q

What is Henoch-Schonlein purpora?

A

IgA-mediated small vessel vasculitis

  • overlap with IgA nephropathy
  • usually seen in children after an infection
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104
Q

What are the features of HSP?

A
  • palpable purpuric rash over buttocks & extensors with localised oedema
  • abdo pain
  • polyarthritis
  • features of IgA nephropathy may occur e.g. haematuria, renal failure
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105
Q

Rx of HSP?

A
  • analgesia for arthralgia
  • Rx of nephropathy is generally supportive
  • self-limiting (esp in children without renal involvement) so there’s good prognosis
  • 1/3 relapse
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106
Q

Renal involvement in HIV - what drugs can precipitate intratubular crystal obstruction?

A

protease inhibitors eg Indinavir

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107
Q

HIVAN = HIV ass nephropathy

  • what alters the course of the disease
  • what are the 5 key features?
A
  • **Antiretroviral therapy
    1. normotension
    2. elevated urea & creatinine
    3. massive proteinuria
    4. normal/large kidneys
    5. FSGS with focal/global capillary collapse on renal biopsy
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108
Q

What is the triad in haemolytic uraemia syndrome?

A
  1. acute renal failure
  2. thrombocytopenia
  3. MAHA
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109
Q

What are the causes of HUS?

A
  • post-dysentery classically E. coli
  • tumours
  • pregnancy
  • ciclosporin, the pill
  • SLE
  • HIV
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110
Q

Ix in HUS?

A
  • anaemia, thrombocytopenia, fragmented blood film
  • U&E AKI
  • stool culture
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111
Q

Rx in HUS?

A
  • supportive: fluids, blood transfusion, dialysis if required
  • plasma exchange in specific severe cases
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112
Q

Which diseases typically present with nephritic syndrome i.e. haematuria & hypertension?

A
  • Rapidly progressive GN = crescenteric glomerulonephritis

- IgA nephropathy aka mesangioproliferative GN, Berger’s disease

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113
Q

Rapid onset nephritic syndrome (haematuria & HTN), often presenting as AKI - what is the cause?

A

Rapidly progressive glomerulonephritis = crescenteric GN

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114
Q

Causes of rapidly progressive GN aka crescenteric GN?

A
  • Goodpasture’s

- ANCA +ve vasculitis

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115
Q

Glomerulonephritides which typically present with nephrotic syndrome (proteinuria, oedema)?

A
  • Minimal change disease (child)
  • Membranous glomerulonephritis (adult)
  • Focal segmental glomerulosclerosis (young adult)
  • Membranoproliferative
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116
Q

A child presents with nephrotic syndrome - what is the most likely disease?
Causes?

A

Minimal change disease

  • Hodgkin’s, NSAIDs
  • good response to steroids
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117
Q

Nephrotic syndrome (proteinuria, oedema) +/- CKD caused by infections/rheumatoid drugs/malignancy - what is the most likely disease?

A

Membranous glomerulonephritis

- 1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop CKD

118
Q

Nephrotic syndrome (proteinuria, oedema) +/- CKD, which may be idiopathic or 2ry to HIV, heroin - what is the most likely disease?

A

FSGS: focal segmental glomerulosclerosis

  • young adults
  • high recurrence rate in renal Tx
119
Q

What diseases lead to a mixed nephritic/nephrotic presentation?

A
  • Diffuse proliferative GN

- Membranoproliferative GN (mesangiocapillary)

120
Q

What is the most common form of renal disease in SLE?

How does it present?

A
  • Diffuse proliferative GN
  • presents as nephritic syndrome/AKI (mixed picture)
  • classically post-strep GN in child
121
Q

Causes of type 1 membranoproliferative GN (mesangiocapillary)?
Presentation?

A
  • mixed nephritic/nephrotic presentation

- cryogobulinaemia, hepatitis C

122
Q

Causes of type 2 membranoproliferative GN (mesangiocapillary)?
Presentation?

A
  • mixed nephritic/nephrotic presentation

- partial lipodystrophy

123
Q

4 disorders ass with glomerulonephritis & low complement levels?

A
  • post-Strep GN
  • Subacute bacterial endocarditis
  • Sle
  • meSangiocapillary GN
124
Q

Rx of predominately voiding LUTS in men?

A
  • cons: pelvic floor muscle training, bladder training, prudent fluid intake, containment products
  • if mod/severe Sx -> ALPHA-BLOCKER
  • if enlarged prostate and at high risk of progression -> 5-ALPHA REDUCTASE inhibitor
  • if enlarged prostate & mod/severe Sx -> BOTH
  • if mixed Sx of voiding & storage not responding to an alpha-blocker, than a ANTIMUSCARINIC(anticholinergic) can be ADDed
125
Q

Rx of predominately overactive bladder in men?

A
  • cons: moderating fluid intake
  • bladder training can be offered
  • if Sx persist -> ANTIMUSCARINIC eg OXYBUTYNIN IR, TOLTERODINE IR, DARIFENACIN OD
  • MIRABEGRON can be considered if 1st line drugs fail
126
Q

Rx of predominately nocturia in men?

A
  • moderate fluid intake at night
  • furosemide 40mg late afternoon can be considered
  • desmopressin may be helpful
127
Q

What is the commonest cause of GN worldwide?

A

IgA nephropathy = Berger’s disease = mesangioproliferative GN

128
Q

What is the cause of IgA nephropathy?

A
  • mesangial deposition of IgA immune complexes
129
Q

What is seen on histology of IgA nephropathy?

A
  • mesangial hypercellularity, +ve immunofluorescence for IgA & C3
130
Q

How does IgA nephropathy present?

A
  • young male, rec visible haematuria
  • typically ass with mucosal infections e.g. URTI
  • nephrotic range proteinuria rare, renal failure unusual
131
Q

Conditions ass with IgA nephropathy?

A
  • alcoholic cirrhosis
  • coeliac disease, dermatitis herpetiformis
  • HSP
132
Q

IgA nephropathy:

  • how many develop ESRF?
  • what is a marker of good prognosis?
  • what are markers of bad prognosis?
A
  • 25% develop ESRF
  • frank haematuria is good
X male
X proteinuria esp >2g/day
X hypertension
X smoking
X hyperlipidaemia
X ACE genotype DD
133
Q

What is the cause of post-strep GN?

when does it occur?

A
  • immune complex deposition (IgG, IgM, C3) in the glomeruli
  • young children most commonly affected
  • 7-14days after a group A beta-haemolytic strep infection
134
Q

Features of post-strep GN?

A
  • headache, malaise
  • haematuria, proteinuria
  • hypertension
  • LOW C3
  • raised ASO titre
  • good prognosis
135
Q

Features on renal biopsy in post-strep GN?

A
  • acute diffuse proliferative GN
  • endothelial proliferation with neutrophils
  • EM: subepithelial humps caused by lumpy immune complex deposits
  • immunofluorescence: granular/starry sky appearance
136
Q

What is rapidly progressive GN?

A

Rapid loss of renal function ass with the formation of epithelial crescents in the glomeruli

137
Q

What are the causes of rapidly progressive GN?

A
  • Goodpasture’s syndrome
  • Wegener’s granulomatosis
  • SLE
  • microscopic polyarteritis
138
Q

Features of rapidly progressive GN?

A
  • nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria
  • features specific to underlying cause
139
Q

How does minimal change disease present?
What is the main cause?
Other causes?

A
  • nephrotic syndrome, 75% of children, 25% of adults
  • majority idiopathic
  • NSAIDs, rifampicin
  • Hodgkin’s lymphoma, thymoma
  • EBV
140
Q

Pathophysiology of minimal change disease?

A
  • T cell & cytokine mediated damage to the glomerular basement membrane -> pollination loss
  • resultant reduction of electrostatic charge -> increased glomerular permeability to serum albumin
141
Q

Features of minimal change disease?

A
  • nephrotic syndrome
  • normotension
  • highly selective proteinuria (only intermediate-sized proteins e.g. albumin & transferrin leak though glomerulus)
  • renal biopsy: EM shows fusion of podocytes
142
Q

Renal biopsy: EM shows fusion of podocytes

- what is the Dx?

A

Minimal change disease

143
Q

Rx of minimal change disease?

Prognosis?

A
  • majority 80% respond to steroids
  • if steroid-resitsnat, consider cyclophosphamide
  • 1/3 1 episode, 1/3 infrequent relapses, 1/3 frequent relapses which stop before adulthood
144
Q

What is the commonest type of glomerulonephritis in adults?

A

Membranous GN

- 3rd most common cause of ESRF

145
Q

How does membranous GN usually present?

A
  • nephrotic syndrome

- or proteinuria

146
Q

What is shown on renal biopsy in membranous GN?

A
  • EM: basement membrane is thickened with sub epithelial electron dense deposits
  • creating a spike & dome appearance
147
Q

Renal biopsy: - EM: basement membrane is thickened with sub epithelial electron dense deposits, creating a spike & dome appearance
What is the Dx?

A

Membranous GN

148
Q

Causes of Membranous GN?

A
  • idiopathic
  • infection: HBV, malaria, syphilis
  • malignancy: lung ca, lymphoma, leukaemia
  • drugs: gold, penicillamine, NSAIDs
  • autoimmune: SLE class V, thyroiditis, rheumatoid
149
Q

What are good prognostic features in membranous GN?

A
  • female
  • young age at presentation
  • aSx proteinuria of a modest degree at time of presentation
  • 1/3 spontaneous remission
  • 1/3 remain proteinuria
  • 1/3 develop ESRF
150
Q

Rx of membranous GN?

A
  • immunosuppression: STEROID + OTHER eg Chlorambucil
  • control BP: ACE-I shown to reduce proteinuria
  • consider anticoagulation
151
Q

What is nephrotic syndrome?

A
  1. proteinuria >3g/24h causing
  2. hypoalbuminaemia <30
  3. oedema
152
Q

What predisposes to thrombosis in nephrotic syndrome?

What happens to thyroxine levels?

A
  • loss of anti-thrombin III, proteins C & S, and ass rise in fibrinogen levels predispose to thrombosis
  • loss of thyroxine-binding globulin lowers the Total (not free) thyroxine levels
153
Q

What are the main causes of nephrotic syndrome?

A
  • 1ry GN 80%
  • systemic disease
  • drugs
  • others: congenital, neoplastic (carcinoma, lymphoma, leukaemia, myeloma), infection (endocarditis, HBV, malaria)
154
Q

Drug causes of nephrotic syndrome?

A
  • gold (sodium aurothiomalate)

- penicillamine

155
Q

systemic disease causes (20%) of nephrotic syndrome?

A
  • diabetes
  • SLE
  • amyloid
156
Q

1ry GN causes of nephrotic syndrome?

A
  • minimal change disease
  • membranous GN
  • FSGS
  • membranoproliferative GN
157
Q

How does membranoproliferative GN present? what is the prognosis?

A
  • nephrotic syndrome, haematuria or proteinuria
  • aka mesangiocapillary GN
  • poor prognosis
158
Q

Type 1 membranoproliferative GN - causes?

- pathology?

A
  • 90% of cases
  • cryoglobulinaemia, hepatitis C
  • sub endothelial immune deposits of electron dense material resulting in tram-track appearance
159
Q

Sub endothelial immune deposits of electron dense material resulting in tram-track appearance - what is the Dx?

A

Type 1 membranoproliferative GN

160
Q

What is type 2 membranoproliferative GN?

causes?

A
  • dense deposit disease
  • reduced serum complement
  • C3b nephritic factor (Ab) found in 70%
  • partial lipodystrophy (loss of SC tissue from face), factor H deficiency
161
Q

Causes of type 3 membranoproliferative GN?

162
Q

Rx of membranoproliferative GN?

A

Steroids may help

163
Q

‘Dense deposit disease’
- presents as nephrotic syndrome, haematuria or proteinuria
- causes: partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face), factor H deficiency
- reduced serum complement
- C3b nephritic factor (Ab) in 70%
What is the Dx?

A

Type 2 membranoproliferative GN

164
Q
  • presents as nephrotic syndrome, haematuria or proteinuria
  • subendothelial immune deposits of electron dense material resulting in a ‘tram-track’ appearance
  • causes: cryoglobulinaemia, hepatitis C

What is the Dx?

A

Type 1 membranoproliferative GN

165
Q

What are the complications of nephrotic syndrome?

A
  • increased risk of infection (urinary Ig loss)
  • increased risk of thromboembolism (loss of anithromb III & plasminogen in urine) -> renal vein thrombosis -> sudden deterioration in renal function
  • hyperlipidaemia
  • hypocalcaemia (vit D & binding protein lost in urine)
  • acute renal failure
166
Q

What is contrast media nephrotoxicity?

How to prevent?

A

25% increase in Cr occurring within 3 days of IV contrast media

  • 12h IV saline pre & post-procedure
167
Q

RFs for contrast media nephrotoxicity?

A
  • known renal impairment, esp diabetic nephropathy
  • age >70
  • dehydration
  • cardiac failure
  • use of nephrotoxic e.g. NSAIDs
168
Q

Causes of papillary necrosis?

A
  • chronic analgesia use
  • sickle cell disease
  • TB
  • acute pyelonephrtis
  • diabetes mellitus
169
Q

Features of papillary necrosis?

A
  • fever, loin pain, haematuria

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

170
Q

What does CAPD: continuous ambulatory peritoneal dialysis involve?

A

4 2litre exchanges/day

171
Q

Complications of peritoneal dialysis?

A
  • peritonitis - commonest cause = coag-negative staph eg staph epidermidis. can also be staph aureus
  • sclerosing peritonitis
172
Q

Indications for plasma exchange/plasmapheresis?

A
  • Guillain-Barre syndrome
  • myasthenia gravis
  • Goodpasture’s syndrome
  • ANCA +ve vasculitis eg GPA, Churg-Strauss
  • TTP/HUS
  • cryogobulinaemia
  • hyperviscosity syndrome eg 2ry to myeloma
173
Q

NICE guidelines when to refer for PSA/prostate cancer?

A

men aged 50-69 with PSA >3 and/or abnormal DRE, after UTI Rx or ruled out

174
Q

What factors cause raised PSA levels?

A
  • prostate ca
  • BPH
  • prostatitis & UTI
  • ejaculation in prev 48h
  • vigorous exercise in prev 48h
  • urinary retention
  • instrumentation of urinary tract
175
Q

Sensitivity & specificity of PSA?

A
  • 20% men with prostate cancer have a normal PSA

- 33% of men with PSA 4-10 have prostate ca, if PSA 10-20 this is 60%

176
Q

Localised prostate cancer T1/T2 - what are the Rx options?

A

Depend on life expectancy & pt choice

  • conservative active monitoring & watchful waiting
  • radical prostatectomy
  • RT: external beam & brachytherapy
177
Q

Localised advanced prostate cancer (T3/T4) - what are the Rx options?

A
  • hormonal Rx
  • radical prostatectomy
  • RT: external beam & brachytherapy
178
Q

Metastatic prostate cancer disease - what are the Rx options?

A
  • hormonal Rx

- orchidectomy

179
Q

What are the hormonal Rx options for prostate cancer?

A
  • Synthetic GnRH agonists eg Goserelin/Zoladex

- Anti-androgen eg cyproterone acetate - prevents DHT binding from intracytoplasmic protein complexes

180
Q

What cover is needed with Goserelin/Zoladex in prostate ca?

What is the MoA?

A

Synthetic GnRH agonist

- cover initially with anti-androgen to prevent rise in testosterone

181
Q

What is renal papillary necrosis?

What are the features?

A
  • coagulative necrosis of the renal papillae
  • visible haematuria
  • loin pain
  • haematuria
182
Q

Causes of renal papillary necrosis?

A
  • severe acute pyelonephritis
  • diabetic nephropathy
  • obstructive nephropathy
  • analgesic nephropathy (classically phenacetin)
  • sickle cell anaemia
183
Q

How should SLE pts be monitored for renal complications?

What is a severe renal manifestation of SLE?

A
  • urinalysis at regular intervals to rule out proteinuria

- lupus nephritis - can result in ESRF

184
Q

What is the WHO classification for SLE renal disease?

A 
I normal kidney
II mesangial GN
III focal &amp; segmental proliferative GN
IV diffuse proliferative GN
V diffuse membranous GN
VI sclerosing GN
185
Q

What is the most common & severe form of renal disease in SLE?

A

class IV diffuse proliferative GN

186
Q

What is shown on renal biopsy in class IV diffuse proliferative GN in SLE?

A
  • glomeruli shows endothelial & mesangial proliferation, with a wire-loop appearance
  • if severe, capillary wall may be thickened 2ry to immune complex deposition
  • EM shows endothelial immune complex deposits
  • immunofluorescent shows granular appearance
187
Q

Renal biopsy EM: subendothelial immune complex deposition
Immunofluorescence: granular appearance
glomeruli: endothelial & mesangial proliferation, ‘wire-loop’ appearance
What is the Dx?

A

SLE class IV diffuse proliferative GN

188
Q

Rx of renal complications in SLE?

A
  • treat HTN
  • corticosteroids if clinical evidence of disease
  • immunosuppressant eg azathioprine (if pregnant)/cyclophosphamide
189
Q

What is the MoA of spironolactone?

Adverse effects?

A
  • aldosterone antagonist
  • acts in the cortical collecting duct
  • hyperkalaemia
  • gynaecomastia
190
Q

Indications for spironolactone?

A
  • ascites (large doses used) - pts with cirrhosis develop a 2ry hyperaldosteronism
  • HTN step 4
  • heart failure (reduces all cause mortality when NYHA III & IV and already on an ACE-I)
  • nephrotic syndrome
  • Conns syndrome
191
Q

Commonest scrotal lump, separate from body of testicle, found posterior to it?
Dx?
Rx?

A

Epididymal cyst
US scrotum
supportive but surgical removal or sclerotherapy may be attempted for larger/Sx cysts

192
Q

Conditions ass with epididymal cysts?

A
  • polycystic kidney disease
  • CF
  • von Hippel-Lindau syndrome
193
Q

What is a hydrocele?

Features?

A
  • accumulation of fluid within the tunica vaginalis
  • soft non-tender swelling of the hemi-scrotum, usually anterior & below the testicle
  • swelling confined to the scrotum, you can get above it on exam
  • transilluminates
  • testis may be difficult to palpate if hydrocele is large
194
Q

What is a communicating hydrocele?

A
  • caused by patency of the processes vaginalis allowing peritoneal fluid to drain down int the scrotum
  • common in newborn males
  • usually resolve within first few months of life
195
Q

What is a non-communicating hydrocele?

A
  • caused by XS fluid production within the tunica vaginalis
196
Q

When may hydroceles develop 2ry to something else?

A
  • epididymo-orchitis
  • testicular torsion
  • testicular tumours
197
Q

Rx of hydroceles?

A
  • infantile: repair if they don’t resolve by age 1-2yrs

- adults: conservative depending on presentation, US to rule out underlying tumour

198
Q

What is a varicocele?
what is the significance?
what are the features?
when may it present as a different disease?

A

Abnormal enlargement of the testicular veins

  • usually aSx but ass with Infertility
  • > 80% are on the LEFT side, feel like a bag of worms
  • renal cell carcinoma may present as a left varicocele due to occlusion of the left testicular vein
199
Q

Dx of varicocele?

Rx?

A
  • US with Doppler studies
  • usually conservative
  • surgery may be required if troubled by pain
200
Q

Features of rhabdomyolysis?

A
  • acute renal failure with disproportionately raised creatinine
  • elevated CK
  • myoglobinuria
  • hypocalcaemia (myoglobin binds to calcium)
  • elevated phosphate (released from myocytes)
201
Q

Causes of rhabdomyolysis?

A
  • collapse, seizure, coma
  • ecstasy
  • crush injury
  • MsArdle’s syndrome
  • drug: statins
202
Q

Rx of rhabdomyolysis?

A
  • IV fluids to maintain good urine output

- urinary alkalinisation sometimes used

203
Q

Presentation of retroperitoneal fibrosis?

A
  • lower back/flank pain is commonest

- fever & LL oedema can be seen

204
Q

Lower back/flank pain + fever + LL oedema - Dx?

A

Retroperitoneal fibrosis

205
Q

Associations of retroperitoneal fibrosis?

A
  • Riedel’s thyroiditis
  • Previous RT
  • sarcoid
  • inflammatory AAA
  • drugs: methysergide
206
Q

Commonest cause of renal vascular disease?
RFs?
How does it present?

A
  • atherosclerosis >95%
  • smoking, HTN -> atheroma etc
  • may present as HTN, chronic renal failure or ‘flash’ pulmonary oedema
207
Q

What to consider in younger pts with renal vascular disease?

A

FMD: fibromuscular dysplasia

- more common in young women

208
Q

Characteristic angiography in fibromuscular dysplasia?

Rx?

A
  • string of beads

- balloon angioplasty

209
Q

Ix of choice in renal vascular disease?

A

MR angiography

renal angio may still have role in planning surgery

210
Q

RFs for urate renal stones?

A
  • gout

- ileostomy: loss of HCO3 & fluid -> acidic urine -> uric acid precipitation

211
Q

RFs for renal stones?

A
  • dehydration
  • hypercalciuria, hyperparathyroidism, hypercalcaemia
  • cystinuria
  • high dietary oxalate
  • renal tubular acidosis
  • medullary sponge kidney, polycystic kidney disease
  • beryllium or cadmium exposure
212
Q

Drug causes of calcium renal stones?

A
  • loop diuretics
  • steroids
  • acetazolamide
  • theophylline
    (thiazides can prevent calcium stones (increase distal tubular calcium resorption))
213
Q

Opaque renal stones on xray?

A
  • calcium oxalate 40%
  • mixed calcium oxalate/phosphate 25%
  • triple phosphate 10%
  • calcium phosphate 10%
214
Q

Radiolucent renal stones on xray?

A
  • urate stones 5-10%

- xanthine stones <1%

215
Q

Semi-opaque, ground-glass appearance of renal stones on X-ray?

A

Cystine stones 1%

216
Q

What are stag horn calculi?
What are they made of?
When do they develop?
What predisposes to their formation?

A
  • involve renal pelvis, extending into >1 calyces
  • struvite (ammonium magnesium phosphate, triple phosphate)
  • they develop in alkaline urine
  • ureaplasma urealyticum & proteus infections
217
Q

Initial Rx of renal colic?

A
  • NSAID for analgesia eg Diclofenac
  • IM for rapid relief of pain, for those who require admission
  • (alpha-blockers may help in pts amenable to conservative Rx, with greatest benefit in those with larger stones)
218
Q

Initial Ix when suspecting renal stones?

A
  • urine dip + culture
  • FBC/CRP ?infection
  • U&Es ?renal function
  • calcium/urate ?underlying cause
  • clotting ?for percutaneous intervention
  • blood mcs if febrile etc
219
Q

Imaging in renal stones - what should be performed in all?

A

CT-KUB within 14h of admission
- 97% sens ureteric stone, 95% spec
(US much lower sens)

220
Q

Imaging in renal stones - if a pt has a fever, just 1 kidney, or there is uncertainty re: Dx, what should be done?

A

Immediate CT-KUB

- exclude other causes e.g. ruptures AAA

221
Q

Rx of renal stone <5mm?

What if severe?

A
  • usually will pass spontaneously within 4wks of Sxonset

- lithotripsy & nephroithotomy if severe

222
Q

When might urgent Rx be indicated with a renal stone <5mm?

A
  • ureteric obsrtuction
  • renal developmental abnormality e.g. horseshoe kidney
  • renal Tx
223
Q

Renal stone + ureteric obstruction + infection - what are the Rx options?

A

Surgical emergency -> Decompression:

  • nephrostomy tube placement
  • ureteric catheter insertion
  • ureteric stent placement
224
Q

What are the options for Rx of renal stone disease when not an emergency but e.g. >5mm?

A
  • extra-corporeal shock wave lithotripsy
  • percutanoeus nephrolithotomy
  • ureteroscopy
  • open surgery remains an option in selected
225
Q

Sx renal stone <2cm in aggregate - Rx of choice?

A

Lithotripsy

226
Q

Sx renal stone <2cm in aggregate in a pregnant female - Rx of choice?

A

Ureteroscopy

227
Q

Complex renal stones or stag horn stones - Rx of choice?

A

Percutanoeus nephrolithotomy

228
Q

What does ureteroscopy involve in renal stone Rx?
When is it indicated?
What happens to the stent?

A
  • ureteroscopy passed retrograde through ureter into renal pelvis
  • indicated where lithotripsy is C/I e.g. pregnancy, or in complex stone disease
  • stent left in situ for 4wks after procedure
229
Q

What does shockwave lithotripsy involve in renal stone Rx?

What are the risks/disadvantages?

A
  • shock wave generated externally to pt -> internal cavitation bubbles & mechanical stress lead to stone fragmentation
  • solid organ injury from the shock waves
  • ureteric obstruction from larger stones fragmenting
  • uncomfortable procedure, analgesia required after
230
Q

What does percutaneous nephrolithotomy involve in renal stone Rx?

A
  • access gained to renal collecting system
  • intra-corporeal lithotripsy or stone fragmentation performed
  • stone fragments removed
231
Q

How to help prevent calcium renal stones?

A

(prevent hypercalciuria)

  • high fluid intake
  • low animal protein, low salt diet
  • thiazide diuretics
232
Q

How to help prevent oxalate renal stones?

A
  • cholestyramine
  • pyridoxine
    (they reduce urinary oxalate secretion)
233
Q

How to help prevent uric acid renal stones?

A
  • allopurinol

- urinary alkalinisation eg oral bicarbonate

234
Q

Where does renal cell carcinoma arise from?

A
  • proximal renal tubular epithelium
  • 85% of 1ry renal neoplasms
  • = hypernephroma
235
Q

Associations of RCC?

A
  • middle-aged men
  • smoking
  • tuberous sclerosis, von Hippel-Lindau syndrome
236
Q

Features of RCC
classic triad?
other?

A
  • haematuria, loin pain, abdominal mass
  • fever unknown origin
  • left varicocele (due to occlusion of left testicular vein)
  • endocrine: may secrete EPO (polycythaemia), PTH (hypercalcaemia), renin, ACTH
  • 25% have mets at presentation
237
Q

Rx of RCC:
confined disease?
what may help reduce tumour size or help treat pts with metastases?

A
  • partial/total nephrectomy depending on tumour size
  • alpha-IFN & IL-2
  • receptor TK inhibitors eg Sorafenib, Sunitinib, have been shown to have superior efficacy to IFN-alpha
238
Q 
Where is the HLA system (human MHC) coded?
what are the class 1 Ag?
what are the class 2 Ag?
A
  • chr 6
  • 1: A B C
  • 2: DP DQ DR
239
Q

What is the relative importance when HLA matching for a renal Tx?

A
  • DR > B > A
240
Q

What are post-op renal Tx problems?

A
  • acute tubular necrosis of the graft
  • vascular thrombosis
  • urine leakage
  • UTI
241
Q

When and why does hyperacute rejection of the graft occur with renal Tx?

A
  • within mins- hours
  • due to pre-existent Abs against donor HLA type 1 Ag (type II hypersensitivity reaction)
  • rarely seen due to HLA matching
242
Q

When & why does acute graft failure occur with renal Tx?

A
  • within 6months
  • due to mismatched HLA - cell-mediated (cytotoxic T cells)
  • other causes inc CMV infection
  • may be reversible with steroids & immunosuppressants
243
Q

Causes of chronic graft failure with renal Tx?

A
  • both Ab & cell-mediated mechanisms cause fibrosis to the Tx kidney = chronic allograft nephorpathy
  • or recurrence of the original disease: MCGN >IgA > FSGS
244
Q

Example initial regime for immunosuppression after renal Tx?

A

tacrolimus/ciclosporin + mAb

245
Q

Example maintenance regime for immunosuppression after Renal Tx?

A

tacrolimus/ciclosporin + MMF/Sirolimus

246
Q

Post-renal Tx - what should be added to immunosuppressant regime if there is >1 acute rejection episode?

A

Add steroids (if the episodes are steroid responsive)

247
Q

MoA of ciclosporin?

A
  • calcineurin inhibitor (phosphatase involved in T cell activation)
248
Q

MoA of Tacrolimus?
What is the benefit of Tac over ciclosporin?
Disadvantage?

A
  • calcineurin inhibitor
  • lower incidence of acute rejection
  • less HTN & hyperlipidaemia
  • but high incidence of impaired glucose tolerance & diabetes
249
Q

MoA of MMF: mycophenolate mofetil?

Side-effects?

A
  • blocks purine synthesis by IMPDH inhibition
  • therefore inhibits proliferation of B & T cells
  • GI & bone marrow suppression
250
Q

MoA of Sirolimus/Rapamycin?

Side-effect?

A
  • blocks IL-2 which blocks T cell proliferation

- hyperlipidaemia

251
Q

monoclonal antibodies which may be used in immunosuppressant regime for renal Tx?

A
  • selective inhibitors of IL-2 receptor
  • daclizumab
  • basilximab
252
Q

Pts on long-term immunosuppression for organ Tx require regular monitoring for what complications?

A
  1. CVD - tacrolimus & cyclosporin can cause HTN & hyperglycaemia, Tac can also cause hyperlipidaemia - therefore monitor for accelerated CVD
  2. Renal failure - nephrotoxic effects of tacrolimus & ciclosporin/graft rejection/recurrence of original disease in Tx kidney
  3. Malignancy - minimise sun exposure etc, reduce risk of SCC & BCC of skin
253
Q

Proteinuria, haematuria, oedema, HTN in a pt with SLE - what is the Dx?

A

Diffuse proliferative GN on renal Bx

254
Q

‘Basket weave’ appearance on EM of renal Bx - what is the Dx?

A

Alport syndrome = mutation in type IV collagen

- eye problems, SNHL, GN

255
Q

Pt had an MI a month ago, is a smoker, started on aspirin, statin, ace-i, beta-blocker, admitted with breathlessness. Acute pulmonary oedema on CXR. Normal ecg & ECHO shows good LV function. What is the Dx?

A

Renal artery stenosis

-> do MR angiography

256
Q

Electrolyte causes of nephrogenic DI?

A
  • hypercalcaemia

- hypokalaemia

257
Q 
Non-idiopathic causes of membranous glomerulonephritis?
infective
malignant
drugs
autoimmune
A
  • malaria, syphilis, HBV
  • lung cancer, lymphoma, leukaemia
  • gold, penicillamine, NSAIDs
  • SLE class V, thyroiditis, rheumatoid
258
Q

What type of GN does cryglobulinaemia cause?

What Rx might be indicated?

A
  • type 1 membranoproliferative/mesangiocapillary GN

- plasma exchange

259
Q

Woman with Hx of membranous GN 2ry to SLE is admitted to hospital
- prev stable renal function has deteriorated rapidly
- left flank tenderness
- ESR 50
- blood ++ & protein +++ in urine dip
What is the likely cause of sudden deterioration in renal function?

A

RENAL VEIN THROMBOSIS

- nephrotic syndrome predisposes to thrombosis, esp of renal veins, which can be bilateral

260
Q

Most common glomerulonephropathy linked tor renal vein thrombosis?

A
  • membranous GN
261
Q

What sort of metabolic acidosis does renal tubular acidosis cause?

A

Normal anion gap

- hyperchloraemic metabolic acidosis

262
Q

What is type 1 (distal) renal tubular acidosis?

Complications?

A
  • inability to generate acid urine (secrete H+) in distal tubule
  • caused HYPOkalaemia
  • nephrocalcinosis & renal stones
263
Q

Causes of type 1 distal RTA?

A
  • idiopathic
  • RA, SLE, Sjogren’s
  • amphotericin B toxicity
  • analgesic nephropathy
264
Q

What is type 2 (proximal) RTA?

what is a complication?

A
  • decreased HCO3- reabsorption in proximal tubule
  • causes HYPOkalaemia
  • OSteomalacia
265
Q

Causes of type 2 proximal RTA?

A
  • idiopathic
  • Wilson’s disease
  • cystinosis
  • as part of Fanconi syndrome
  • carbonic anhydrase inhibitors, outdated tetracyclines
266
Q

What is type 4 RTA?

A
  • HYPERkalaemia

- reduction in aldosterone leads in turn to a reduction in proximal tubular ammonium excretion

267
Q

Causes of type 4 RTA?

A
  • hypoaldosteronism

- diabetes

268
Q

What type of renal impairment down gentamicin cause?

A

intrinsic renal AKI

- therefore proteinuria on urine dip

269
Q

What type of GN is characteristically ass with partial lipodystrophy?

A

Mesangiocapillary = membranoproliferative type 2 GN

270
Q

What type of GN is ass with Wegener’s & Goodpasture’s?

A

Rapidly progressive

271
Q

What is most likely finding on renal biopsy in HSP?

A

mesangial hypercellularity (IgA deposition)

272
Q

Child presents with anaemia, low platelets, protein & blood in urine. No Hx of diarrhoea

  • Dx?
  • Rx?
A

HUS

  • supportive
  • plasma exchange
273
Q

What is on renal biopsy in Wegener’s?

A

rapidly progressive GN

= CRESCENTERIC GN

274
Q

32y.o. man presents with LL oedema, feeling lethargic with pitting LL oedema & periorbital oedema + ascites & coarse crackles in lung bases
Urin dip: protein +++, negative for blood urine nitrites glucose

What is most likely underlying pathology?

A

FSGS: focal segmental glomerulosclerosis

  • nephrotic syndrome
  • generally presents in young adults
275
Q

EM of renal biopsy: the basement membraneis thickened with subepithelial electron dense deposits - a ‘spike and dome’ appearance
What is the Dx?
What is the Ab most ass with this condition?

A

Membranous GN

- anti-phospholipase A2 is ass with idiopathic membranous GN

276
Q

What Ab is ass with idiopathic membranous GN?

A

anti-phospholipase A2

277
Q

What is Goodpasture’s syndrome?

What HLA is it ass with?

A
  • pulmonary haemorrhage then rapidly progressive GN
  • caused by anti-GBM antibodies against type IV collage
  • more common in men 2:1, with bimodal age distribution of 20-30 & 60-70
  • HLA-DR
278
Q

Factors which increase likelihood of pulmonary haemorrhage in Goodpasture’s syndrome?

A
  • smoking
  • LRTI
  • pulmonary oedema
  • inhalation of hydrocarbons
  • young males
279
Q

Ix in Goodpasture’s syndrome inc renal Bx?

A
  • linear IgG deposits along basement membrane

- raised transfer factor

280
Q

Rx of Goodpasture’s syndrome?

A
  • plasma exchange (plasmapheresis)
  • steroids
  • cyclophosphamide
281
Q

Podocyte fusion on renal biopsy - what is the Dx?

A

Minimal change GN

occ FSGS

282
Q

What is a known iatrogenic complication of using 0.9% NaCl in large volumes?

A

hyperchloraemic metabolic acidosis

283
Q

MoA of Abiraterone acetate, used in prostate ca?

A
  • selective androgen synthesis inhibitor, blocks cytochrome p450 17-alpha-hydroxylase
  • blocks androgen production in testes & adrenal glands & in prostatic tumour tissue
  • given orally with prednisolone
  • has survival benefit in men with castrate refractory prostate ca who are yet to receive chemo
  • indicated in metastatic castration-resistant (hormone-relapsed) prostate ca who are aSx or mildly Sx after failure of androgen deprivation Rx in whom chemo is not yet clinically indicated
  • and in metastatic castration resistant prostate ca when disease has progressed on/after docetaxel-based chemo regimen
284
Q

What is useful in the prevention of oxalate renal stones?

A

cholestyramine

pyridoxine

285
Q 
Pt has HTN refractory to ACE-I &amp; calcium channel blocker at 170/100
K 2.9
aldosterone 600 (high)
renin 6.8 (high)
What is the Dx?
A

BL renal artery stenosis

1ry hyperaldosteronism is ass with LOW renin due to negative feedback

286
Q

What type of GN do malignancies cause when ass with nephrotic syndrome?

A

membranous GN
- paraneoplastic
- HLA-DR3
(lymphomas - minimal change)

287
Q

middle-aged man with nephrotic syndrome & HTN with renal biopsy showing: thickened capillary walls, & sub endothelial deposits

  • what is the Dx?
  • what is most likely to be beneficial to reduce proteinuria?
A

Membranous GN

  • ACE-I
  • (steroids may help in combo with something else)
288
Q

ACR of 30 is approx equivalent to a PCR of?

And ACR 70?

A 
30 = 50 (0.5g protein/24h)
70 = 100 (1g protein/24h)
289
Q

What Ig is involved in hyper acute graft rejection?

290
Q

What is thin basement membrane disease?

A
  • inherited disorder of type IV collagen causing thinning of the basement membrane
  • may affect 5% of people, 30% of them report FHx of haematuria
  • Dx on Hx of persistent haematuria, normal kidney function, FHx of haematuria without kidney failure
  • benign, biopsy rarely indicated

EXAM (21 decks)

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