Renal Flashcards

1
Q

Causes of hypernatraemia? (4)
How may this present in an infant?
Rx?

A

Dehydration (e.g. D&V, high fever)
Osmotic diuresis (e.g. DKA)
Diabetes insipidus
Excessive saline infusion

In an infant: jittery, increased muscle tone, hyperreflexia, sunken fontanelles, drowsiness, eventually coma

Rx: Oral rehydration solution 1st line
Slow infusion IV 0.9% NaCl if cannot tolerate oral (D&V), sepsis/shock suspected, or if oral not working

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2
Q

Drugs to stop in AKI as they will cause worsening? (3)

A

DAAAMN

Diuretics
ACEI/Aminoglycoside/ARB
Metformin
NSAIDs

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3
Q

Drugs that may have to be stopped in AKI as they will build up?

A

Metformin
Digoxin
Lithium

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4
Q

Is aspirin safe in AKI?

A

At cardioprotective dose 75mg

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5
Q

Is paracetamol safe in AKI?

A

Yes

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6
Q

Is warfarin safe in AKI?

A

Yes

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7
Q

Are statins safe in AKI?

A

Yes

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8
Q

Is clopidogrel safe in AKI?

A

Yes

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9
Q

Are B Blockers safe in AKI?

A

Yes

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10
Q

Diagnosis of AKI?

4 symptoms, 3 bloods

A

Symptoms:

  • oliguria
  • oedema
  • arrhythmias (from K/acid build up)
  • features of uraemia (pericarditis, encephalopathy)

Bloods:

  • rise in serum creatinine by 26 mol/l in 48 hours
  • rise in serum creatinine by 50% in 7 days
  • fall in urine output less than 0.5 ml/kg/hr for 6 hours
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11
Q

What usually increases during an AKI?

A

Things that the kidney normally excretes

  • K
  • Creatinine
  • Urea

Also usually acidosis

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12
Q

SE of EPO therapy?

Why might someone not respond?

A
  • Accelerated hypertension (encephalopathy and seizures)
  • Bone ache
  • Flu-like symptoms
  • Pure red cell aplasia
  • Iron deficiency due to increased erythropoiesis

Non-responsive:

  • iron deficiency
  • inadequate dose
  • infection
  • hyperparathyroid bone disease
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13
Q

Alport’s Syndrome:

  • inheritance?
  • presentation?
  • diagnosis?
  • why might a transplant fail in an alport’s pt?
A

X-linked dominant

In childhood:

  • microscopic haematuria
  • progressive renal failure
  • bilateral sensorineural deafness
  • Lenticonus: lens protrudes into anterior chamber (needs glasses)
  • Retinitis pigmentosa

Diagnosis:

  • genetic testing
  • renal biopsy: EM - longitudinal splitting of lamina dense of GBM, causing ‘basket-weave’ appearance

Fail: due to anti-GBM antibodies against normal GBM

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14
Q

Minimal change disease:

  • presentation? (1)
  • renal biopsy? (2)
  • Management?
A
  • Nephrotic syndrome (normotension)

Biopsy:

  • LM: normal glomeruli
  • EM: fusion of podocytes, effacement of foot processes

Rx:

  • Oral pred + urgent referral
  • Cyclophosphamide if resistant
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15
Q

Why can nephrotic syndrome cause blood clots?
What must happen?
How can it cause infection?
How can it cause hypocalcaemia?

A

Clots:

  • ATIII and plasminogen lost to urine
  • Can cause DVT and renal vein thrombosis
  • LMWH

Infection: Ig lost to urine

Hypocalcaemia: VitD and binding protein lost in urine

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16
Q

ADPKD:

  • presentation? (4)
  • extra-real manifestations? (4)
A

As a young adult:

  • hypertension
  • abdo pain
  • CKD
  • loin mass
  • haematuria

Extra-renal:

  • liver cysts (most common) - hepatomegaly
  • berry aneurysm
  • mitral/tricuspid incompetence
  • pancreatinc/splenic cysts
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17
Q

IgA nephropathy vs post-strep glomerulonephritis?

A

IgA:

  • 1-2 days after URTI
  • haematuria
  • caused by IgA

Post-strep:

  • 1-2 weeks after URTI
  • Proteinuria
  • haematuria
  • low complement count
  • caused by IgG, IgM and C3 deposition in glomeruli

Caused by GAS

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18
Q

Renal biopsy of post-strep?

A
  • Acute, diffuse, proliferative glomerulonephritis
  • Endothelial proliferation with neurtophils
  • EM: subaopithelial ‘humps’ caused by lumpy immune complex deposition
  • IF: granular or ‘starry sky’ appearance
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19
Q

How to tell intrinsic AKI from pre/post renal?

A

Protein present in intrinsic

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20
Q

How to tell primary from secondary hyperaldosteronism?

A

Pt with refractory hypertension, low K and high Na (since high aldosterone)

Look at renin activity. If renal artery stenosis then low afferent blood flow will stimulate renon release and cause they hyperaldosteronism

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21
Q

3 things renal artery stenosis can cause?
Renal artery stenosis due to atherosclerosis is most common cause of renal vascular disease (90%), what is next most common cause?

A
  • hypertension
  • CKD
  • flash pulmonary oedema

Fibromuscular dysplasia

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22
Q

50 y/o patient with progressive weakness, and dyspnoea, hepatomegaly, reduced renal function, T2DM, COPD, no FHx?
Diagnosis?

A

Amyloidosis

Rectal biopsy - congo red staining shows apple-green birefringence

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23
Q

What should you think of in young woman who develops AKI in response to ACEI?
What is seen on renal USS?
What is seen on duplex scan?
What is next Ix?

A

Fibromuscular dysplasia

USS: normal kidneys and urinary system

Duplex: stenotic arteries

MR angiography: ‘string of beads’ appearance

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24
Q

HSP:

  • what is it?
  • features? (4)
  • treatment?
A
  • IgA small-vessel vasculitis after URTI - degree of overlap with IgA nephropathy
  • palpable purpuricrash with localised oedema over buttocks, extensors and legs
  • abdo pain
  • polyarthritis
  • features of IgA nephropathy (haematuria, renal failure)

Rx: supportive. Good prognosis

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25
Q

If someone with CKD and low GFR needs contrast scan?

A

Offer Iv hydration before and after contrast infusion

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26
Q

Why is lupus nephritis different from other nephritic syndromes?
There are 6 different types of lupus nephritis - what is the most common?
What is seen on renal biopsy with this?

A

All patients with lupus nephritis will have proteinuria

Diffuse proliferative glomerulonephritis

endothelial and mesangial proliferation, ‘wire-loop’ appearance
EM: sub endothelial immune complex deposits
IF: granular appearance

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27
Q

Management of rhabdomyolysis causing myoglobinaemia?
What dangerous electrolyte disturbance may occur with this, and may appear before AKI?
Among other causes, e.g. prolonged collapse, seizure, ecstasy etc, what 2 common drugs may interact to cause this?

A

Lots of IV fluids to maintain good urine output, urinary alkalisation sometimes used

Hyperkalaemia

Statins with clarithromycin - don’t prescribe together

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28
Q

4 causes of transient non-visible haematuria?
5 causes of persistent non-visible haematuria?
2 causes of spurious red/orange urine where blood not present on dipstick?

A
  • UTI
  • menstruation
  • vigorous exercise (settles after 3 days)
  • sex
  • cancer (kidney, renal, prostate)
  • stones
  • BPH
  • prostatitis/urethritis (e.g. chlamydia)
  • renal e.g. IgA nephropathy

Food: beetroot, rhubarb
Drugs: rifampicin, doxorubicin

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29
Q

Define persistent non-visible haematuria?

What else should be tested? (3)

A

Non-visible haematuria present on 2/3 samples tested 2-3 weeks apart

Renal function
ACR or PCR
BP

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30
Q

Who gets urgent cancer referral for haematuria?

A

Age 45+ AND:

  • visible haematuria without UTI
  • visible haematuroa that persists past UTI

Age 60+ AND:
- unexplained non-visible haematuria with dysuria/raised WBC on bloods

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31
Q

Who gets non-urgent cancer referral for haematuria?

A

Age 60+ AND:

- recurrent/persistent UTI

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32
Q

Acute interstitial nephritis:

  • what is it?
  • causes?
  • features?
  • Ix?
A

allergic-type reaction involving kidneys, causing interstitial oedema and infiltrates in the connective tissue between renal tubules - accounts for 25% of all drug-induced AKI

Most commonly drugs, usually antibiotics (penicillin, rifampicin) - also NSAIDs, allopurinol, furosemide

Features:

  • fever, rash, arthralgia
  • Eosinophilia
  • mild renal impairment
  • hypertension

Ix:

  • sterile pyuria (WCC on dipstick but no culture)
  • white cell casts
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33
Q

How long for fistulas to develop for dialysis?

3 complications?

A

6-8 weeks

  • infection
  • thrombosis (bruit)
  • stenosis (limb pain, ischaemia)
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34
Q

What is the most common cause of nephrotic syndrome in adults?
What is seen on biopsy?
Causes?

A

Membranous glomerulonephritis

  • LM: thickened basement membrane
  • EM/silver staining: ‘spike and dome appearance’ due to sub epithelial deposits

Causes:

  • anti-phospholipase A2 Ig
  • hepB, malaria
  • malignancy (prostate, lung, blood)
  • autoimmune diseases
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35
Q

Management of membranous glomerulonephritis?

A

All its receive ACEI/ARB
Immunosuppression
Anticoagulation for high risk pts

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36
Q

Stages of CKD?

Definition of CKD?

A
1 - GFR >90
2 - GFR 60-90
3a - GFR 45-59
3b - GFR 30-44
2 - GFR 15-29
1 - GFR <15 - RRT if uraemia present

Reduced GFR and evidence of kidney damage for at least 3 months. Evidence:
proteinuria, haematuria, abnormal U&E, abnormal imaging. More proteinuria = more damage

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37
Q

6 things that can cause CKD

A
Diabetes - commonest
Glomerulonephritis - 2nd
Hypertension
Chronic pyelonephritis
Renovascular disease
PKD
Idiopathic - small, scarred kidneys unknown cause
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38
Q

At what GFR do symptoms usually become apparent for CKD?
Mild symptoms
Mod?
Sev?

A

GFR <20 - due to altered conc of electrolytes and urea

Mild - nocturia (unable to concentrate urine)

Mod - non-specific: fatigue, weakness, loss of appetite, nausea, abdominal cramps, gout, bad taste in mouth

Sev - Restless leg, yellow/brown tinge in skin, paraesthesia/cramps, encephalopathy, pericarditis,, itch, halitosis, seizures, uraemia frost

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39
Q

General management of CKD?

A

Slow progression with ACEI/ARB +/- Spironolactone

Aim for BP <130/80 to reduce proteinuria

Optimise glycaemia

Counsel on RRT once GFR <15

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40
Q

Anaemia of CKD - what type normally?

Management?

A

Normochromic normocytic (due to decreased EPO) - can also have malabsorption of Fe/B12/folate, decreased cel survival (dialysis), concurrent GI blood loss etc

Target Hb 10.5-12.5
Optimise Fe status - many require IV Fe
EPO injections weekly

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41
Q

How does renal bone disease occur?
What are the manifestations?
Management?

A
  1. high phosphate ‘drags’ Ca from bones –> osteomalacia
  2. Low vitD (no activation in kidney) causing low Ca –> secondary hyperparathyroidism

Manifest:

  • osteoporosis
  • osteomalacia
  • osteitis fibrosa cystica (due to unchecked hyperparathyroidism)
  • osteosclerosis

Rx:

  • reduce dietary phosphate
  • phosphate binders (calcium carbonate, sevelamer)
  • VitD (calcitriol)
  • parathyroidectomy in some cases
  • Alendronic acid to prevent osteomalacia/osteoporosis

Calcium based phosphate binders risk hypercalcaemia and vascular calcification, so sevelamer may be better option

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42
Q

3 options of RRT?

A

Haemodialysis:

  • most common, usually 3-4 sessions a week
  • AV fistula

Peritoneal dialysis:

  • filtration in patient’s abdo
  • CAPD or APD (overnight)

Renal transplant

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43
Q

Life expectancy of renal transplant?
Anti-rejection meds?
What type of matching is best?
Risks of immunosuppression? (3)

A

10-12 years

ciclosporin/tacrolimus + MMF
Steroids in acute rejection

HLA most important (DR>A>B surface antigens)

CVD, renal failure, SCC of skin

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44
Q

3 types of transplant rejection?

A

Hyperacute - mins-hours - type II hypersensitivity from pre-existing Ig to HLA (rare - immediate removal)

Acute (<6 months) - HLA mismatching - Tc cell mediated - can be reversed with steroids

Chronic (>6 months) - chronic allograft nephropathy (renal fibrosis)

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45
Q

Peritoneal dialysis, fever, cloudy dialysis?

How does PD work?

A

Staph epidermidis

Inject high dextrose solution into abdominal cavity which draws out waste products from blood, drained after several hours dwell time and exchanged for new dialysis solution (so risk of hyperglycaemia as well)

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46
Q

What is seen on biopsy of diabetic nephropathy?
Does it cause nephritic/nephrotic syndrome?
What should be checked annually?
3 main management points in diabetic nephropathy?

A

Nodular glomerulosclerosis - kimmelstein-wilson lesions

Nephrotic syndrome

Urinary albumin:creatinine ratio

  1. Tight glycaemic control
  2. BP <130/80 (ACEI)
  3. Statin
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47
Q

What is microalbuminuria?

What is clinical proteinuria?

A

ACR 2.5-30
Lose 0.15g protein each day in urine
Dipstick will be negative
Regard >2.5 as clinically significant proteinuria. If ACR >70 start ACEI regardless of BP

ACR >30 - will show up as + on dipstick (loss of 0.45g protein per day)

48
Q

Presentation of chronic pyelonephritis?
What does it cause to the kidney?
Most common cause?
Other causes?

A

Can be vague - hypertension/CKD, maybe hydronephrosis

Asymmetrical scarring, fibrosis and contraction of the kidney

Vesicoureteric reflux causing reflux nephropathy (name of chronic pyelonephritis due to reflux)

Others: recurrent acute infection, chronic obstruction, xantho-granulomatous abscess

49
Q

Presentation of vesicoureteric reflux?

Ix?

A
  • May be hydronephrosis in antenatal scan
  • Recurrent childhood UTI
  • Reflux nephropathy
    (renal scarring may increase renin release causing hypertension)
  • Normally diagnosed with micturating cystourethrogram
  • DMSA scan can look for renal scarring
50
Q

Causes of ischaemic nephropathy?

A
Essential hypertension
Renovascular disease (atherosclerosis 90%, FMD 10%)
51
Q

Features of renal artery stenosis? (6)
Ix?
Medical Rx?
Surgical Rx?

A
Hypertension
AKI (due to ACEI initiation)
Flash pul oed
CKD
Renal bruit
Discrepency in size of kidneys on USS as usually unilateral

Renal US –> Duplex US –> CT angiography

Med: Statin, ACEI (contraindicated in bilateral renal artery stenosis), anti-platelet (same as atherosclerotic disease)

Surgical: angioplasty +/- stent

52
Q

In GN, what leads to haematuria?

What leads to proteinuria?

A

Haematuria - due to endothelial/mesangial damage (proliferative)

Proteinuria - due to podocyte damage (non-proliferative - atrophy)

53
Q

What 3 things cause nephritic syndrome (haematuria, hypertension)?

A

Rapidly progressive GN
IgA nephropathy
Alport syndrome

54
Q

What 5 things cause nephrotic syndrome (proteinuria, oedema)?

A
Minimal change
Membranous GN
Focal segmental glomerulosclerosis
Amyloidosis
Diabetic nephropathy
55
Q

What 3 things can cause a mixed picture of nephritic/nephrotic syndrome?

A

Diffuse proliferative GN
Membranoproliferative GN
Post-streptococcal GN

56
Q

Biopsy for IgA nephropathy?

Rx?

A

LM: mesangial cell proliferation (nephritic)

IF: IgA and C3 deposition

Rx: BP control (ACEI/ARB) and fish oil
(steroids/immunosuppression NOT useful)

57
Q

Biopsy of minimal change?

A

LM: normal

EM: podocyte fusion and foot process effacement

Rx: steroids, cyclophosphamide if steroid resistant

58
Q

Focal segmental glomerulosclerosis:

  • typical Hx?
  • assoc?
  • biopsy?
  • Rx?
A

young adult with nephrotic syndrome and CKD

HIV, reflux nephropathy, heroin, sickle cell

LM: focal/segmental sclerosis + hyalinosis

EM: effacement of foot process

IF: minimal Ig/complement deposition

Rx: steroids +/- immunosuppression - 60% steroid sensitive, 50% progress to ESRF

59
Q

Membranous nephropathy:

  • typical Hx?
  • Assoc?
  • biopsy?
  • Rx?
  • Rule of 1/3?
A

Adult with proteinuria and nephrotic syndrome

Primary - anti-phospholipid A2 Ig (PLA2R)
Secondary - cancer, infection, systemic disease

EM: thick BM, sub-epithelial deposits causing spike and dome appearance

Rx: ACEI, steroids + cyclophosphamide +/- B-cell monoclonal AB

1/3 resolve spontaneously
1/3 respond to Rx
1/3 –> ESRF

60
Q

Rapidly progressive GN:

  • Typical presentation?
  • Biopsy?
  • Rx?
A
  • AKI, nephritic syndrome with features of underlying condition (SLE, ANCA, Goodpasture’s)
  • treatable cause of AKI +/- granular casts

Biopsy: crescentic glomeruli

Rx: Immunosuppression (steroids, cyclophosphamide, azathioprine) +/- plasmapheresis +/- temporary RRT

61
Q

Membranoproliferative GN:

  • Typical Hx?
  • Biopsy?
  • Rx?
A

Nephritic and nephrotic syndrome –> poor prognosis

Depends on subtype:

  • Type 1 - ‘tram track’ appearance on EM (most common)
  • Type 2 - intramembranous immune complex deposition with dense deposits

Rx: Steroids may help

62
Q

Post-strep GN:

  • typical Hx?
  • Biopsy?
  • Rx?
A

Kid with GABHS infection (usually pyogenes) 7-14 days prior
Haematuria, proteinuria, hypertension, LOW C3, headache, malaise

Biopsy:

  • EM - sub epithelial humps by lumpy immune deposits
  • IF - granular/starry sky appearance (neutrophilic)

Rx: supportive - good prognosis

63
Q

Goodpastures:

  • typical Hx?
  • Ig?
  • Renal biopsy?
  • Other thing in blood?
  • Rx?
A

Pulmonary haemorrhage and rapidly progressive GN

Anti-GMB Ig against type IV collagen

Biopsy: linear IgG deposits along basement membrane

Raised transfer-factor

Rx: steroids/cyclophosphamide +/- plasmapheresis

64
Q

Rx for lupus nephritis?

A

Azathioprine/MMF (organ involvement)
Hydroxychloroquine (arthritis)
IV steroids/cyclophosphamide if flare

65
Q

ANCA diseases?
Other, similar disease?
Rx?

A

cANCA (anti-PR3) - Wegener’s (GPA) - ENT/resp involvement, saddle nose

pANCA (anti-MPO) - microscopic polyangitis - no granuloma

Eosiniphilic GPA (eosinophilia + late-onset asthma)

Rx: Immunosuppression, plasma exchange, dialysis, supportive care

66
Q

Primary AL amyloid vs Secondary AA?

A

AL light chain - age of diagnosis 50-60 - heart, kidneys, bowels, skin, nerves

AA (systemic inflammatory IBD/RA etc) - liver, spleen, kidneys, adrenals

67
Q

How to tell AKI from longstanding CKD in patient who newly presents?

A

Renal US - bilateral small kidneys <9cm suggests longstanding CKD

Exceptions - ADPKD, diabetic nephropathy, amyloid - kidneys may enlarge/stay normal size

In which case: high phosphate, low calcium, high PTH

Only true way to tell is previous blood tests

68
Q

What drug can help with symptoms ADPKD?
If someone wants screening?
ARPKD?

A

Tolvaptan

Renal US (better than genetic)

Polycystic kidneys may be felt/seen at birth - ESRF in childhood

69
Q

Anderson-Fabry:

  • genetics?
  • Hx?
  • Rx?
A

X-linked - a-galactosidase metabolism error

renal failure, cardiac myopathy, neuropsychiatric, angiokeratomas

Fabryzyme

70
Q

Medullary cystic kidney:

  • inheritance?
  • what does it cause?
  • age of renal transplant?
A

AD

renal tubular necrosis
small kidneys
cysts
(seen on ct)

28

71
Q

Medullary sponge kidney:

  • genetics?
  • what does it cause?
  • prognosis?
A

sporadic mutation

Cystic dilation of collecting ducts (bunch of grapes)

Asymptomatic/incidental finding - increased risk of calculi

Good prognosis - rarely progresses to ESRF

72
Q

What is Fanconi syndrome?
Causes?
Typical Hx?

A

Inadequate reabsorption occurring in PCT

Causes: Wilson’s, cystinosis, myeloma, Sjrogen’s
(cystinosis most common in kids - AR disorder)

failure of growth, osteomalacia, renal tubular acidosis, polyuria, glycosuria, phosphaturia

73
Q

Grading of AKI?

A

1 - creatinine rise of 26mmol in 48 hrs, or rise of 50% in a week, or oliguria <0.5ml/kg/hr for 6 hours

2 - creatinine 2-2.99x baseline in 7 days OR oliguria <0.5ml/kg/day for 12 hours

3 - creatinine >3x baseline in 7 days OR oliguria <0.3ml/kg/hr for 24 hrs OR anuria for 12 hours

74
Q

Symptoms of AKI?

Important assessment steps?

A

early may be asymptomatic
Oliguria, pul/per oed, uraemia (itch, pericarditis, encephalopathy), arrhythmia (hyperkalaemia)

Assess:
- Hx - disease, fluid, drugs, chemo, rheum, cough etc

  • examine - euvolaemia, bladder, kidneys, renal bruit
  • Ix: dipstick + culture, microscopy (cells, casts), U&E, FBC, LFT, clotting, CK, ESR, CRP. Consider electrophoresis, Ig (ANCA, ANA, GBM)

Image: renal US

75
Q

4 indications for dialysis in AKI?

A

Hyperkalaemia >7 resistant to Rx

Severe acidosis ph <7.15

Fluid overload

Urea >40

76
Q

5 pre-renal causes of AKI?
4 intra?
4 post?
Most common causes?

A
Pre:
Cardiac failure
Sepsis
Blood loss
Dehydration
Vascular occlusion

Intra:
GN
Small-vessel vasculitis
Acute tubular necrosis (drugs, toxins, prolonged hypotension, myoglobin)
Interstitial nephritis (drugs, inflammation, infection)

Post:
calculi
BPH
Cancer (prostate, cervix, ureter)
Stricture

90% pre-renal and acute tubular necrosis

77
Q

Causes of hyperkalaemia?
Symptoms:
Risk?
ECG?

A

AKI, metabolic acidosis, drugs (ACEI, ARB, spironolactone), Addison’s, massive blood transfusion, tumour lysis syndrome)

Non-specific - fatigue, weakness

Can go into VF

ECG: 
- loss of P waves
- Prolonged QRS
- tall, tented T waves
- ectopics/escapes
If severe: sine wave
78
Q

Rx hyperkalaemia?

A

ECG + IV access

Protect myocardium - 10ml 10% Ca gluconate

Short-term shift - act rapid 10 units, 50ml 50% dextrose, nebuliser salbutamol

Removal - Ca resonium, loop diuretics, dialysis

Ca resonium enema better than oral

79
Q

Management of AKI?

A

Assess volume status

Aim for euvolaemia
STOP nephrotoxic drugs (DAAAMN)

Treat underlying cause:
Pre-renal: fluid challenge
Post: catheter + consider CT KUB
Intra: renal assessment

Remember indications for dialysis:

  • urea >40
  • K >7 and refractory
  • pH <7.15
  • fluid overload (pul oed)
80
Q

Acute tubular necrosis:

  • How does it present?
  • urine Na content?
  • urine osmolality?
  • serum urea:creat ratio?
  • response to fluid challenge?
A

AKI + muddy brown casts (pre-renal = normal/’bland’ sediment)

Na content HIGH (low in pre-renal as trying to conserve volume)

Urine osmolality LOW (high in pre-renal as again trying to conserve volume)

Serum urea:creat normal (raised in pre-renal)

Poor response to fluid challenge (good in pre-renal)

81
Q

Acute tubular necrosis:

  • causes?
  • reversible?
A
  • nephrotoxic drugs
  • rhabdomyolysis
  • ethylene glycol poisoning
  • ischaemia (prolonged hypoperfusion)

Reversible if detected early and treatment started

(ethylene glycol = anti-freeze. Rx = fomepizole or ethanol

82
Q

What is renal papillary necrosis?
Triad of symptoms?
Causes?

A

Coagulative necrosis of renal papillae (base of pyramids)

Haematuria, loin pain, proteinuria

Causes: acute pyelonephritis, diabetic/obstructive nephropathy, NSAIDs, sickle cell

83
Q

What is renal tubular acidosis?

A

Normal anion gap metabolic acidosis caused by impaired H+ secretion by the kidney

There are 4 types, 1 and 2 being the most common. They can be inherited or acquired from e.g. SLE, amphotericin, Wilson’s.

84
Q
Coliforms that can cause UTI?
Gm +ve cocci?
What is pseudomonas UTI assoc w?
What is CPE UTI assoc w?
What are staph saphrophyticus, staph aureus and proteus UTI assoc w?
A

E coli, proteus, enterobacter

Enterococcus, staph saphrophyticus, staph aureus

Pseudomonas - catheters

Carbapenemase producing enterobacter - travel to India

Staph saph - pregnancy

Staph aureus - bacteraemia - pyelonephritis

Proteus - foul smell (urea breakdown –> ammonia –> alkaline urine) and struvite stones

85
Q

When should asymptomatic bacteriuria be treated?

A

Pregnancy

Do not treat in anyone else, esp older folk as it’s very common

86
Q

Why is urinalysis not routinely performed in older people?

When else is it nor routinely used?

A

False positives of leukocytes, nitrite (coliform) and protein/blood

Perform urine culture/microscopy if >65 and suspect

Do not use urinalysis for catheterised patients either. Also will commonly get colonisation. In both cases, do not treat unless clinical signs/symptoms. Treat catheter as complicated UTI

87
Q

Kass criteria for UTI?

A

Must have symptoms
>10^5 organisms per ml probable UTI
Or <10^5 but significant pyuria

88
Q

Uncomplicated female UTI?

A

Trimethoprim or Nitrofurantoin 3 days

89
Q

Uncomplicated male UTI?

A

Trimethoprim or Nitrofurantoin 7 days

90
Q

Complicated UTI/pyelonephritis/urosepsis?

A

IV amox + gent

Step down PO co-trimoxazole or as per sensitivities

91
Q

Abacterial cystitis causes?

A

UTI symptoms with no significant culture or sterile pyuria

Honeymoon cystitis - trauma (shagging)
Urethritis (STI)

Test for STI
Alkalinising urine may help

92
Q
What is emphysematous pyelonephritis?
Assoc and cause?
Features?
Ix?
Rx?
A

Necrotising infection causing gas accumulation in renal parenchyma - high mortality

Diabetes - E. Coli

Classic pyelonephritis (dysuria, fever/rigors, loin pain, N&V)
AKI, rapid sepsis, crepitations in flank/scrotum

Abdo CT most sensitive

Rx: percutaneous drainage and Abx –> nephrectomy

(urgent CT if not responding to standard therapy)

93
Q

What bacteria causes of bacterial prostatitis?
Symptoms?
PR exam?

Rx?

A

E coli

Referred pain - perineum, rectum, penis, back
Fever/rigors
Urinary obstruction maybe present

DRE - tender, boggy

Ofloxacin 28 days
Trimethoprim if unsuitable
(quinolone risk tendon rupture, AA dissection, QT, C diff)

94
Q

Epididymo-orchitis:

  • features?
  • what is seen on doppler?
  • Rx?
A

unilateral testicular pain and swelling
May be urethral discharge present

Doppler may be needed to rule out torsion
- increased blood flow and present cremasteric reflex

STI suspected - Doxycycline 14 days
STO NOT suspected - Ofloxacin 14 days

95
Q

Balanitis:

  • causes?
  • Rx?
A

Inflammation of the glans

Infective:
- Candiasis (assoc w intercourse) - itch +/- white discharge
- Staph - pain, itch, yellow discharge
(swab may be helpful if unclear)
- anaerobic - foul smelling yellow discharge

Rx: topical clotrimazole (2 weeks), oral Flucloxacillin, or topical/oral metronidazole respectively respectively

Other causes: dermatitis, lichen plans/sclerosus, circinate balanitis etc

Role for circumcision in these

96
Q

Haemolytic uraemic syndrome:

  • Ix?
  • What is seen on bloods?
  • Management?
A

HUS = triad of AKI, thrombocytopenia and MAHA following E. Coli O157 infection

FBC - normocytic anaemia, thrombocytopaenia, AKI (high urea and creatinine)

Other Ix:

  • stool culture for STEC
  • stool PCR for shiva-like toxin
  • film - fragmented cells

Rx:

  • supportive - fluids, blood transfusion or dialysis if required
  • NO ROLE for Abx
97
Q

Aspirin/salicylate OD:

  • symptoms?
  • how does it develop over time?
  • Rx?
A

N&V, tinnitus, headache

Initially hyperventilation causing resp alkalosis

Then over about 24 hours causes raised anion gap metabolic acidosis

Rx: IV sodium bicarbonate (alkalinises urine, promotes excretion)

98
Q

If someone has eGFR 65 but no symptoms is it CKD?

A

Not CKD

Need symptoms to diagnose stage 1&2

Also one off test means nothing, must be present for 3 months

99
Q

When should ACEI be stopped in CKD?

What other drug may be useful as an antihypertensive?

A
  • fall in GFR by 25%
  • rise in creatinine by 30%
  • GFR <15

Furosemide - has added benefit of lowering K - higher doses usually needed in CKD

100
Q

When to suspect renal vein thrombosis?

A

Flank pain and haematuria in background of nephrotic syndrome of hyper coagulable state

101
Q

When to suspect renal TB?

A

Symptoms of UTI
Sterile pyuria (i.e. leukocytes but no growth on MSSU)
Elevated CRP
No response to trimethoprim

102
Q

What diuretic should be used for ascites?

A

Spironolactone

103
Q

Dip shows +++ protein, ++ leukocytes and trace blood, no nitrites, is it likely IgA nephropaty, interstitial nephritis or UTI?

A

Interstitial nephritis

IgA nephropathy would cause more than trace blood
UTI would cause nitrites

104
Q

What electrolyte disturbance may be seen in nephrogenic DI?

A

Hypokalaemia
Hypernatraemia
Hypercalcaemia

105
Q

A few weeks post-renal transplant a patient presents feeling generally unwell and fatigued with anorexia and arthralgia. O/E jaundice and hepatomegaly. Widespread lymphadenopathy.

  • Cause?
  • Rx?
A

CMV - most common viral infection of solid organs

Rx: Ganciclovir

106
Q

Why do the first few dialysis sessions need to be short at around 90 mins?

A

To prevent dysequilibrium syndrome - the toxins which accumulate have osmotic potential, removing them all too quickly can cause oedema, cerebral oedema can lead to confusion, convulsions and death

107
Q

Differentials and respective Ix when someone presents in AKI with no Hx of note ie no signs of sepsis/hypovolaemia? (7)

A

Sepsis - blood and urine culture, suptum if expectorating

Obstruction - inflow/outflow? Renal tract imaging

Acute GN - pANCA, cANCA, Complements (C3&C4), CTD screen, anti-GBM, PLA2 (membranous nephropathy)

Tubulointerstitial nephritis - recent doxy/clarith/omeprazole/naproxen?

Myeloma - Serum Ig and protein electrophoresis, urinary BJP

Thrombotic microangiopathy - HUS/TTP? DIC? Haemolysis screen - film, haptoglobins, reticulocyte count, LDH

ESRF - chronic? Check PTH, iron studies, haematinics, kidney size and appearance
HELLP if pregnant?

Nephrotoxic drugs? OTC nephrotoxins (NSAIDs, alcohol, illegal drugs)

Acute renal artery stenosis? USS/CT angio
(difference in size >1.5cm suggestive of potential RAS)

108
Q

Below which eGFR should patients not be given bisphosphonates?

A

35

109
Q

Protective /prophylactic medication given with steroids/cyclophosphamide for GN?
Other than cyclophosphamide what else can be given as immunosuppression?

A

Adcal D3 (osteoporosis)
Omeprazole (gastritis)
Co-trimoxazole (pneumocystis jirovicii)

usually given for 6 months-3 years

Rituximab

110
Q

What chronic conditions give enlarged kidneys instead of small ones? (4)

A

ADPKD
Diabetic nephropathy
HIV-associated nephropathy (IVDU)
Amyloidosis

111
Q

What biochemical disturbance points to chronic rather than acute kidney disease?

A

Low Ca (due to low VitD)

112
Q

Classic presentation of henoch schonlein purpura?

A
Purpuric rash
Haematuria
Abdo pain
Joint pain
Raised WCC and ESR
113
Q

Plasma and urine osmolality and sodium levels in pre-renal and renal AKI?
How can you tell if it’s post-renal?

A

Pre-renal:

  • try to retain sodium and water, so:
  • urine osmolality high, urine Na low

Renal:

  • loss of ability to concentrate urine or retain sodium, so:
  • urine osmolality low, urine Na high

(most common = ATN due to hypoxia/toxins, rarer causes are acute GN and acute IN)

Post-renal:
Hydronephrosis on renal USS

114
Q

In what people may eGFR be inappropriately low?

A

Bodybuilders in extremes of muscle mass

115
Q

Treatment of hyper acute kidney transplant rejection?

A

Removal of transplant

116
Q

How to guess from U&E if AKI is pre-renal or renal?

A

Pre-renal: raised urea:creatinine ratio

Renal: normal