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Phase 4 > Renal > Flashcards

Renal Flashcards

1
Q

Where in the kidney is most of the filtered Na reabsorbed?

A

Proximal convoluted tubule

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2
Q

How does RAAS system work to raise BP?

A

Renin produced by juxtraglomerular apparatus- triggered by a low BP/decreased Na. It converts angiotensinogen to angiotensin I. ACE converts angiotensin I to angiotensin II which produces aldosterone. This reabsorbs Na and water in the kidney and vasoconstricts to raise the BP.

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3
Q

What is the definition of a stage 1 AKI?

A

Creatinine rise >26umol/L in 48h or 1.5 x from baseline.

AND Urine output <0.5ml/kg/hour for > 6hours

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4
Q

What is the definition of a stage 2 AKI?

A

Creatinine rise 2 x baseline AND urine output <0.5ml/kg/hour for >12 hours

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5
Q

What is the definition of stage 3 AKI?

A

Creatinine rise 3 x baseline AND urine output <0.3ml/kg/hour >24 hours or anuria >12 hours

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6
Q

What are the causes of AKI? And the headings they fall under?

A

Pre renal:

  • Hypovolaemia - dehydration, shock, sepsis
  • Heart failure (hypervolaemia)
  • Renal artery stenosis

Renal:

  • Acute tubular necrosis
  • Rhabdomyolysis
  • Acute interstitial nephritis- NSAIDs
  • Drugs- DAMN- diuretics (furosemide, thiazide, spironolactone- causes a hyperK–> AKI), ACEi, metformin, NSAIDs, contrast, anticonvulsants eg. lamotrigine and valproate, lithium,
  • Glomerulonephritis
  • Vasculitis

Post-renal:
-Obstruction: ureteric/renal calculi, tumour (bladder/ureter), infection, enlarged prostate

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7
Q

What happens in acute tubular necrosis? What is the cause?

A

Cause is prolonged hypoperfusion/prolonged use of nephrotoxic drugs. The potassium and hydrogen ions don’t filter through into the urine- so they create an acidosis which causes tubules to die.

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8
Q

What are the causes of rhabdomyolysis?

A 
Prolonged immobilisation after a fall
Crush injury 
Burns
Trauma
Embolism
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9
Q

What signs may you see in a patient with rhabdomyolysis?

A

Brown coloured urine, muscle pain, swelling

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10
Q

What investigations would you do in a patient with suspected rhabdomyolysis?

A

Creatinine kinase- raised
U&Es- AKI?
Phosphate- raised and potassium- raised

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11
Q

How do you treat rhabdomyolysis?

A

Treat the hyperkalaemia- calcium gluconate and insulin + dextrose
IV fluids
Catheterise
IV sodium bicarbonate

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12
Q

What is the biggest cause of acute interstitial nephritis?

A

NSAIDs

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13
Q

What are the symptoms to ask about in a patient with an AKI?

A

Dehydration- oliguria, dizziness, dry mucous membranes
Abdominal pain (loin to groin if stones)
Nausea and vomiting
LUTS symptoms- frequency, hesitancy, straining, urgency- prostate cancer/BPH
Weight loss, night sweats - malignancy
Rashes, joint pains, fevers- renal cause (vasculitis, glomerulonpehritis)
Recent illness
Previous AKI
MEDICATIONS
FMH- kidney failure? Polycystic kidneys?
Sx of hyperkalaemia- muscle cramps/weakness, respiratory distress, decreased reflexes

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14
Q

What investigations would you do in a patient who’s coming in with oliguria, abdominal pain and a raised creatinine? He has been taking ibuprofen for his back pain for a year now and sometimes takes too much.

A

Suspecting AKI

  • urine dip and MC&S (rule out urinary sepsis): if renal cause- protein and blood
  • Bloods- FBC (infection), U&Es (monitor creatinine, dehydrated?), LFTS, CRP, clotting, Na and K (hypo Na, hyper K), Ca, phosphate, creatinine kinase
  • ECG- hyperkalaemia (kidneys usually reabsorb Na and excrete K)
  • May do ABG for hyperkalaemia
  • If suspected obstruction- USS KUB - anuria
  • Later on- Autoimmune profile (anti-dsDNA-SLE, ANCA- granulomatosis with polyangiitis, anti-GBM- good pastures)
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15
Q

What would you treat a patient who was in AKI? and hyperkalaemia?

A

Catheterise - monitor fluid balance
Stop nephrotoxic drugs
Regular U&Es - daily
Treat cause:
- Pre renal: IV fluids- monitor, IV Abx - sepsis
-Obstruction: USS KUB and may need nephrostomy
-Hypervolaemia (HF)- fluid restrict and IV furosemide
- Treat hyperkalaemia- IV 10ml of 10% calcium gluconate, IV insulin (actrapid) + dextrose, nebs salbutamol

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16
Q

If a patient was in AKI- when would you refer for dialysis/to the renal team?

A 
Refractory hyperkalaemia
Refractory pulmonary oedema
Severe metabolic acidosis
Uraemia complications- encephalopathy, pericarditis, seizures
Drug overdose
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17
Q

What is the definition of CKD?

A

Imapired kidney function for >3 months (based on abnormal kidney results- proteinuria) or eGFR <60ml/min/1.73m2.

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18
Q

Name 5 causes of CKD?

A

Glomerulonephritidies- IgA nephropathy, membranous, SLE
Diabetes
Hypertension
AKI
Obstruction- stones, prostatic hyperplasia
Polycystic kidney disease
Pyelonephritis

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19
Q

What would you ask in a history in a patient with CKD?

A

Symptoms- changes in urine output? Abdominal pain? LUTS symptoms- frequency, urgency, hesitancy, poor steam? signs of overload- SOB, ankle oedema. Uraemic symptoms- confusion, vomiting, asteriks tremor, seizures
Cause- well controlled diabetes? well controlled HTN? recent UTI?
Medication review

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20
Q

What would you look for on examination in a patient with CKD?

A

Uraemia- yellow skin, flapping tremor,
Pallor - anaemia
Fluid overload (complication of CKD) - ankle oedema, consolidation in lungs
Ballotable kidneys- polycystic kidneys

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21
Q

What investigations would you do in a patient with CKD?

A

Urine dip- proteinuria, haematuria?
Albumin: creatinine ratio
Bloods- FBC- anaemia?, U&E- monitor regularly, clotting, glucose, low calcium & high phosphate, high PTH (tertiary hyperPTH- if CKD stage 3 higher), iron studies (needs to be done before giving EPO)
USS kidneys - usually small in CKD

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22
Q

How would you treat a patient with CKD?

  • How would you treat potential causes?
  • How would you limit complications? And what are these?
  • How would you treat symptoms eg. anaemia, oedema, acidosis
A

Treating cause:

  • Stop nephrotoxic drugs
  • Tighter control of diabetes and HTN
  • USS KUB and nephrostomy if obstruction
  • Stop smoking, healthy diet- low salt and phosphate

Limiting complications:

  • Renal osteodystrophy- check PTH. Tx: vitamin D and calcium supplements. Bisphophonates.
  • BP control - ACEi if <55 (best for proteinuria), >55 /black=CCB
  • Treat any hyperkalaemia
  • Statins- reduce cardiac risk

Treating symptoms:

  • Anaemia- IV Fe supplementation + B12, folate. IF this doesn’t work- EPO
  • Oedema- fluid restrict, furosemide
  • Acidosis- sodium bicarb
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23
Q

What is the last line if all the initial treatments of CKD don’t work?

A

Renal replacement therapy

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24
Q

What are the 3 types of RRT?

A

Haemodialysis
Peritoneal dialysis
Transplant

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25
Q

What are the benefits of peritoneal dialysis over Haemodialysis?

A

Haemodialysis- can be done at a centre or home. 3 times a week.
Peritoneal dialysis- can do it at home - allows patients more independence.

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26
Q

What needs to be done/given before a kidney transplant can go ahead?

A

Cross matching of organs- must be negative

Immunosuppresion has to be given- tacrolimus/ciclo, azathioprine/ mycophenolate, prednisolone

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27
Q

What complications can occur from kidney transplant?

A

Rejection, infection, thrombosis, bleeding

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28
Q

What is the main inheritance pattern of polycystic kidney disease?

A

Autosomal dominant

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29
Q

What are the main symptoms/signs of polycystic kidney disease?

A

Bilateral renal enlargement with fluid filled cysts
Hypertension
Abdominal pain
Haematuria- if cyst haemorrhages

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30
Q

What is the main extra-renal association of polycystic kidney disease? What test is used to screen for this?

A

Sub-arachnoid haemorrhage - screen with MRA

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31
Q

What investigations would you do for a patient with polycystic kidney disease?

A

Genetic screening - USS
Urine dip- proteinuria ? haematuria? infection ?
FBC, U&E, LFTs, clotting, potassium, eGFR
ULTRASOUND

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32
Q

How do you treat polycystic kidney disease?

A

Monitor U&Es regularly
Treat HTN - ACEi/ARB
If in end stage - transplant/dialysis
If severe pain: analgesia, laparoscopic cyst removal, nephrectomy

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33
Q

What are the cardinal symptoms/signs of nephrotic syndrome?

A

Hypoalbuminaemia
Oedema- periorbital, scrotal , leg, ascites
Proteinuria- frothy urine- loss of >3.5g in 24h
Hyperlipidaemia
Breathlesness- pleural effusions
Infections - loss of protective Ig in urine
DVT/PE- lose clotting factors in urine

34
Q

How does oedema develop in nephrotic syndrome?

A

Loss of albumin through leaky podocytes into urine (proteinuria), reduces the oncotic pressure so lose water to extravascular space –> oedema

35
Q

What are the causes of nephrotic syndrome? renal and extra-renal?

A

‘M’s
Renal- minimal change disease (kids), membranous nephropathy (adults) , focal segmental glomerulosclerosis, mesangiocapillary/membranoproliferative
Extra renal: diabetes, SLE, hepatitis B/C, drugs, myeloma

36
Q

What investigations are done in nephrotic syndrome?

A

Urine dipstick- proteinuria? albumin:creatinine ratio
Bloods- FBC, U&E, clotting, LFTs, hepatitis screen, autoantibodies
KIDNEY BIOPSY !

37
Q

How would you treat nephrotic syndrome? (think of the symptoms/signs)

A 
Oedema- fluid restrict, furosemide
Proteinuria - ACEi /ARB
Anticoagulate, treat infections promptly 
Stop nephrotoxic drugs
Treat underlying cause
38
Q

A patient presents with frothy urine, has not passed urine for 2 days and has noticed blood in her urine. Is this a nephritic or nephrotic syndrome?

A

Nephritic: haematuria, proteinuria, oliguria, HTN

39
Q

What are the causes of nephritic syndrome?

A

‘A’s
Renal:
Post- strep glomerulnephritis- ASOT +
IgA nephropathy - IgA +

Extra renal:
Granulomatosis with polyangitis - ANCA +
SLE- anti-dsDNA +
Goodpastures- antiGBM 
HSP
40
Q

What investigations would you do for nephrotic syndrome?

A

Urinalysis- proteinuria, RED CELL CASTS, haematuria

Bloods- FBC, U&E, LFTs, clotting, autoimmune profile,

41
Q

Does minimal change disease come under nephrotic or nephritic syndrome? and what features make it so?

A

Nephrotic- heavy proteinuria, no haematuria.

Oedema, hypoalbuminaemia

42
Q

What would you see on light microscopy in minimal change disease?

A

Nothing

43
Q

What would you see on electron microscopy in minimal change disease?

A

Podocyte effacement

44
Q

How do you treat minimal change disease?

A

Steroids- prednisolone

Diuetics- furosemide for the oedema

45
Q

Is membranous nephropathy a type of nephrotic or nephritic syndrome or mixed?

A

Nephrotic - heavy proteinuria, no haematuria.

Oedema, hypoalbuminaemia

46
Q

What demographic is affected by membranous nephropathy?

A

Caucasian adults

47
Q

What are some causes of membranous nephropathy?

A

Idiopathic
Malignancy - lung, colon
Connective tissue disorders- SLE,
Drugs

48
Q

What would you see on biopsy in membranous nephropathy?

A

Basement membrane thickening

49
Q

How do you treat membranous nephropathy?

A

Immunosuppression- steroids
Diuretics- oedema
ACE/ARB

50
Q

Is focal segmental glomerulosclerosis a type of nephrotic or nephritic syndrome or mixed?

A

Nephrotic- HOP - proteinuria, renal failure

51
Q

What demographic is affected by focal segmental glomerulosclerosis?

A

Black adults

52
Q

What are some causes of focal segmental glomerulosclerosis ?

A

Heroin abuse, HIV, sickle cell disease

53
Q

What would you see on biopsy in focal segmental glomerulosclerosis ?

A

Segmental areas of sclerosis

54
Q

How do you treat focal segmental glomerulosclerosis ?

A

Initially - steroids but commonly progresses to end stage renal failure
If steroid resistant: cyclophosphamide
ACEi/ARB

55
Q

Is mesangiocapillary/membranoproliferative GN nephrotic, nephritic or mixed?

A

Mixed picture- more commonly nephrotic.

56
Q

What is the most common cause of mesangiocapillary/membranoproliferative GN?

A

Hepatitis C & B

57
Q

What do you see on biopsy in mesangiocapillary/membranoproliferative GN ?

A

Double membrane - basement membrane thickening.

58
Q

How do you treat mesangiocapillary/membranoproliferative GN?

A

Treat underlying cause eg hepatitis
ACEi - proteinuria
Steroids- to stop progression

59
Q

Kimmelstein-Wilson nodules and Congo red staining negative are signs of what type of nephropathy?

A

Diabetic

60
Q

How do you treat diabetic nephropathy?

A

Monitor regularly for symptoms and urine dip for proteinuria etc
Tight control of diabetes
Tight control of HTN : ACE/ARB- proteinuria

61
Q

Apple green birefringence under polarised light on Congo staining and nodules are signs of what type of nephropathy?

A

Amyloid

62
Q

Is Goodpasture’s syndrome a type of nephritic, nephrotic of mixed picture?

A

Nephritic

63
Q

What antibodies are implicated in Goodpasture’s syndrome?

A

Anti-glomerular basement membrane- target type 4 collagen in b.m

64
Q

What would be seen on biopsy in Goodpasture’s syndrome?

A

Cresenteric picture

65
Q

What symptoms would a patient with Goodpasture’s syndrome present with?

A 
Haematuria
Proteinuria 
HTN 
Renal failure - crescenteric
Pulmonary haemorrhage- haemoptysis
66
Q

How do you treat Goodpasture’s syndrome?

A

Steroids
Plasma exchange
Immunosuppressants- cyclophosphamide

67
Q

What antibody is implicated in Granulomatosis with polyangiitis?

A

C-ANCA

68
Q

Is Granulomatosis with polyangiitis a type of nephrotic, nephritic or mixed picture?

A

Nephritic

69
Q

What symptoms do you get with Granulomatosis with polyangiitis?

A

Haematuria, proteinuria, HTN
Pulmonary haemorrhage - haemopytsis, SOB
Saddle nose- destroyed nasal septum, epistaxis, sinusitis
Otitis media

70
Q

How do you treat Granulomatosis with polyangiitis?

A

Steroids + cyclophosphamide

71
Q

What antibodies are implicated in SLE?

A

Anti-DsDNA, ANA+, anti-phospholipid

72
Q

What are the main symptoms of SLE?

A 
Malar, photosensitive rash 
Discoid rash 
Lupus nephritis- proteinuria, RBC casts/haeamturia, HTN 
Arthritis - joint pains 
Oral ulcers
73
Q

What is the diagnostic investigation for lupus nephritis?

A

Renal biopsy

74
Q

How do you treat SLE/lupus nephritis?

A

Steroids - pred
Cyclophosphamide/mycophenalate
Rituximab- if not responding to either

75
Q

A patient presents with a 2 week history of sore throat, cold symptoms. In the last two days, he has now noticed his urine being darker ‘coke coloured’ and he’s urinating less. What is the likely diagnosis?

A

Post-strep glomerulonephritis

2-3 weeks post group strep A infection

76
Q

What investigations would you do for a patient with post-strep glomerulonephritis?

A

ASOT +
Complement C3 levels low
FBC, U&Es, cultures
Urine - proteinuria, haematuria - RBC casts

77
Q

How would you treat post-strep glomerulonephritis?

A

Supportive

Treat the HTN, treat strep infection, if much oedema- diuretics

78
Q

A patient presents with a 3 day history of SOB, cough, fever and has now noticed dark coloured urine on occasion and slightly frothy. What is the likely diagnosis?

A

IgA nephropathy- 2/3 days post sore throat

Nephritic syndrome- EPISODIC haematuria and proteinuria

79
Q

What investigations would you do in a patient with IgA nephropathy?

A

Raised IgA
Raised ESR/CRP, FBC, U&Es, cultures
Renal biopsy- mesangial proliferation (IGA forms immune complexes and deposits in mesangium)

80
Q

How do you treat IgA nephropathy?

A

ACE/ARB - BP control works well

If still worsening- steroids/cyclophosphamide

81
Q

What is HSP?

A

Small vessel vascultiis- Systemic form of IgA nephropathy, ANCA -

82
Q

What symptoms do you get in HSP?

A

Arthritis + rash on buttocks/shins + abdo pain + haematuria

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