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Clinical > Renal > Flashcards

Renal Flashcards

1
Q

What are the hallmarks of a nephrotic syndrome?

A

Proteinuria, peripheral oedema, and hypoalbuminaemia.

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2
Q

Why might a nephrotic syndrome cause a hypercoagulable state?

A

Increased protein excretion includes loss of anticoagulants.
Increases risk of VTE.

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3
Q

Why can nephrotic syndromes cause Secondary Hyperaldosteronism?

A

Decreased circulating fluid = decreased renal perfusion = upregulation of RAAS

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4
Q

A membranous nephropathy causes deposition of immune complexes where in the kidney?

A

Subepithelial layer of Glomerular base membrane.

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5
Q

Risk factors for membranous nephropathy?

A

Adults age 40-60, hep B and C, drugs (penicillamine, NSAIDs), other autoimmune conditions (SLE) and malignancies (colon, lung, breast).

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6
Q

What do you see on microscopy of the glomeruli in a membranous nephropathy?

A

Thickening of basement membrane and silver spikes on staining.

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7
Q

How do pts present with minimal change disease?

A

Often in children post URTI.
Oedema, proteinuria.

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8
Q

How can you view changes in minimal change disease?

A

Electron microscopy

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9
Q

Who is focal segmental glomerulosclerosis seen in most commonly?

A

Afro-Caribbean descent, hx of other disease such as Berger’s, sickle cell, and HIV.

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10
Q

What proportion of minimal change disease pts progress to to end-stage renal failure?

A

1%

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11
Q

What proportion of focal segmental-glomerulosclerosis pts progress to to end-stage renal failure?

A

30-50%

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12
Q

What proportion of membranoproliferative glomerulonephritis pts progress to to end-stage renal failure?

A

50%

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13
Q

What co-morbidities are associated with membranoproliferative glomerulonephritis?

A

Hep b and C, and endocarditis

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14
Q

Which medications are associated with acute interstitial nephritis?

A
  • Antibiotics: B-lactams, cephalosporins, rifampicin, fluoroquinolones,
  • Others: NSAIDs, diuretics, allopurinol, PPIs.
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15
Q

What is the typical presentation of acute interstitial nephritis? What do you seen in urine microscopy?

A
  • Urinary sx: haematuria, worsening renal function.
  • Non Urinary sx: Rash, fever, eosinophilia,
  • Microscopy: White casts.
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16
Q

What causes post-streptococcal glomerulonephritis?

A

Group A beta haemolytic strep most commonly.

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17
Q

How does post-streptococcal glomerulonephritis present? What happens to C3 levels?

A

3 weeks post infection with haematuria, proteinuria, HeTN.
Often decreased C3 levels in serum due to deposition.

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18
Q

What do you see on electron microscopy of post streptococcal glomerulonephritis?

A

IgG and C3 subepithelial deposition

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19
Q

Rapidly progressing glomerulonephritis is also known as what? Why?

A

Crescentic glomerulonephritis - you get epithelial crescents in the glomeruli.

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20
Q

What type of acidosis is seen in renal tubular acidosis?

A

normal anion gap metabolic acidosis

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21
Q

What is the problem in Type 1 renal tubular acidosis? What happens to the urine pH and serum K+?

A

Distal: Poor hydrogen secretion into urine, generally caused by genetic disorders, medication toxicity, or obstruction such as with renal stones.
pH >5.5 and K+ high-normal

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22
Q

What sx are seen in Type 1 renal tubular acidosis?

A

Muscle weakness, hyperventilation, cardiac arrhythmias, bone pain.

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23
Q

What is the problem in Type 2 renal tubular acidosis? What happens to urine pH and serum K+?

A

Proximal: Poor bicarb reabsorption, most commonly caused by Fanconi syndrome.
Urine pH <5.5, low to normal K+.

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24
Q

What are the key sx of Type 2 renal tubular acidosis?

A

Polyuria, polydipsia, proximal myopathy.

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25
Q

What is the problem in Type 4 renal tubular acidosis? What happens to urine pH and serum K+?

A

Aldosterone resistance most commonly caused by obstructive uropathy and congenital syndromes.
Urine pH <5.5,
High serum K+.

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26
Q

What are the main sx of Type 4 renal tubular acidosis?

A

Dizziness, infrequent urination.

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27
Q

What is the problem in Type 3 renal tubular acidosis?

A

Hyporeninaemic hypoaldosteronism: mixed type 1 and 2 - very rare.

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28
Q

What are the boundaries for eGFR in each CKD stage?

A

45-59: stage 3a
30-44: stage 3b
15-29: stage 4
<15: stage 5

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29
Q

What are the supporting factors for CKD in a pt with a GFR >60?

A

Biopsy proven glomerulonephritis, persistent albuminuria, proteinuria, or haematuria, and hereditary PKD

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30
Q

What are the eGFR ranges for CKD?

A

Stage 3a: 45-59
Stage 3b: 30-44
Stage 4: 15-29
Stage 5: <15

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31
Q

What are the ACR (albumin: creatinine ratio) ranges for CKD?

A

A2: 3-30
A3: >30

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32
Q

What causes albuminuria?

A

Damage to the glomerular filtration barriers allows leakage of albumin.
This is the smallest protein so is an early sign of damage.

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33
Q

What dose of statin is given to CKD pts? Why? What if their GFR is very low?

A

20mg/day as CKD pts have increased CV risk.
If their GFR is extremely low, can give bempoic acid instead as this is metabolised in the liver.

34
Q

What is the target Haemoglobin for CKD pts?

A

100-120 as higher than this can cause complications.

35
Q

What do you prescribe for CKD pts instead of bisphosphonates?

A

Denosumab

36
Q

Why do CKD pts experience hypocalcaemia and secondary hyperparathyroidism?

A

They have reduced calcidiol levels. This is a metabolite of cholecalciferol which promotes active transport of calcium from the gut.
Without it, you get hypocalcaemia.
Cholecalciferol supresses PTH, with less of it you become hyperparathyroid.

37
Q

What are the signs/sx of hypercalcaemia? Mx?

A

Hyper = Ca >2.65
- Stones: renal stones
- Bones: steoporosis and fractures
- Groans: GI sx due to reflux and pancreatitis
- Moans: Neuropsychiatric manifestations,
Mx: IV fluids, bisphosphonates, treat underlying cause.

38
Q

What is the physiological response to hypercalcaemia?

A

Parafollicular cells release calcitonin to inhibit osteoclastic activity and increase renal excretion of Ca and phosphate.

39
Q

Why can CKD pts become hyperkalaemic?

A

K+ is renally excreted, if they are not functioning properly, it can build up.

40
Q

What are the 3 types of AKI?

A

Pre-renal: shock, renovascular disease.
Renal: dysfunction of glomeruli, tubules, interstitium, or vessels.
Post-renal: obstructive AKI which can be intra-renal (uric acid nephropathy) or extra-renal (stones).

41
Q

How do we stage AKI?

A

Stage 1: creatinine 1.5x baseline OR urine output <0.5ml/kg/hr over 6 hours
Stage 2: creatinine 2x baseline OR urine output <0.5mls/kg/hr over 12 hours
Stage 3: creatinine 3x baseline OR creatinine >354 OR urine <0.3mls/kg/hr for 24 hours OR anuria for 12 hours.

42
Q

What is the most common cause of renal AKI?

A

Acute tubular necrosis

43
Q

What is acute tubular necrosis?

A

Prolonged ischaemia to kidneys causes toxicity to the tubular epithelium.

44
Q

What are some causes of acute tubular necrosis?

A

Drugs: aminoglycosides
Ethylene glycol poisoning
Long lies

45
Q

What is seen on urinalysis for acute tubular necrosis?

A

Granular, muddy brown casts

46
Q

What are the main 3 components of haemolytic uremic syndrome?

A

Haemolytic anaemia, thrombocytopenia, AKI.

47
Q

What pathogen is most commonly associated with HUS?

A

E.coli 0157:H7

48
Q

What are the indications for dialysis in AKI?

A

AEIOU: acidosis (<7.2), electrolyte imbalance (K+ >7), intoxication (poisoning), oedema (refractory pulmonary oedema), uraemia (encephalitis, pericarditis).

49
Q

What is uraemia?

A

The clinical syndrome as a result of high uric acid.

50
Q

What are the most common sx of uraemia?

A

N+V, itching, tiredness, muscle cramps

51
Q

What are the serious complications of uraemia?

A

Pericarditis and encephalopathy

52
Q

Hyperphosphatemia can be caused by reduced kidney function, what are the complications?

A

Cardiovascular tissue calcification, bone disease, secondary hyperparathyroidism.

53
Q

How can we manage hyperphosphataemia?

A

Calcium acetate: binds to phosphate to be excreted.

54
Q

How does vesicoureteral reflux cause worsening renal function?
How is it investigated?

A

Recurrent UTIs cause inflammation and damage to renal parenchyma which causes scarring of the kidney and deterioration in function.
Micturating cystography.

55
Q

Why are renal artery sclerosis pts CI to using ACEis and ARBs?

A

Both these medications dilate the efferent arteriole.
Normally the body then constricts the afferent to maintain eGFR.
However, in these pts, the afferent is already narrowed so this worsens this narrowing.

56
Q

What is the effect of fibromuscular dysplasia on the kidneys?

A

Renal arteries become stenosed so pts may may present with HeTN and real bruits.

57
Q

What demographic is fibromuscular dysplasia most commonly seen in?

A

Young women

58
Q

What is an angiomyolipoma? When should they be treated?

A

Benign tumour of the kidney.
>4cm due to bleeding risk.

59
Q

What is reflux nephropathy?
Who does it present in?

A

Retrograde flow of urine from bladder into ureters. Causes raised creatinine and urea.
Women of childbearing age.

60
Q

ADPKD is caused by what mutation?

A

Chromosome 16 of PLD1 gene.

61
Q

How does ADPKD present?

A

Loin/abdo pain, painless haematuria, HeTN, urinary frequency, renal colic.

62
Q

What are the extra-renal effects of ADPKD?

A

Hepatic cysts, cerebral aneurysms, pancreatic cysts, valvular regurgitation, diverticular disease, hernias.

63
Q

How does renal cell carcinoma present?

A

Haematuria, flank pain, flank mass.
Also get varicoceles in males due to interrupted lymphatic drainage.

64
Q

Where do mets spread in a renal cell carcinoma?

A

Blood vessels then lymph nodes.

65
Q

What happens in a scleroderma renal crisis?

A

Abrupt onset of HeTN and decline in renal function.
Can lead to hypertensive encephalopathy, congestive heart failure, and microangiopathic haemolytic anaemia.

66
Q

What is the management of a scleroderma renal crisis?

A

ACEis

67
Q

What is Goodpasrure’s Syndrome?

A

Anti-GBM disease causing renal and pulmonary pathology: haemoptysis, pulmonary haemorrhage, and severe AKI.

68
Q

What is the management for Goodpasture’s?

A

High dose corticosteroids, cyclophosphamide, and plasmapheresis.

69
Q

What is the presentation of IgA nephropathy?

A

Haematuria proteinuria, and HeTN.
If it presents after URTI it is known as Berger’s syndrome.

70
Q

How is IgA nephropathy managed?

A

ACEi or ARB, may also need steroids.

71
Q

What are the manifestations of hypocalaemia?

A

SPASMODIC:
- Spasms (elicited by trousseau’s sign: inflated BP cuff around arm)
- Perioral paraesthesia
- Anxiety/irritability
- Seizures
- Muscle tone increase
- Orientation impairment
- Dermatitis
- Impetigo herpetiformis
- Chvostek’s sign (facial nerve tap = facial contraction)

72
Q

What is a pseudo hyponatreamia?

A

low sodium (<135) but normal serum osomolality (>275).
Caused by hyperlipidaemia, paraproteinemia, high blood glucose, use of mannitol/glycine.

73
Q

What happens if you replace sodium too quickly?

A

Central pontine myelinolysis (damage to the myelin sheath of the pons):
- confusion, delirium, hallucinations
- balance instability, tremor
- dysphagia
- reduced consciousness, lethargy, poor responses
- slurred speech
- weakness usually affecting arms, legs, face on both sides of the body

74
Q

How is UTI diagnosed on MSU?

A

E.Coli (normally) 10^5 colony forming units/mL of pure growth bacteria

75
Q

Recurrent UTIs due to proteus is a RF for what?

A

Struvite stones: staghorn calculi

76
Q

How do you treat pseudomonal UTIs?

A

Gentamicin or quinolones

77
Q

What medications are given post renal transplant?

A
  • Induction antibodies (basiliximab)
  • Corticosteroid (prednisolone)
  • Calcineurin inhibitor (tacrolimus)
  • Anti-proliferative agent (mycophenolate mofetil)
78
Q

In which pts with ADPKD do you screen for aneurysms? How/When?

A
  • Known aneurysm
  • Familial hx of SAH/aneurysms
    Every 5 years with MRA
79
Q

What is the most common cause of nephrotic syndrome in a non-diabetic adult?

A

Membranous nephropathy.

80
Q

How do you manage membranous nephropathy?

A
  • ACEi/ARB
  • Corticosteroid + cyclophosphamide in advanced cases
81
Q

What is the prognosis for membranous nephropathy? (Rule of 1/3s)

A
  • 1/3 spontaneously resolve
  • 1/3 persistent proteinuria
  • 1/3 progress to end stage CKD
82
Q
A

Clinical (27 decks)

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