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Renal Flashcards

1
Q

How is AKI defined by KDIGO?

A
  • increase in serum creatinine by >0.3mg/dL in 48hr
  • increase in serum creatinine to >1.5x baseline, known or presumed to have occurred in the past 7 days
  • urine output <0.5ml/kg/hr for six hours
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2
Q

How do KDIGO classify the stages of AKI?

A
  • based on SCr or urine output (whichever is worst)
  • stage 1: SCr 1.5-1.9x baseline or UO <0.5ml/kg/hr for 6-12 hours
  • stage 2: SCr 2-2.9x baseline or UO <0.5ml/kg/hr for >12 hours
  • stage 3: SCr >3x baseline or UO <0.3ml/kg/hr for 24 hours or anuria for >12 hours
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3
Q

What meds should be withheld is AKI is suspected?

A
  • nephrotoxins
  • hypotensives
  • diuretics
    (DAMN-AKI mnemonic)
  • diuretics
  • ACEi / ARBs
  • metformin
  • NSAIDs
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4
Q

How can causes of AKI be classified?

A
  • prerenal: decreased perfusion to the kidney
  • intrinsic: renal disease
  • postrenal: obstruction to the urine flow
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5
Q

How common is AKI?

A
  • 18% of hospital patients

- up to ~50% of ICU patients

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6
Q

What are the risk factors for AKI?

A
  • CKD
  • age
  • male sex
  • comorbidities e.g.DM, CVD, malignancy liver disease)
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7
Q

What are the most common causes of AKI?

A
  1. Sepsis
  2. Major surgery
  3. Cardiogenic shock
  4. Other hypovolaemia
  5. Drugs
  6. Hepatorenal syndrome
  7. Obstruction
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8
Q

What are the key factors to manage in AKI?

A
  • fluid balance
  • acidosis
  • hyperkalaemia
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9
Q

How would you manage hyperkalaemia in AKI?

A

1) calcium gluconate or calcium chloride IV until ECG normalises (cardioprotective because it stabilises the membrane but it doesn’t actually treat K+ level)
2) IV insulin in glucose OR salbutamol nebs
3) if underlying pathology cannot be corrected then renal replacement therapy may be indicated

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10
Q

In those with existing renal disease NSAIDs and ACEi can interact to cause an AKI, how does this happen?

A
  • NSAIDs constrict the afferent arteriole
  • ACEi dilate the efferent arteriole
  • result is decreased filtration
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11
Q

How would you investigate a patient with AKI after they had been stabilised?

A
  • urine dip (pre-catheter)
  • USS KUB
  • LFTs
  • platelets plus a blood film if low
  • specific tests for intrinsic renal disease if indicated (e.g. Igs, paraproteins, autoantibodies etc)
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12
Q

What stages form the immediate management of AKI?

A

Look for life threatening complications:

  • examine: HR, BP, JVP, cap refill, palpate bladder - calculate NEWS
  • pulmonary oedema?
  • VBG for K+

Treat hypovolaemia:

  • initial fluid challenge
  • fluid management (consider catheter and hourly UO measurements)

Observations:

  • every 4 hours as minimum
  • more frequently if clinically indicated

Investigations:

  • check K+ at least daily until creatinine falls
  • daily creatinine until it decreases
  • check lactate if signs of sepsis
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13
Q

Which drugs interfere with renal perfusion?

A
  • ACEi
  • ARBs
  • NSAIDs
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14
Q

Which drugs require dose reduction or may be unsuitable for patients with renal disease?

A

All medications that are metabolised and excreted by the kidneys (~20% of meds, mainly water soluble ones) including:

  • fractioned heparins
  • opiates
  • penicillin-based antibiotics
  • sulphonylurea-based OHAs
  • aciclovir
  • metformin
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15
Q

Which drugs require closer monitoring in renal disease?

A
  • warfarin
  • aminoglycosides (e.g. gentamicin)
  • lithium
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16
Q

Which drugs can aggravate hyperkalaemia?

A
  • trimethoprim
  • spironolactone
  • amiloride
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17
Q

Do loading doses need dose adjustment in patients with renal disease?

A

Not usually, especially if it’s important to get to the therapeutic dose quickly

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18
Q

If a patient has renal disease, what figures should you use to calculate their dose adjustment?

A
  • eGFR

- if unknown then assume <10ml/min/1.73m2

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19
Q

What are the potentially fatal complications of renal failure?

A
  • hyperkalaemia
  • pulmonary oedema
  • intravascular volume depletion
  • uraemic encephalopathy
  • pericardial effusion
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20
Q

What are the functions of the kidney?

A
  • elimination of waste products
  • electrolyte homeostasis
  • acid base balance
  • fluid balance and BP control
  • metabolism of vitamin D
  • endocrine (EPO, vitD, RAAS)
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21
Q

What are the ECG signs that are indicative of hyperkalaemia?

A
  • tall, tented T waves
  • wide QRS
  • sine wave pattern
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22
Q

What clinical methods can be used to assess intravascular volume?

A
  • body weight
  • skin turgor
  • postural BP
  • mucosal membrane hydration
  • JVP
  • lung base sounds
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23
Q

What are the main complications of CKD?

A
  • anaemia
  • renal bone disease
  • acidosis
  • hypertension
  • malnutrition
  • uraemia
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24
Q

What are the categories of CKD as classified by GFR?

A 
>90 = G1
60-89 = G2
45-59 = G3a
30-44 = G3b
15-29 = G4
<15 = G5
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25
Q

What are the categories of CKD as classified by ACR?

A 
<3 = A1
3-30 = A2
>30 = A3
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26
Q

What are the negative impacts of chronic dialysis on a patient?

A
  • heavy time burden
  • high morbidity of psychological illness
  • limitation on travel
  • diet restrictions
  • complications can result in frequent hospital admissions
  • home dialysis may require changes to the home and requires another person to be present during dialysis
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27
Q

What is the triad of nephrotic syndrome?

A
  • proteinuria (>3g/day)
  • hypoalbuminaemia
  • oedema
  • hypercholesterolaemia and hyperaldosteronism are secondary phenomena
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28
Q

What symptoms form nephritic syndrome?

A
  • haematuria
  • proteinuria
  • mild hypertension
  • reduced urine output (<300ml/day)
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29
Q

What investigations can show proteinuria? Which are preferred?

A
  • dipstick
  • albumin/creatinine ratio (preferred screening test)
  • protein/creatinine ratio (used for monitoring proteinuria in patients with established proteinuria)
30
Q

What are the potential consequences of loss of function of the glomerular basement membrane?

A
  • protein loss

- blood loss

31
Q

What are the most common causes of nephrotic syndrome in children?

A
  1. minimal change glomerulonephritis

2. focal segmental glomerulosclerosis

32
Q

What are the most common causes of nephrotic syndrome in adults?

A
  • membranous glomerulonephritis
  • IgA nephropathy
  • Diabetic nephropathy
  • SLE
  • Amyloidosis
33
Q

Describe minimal change glomerulonephritis

A
  • patient has nephrotic syndrome
  • light microscopy would show all normal glomeruli
  • electron microscopy would show fusion of podocyte foot processes and therefore loss of the filtration barrier
34
Q

What is the initial management for a child with nephrotic syndrome? Why?

A
  • steroid treatment without a biopsy
  • most children would have minimal change GN on histological sample
  • most minimal change GN responds to steroids
  • diagnosis is clinical and dependent on response as there is no histological diagnosis (steroid responsive nephrotic syndrome // relapsing nephrotic syndrome // steroid dependent nephrotic syndrome // steroid resistant nephrotic syndrome
35
Q

What is the next step in management for a child diagnosed with steroid resistant nephrotic syndrome?

A
  • biopsy (likely inherited podocyte protein abnormality or other cause of GN e.g. FSGS
36
Q

What is the prognosis for membranous glomerulonephritis in adults?

A
  • 1/3 spontaneous recovery
  • 1/3 persistent proteinuria
  • 1/3 progress to end stage renal failure (ESRF)
37
Q

What is the most common cause of membranous glomerulonephritis?

A
  • autoimmune response
38
Q

What underlying diseases may be associated with membranous glomerulonephritis?

A
  • adenocarcinoma (lung or GI)
  • hepB
  • SLE (Class V lupus nephritis)
39
Q

The use of which drugs have been associated with membranous glomerulonephritis?

A
  • gold/penacillamine
40
Q

What kind of treatment may be helpful in membranous glomerulonephritis?

A
  • immunosuppressants
41
Q

How is IgA nephropathy diagnosed?

A
  • biopsy with fluorescent anti-IgA staining of biopsy specimen
42
Q

What is the classical presentation of IgA nephropathy?

A
  • visible haematuria
  • 1 to 2 days after URTI
  • in younger patients
43
Q

What factors worsen the prognosis of IgA nephropathy?

A
  • proteinuria
  • hypertension
  • scarring on biopsy
  • male
  • abnormal renal function
44
Q

What is the prognosis for patients with IgA nephropathy?

A
  • very variable
  • can be relatively benign
  • 36% of patients progress to end stage renal failure or death within 20 years
45
Q

What is Alport’s syndrome?

A
  • genetic disorder affecting Type IV collagen
  • can be x-linked so severity in men > women
  • generally presents in childhood with: haematuria, proteinuria, progressive renal failure, sensorineural deafness, anterior lenticonus
46
Q

What are the common causes of nephritic syndrome in children?

A
  • haemolytic uraemia syndrome
  • henoch-schonlein purpura
  • post-streptococcal glomerulonephritis (most common)
47
Q

What are the common causes of nephritic syndrome in adults?

A
  • Goodpasture’s*
  • ANCA-associated vasculitis*
  • SLE
  • primary or secondary mesangiocapillary glomerulonephritis

*most common

48
Q

Describe the typical presentation, histology, management and prognosis of post-streptococcal glomerulonephritis

A
  • haematuria 10-14 days post streptococcal throat infection
  • diffuse, global, proliferative glomerulonephritis
  • supportive care
  • spontaneous recovery
49
Q

Describe the typical presentation, histology, serology, management and prognosis of rapidly progressive glomerulonephritis

A
  • AKI (days to weeks)
  • crescentic glomerulonephritis and vascular necrosis
  • antineutrophil cytoplasmic antibodies (ANCA): two forms cANCA and pANCA
  • steroids/cyclophosphamide +/- plasma exchange
  • rituximab may also be used
  • early treatment = better outcome
50
Q

What is the eponymous name for antiglomerular basement membrane antibody disease?

A

Goodpasture’s

51
Q

Describe the typical presentation, histology, serology, management and prognosis of antiglomerular basement membrane antibody disease

A
  • AKI +/- pulmonary haemorrhage
  • crescentic glomerulonephritis, linear IgG deposition along basement membrane
  • anti-GBM antibody +ve
  • treat with steroids / cyclophosphamide / plasma exchange
  • early treatment = better outcome
52
Q

What is another name for mesangiocapillary glomerulonephritis?

A
  • membranoproliferative glomerulonephritis
53
Q

Give examples of causes of mesangiocapillary glomerulonephritis

A
  • infection
  • collagen vascular disease
  • monoclonal gammopathies
  • genetic and acquired complement disorders
54
Q

What is the eponymous name for the amorphous histological features in the glomerulus, common in diabetic nephropathy?

A
  • Kimmelsteil-Wilson lesions
55
Q

What histological stain would confirm a diagnosis of glomerular amyloidosis?

A
  • congo red stain
56
Q

What diseases commonly underlie AA amyloidosis?

A
  • chronic inflammatory conditions e.g. RA, Crohn’s, ankylosing spondylitis
  • chronis pyogenic infections e.g. bronchiectasis, osteomyelitis
57
Q

What is AA amyloidosis also known as?

A
  • secondary amyloidosis
58
Q

What is primary amyloidosis associated with?

A
  • AL amyloid
  • multiple causes e.g. myeloma, lymphoma
  • 90% of patients have paraprotein in blood or urine
59
Q

Which organs are predominantly affected by AA amyloidosis and AL amyloidosis?

A
  • AA = kidneys

- AL = kidneys and heart

60
Q

Pros of kidney transplant?

A
  • removes or alleviates burden of dialysis
  • improves renal clearance (dialysis GFR usually only ~10ml/min)
  • restores endocrine functions of kidney (e.g. EPO production, hydroxylation of vitD)
  • improves patient life expectancy (if patients are appropriately selected)
61
Q

Cons of kidney transplant?

A
  • significant peri-operative mortality risk: ~2% but higher with comorbidity (particularly due to cardiovascular risk and sepsis)
  • lifelong burden of immunosuppression (risk of infections, risk of cancers (esp non melanoma skin ca, cervical ca, lymphoma), risk of new-onset post-transplant diabetes = 12-20%)
62
Q

What are the contraindications for renal transplant?

A
  • active infection
  • active cancer
  • short life expectancy due to other conditions
  • circumstances which are likely to make post-transplant care challenging e.g. previous non-compliance with follow-up/treatment, active drug ‘misuse’, uncontrolled major psychiatric disorders, chaotic lifestyle including homelessness or frequent moves out of area
63
Q

What are the sources of kidney transplants?

A

Cadaveric donor:
- deceased, brain dead (DBD)
- deceased, cardiac death (DCD)
Living donor:
- related e.g. blood relative, spouse, friend, colleague
- unrelated e.g. paired/pooled system match, altruistic donor

64
Q

What’s the average waiting list time for kidney transplantation?

65
Q

Which transplant immunosuppressants act on Calcineurin?

A
  • tacrolimus

- cyclosporine A

66
Q

Which transplant immunosuppressants inhibit de novo purine synthesis?

A
  • azathioprine

- mycophenolate

67
Q

Which transplant immunosuppressant targets mTOR?

A
  • sirolimus (rapamycin)
68
Q

What is the target of the Daclizumab?

69
Q

Which complex presents alloantigens from APCs to T cells?

70
Q

What is the role of Calcineurin in T cell activation?

A
  • dephosphorylates NFAT
  • complexes with NFAT and translocates to the nucleus
  • unregulated transcription of pro-inflammatory cytokines including IL-2

0Finals Revision (21 decks)

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