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Renal Flashcards

1
Q

Describe the RAAS system?

A

Angiotensinogen released by liver

RENIN enzyme secreted by kidneys converts Angiotensinogen to Angiotensin I

ACE enzyme secreted by the lungs conversts Angiotensin I to Angiotensin II

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2
Q

What does Angiotensin II do?

A
  • Vasoconstriction at arterioles - this increases calcium in cells
  • Noradrenaline release
  • Aldosterone release by adrenals –> Na reabsorption and K secretion in DCT and collecting ducts
  • ADH release –> increases water reabsorption at collecting ducts
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3
Q

In acute and chronic kidney patients, what should you use to measure function?

A

Acute - Serum creatinine

Chronic - eGFR

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4
Q

What are the three categories for AKI?

A

Pre-renal
Renal
Post-renal

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5
Q

What are the common pre-renal causes of AKI?

A

Anything that reduces blood flow to arteries:

  • Sepsis, Haemmorhage, Hypovolemia, heart failure
  • Renal Artery Stenosis
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6
Q

What are the common Renal causes of AKI?

A

Acute Tubular Necrosis (ATN)

      - Ischaemic ATN
      - Nephrotoxic - aminoglycoside ABs and cisplatin

Acute Intersititial Nephritis (AIN)
- Nephrotoxic - beta-lactam ABs, NSAIDs

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7
Q

what is DRESS syndrome?

A

Drug Rash with Eosinophilia and Systemic Symptoms

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8
Q

What drugs cause DRESS syndrome?

A

Anti-epileptics
Antibiotics - esp B-lactams
Allopurinol

NSAIDs
Captopril

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9
Q

Management of DRESS syndrome?

A

Stop offending drug and give steroids

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10
Q

What are some post-renal causes of AKI?

A

Anything that causes a blockage to outflow, such as tumours, clots, calculi –> causes cytokine release and leukocyte infiltration

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11
Q

Features of AKI?

A

Increased urea in blood causes:
general malaise, lethargy, pruritis, altered mental state, pericarditis

Hyperkalaemia causes:
palpitations, chest pain

Acidosis causes: kussmaul breathing, confusion

Fluid overload causes: oedema, breathless, raised JVP

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12
Q

What are the criteria for diagnosing AKI?

A

Rise in serum creatinine of 26.5 mmol/L or more within 48 hours

1.5x increase from baseline serum creatinine in the last 7 days

<0.5ml/kg/hour urine output for at least 6 hours

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13
Q

Management of AKI?

A

1) Fluid balance chart - consider catheter
2) Review medicines
3) Refer to Nephrologist if unresponsive or requires renal replacement therapy

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14
Q

When to refer for renal replacement therapy?

A

POAU

Potassium
Oedema
Acidosis
Uremia complications - pericarditis, encephalopathy

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15
Q

What is rhabdomyolosis?

A

When skeletal muscle breaks down and releases contents into bloodstream - particularly myoglobin, which is toxic to kidneys

Also causes high potassium and phosphatemia, and lower calcium in blood - as myoglobin binds to calcium and mops it up

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16
Q

Risk factors for rhabdomyolosis?

A

Anything that causes muscle death

Alcohol, DKA, trauma, long lie, compartment syndrome

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17
Q

Features of Rhabdomyolosis?

A

Red-brown urine
muscle pain and swelling
fever, nausea, vomiting

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18
Q

Electrolyte abnormalities in rhabdomyolosis?

A

high potassium and phosphate
low calcium
CK high (5x basline)

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19
Q

Treatment for rhabdomyolosis?

A

FLUIDS! - normal saline or lactated Ringer’s

Correct electrolytes if life-threatening hyperpotassium or hypocalcaemia

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20
Q

When to consider haemodialysis in rhabdomyolosis?

A

If not urinating at all or if no response to fluids first

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21
Q

What is the definition of CKD?

A

Kidney damage for 3 or more months, secondary to structural disorders

eGFR <60 on two separate occasions

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22
Q

Classify CKD based on eGFR

A

Stage 1) Normal/ high >=90

2) Mild reduction 60-90
3a) Mild/Moderate 45-59
3b) Moderate/severe 30-44
4) Severe 15-29

5) Kidney failure <=15 –> transplant or dialysis

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23
Q

KDIGO guidelines also include albumin in urine in CKD stratification.

Classify CKD based on Albuminuria

A

Mild <30 mg/g
Moderate 30 - 300 mg/g
Severe >300mg/g

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24
Q

Which patients should you be careful about eGFR rates as they may not be accurate?

A

Bodybuilders

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25
Which two conditions go hand in hand with CKD?
Hypertension and T2DM
26
Other causes of CKD?
GN, SLE! | Polycistic kidney disease
27
Ix for CKD?
1) Kidney function assessment - eGFR - no meat in 12 hours before eGFR measurement 2) Blood test and urine dipstick: will show normochromic normocytic anaemia 3) Renal ultrasound - espeically if chance of obstruction
28
Mx of CKD?
- Manage HTN - Ace inhibitors: <140/90 - Manage cardiovascular risk - statins and antiplatelets - If eGFR <30, check for calcium, phosphate, PTH and Vit D levels - Manage Anaemia - erythopoetin if needed - Manage Oedema - loop dieuretics
29
eGFR can be influenced by?
pregnancy, eating red meat, muscle mass
30
What kind of CKD patients need a nephrologist referral?
If eGFR falls below 30 or by more than 15 in one year OR if ACR ratio >70
31
What do you do with a Post-menopausal woman with iron deficiency anaemia?
Refer to gastro for colonoscopy in 2ww!
32
How can CKD cause bone disease?
Normally, kidneys hydroxylate Vitamin D into calcitriol which helps absorb calcium In CKD, kidneys can't hydroxylate Vitamin D --> low Vit D and low Calcium. In CKD, kidneys can't excrete phosphate either --> high phosphate --> high phosphate drags calcium out of bones --> even lower calcium
33
How does CKD affect calcium?
CKD --> kidneys can't hydroxylate vitamin d --> lower calcium and vitamin D kidneys cant excrete phosphate --> high phosphate and PTH High PTH causes bone breakdown = SECONDARY HYPERPARATHYROISISM Which is the most common type of renal osteodystrophy
34
Management of Renal osteodystrophy?
Reduce Phosphate and PTH, and increase calcium and Vit D - reduce phosphate in diet - phosphate binders - sevelamer or calcichew - Add calcium and Vitamin D supplement - maybe cinacalcet, calcium mime that reduces PTH levels
35
What is tertiary Hyperparathyroidism?
After prolonged Secondary Hyperparathyroidism (and low calcium), adenoma forms in parathryroid gland releasing LOTS of PTH - even if kidney is treated, the PTH gland is autonomous --> surgery
36
What are the two main types of glomerulonephritis?
NephrOtic and NephrItic
37
What is Nephrotic syndrome?
Triad of: ``` - ProteinURIA: >3g in 24 hours or PCR >300 or ACR >250 - HypoAlbuminAEMIA: <25g / L - Oedema ``` + Hyperlipidaemia
38
What are the common types of NephrOtic disease?
- Minimal change nephropathy - Focal segmental Glomerulosclerosis - Membranous Nephropathy
39
What is minimal change nephropathy?
Podocyte fusion on electron microscopy Treat with prednisolone Good prognosis
40
What is FSGS?
Parts of glomerulus damaged Associated with black people, HIV and heroin users Treat with steroids and immunosuppressants Half people go into remission, half progress
41
What would an FSGS biopsy show?
IgM deposition
42
What is membranous nephropathy?
Most common cause of nephrotic syndrome in adults - idiopathic damage to podocytes
43
What would histology show in membranous nephropathy?
"spike and dome" pattern caused by igG deposits enveloped by basement membrane
44
How many people with membranous nephropathy recover?
1/3 spontaneous remission 1/3 respond treatment 1/3 end stage disease
45
What are the characteristics of NephrItic syndrome?
Haematuria Hypertension Proteinuria with oedema
46
Types of NephrItic syndrome?
Thin basement membrane disease IgA nephropathy, or Berger's disease Post-strep glomeulonephritis Rapidly progressing glomerulonephritis Granulomatosis w polyangiitis
47
What is thin membrane disease?
Autosomal dominant, usually presents incidently w microscopic haematuria - Fine prognosis, reassure patient
48
What is IgA nephropathy also known as?
Berger's disease
49
What is the classic Berger's disease patient?
Frank haematuria days after a Respiratory or gastro infection Associated with cirhossis, coeliac/ dermatitis herpetiformis, HSP
50
First and Definitive Investigation for Berger's?
Urinalysis is first Renal biopsy showing mesangial IgA deposits is definitive
51
What is Henoch Schonlein purpura a variant of?
IgA nephropathy
52
What is Post-streptococcal glomerulonephritis (PSGN)?
Kidney damage caused by strep virus a week after strep infection Ix with Anti-streptolysin O titre (ASOT) w low c3 Supportive treatment, good prognosis
53
What is Rapidly Progressing Glomerulonephritis?
Aggressive decline in kidney function associated with epithelial crescents
54
What antibody in Goodpastures?
Anti-GBM antibodies which bind to Type 4 collagen
55
Investigation for Goodpastures?
Biopsy shows IgG deposits
56
Treatment for Goodpastures?
Plasmapheresis to remove antibodies | - Steroids and Immunosuppressants
57
Types of RPGNs?
Type 1 = goodpastures Type 2 = Immune complex: SLE, PSGN Type 3 = Pauci-immune: Microscopic pol, Churg- Strauss, Gran w Pol,
58
What antibody in Gran w Pol?
cANCA
59
What is Gran w Pol?
systemic vasculitis that causes inflammation of small and medium vessels
60
Features of Gran w Pol?
Haemoptysis, otitis, nose-bleeds, rashes Saddle shaped nose Conjuctivitis, episcleritis
61
Treatment for Gran w Pol?
Induce remission with steroids and Cyclophosphamide or 2nd line rituximab (if fertility needed) + give ergocalciferol + alendronate/risendronate for osteoporosis prophylaxis cos of the steroids

Finals RP (11 decks)

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