RENAL Flashcards

1
Q

RTA Type 2
- Mechanism
- Associations

A

PCT

Mechanism
- no reabsorption of bicarb/uric acid/glucose

Associations
- MM
- Drugs: Tenofovir!!!!!!!!!!!!!!!!!!!
- Fanconi

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2
Q

RTA Type 1
- Mechanism
- Associations

A

DCT

Mechanism
- Hypokalemia, hypercalciuria

Associations
- Sjogrens
- RA
- Urine stones
- Glue sniffing

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3
Q

RTA Type 4
- Mechanism
- Associations

A

CD

Mechanism
- Hyperkelamia
acidosis

Associations
- Addisons
- Sjogrens
- Drugs: Angiotensin II inhibitors, NSAIDs, trimeth, heparin

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4
Q

Features of nephrotic syndrome?

A

Proteinuria > 3.5 g / day
Hypoalbuminema
Hyperlipidemia + lipiduria
Edema
Frothy urine
Hypercoagulable state (loss of antithrombin, Protein C + S)

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5
Q

Features of nephritis syndrome?

A

Haematuria
Hypertension (salter + water retention -> filtered proteins stimulate reabsoption of Na + H2O)
RBC casts in urine
Incr BUN + Creatinine (Azotemia)
Oliguria
Proteinuria < 3.5 g / day

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6
Q

Causes for RPGN? What do you see on LM?

A

GBM
Immune complex
Pauci immune

LM: crescents

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7
Q

What are the causes of immune complex GN? Which ones are complement mediated and which ones are antibody mediated?

A

COMPLEMENT is LOW
SLE
Cryglobulinemia
Infection assoc
MGUS

ANTIBODY
IgA
HSP

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8
Q

Which causes of GN cause mesangial deposition?

A

IgA
MPGN
Diabetes
Lupus

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9
Q

Types of GN lupus?

A

I: minimal mesangial
II: proliferative mesangial

III: focal proliferative < 50%
IV: diffuse proliferative > 50%

V: diffuse membranous –> NEPHROTIC
VI: adv sclerosing

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10
Q

When are PLA2R antibodies seen? Primary or secondary?

A

Membranous Nephropathy - primary AND secondary

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11
Q

Treatment for IgA nephropathy? What is this dependent on?

A

Proteinuria < 3.5g + normal eGFR: supportive
Proteinuria > 3.5g + normal eGFR: Ritux/calcineurin/ cyclophosphamide
Proteinuria > 3.5g + eGFR < 60: Add steroids to above
Life threatening proteinuria / rapidly reducing kidney function: Steroids + cycle

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12
Q

Treatment for MCD/FSGS?

A

MCD: steroids resistance, supportive

FSGS: not as responsive to steroids, yclo/tac

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13
Q

Treatment for MCD/FSGS?

A

MCD: steroids resistance, supportive

FSGS: not as responsive to steroids, yclo/tac

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14
Q

Treatment for RPGN?

A

Cyclo
Steroids
Plasmapheresis if GBM

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15
Q

Pathophys of IGA nephropathy?

A

IgA lacks galactose in hinge region –> body does not recognise as self and produces IgG antibodies against IgA1

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16
Q

Causes of nephritic syndrome with low complement?

A

Lupus III/IV
Infection
Cryoglobulinemia
MPGN
Endocarditis

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17
Q

Treatment for IgA nephropathy?

A

Supportive
- steroids if required
ACEI/ARB

18
Q

Anti-GBM GN is against what?

A

Type IV collagen

19
Q

Px of IgA vasculitis (HSP)?

A

Arthralgia
Abdominal pain
Rash
GN

20
Q

Tx Iga vasculitis?

A

Steroids
Immunosupressive

21
Q

What does each type of lupus nephritis correlate to?

A
  • I: minimal mesangial
    - II: mesangial proliferative
    - III: focal proliferative < 50% involved
    - IV: diffuse proliferative GN ? 50% involved
    - V: diffuse membranous
    - VI: adv sclerosing >90% gloms involved
22
Q

When to treat lupus nephritis?

A

I II: RAAS blockafe
II, IV, V: steroids, cyclo

23
Q

Causes of cryoglobulinemia types?

A

I: MM, haematological malignancy
II: hepatitis
III: AI

24
Q

Causes of cryoglobulinemia types?

A

I: MM, haematological malignancy
II: hepatitis
III: AI

25
Q

How do you decide when to treat Membraneous Nephropathy? Treatment options?

A

Based on proteinuria and eGFR

Options
- Cyclo
- Ritux
- Calcineurin
- Steroids

26
Q

How to differentiate primary vs secondary FSGS?

A

Primary: proteinuria and hypoalbuminemia
Secondary: slowly progressing proteinuria, no hypoalbuminema

27
Q

When do you treat FSGS? What do you use?

A

Proteinuria

Not as responsive to steroids; may need immunosupression

28
Q

Post transplant lymphproliferative disorder: causes, manifestation and treatment?

A

Cause
- EBV
- Uncontrolled B cell proliferation

Clin
- Splenomgaly
- Lymphadenopathy
- Extranodal

Treatment
- Reduce immunosuppression
- mTOR
- Ritux

29
Q

Poor prognostic factors of post transplant lymphoproliferative disorder?

A

Older age
Poor response ritux
CNS involvement

30
Q

Use of Finerenone in CKD?

A

Reduces progression of CKD, albuminuria
in eGFR as low as 25

31
Q

Which causes of nephrotic/nephritic syndrome demonstrate mesangial hypercellularity on biopsy?

A

IgA
Diabet
SLE
MPGN

32
Q

How does ACEI/ NSAIDs/ SLGT2I cause an AKI?

A

SLGT2: impaired aff vasodilation
NSAIDs: impaired aff vasodilation
ACEI: impaired eff vasoconstriction

33
Q

How to tell if an AKI is pre renal?

A

Ur Na low
Ur osm high
Ur:Cr > 20

34
Q

How to tell if an AKI is due to ATN?

A

Muddy brown casts
Ur Na high and Ur Osm low because the kidney is not concentrating urine

35
Q

HTN treatments?

A

ACEI/ARB
Thiazide
CCB
Spiro
BB

36
Q

Renal artery stenosis investigations and treatment

A

Renal duplex doppler ultrasonography
CT angiography
MRI angiography
Nuclei ACEI scintigraphy

Medical therapy just as good as stenting
- Those with more rapidly decling renal function pre angioplasty had better outcomes after

37
Q

RAAS: decribe

A

Check notes

38
Q

Ca stones: risk factors and treatment

A

Causes
- Increased Ca intake
- RTA
- Reduced Ca reabsorption
- loop diuretics, steroids, acetazolamide, theophylline

Risk factors
- Hypercalciuria
- Hypercalcemia
- Fat malabsorption
○ Gastric bypass
○ Crohns
○ Fat not absorbed and binds to Ca
- Low citrate

Tx
- thiazides

39
Q

Struvite stones: risk factors and treatment

A
  • Infection stones: can present with UTI as often caused by urease positive bugs
    • Klebsiella/ proteus/ staph saprophyticus has urease which breaks down urea to NH3, which can precipitate stones
40
Q

Uric acid stones: risk factors and treatment

A

Risk factors
- Hyperuricemia
- Dehydration
- Leukaemia: incr tissue breakdown + more uric acid

Tx
- Alkalinisation of urine
Allopurinol

41
Q

Cysteine stones: risk factors and treatment

A

Risk factors
- Cystinuria: autosomal recessive
- Defect in cystine reabsorping PCT transporter

Treatment
- Low Na diet
- Alkalinisation of urine
- Chelating agents