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
How do you decide when to treat Membraneous Nephropathy? Treatment options?
Based on proteinuria and eGFR Options - Cyclo - Ritux - Calcineurin - Steroids
26
How to differentiate primary vs secondary FSGS?
Primary: proteinuria and hypoalbuminemia Secondary: slowly progressing proteinuria, no hypoalbuminema
27
When do you treat FSGS? What do you use?
Proteinuria Not as responsive to steroids; may need immunosupression
28
Post transplant lymphproliferative disorder: causes, manifestation and treatment?
Cause - EBV - Uncontrolled B cell proliferation Clin - Splenomgaly - Lymphadenopathy - Extranodal Treatment - Reduce immunosuppression - mTOR - Ritux
29
Poor prognostic factors of post transplant lymphoproliferative disorder?
Older age Poor response ritux CNS involvement
30
Use of Finerenone in CKD?
Reduces progression of CKD, albuminuria in eGFR as low as 25
31
Which causes of nephrotic/nephritic syndrome demonstrate mesangial hypercellularity on biopsy?
IgA Diabet SLE MPGN
32
How does ACEI/ NSAIDs/ SLGT2I cause an AKI?
SLGT2: impaired aff vasodilation NSAIDs: impaired aff vasodilation ACEI: impaired eff vasoconstriction
33
How to tell if an AKI is pre renal?
Ur Na low Ur osm high Ur:Cr > 20
34
How to tell if an AKI is due to ATN?
Muddy brown casts Ur Na high and Ur Osm low because the kidney is not concentrating urine
35
HTN treatments?
ACEI/ARB Thiazide CCB Spiro BB
36
Renal artery stenosis investigations and treatment
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
RAAS: decribe
Check notes
38
Ca stones: risk factors and treatment
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
Struvite stones: risk factors and treatment
- 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
Uric acid stones: risk factors and treatment
Risk factors - Hyperuricemia - Dehydration - Leukaemia: incr tissue breakdown + more uric acid Tx - Alkalinisation of urine Allopurinol
41
Cysteine stones: risk factors and treatment
Risk factors - Cystinuria: autosomal recessive - Defect in cystine reabsorping PCT transporter Treatment - Low Na diet - Alkalinisation of urine - Chelating agents