Renal 2

Question 1

Unilateral Renal artery stenosis

when indicated to stent it?

Answer 1

1. Short duration of High BP prior to dx renovascular disease (strongest factor)
2. intolerance/failure medical therapy
3. Flash oedema/heart failure

Question 2

CaSR apart from parathyroid, where is it found?

Answer 2

Ascending LOH

• blocks NAKatp channel
• secrets Ca/Mg and lowers serum hypercalcemia

Question 3

In old age, renal cortical or medulla mass is lost?

Answer 3

Cortical part of renal is lost

Medulla is spared

Question 4

Commonest bone disease in renal dialysis patients?

Answer 4

Adynamic bone disease ( low bone turnover)

Question 5

2 Inhibitors of vascular calcification in HD?

Answer 5

Fetuin-A = Binds Ca and Phosphate ( low in dialysis patient)

Matrix GLA protein = Inhibits vascular mineralization ( inhibited by warfarin)

Question 6

Treatment for calciphylaxis?

Answer 6

Sodium thiosulphate - chelates calcium, produce NO - vasodilatation = better perfusion

Question 7

Nephrogenic systemic fibrosis - pathogenesis? Treatment?

Answer 7

Free Gadolinium dissociated from it’s chelated form

• absorbed into tissue
• phagocytosed by macrophage and express CD34
• Fibrocytes and makan it and transform into fibroblast = fibrosis

Treatment = urgent HD and repeat after 24 hours

Question 8

Loop diuretics can cause hyponatremia?

Thiazide diuretics can cause hyponatremia?

Answer 8

No, because it blocks NakCI channel, interfering with osmotic gradient - ADH can’t actively absorb water in CD

Yes, blocking of NACI in DCT, upregulates all other channels in the renal tract = Increase NA reabsorption, increase ADH can water reabsorption = DILUTIONAL HYPONATREMIA

Question 9

When remove catheter in Peritoneal dialysis?

Answer 9

Fungal/mycobacterium peritonitis
Refractory peritonitis ( 4 days ABX - no improvement)
Relapsing peritonitis ( 4 weeks later, same bug)
Peritonitis + intra-abdominal pathology
Peritonitis + Exit site/tunnel infection

Question 10

PD adequacy has 2 factors - name it?

Answer 10

Small solute clearances

Ultrafiltration - 1L/day

Question 11

Cardiopulmonary recirculation does what?

Answer 11

Reduces effectiveness of HD ( blood recirculate due to fistula)
It’s 40% of Total cardiac output

Question 12

For HD - vascular access needs to support what in order to work?

AV fistula - flow rate?

Answer 12

Dialysis flow of 300 ml/minute without recirculation

AV fistula = 500 ml/minute

Question 13

MCD and FSGS - difference?

Answer 13

FSGS = suPAR protein - increase ab-integrin activity that destroy podocytes so proteinuria

MCD = IL 13 leads to high CD80 expression on podocytes - decreases nephrin protein ( negatively charged)
so proteinuria

Question 14

Membranous nephropathy a/w what infection, drugs, connective tissue disease most?

Antibodies are?

A/w what demographic?

Answer 14

Infection = Hep B
Connective tissue disease = SLE
Drugs = Penicillamine/NSAIDS/Gold
MALIGNANCY

Antibodies - THSD7A if anti-PLAR2 is negative

most common cause of Nephrotic syndrome in Caucausian

Question 15

Pathogenesis of Membranous nephropathy?

Answer 15

Immune-antibody complexes ( IgG and anti-PLAR2) at podocytes - triggers complement mediated injury

Podocytes rebuild wall membrane via Type IV collagen

Question 16

FSGS commonly seen in what population?

Answer 16

African origin - Nephrotic syndrome

APOL1 gene polymorphism to combat trypanosomiasis but somehow kena FSGS

Question 17

Best FSGS prognosis and worst prognosis?

Answer 17

Tip segmental lesion of glomerular near PCT = GOOD

Collapsing tuft of glomerular = BAD

Question 18

MPGN has 2 types - name it and difference?

Answer 18

Immune mediated
Hep C/B , SLE , Monoclonal gammopathies (MM)
Treat underlying cause and NO immunosuppression

-Tram-track appearance, subendothelial and mesangial deposits

Complement mediated (antibodies towards C3 convertase) - C3GN or Dense Deposit Disease
Treatment - like nephrotic syndrome

Subendothelial and subepithelial deposits

Question 19

Difference between staph GN and Strep GN?

Answer 19

Staph GN - IgA staining = IgA nephropathy
-rapid onset and poor prognosis, ESRF

Strep GN = C3 staining
-2 weeks post infection , good prognosis

Question 20

IgA pathogenesis?

Answer 20

Mucosal IgA2 excess production post infection
-translocate to Bone marrow ( which have IgA1) and knock off IgA1 in bone marrow

IgA1 ( defectively glycosylated) run to liver and not cleared
- go to kidneys mesangial and deposited there

IgG antibodies attack IgA1 in kidneys

Question 21

IgA good prognosis marker according to MEST classification?

IgA poor prognosis marker?

Answer 21

Endocapillary hypercellularity = good response to steroids

Crescents, proteinuria > 1g/day, elevated serum creatinine

Question 22

Anti GBM antibody targets what in the collagen IV chain?

Answer 22

Alpha 3

Question 23

GBM syndrome vs GBM disease?

Answer 23

GBM syndrome = Lung hemorrhage + RPGN of ANY CAUSE

GBM disease = Lung hemorrhage + RPGN + Antibodies

Question 24

Treatment of anti-GBM

Answer 24

PLEX + CYP ( esp. if pulmonary hemorrhage)

Question 25

RPGN on kidney biopsy shows?

Answer 25

> 50% crescents in bowman space
Circumferential crescents (> 805 of glomeruli) respond poorly

Question 26

PLASMIC score for suspected TTP?

Answer 26

Platelets < 30
Lysis-hemolysis
no Active cancer/Stem cell transplant
MCV< 90
INR < 1.5
Creatinine < 170

Question 27

In Australia what causes STEC - HUS?

Answer 27

E. Coli 0111

worldwide is 0157.H7

Question 28

Commonest cause of drug-induced TMA

Answer 28

Quinine

Question 29

PAN vasculitis histology shows?

Answer 29

Fibrinoid necrosis arteries + leucocytes and aneurysms

Question 30

Treatment of GPA and MPA?

Answer 30

IV methylprednisolone then oral prednisolone
Maintenance with Rituximab!

Pulmonary hemorrhage, hemoptysis, anti-GBM antibodies, RPGN = PLEX

Question 31

Treatment of Churg-Strauss syndrome?

Answer 31

IV Methylprednisolone then oral prednisolone
AZA as maintenance

CYP if have CNS component