LAPORAN KEGIATAN KERJASAMA

LAPORAN KEGIATAN KERJASAMA

BIDANG : PERTUKARAN MAHASISWA

TEMPAT : Internal Medicine-Nephrology,

Hospital Clínico, Spain (IFMSA-Spain) – Valencia City,

Spain, IFMSA-Spain

PERIODE : 01/04/2019 sampai 29/04/2019

AF Number 83763

Exchange Contract Information

AF Number 83763

Origin NMO Indonesia (CIMSA-ISMKI)

Exchange is unilateral No

Contract signed 11/10/2018

Personal Student Information

Family name (as written in passport) Suryanto

First name (as written in passport) Nandhan Seftiyan

Sex Male

Date of birth (dd/mm/yyyy) 14/09/1994

Email [email protected]

Alternative Email [email protected]

Acceptance details

Accepted in city/LC Spain (IFMSA-Spain) - Valencia

Accepted at Department of Internal Medicine-Nephrology

Accepted in hospital Hospital Clínico

Accepted start date (dd/mm/yyyy) 01/04/2019

Accepted end date (dd/mm/yyyy)) 29/04/2019

Boarding 1 time(s) per day, at Pocket Money, at the cost of Hosting association

Other Boarding Tickets for take away dish at a restaurant

Lodging At Student flat, at the cost of Hosting association

Other Lodging

Lodging Address Avenida Gaspar Aguilar 9

Social Program Yes

Social Program Information more info soon by email or WhatsApp group

Pocket money No

Pickup Yes “Please contact your contact persons as soon as possible”.

Special remarks Department and/or hospital might still change, we will confirm by email as soon as we know.

mailto:[email protected]


AF Number 83763

Contact Person 1

First Name Carla

Last Name Sanchez Hidalgo

Street & Number Av. Blasco Ibanez 17

City Valencia

Post Code 46010

Region

Country Spain

Phone +34 628154377

Cellular +34 963695568

E-mail [email protected]

Role LEO/NEO

Contact Person 2

First Name

Last Name

Street & Number

City

Post Code

Region

Country

Phone

Cellular --

E-mail

Role

Additional notes

Notes from LEO

Notes from NEO Welcome to your exchange in Valencia! We will send you an email soon with more information :)


AF Number 83763


AF Number 83763

Origin NMO Indonesia (CIMSA-ISMKI)


Contract signed 11/10/2018


Family name (as written in passport) Suryanto

First name (as written in passport) Nandhan Seftiyan

Sex Male



Alternative Email [email protected]

Acceptance details

Accepted in city/LC Spain (IFMSA-Spain) - Valencia

Accepted at Department of Internal Medicine-Nephrology

Accepted in hospital Hospital Clínico

Accepted start date (dd/mm/yyyy) 01/04/2019

Accepted end date (dd/mm/yyyy)) 29/04/2019

Arrival details

Do you need pick up by the Hosting Comittee Yes

Arrival date and time 31/03/2019 14:15

Arrival Location Bus station

Flight/Bus/Train number ALSA

Arrival location details Valencia estacion bus

Departure date 30/04/2019

Other details I arrive with with Wiryanti Ambarita, thank you :)



AF Number 83763

Other

Diet No

Do you have any allergies? No

In case of emergency, please contact :

Suryanto / +6282244939300 / [email protected]

Insurance Information

Insurance Company Tokio Marine

Policy Number TM/VOTP/19-V8003672

Contact telephone +625725772

Other comments


IgA

NEPHROPATHY CURRENT TREATMENT

Valencia – April 22th 2019

Nandhan Seftiyan Suryanto

(Wijaya Kusuma Surabaya University)

Nephrology Department

Hospital Clinico Universitario de Valencia

1

Glomerular Disease Classification

Robbins Cotran Pathologic basic disease 8th edition

Primary Glomerular Diseases

1. Minimal-change disease

2. Focal and segmental glomerulosclerosis

3. Membranous nephropathy

4. Acute postinfectious GN

5. Membranoproliferative GN

6. IgA nephropathy

7. Chronic GN

Glomerulopathies Secondary to

Systemic Diseases

1. Lupus nephritis (systemic lupus

erythematosus)

2. Diabetic nephropathy 3. Amyloidosis

4. GN secondary to

lymphoplasmacytic disorders

5. Goodpasture syndrome

6. Microscopic polyangiitis

7. Wegener's granulomatosis

8. Henoch-Schonlein purpura

9. Bacterial endocarditis-related GN

10. GN secondary to extrarenal

infection

11. Thrombotic microangiopathy

Hereditary Disorders

1. Alport syndrome

2. Fabry disease

3. Podocyte/slit-diaphragm protein

mutations

2

1. Epidemiology

2. Pathogenesis

3. Clinical features

4. Cause

5. Diagnosis

6. Prognosis

7. Treatment

3

1.Epidemiology

4

doi: 10.1111/nep.13592

Prevalence of IgA Nephropathy worldwide

Africa;

America; 5% 12%

Asia; 40%

Europe; 25%

5

(Yeo, et al. 2019)

5

doi: 10.1093/ndt/gfp620

Distribution of glomerular diseases

(Schena, Francesco Paolo, 2010)

(Sociedad Espanola de Nefrologia, 2018)

6

Most common form of primary glomerulonephritis

The peak age : second and third decades

Epidemiology 0.2 to 2.9 per100.000 annual incidence

More common in Asia and Australia

Less common in blacks both in the United States and in Africa

2 : 1 male to female ratio in North America and Western Europe

(Naimeh Tashakkorinia and Maria E. Tudor, 2018)

7

2. Pathogenesis

8

'

•

Genetic predisposition(s)

Hit 1 Increased production of

galactose-deficient lgAl Hit 2 Production of

autoantibodies

Lectin pathway

complement

activation /

' I

Formation of pathogenic

Hit 3 circulating immune

complexes

Renal deposition and

Alternative pathway • complement

activation

Hit 4 injury

FIGURE 1 IProposed four-hit pathogenesis of lgAN. Circulatory galactose-deficient lgA1 (Gd-lgA1) (Hit 1) is recognized by specific autoant ibodies (Hit 2) to form

circulating immune complexes (Hit 3). Some of these immune complexes deposit in the kidneys, thereby leading to mesangial activation, enhanced proliferation of

mesangial cells, and ult imately kidney injury (Hit 4) . Certain genetic loci have been associated with increased risk for developing lgAN. The activation of the alternative

and, at least in some patients, mannan-binding lectin (MBL) pathways by immune complexes is involved in disease pathogenesis .

PATHOGENESIS

Genetic Factors

Pre-Existing Medical Conditions

Environmental Factors

Increased

Production of Gd-IgA

Antibody Formation

Against Gd-IgA (Anti Gd-IgA)

Immune Complex Formation

(Gd-IgA & Anti Gd-IgA)

Immune Complex Deposition

Causing Renal Inflammation/Injury

A locus at chromosome 1q32 corresponding to deletion

of CFHR3,1 has been found to protect against renal

scarring in patients with IgAN (Xie et al, 2016).

(Renato C Monteiro, 2018)

Abnormal Gl

cosilation

PATHOGENESIS

Genetic Factors



IgA1

Hinge Region

Normal Glycosilation

(Galactose)

O-Linked Glycosilation O-Linked Glycosila2on

O-Linked Glycosilation


Amino acid O-Linked Glycosila2on

Glycosilated IgA1

↓

Identifed by body

↓

Degraded when (Gives Flexibility to bind antibgen)

O-Linked Glycosilation accumulated too much

Increased


Ser = Serine Thr = Threonine

O-Linked Glycosila2on



Antibody Formation


IgA1

(Galactose deficient) = Gd → Gd-IgA (Galactose)

O-Linked Glycosilation O-Linked Glycosila2on



Hinge Region

O-Linked Glycosila2on


Amino acid O-Linked Glycosila2on

Abnormal Glycosilated

IgA1

↓

Not Identifed by body



(Gives Flexibility to bind antigen)

Ser = Serine Thr = Threonine





↓ Not Degraded when

accumulated too much

↓

ACCUMULATES

10

PATHOGENESIS

Genetic Factors



Gd-IgA1 accumulates

Not Recognized as self

Body generates

IgG

Increased


Antibody Formation






An# Glycan An# body IgG

11

PATHOGENESIS

Genetic Factors



Gd-IgA1 accumulates

Not Recognized as self

Body generates

IgG

Increased


Antibody Formation




Anti Glycan Anti body IgG



Gd-IgA1

Immune complex 12

PATHOGENESIS

Genetic Factors



Increased


Antibody Formation






13

fGJE

Renal corpuscle

Efferent art riot

oot process

Bas m nt m mbran

Bowman's space

Distal convolu ed tubul

r====

Pro imal tubule

H ealthy

lgAN

Afferent arteriofe matrix ,

Proliferation of mesangial cells

,.

lit

diaphragm

GBM

ndothelial cells I

---------------------

pith lialc II

It; II esangial cell

r cell

acroph ge

onocy

Podocyte

Protein

lgA

Gd·l gA1

lgG

N ture Review: I Di e Prim r

(Lai, Kar Neng, et al. 20"16) 14

Also produced by mesangial

Immunohistochemical findings on IgAN

biopsy : C3, properdin, C4d, MBL and C5b-9

deposits in mesangium, coupled with the

general absence of C1q

Probably Lectin and alternative pathways influence in IgAN

In an experimental model of IgAN, mice

deficient for C3 and C5 receptors had less

proteinuria, mesangial IgA deposition,

mesangial matrix expansion and

hypercellularity than normal mice

Activate mesangial cell

to produce matrix protein 15

16

3. Clinical Features

1. Micro/Hematuria – during/after

infection – mostly mucosal infection

2. Proteinuria

3. High blood pressure

4. Nephrotic Syndrome

(Naimeh Tashakkorinia, Maria E. Tudor, 2018) 17

18

4. Cause

Cause? Unknown, Risk associated

• Genes

• Liver diseases

• Celiac disease,

• Dermatitis herpetiformis

• Infections

• Family History

19

20

5. Diagnosis

A. KIDNEY BIOPSY

Light Microscopy

↓

Clinical diagnostic suspicion

↓ Kidney biopsy

↓ Electron Microscopy

↓

Immunofluorescence

↓ 1. Focal or diffuse mesangial

proliferation

2. Increased mesangial matrix

and cellularity 3. Interstitial fibrosis with

tubular atrophy

1. Deposits of IgA in the mesangium

1. Deposits (mainly IgA1, but also IgG and IgM) in

mesangium and capillary

walls. 2. C3

(Manish, et al. 2018)

(Naimeh Tashakkorinia, Maria E. Tudor, 2018) 21

22

HISTOPATOLOGY

B .BIOMARKERS doi:10.1371/journal.pone.0098081

A Panel of Serum Biomarkers Differentiates IgA Nephropathy from Other Renal Diseases

(Yanagawa, Hiroyuki. et al, 2014)

23

24

A Panel of Serum Biomarkers

Differentiates IgA Nephropathy

from Other Renal Diseases (Yanagawa, Hiroyuki. et al, 2014)

doi:10.1371/journal.pone.0098081

1. Serum Gd-IgA1

2. Serum Gd-IgA1 specific

IgG

3. Serum Gd-IgA1 specific

IgA

25

In IgA Nephropathy, Glomerulosclerosis

Is Associated with Increased Urinary CD80 Excretion and Urokinase-

Type Plasminogen Activator Receptor-Positive Podocyturia

(Trimachi, et al. 2017)

DOI.10.1159/0004738

4. CD80 5. Podocyte urokinase

type plasminogen activator

receptor.

26

Predict renal outcome independent of proteinuria, BP, and eGFR.

27

6. Prognosis

Prognosis

IgA nephropathy reduces life expectancy by more than 10 years and leads to kidney failure in 20–40% of patients within 20 years of diagnosis

CLINICAL

1. Hypertension >140/90

2. Reduce GFR

3. High creatinine

4. Persistence hematuria

5. High Trigliserida

6. High ureum

7. Proteinuria >1g/24hour

8. Obesity

HISTOPATOLOGY

1. Cresent (>30%)

2. Sclerotic glomerulus

3. Tubular atrophy

4. Interstitial tissue fibrotic

5. Mesangial Hypercelullarity > 50%

(Naimeh Tashakkorinia, Maria E. Tudor, 2018)

(Dana, et al. 2019) 28

29

7. Treatment

recurrence rate is high after tranplantation

30

31

Conservative therapy

1. Angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers, adequate blood pressure control <125/75

2. Low-sodium intake diet

3. Physical exercise

4. Adequate loss of weight

5. Lipid control

6. Tobacco avoidance

Current Study

1. Intensive Supportive Care plus Immunosuppression in IgA Nephropathy (STOP-IgAN)

2. Rituximab

3. Targeted-release budesonide versus placebo in patients with IgA nephropathy (NEFIGAN)

4. Tonsilectomy (Japan), european? 5. Effect of Oral Methylprednisolone on Clinical Outcomes in Patients With IgA Nephropathy

The TESTING Randomized Clinical Trial

6. US trials mycophenolat mofetil (MMF) terminated early – not proven

7. Chinese MMF + low dose Steroid = Endocapillary hypercellularity, crescents, and necrosis lesions in glomeruli had improved or disapeared after immunosuppressive therapy (KDIGO Basic)

8. Tacrolimus – decrease proteinuria, in China

9. Fish Oil = remain unclear, some research failed to show benefit but a European trial of 30 patients

suggested that a RAS blocker combined with polyunsaturated fatty acids reduced proteinuria more

than a RAS blocker alone

32

Intensive Supportive Care plus Immunosuppression in IgA Nephropathy (STOP-IgAN)

(Raumen, et al. 2015) Comparing

a. Supportive (RASB)

b.RASB + Cyclophosphamide + azathioprine + prednisolon

Conclusion : The addition of immunosuppression did not significantly improve the outcome 33

A R

doi: 10.1681/ASN.2016060640

andomized, Controlled Trial of Rituximab in IgA Nephropathy with Proteinuria and Renal Dysfunction (Laffayete, Richard. et al. 2017)

Rituximab

1-year follow-up

34 adult patients with

biopsy–proven IgA nephropathy

Conclusion : Neither eGFR and Proteinuria not statistically significant, otherwise more adverse effect 34

Tonsillectomy reduces recurrence of IgA nephropathy DOI 10.1007/s10157-015-1170-7

in mesangial hypercellularity type categorized by the Oxford classification (Hirano, keita. et al, 2016)

Conclusion : Tonsillectomy reduce recurrence of IgAN (proteinuria and IgA/C3)

Meeting report 15th International Symposium on IgA Nephropathy 2019 Argentina: Tonsillectomy may

considered in recurrent tonsillitis 35

dx.doi.org/10.1016/S0140-6736(17)30550-0

Targeted-release budesonide versus placebo in patients with IgA nephropathy

(NEFIGAN): a double-blind, randomised, placebo-controlled phase 2b trial

(FellstrOm̈ , Bengt C. et al, 2017)

UPCR

36

eGFR

37

Placebo

(n=50)

TRF-budesonide 8 mg/day

(n=51)

TR F-budesonide 16 mg/day

(n=49)

Total

(n=150)

Patients {%) Events Patients {%) Even ts Patients {%) Events Patients {%) Events

Any adverse event 42{84%) 162 48(94%) 270 43{88%) 305 133 (89%) 737

Nasopharyngi tis 10 {20%) 14 8{16%) 16 10 {20%) 16 28 {19%) 46

Acne* 3{6%) 3 8{16%) 9 9 {18%) 10 20 {13%) 22

Joint swelling 2 (4%) 2 8(16%) 8 9 {18%) 14 19 (13%) 24

Cushingoid* 3{6%) 3 5 {10%) 5 8{16%) 8 16 {11%) 16

Insomnia* 2 {4%) 2 6 {12%) 6 8{16%) 9 16 {11%) 17

Diarrhoea 7 {14%) 9 1{2%) 1 5 {10%) 5 13{9%) 15

Dyspepsia t 4{8%) 5 2 {4%) 2 7 {14%) 9 13{9%) 16

Headache 3{6%) 4 3{6%) 3 6 {12%) 6 12 {8%) 13

Alopecia* 2 {4%) 2 4{8%) 5 4{8%) 4 10 {7%) 11

Back pain 1{2%) 1 6 {12%) 8 3{6%) 3 10 {7%) 12

Mood swings* 2 {4%) 2 3{6%) 3 5 {10%) 5 10 {7%) 10

Oedema peripheral 2{4%) 3 2{4%) 3 6 {12%) 9 10 {7%) 15

Blood creatine 3{6%) 3 3{6%) 4 3{6%) 3 9 {6%) 10 phosphokinase increased Hirsu tism* 1{2%) 1 3{6%) 3 5 {10%) 5 9 {6%) 9

Hypertension 1{2%) 1 3{6%) 3 5 {10%) 5 9 {6%) 9

Muscle spasms 2{4%) 3 5 {10%) 5 2{4%) 2 9 {6%) 10

Abdominal pain t 1{2%) 1 4{8%) 4 3{6%) 4 8{5%) 9

Nausea 1{2%) 1 4{8%) 4 3{6%) 5 8{5%) 10

Upper respi ratory tract

infection 3{6%) 3 2 {4%) 3 3{6%) 3 8{5%) 9

Adverse events reporte d by ;.:5% ofthe total pat ient population. TRF-budesonide=targeted-release formulation-budesonide. •corticosteroid-related adverse events solicited

by questionnaire at every visit. tGastrointestinal-related adverse events solicited by q uestionnaire at every visit

Table 2: Treatment-emergent adverse events reported by l!:5% of all pat ients by preferred term (safety set)

Conclusion : Budesonide 8 mg or 16 mg reduce UPCR and stabilize eGFR 38

40

doi:10.1001/jama.2017.9362

Effect of Oral Methylprednisolone on Clinical Outcomes in Patients With IgA Nephropathy

The TESTING Randomized Clinical Trial (Jicheng, et al. 2017)

All patient Proteinuria >1 g/d

Methylprednisolon 0.6 to 0.8 mg/kg/d reduce proteinuria (P<0.001) + GFR p(<0.01)

Plan for 5 years, Stopped at 3rd year due to adverse event infection

including lethal Pneumocystis jirovecii pneumonia

TESTING 2 – Lower doses 0.4 mg, complete in 2023

40

Conclusion : Final conclusian cannot be made

40

Table 1. From the KDIGO guidelines for corticosteroids in lgAN34

(A) Supportive care with antiproteinuric and antihypertensive drugs (statement 10.2). We recommend long-term ACE-I or ARB (RASBs) treatment

when proteinuria is >1 g/d, with uptitration of drug depending on BP (1B). Suggestions to uptitrate RASBs as far as tolerated to achieve

proteinuria <1 g/d (2C). Target BP <125/75 mmHg when proteinuria is >1 g/d (not graded).

(B) Corticosteroids (statement 10.3.1). We suggest that patients with persistent proteinuria >1 g/d, despite 3-6 mo of optimized supportive care

(including RASBs and BP control) and GFR>50 ml/min per 1.73m2 , receive a 6-mo course of corticosteroid therapy (2C) .

(C) Corticosteroid regimens

(a) iv Bolus injection of 1 g methylprednisolone for 3d each at months 1, 3, and 5 followed by oral steroid (0.5 mg/kg prednisone) on alternate

days for 6 mo.26

(b) Oral prednisone starting with 0.8-1 mg/kg per d for 2 mo and then reduced by 0.2 mg/kg per d permo for the next 4 mo.27 •28

(D) Immunosuppressive agents cyclophosphamide and azatiophrine (statement 10.4.1). We suggest not treating with corticosteroids combined

with cyclophosphamide or azathioprine in patients with lgAN (unless there is a crescentic lgAN with rapidly progressive course; 2D).

Evidence is graduated in levels: 1, recommendations; 2, suggestions; A to D indicates high quality to very low quality, respectively.34

42

Future Therapy

42

(Barrat, et al 2018)

Short story:

1. 16-year-old male with crescentic IgAN who had failed

treatment with corticosteroids, cyclophosphamide, and

plasma exchange subsequently had transient

improvement in renal function with eculizumab

2. Sweden; a young 16-year-old white male with biopsy-

proven crescentic IgAN had failed to respond to

corticosteroids and mycophenolate but stabilized when

treated with eculizumab 43

Future therapy

1. Modulation of mucosal B-cell programming (TLR antagonist) Hydroxychloroquine –TLR-9 inhibitor –

China – reduction proteinuria in 24 weeks significantly 200 mg twice daily compare to RASB only, 2

more RCT’s on going in China 2. Modulation of mucosal B-cell programming (BAFF/APRIL antagonist) - BAFF is necessary for B-cell

maturation - Tonsillar mononuclear cells from IgAN patients exposed to CpG-oligodeoxynucleotide

produce high levels of BAFF and IgA. TLR-9 stimulation induces APRIL (TNF) expression in tonsillar

B cells.

a. Blisibimod = antagonist BAFF (started in 2013, Study completed. Not yet published)

b. Atacicept = BAFF/APRIL dual inhibitor (started in 2017, complete in 2020)

3. Spleen tyrosine kinase (Syk) inhibitor Fostamatinib – Syk mediates maturation and survival of the B-

cell lineage (started in 2014) 4. Proteasomal ihibition = bortezomib (completed in 2017, not yet published)

5. B-cell activating factor = inhibition (LNP023)

6. Complement inhibition (lectin and alternative pathway)

a. Eculizumab = antibody monoclonal C5

b. APL-2 = C3 inhibitor c. CCX168 = C5a Receptor antagonist

d. LNP023 = Factor B inhibitor

e. OMS721 = mAb MASP-2

44

Mbl serine association protease

doi: 10.3389/fimmu.2019.00504

The Emerging Role of Complement Proteins as a Target for Therapy of IgA Nephropathy

(Dana Rizk V., et al. 2019)

45

Conclusions

IgA Nephropathy the most common form GN in worldwide, 40% in Asia, in Spain (2018) 14,2 -19.6%

Pathogenesis influenced by genetic factor chromosome 1q32 corresponding to deletion of CFHR3, 4 hits mechanism, Complement, MALT

Prognosis based on proteinuria, eGFR and MEST-C

46

47

Conclusion

Conservative therapy is basic for IgAN

Systemic Steroid use IgAN may be considered when the patient has persistent proteinuria

The addition of immunosuppression neither cyclophosphamide and azathioprine nor MMF did not significantly improve the outcome

MMF in cresent may be considered

Tonsilectomy may be considered in recurrent tonsilitis with IgAN

Renal transplant may be preferred for the last choice but considered that IgA nephropathy recurrence rate is high after tranplantation

Conclusion

Awhile, budesonide has better prognostic for the steroid therapy

We are still waiting for the published of these study

- Complement inhibition

- Modulation of mucosal B-cell programming

- Spleen tyrosine kinase (Syk) inhibitor

- Proteasomal ihibitor

- B-cell activating factor

48

49

Thank You

1st February, 2019

To whom it may concern, This is to confirm that the following student is accepted to participate in our bilateral exchange program for medical students:

NAME OF STUDENT: Suryanto Nandhan Seftiyan DATE OF BIRTH: 14-09-1994 NATIONALITY: Indonesia COUNTRY OF ORIGIN: Indonesia PASSPORT NUMBER: C1063625

Our organization, which is a member of International Federation of Medical Students’ Associations(IFMSA), will arrange a clerkship at one of our universities or affiliated university hospitals. We will, during the mentioned period, provide full board and lodging at no charge. The student will be placed under supervision of the administrating chief doctor at the department and will not get any salary.

DEPARTMENT: Internal Medicine-Nephrology HOSPITAL: Hospital Clínico UNIVERSITY, CITY: Spain (IFMSA-Spain) - Valencia HOST COUNTRY: Spain HOST ORGANISATION: IFMSA-Spain PERIOD: 01/04/2019 at 29/04/2019

We urge all authorities to be helpful in order for the medical student to acquire a visa for the arranged Clerkship.

Any further questions regarding the mentioned student’s clerkship should be directed to the National Exchange Officer:

NATIONAL EXCHANGE OFFICER: Jose Antonio Hurtado Aguilar TEL: +34 665965901 EMAIL: [email protected]

Stamp and signature of the NEO

Yours sincerely,


AF Number 95527


AF Number 95527

Hosting NMO Serbia (IFMSA-Serbia)

Contract signed 21-09-2019


Exchange is for a specific month No


Family name Adetasia

First name Tesa

Sex Female


Nationality Indonesia

Language spoken English (Good)

Serbian (Unknown)

Passport number C5880199

Passport valid until (dd/mm/yyyy) 06/01/2025

Student's Medicine Related Information

Medical School Wijaya Kusuma Surabaya

# Medical student since 2016

# Clinical student since 2021

Expected day of graduation 09-2023

AF Number 95527

Student's Mailing and Electronic Information

Street & Number Jl. Parang Tirto RT 16/RW 08 Tambakrejo, Krembung

City Sidoarjo

Post Code 61275

Country Indonesia

Phone Number 082231801976

Alternative phone number


Alternative Email

Exchange Preferences

1st Desired City Serbia (IFMSA-Serbia) - Beograd

2nd Desired City Serbia (IFMSA-Serbia) - Novi Sad

3rd Desired City Serbia (IFMSA-Serbia) - Kragujevac

1st Desired Department Surgery-Plastic Surgery

Field studied : Yes

Exam passed : Yes

2nd Desired Department Gynaecology/Obstetrics Field studied : Yes

Exam passed : Yes

3rd Desired Department Radiotherapy Field studied : Yes

Exam passed : Yes

4rt Desired Department Physical Medicine and Rehabilitation

Field studied : Yes

Exam passed : Yes

Exchange Details

# Duration (in weeks) 4

Exchange Start Date (dd/mm/yyyy) 01/10/2021

Exchange End Date (dd/mm/yyyy) 31/10/2021

Type of Clerkship Clinical Clerkship

Do you need an official invitation letter? (for visa or other purpose)

“I will obtain insurance coverage for the Exchange period. Otherwise my exchange will be cancelled

Yes

Yes

Would like to be placed together with this student No

Would like to be placed based on City first


AF Number 95527

Student Remarks

Space for notes/messages to the Exchange Officer of your Country/Local Committee

Notes from the student : The reasons because of my religion, I cannot eat a certain food or drink that contains pork or alcohol. Thank you.

Note

LAPORAN KEGIATAN KERJASAMA

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