NEPHROTIC SYNDROME

Definition Nephrotic syndrome is a group of clinical manifestation consist of Proteinuria, Hypoalbuminuria, Hyperlipidemia and General swollen (oedema anasarka). If protein loss from urine has reached more than ,! gram"day it will be Hypoalbuminemia with the side effects are li#uid and salt endured and general swollen. $hat symptom caused by glomerular function defect as a filter. Glomerular basalis membran has a role as protein filter. If there are some damages, protein reabsorbtion in pro%imal tubular become limited, it caused proteinuria. $his condition initiated by upper respiratory tractus infection, allergy reaction, contact dermatitis wicth is e%pand become swollen and proteinuria.

Etiology: &. Primary renal parenchyme damage a line with idiopatic primary damage in renal parenchyme (Nephrotic syndrome primary) ' ' ' ' Post streptococcus glomerullonefritis acute (embranosa glomerulonefritis (inimal lesion glomerulonefritis (embranoproliferati)e glomerulonefritis

*. +istemic and metabolic diseases ' ' ,( -myloidosis

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Henouch schonlein purpura +./

. (echanical circulation damage ' ' ' ' 0ight heart syndrome (0H+) $ricuspidal )al)e damage, pericarditis and heart tamponade 0efracter congesti)e heart diseases 0enalis )ein $rombosis

1. (alignancy ' ' ' Hodgkin disease .ymfosarcoma (ieloma multiple

!. Infection diseases (alaria, sifilis, herpes 2oster, typhoid abdominalis and hepatitis type 3 4. +pecific to%in ' ' Hg, 3ismuth, (ercury ,rugs 5 $rimetadion, Parametadion, Penisilamin and 6aptopril.

7. 6ongenital Nephrotic syndrome herediter 8. 9thers Pregnancy, sirrosis hepatis, obesity and renal transplantation.

Patofisiology Hepar ha)e a important role in protein syntesa. If body protein losing was increase from renal or e%tra renal. In nefritic syndrome patient, Protein syntesa was increased but it is not enough to e#ual the protein loossing. $his condition caused total body protein was decreased. $he decrease of 0enal function suddently has some effects, there are5 ' ' ' Hypoalbuminemia : oncotic pressure : plasma )olume (hypo)olemia)

abo)e condition caused patofisiologic changes, such as5 ' ' ' : cardiac out put : 0enal blood flow : Glomerular filtration rate

In a large of nephrotic syndrome patient was founded total cholesterol, trigliceride and fosfolipide increase (hyperlipidemia) it make the urine foam up. +wollen is the first complaint, it is a line with li#uid accumulation in interstitial space in the body and oncotyc pressure decrease because of hypoalbuminemia.

Clinical Manifestation $he main symptom from nephrotic syndrome are 5 ' ' ' ' Proteinuria ; ,! g"day for adult or <,<! g"kg 3="day for child Hypoalbuminemia > < g"l General swollen, specially in face, feet, ascites and pleural effution Hyperlipidemia specially hypercholesterolemia

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Hypercoagulabilitas, this condition make the )ein and artery trombosis risk increase

The Support In estigation ?rinalisa, the in)estigation for urine and blood is needed to confirm proteinuria, proteinemia, hypoalbuminemia and hyperlipidemia. Hematuria, 0enal function e%emination and 6alsium in plasma decrease. $he definite diagnosis will be founded by renal biopsy.

Co!plication ' ' ' ' -cute renal failure $rombosis Infection (alnutrition

Manage!ent ' ' @ind the etiology by renal for all adult patient +wollen management 5 take a bed rest and using the pressure stocking specially for old patient. ' 3e carefull in use anti dyuretic drug because the se)ere proteinuria condition caused renal failure or hypo)olemic ' Pay attention to the li#uid balance specially to A, Na, 6reatinin and plasma ureum concentration, if needed gi)e more potassium.

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?se the dyuretic drug e%amples 5 $ia2id or furosemid with lower dose, the dose can be increase a line with patient condition

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3uilt up the nutritional condition with hight calory and lower salt diet Pre)ention of infection by using profila%is antibiotic to a)oid infection specially to pneumococcus.

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@inally we must reordering the etiology ?sing the steroid drug ?sing the anticoagulantia to to pre)ent the complication, such as 5 heparin, warfarin, fenindion or combination with sitostatic drug siklophosfamid -nti trombocyte agregation, such as 5 indometasin *' mg"kgbw"day

specially to nephrotic syndrome with minimal lession and dipiridamol"aspirin.

C"SE REPORT

- < years old man was admitted to the internal medicine departement of ,r. -hmad (ochtar hospital 3ukittinggi on 9ctober *4th,*<< with 5 Chief Co!plaint : ,yspnea since & day before hospitali2ed Present Illness History :

,yspnea since & day before hospitali2ed, not influence by weather, emotion and food

+tomach become enlargement since * month before hospitali2ed, influence with position changes

@ace, hand and feet was swollen since * month before hospitali2ed, swollen was increase in the morning

Bomitting (C) after eating and filling whate)er be eating Nausea (C), @e)er (') ,ecrease in appetite ,ecrease in urine production since * months before hospitali2ed and foam up

,efecation is bleeding since &! days before hospitali2ed

Pre ious Illness History : $here was no history of suffering any disease that need hospitally #a!ily Illness History : None of his family members got the same illness

Social$ econo!ic$ an% e%ucational &ac'groun% : Patient is a dri)er

PHYSIC"( E)"MIN"TION *ital Sign : S'in General -ppearance 5 moderate illness 6onsciousness 3lood Pressure Pulse 0ate 0espiratory 0ate 3ody temperature +kin 9edema Nutrient condition -nemia : Normal 5 composmentis cooperati)e 5&*<"8< mmHg 5 88 %"min 5 4 %"min 5 7< 6 5 cyanosis ('), sweating (') 5 (C) 5 3ody weight5 7& kg 5 (') 3ody length 5 &4* cm

(y!ph no%e : No enlargement Hea% : 6onDuncti)a was not anemic +clera was not icteric Nec' : No enlargement of lymph nodes and thyroid gland EBP ! ' * cmH*9

Thora+ @orm 5 normochest. ' (ungs I 5 +ymetric mo)ement P5 @remitus was the same on the right and left side P5 +onor on the right and left side -5 Besicular normal, rales ('), whee2ing (') ' Heart I 5 Ictus was not )isible P 5 Ictus was palpable at one finger medial at .(6+ B I6+, not strong lift P 5 .eft border 5 one finger medial at .(6+ B I6+ 0ight border 5 right sternalis line. ?pper border 5 *nd I6+. -5 0egular rhythm, murmur (') "&%o!en I 5 /nlargement (C) with F* cm of bundle P 5 Hepar and spleen not palpable, tenderness (C), ballottement (') P 5 ,ullness, shifting dullness (C) -5 Normal peristaltic sound ,ac' I 5 +imetric mo)ement P 5 @remitus was the same on the right and the left side P 5 +onor on the right and the left side

- 5 Besicular normal, rales ('), whee2ing (') E+tre!ities ' ' ' Pitting edema (C) Physiologic reflect 5 C"C N Pathologic reflect 5 '"'

-OR.IN/ DI"/NOSIS Nephrotic +yndrome

TRE"TMENT 3ed 0est 9* High calory and low salt diet .asi% @urosemid -spar A

S0//EST E)"MIN"TION 3?@ routine $otal Protein -lbumin and Globulin serum ?reum 6reatinine $otal 6holesterol

#O((O- 0P On Oct 12th 1334 Laboratory Findings 3lood 5 Hb 5 F,& mgG .eukocyte 5 8F<<"mm /rytrocyte 5 *,4 million"mm Hematocrit 5 * ,7 )olG $rombocyte 5 1<.<<<"mm $otal protein 5 1,8 mgG -lbumin 5 &,& mgG Globulin 5 ,7 mg G $otal bilirubin 5 <,*1 mgG ,irect 3ilirubin 5 <,&* mgG Indirect 3ilirubin 5 <,&* mgG ?reum 5 81, mgG 6reatinin 5 <,8 mgG +GP$ 5 &* mgG +G9$ 5 &&mgG

On Oct 15th 1334 Laboratory Findings 3lood 5 Hb 5 F, mgG .eukocyte 5 &&.!<<"mm ./, 5 <"hr /rytrocyte 5 million"mm $otal 3ilirubin 5 <,& mgG ,irect 3ilirubin 5 <,!* mgG Indirect 3ilirubin 5 <, < mgG ?reum 5 47,1 mgG 6reatinine 5 &,4 mgG +G9$ 5 *< mgG +GP$ 5 &< mgG Globulin 5 <,& mgG

Hematocrit 5 *1 )olG ,iff. 6ount <"<"1"4 "*7"4 $rombocyte 5 1*4.<<<"mm $otal Protein 5 ,4 mgG -lbumin 5 ,! mgG

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On Oct 16th 1334 "7 : ,yspnea (C) Nausea (C) +wollen (C) PE : G(oderate 6onsc 6(6 3P &*<"8< P0 8*%"mnt 00 *8%"mnt $ 7H6

-bdomen 5

/nlargement (C) with F* cm of bundle Hepar and spleen not palpable +hifting dullness (C)

D7 : st# Th7 : 3ed rest 9* .asi% -spar A

On Oct 18th 1334 "7 : ,yspnea (C) Nausea (C) +wollen (C) +tomach pain (C) 3leeding defecation

PE :

G6onsc (oderate 6(6 -bdomen 5

3P & <"7<

P0 8<%"mnt

00 <%"mnt

$ 7H6

/nlargement (C) with 87 cm of bundle Hepar and spleen not palpable

&&

+hifting dullness (C)

(a&oratory #in%ings : $otal 6holesterol 5 ,8 mgG $rigliceride 5 4* mgG D7 : Nephrotic syndrome -cute Gastritis Th7 : 3ed rest 9* +pirolacton .asi% -spar A -ntacid

On Oct 49st 1334 "7 : ,yspnea (C) Nausea (C) +wollen (C) PE : G6onsc (oderate 6(6 =eight 5 47 kg .ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) with 84 cm of bundle Hepar and spleen not palpable +hifting dullness (C) 3P &&<"7< P0 4<%"mnt 00 *%"mnt $ *H6

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R: : +usp. Pleural /fussion D7 : Pleural efussion e.c. Nephrotic syndrome -cute Gastritis Th7 : continue

On No 9st 1334 "7 : ,yspnea (C) Nausea (C) +wollen (C) PE : G6onsc (oderate 6(6 3P &&<"7< P0 4<%"mnt 00 *1%"mnt $ 7H6

.ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) with 8F cm of bundle Hepar and spleen not palpable +hifting dullness (C) (a&oratory #in%ings : /sbach 5 !,<F gG per *1 hr (!&! cc) D7 : Nephrotic syndrome e.c. nephropati membranosa Pleural efussion -cute Gastritis DD7 : Nephrotic syndrome e.c. nephrosis lipoid Th7 : continue

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Suggest E+a!ination : 0enal 3iopsy

On No 4th 1334 "7 : ,yspnea (C) Nausea (C) +wollen (C) PE : G6onsc (oderate 6(6 3P &&<"7< P0 48%"mnt 00 *4%"mnt $ 7H6

.ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) Hepar and spleen not palpable +hifting dullness (C) D7 : st# Th7 : continue

On No ;th 1334 "7 : ,yspnea (C) 6ough (C) Nausea (C) +wollen (C)

&1

PE :

G6onsc (oderate 6(6

3P &&<"7<

P0 &<<%"mnt

00 *8%"mnt

$ 7H6

.ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) Hepar and spleen not palpable +hifting dullness (C) D7 : st# Th7 : continue

On No <th 1334 "7 : ,yspnea (C) 6ough (C) Nausea (C) +wollen (C) PE : G6onsc (oderate 6(6 3P &1<"8< P0 &&4%"mnt 00 *1%"mnt $ 7H6

.ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) Hepar and spleen not palpable +hifting dullness (C)

&!

(a&oratory #in%ings : ?rine 5 Protein C* 0eduction C* ?robilin C& 3ilirubin (') D7 : st# Th7 : continue

On No 2th 1334 "7 : ,yspnea (C) 6ough (C) Nausea (C) +wollen (C) PE : G(oderate 6onsc 6(6 3P &!<"F< P0 &&*%"mnt 00 *8%"mnt $ 7H6

=eight 5 41 kg .ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) with F7 cm of bundle Hepar and spleen not palpable +hifting dullness (C) (a&oratory #in%ings : ?rine 5 Protein C*

&4

0eduction C D7 : st# Th7 : 3ed 0est .asi% -ntacid Basotin ,(P +yrup 9* -spar A Prednison -minophyllin

On No 5th 1334 "7 : ,yspnea (C) 6ough (C) PE : G6onsc (oderate 6(6 =eight 5 44 kg .ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) Hepar and spleen not palpable +hifting dullness (C) D7 : st# Th7 : continue 3P &!<"F< +wollen (C) Nausea (C) P0 8<%"mnt 00 *%"mnt $ !,7H6

&7

On No 6th 1334 "7 : ,yspnea increase 6ough increase PE : G6onsc (oderate 6(6 =eight 5 44 kg .ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) with F7 cm of bundle Hepar and spleen not palpable +hifting dullness (C) (a&oratory #in%ings : ?rine 5 Protein C 0eduction C /sbach 1, gG per *1 hr (!&<cc) D7 : st# Th7 : continue 3P &!<"&<< +wollen (C) Nausea (C) P0 &<<%"mnt 00 %"mnt $ !H6

On No 93th 1334 "7 : ,yspnea (C) 6ough (C) Nausea (C) PE : G6onsc (oderate 6(6 3P &!<"&&< P0 F4%"mnt 00 %"mnt $ 4H6 +wollen (C) 3leeding defecation

&8

.ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C) Hepar and spleen not palpable +hifting dullness (C) D7 : st# Th7 : 3ed rest .asi% -ntacid Basotin ,(P +yrup Bit A 9* -spar A Prednison -minophyllin $ransamin Bit 6

On No 99th 1334 "7 : ,yspnea (C) 6ough (C) Nausea (C) PE : G6onsc (oderate 6(6 3P &1<"&<< +wollen (C) 3lood )omitting (C) 3leeding diarrhoea P0 81%"mnt 00 *%"mnt times I J glass $ 4H6

.ung 5 Prolonged e%piration (') =hee2ing (') 0ales (C) -bdomen 5 /nlargement (C)

&F

Hepar and spleen not palpable +hifting dullness (C) D7 : st# Th7 : continue P-$I/N$ P-++ -=-K IN 96$ &&th, *<< at &&. < pm

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DISC0SSION - < years old man was admitted to the internal medicine department at the ,r. -hmad (ochtar Hospital on 9ctober *4th,*<< with chief complaint was dyspnea since & day before hospitali2ed, enlargement of stomach since * months before hospitali2ed, influence with position change. @ace, hand and feet was swollen since * months before, swollen was increase in the morning and the urine production was decrease since * months before hospitali2ed and foam up. @rom physical e%amination found that pulse rate was 88%"mnt, blood pressure &*<"8< mmHg, stomach, face, hand and feet was swollen. 3y percussion of abdomen we found that shifting dullness was positi)e. $here is pleural efussion as a complication of nephrotic syndrome. @rom laboratory datas, we found hypoproteinemia, hyperlipiduria, proteinuria. - line with the datas abo)e the diagnosis was nephrotic syndrome caused by nephropaty membranosa and the differential diagnosis was nephrotic syndrome caused by nephrosis lipoid (minimal change lession) and therapy was bed rest, high calory and low salt diet, .asi% inDection, -spar A, +pirolacton, -ntacid, Prednison, Basotin, -minophyllin, ,(P +yrup, $ransamin, Bit A, Bit 6. $o make sure with ," we recomanded to e%amination of 0enal 3iopsy.

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