PEMICU 1

BLOK UROGENITAL
Cindy Claudia
405140139
LO 1
MM Anatomi Ginjal ,VU ,Traktus urinarius
,Genitalia Laki laki & Perempuan
Embriologi
 Komponen sistem urogenital :Urinary system & genital system
 Keduanya berasal dari :mesoderm intermediate bersama dgn
dinding posterion dari rongga abdominal ,duktus ekskretorius
,cloaca
 Urinary System

Kidney System
Sistem terbentuknya ginjal dimulai dari cranial ke kaudal saat
masa intrauterine
a) Pronephrospd sistem ini belum sempurna & blm berfungsi
b) Mesonephros mngkin dapat berfungsi dalam wktu singkat
pd tahap fetus awal
c) Metanephros permanent kidney
a)Pronephros
pd tahap mnggu ke 4 ,pronephros ditandai
munculnya 7-10 solid cell group di regio cervical
Solid Cell Group akan membentuk vestigial
excretory unit ,nephrotomes (yg akan regresi)
 Pd akhir mnggu ke 4 sistem pronefros akan hilang
Mesonephros
 The mesonephros and mesonephric ducts are derived
from intermediate mesoderm from upper thoracic to
upper lumbar (L3) segments.

 Early in the 4th week of development,during

regression of the pronephric system the 1st
excretory tubules of the mesonephros appear.

 They lengthen rapidly, form an S-shaped loop&

acquire a tuft of capillaries will form a glomerulus
at their medial extremity
 Around the glomerulus, the tubules form Bowman’s
capsule, and together these structures constitute a
renal corpuscle.
 the tubule enters the longitudinal collecting duct
known as the mesonephric or wolffian duct.

In the middle of the 2nd month, the mesonephros forms

a large ovoid organ on each side of the midline
 Developing gonad is on its medial side, the ridge formed by
both organs is known as the urogenital ridge

 Caudal tubules are still differentiating, cranial tubules and

glomeruli show degenerative changes, and by the end of
the 2nd month, the majority have disappeared.

 In the male, a few of the caudal tubules and the

mesonephric duct persist & participate in formation of the
genital system, but they disappear in the female.
Metanephros: The Definitive Kidney
 The third urinary organ: the metanephros or
permanent kidney, appears in the 5th week.

 Its excretory units develop from metanephric

mesoderm in the same as in the mesonephric system.

 The development of the duct system differs from that

of the other kidney systems.
Collecting System
 Collecting ducts of the permanent kidney develop from the
ureteric bud, an outgrowth of the mesonephric duct close to
its entrance to the cloaca.

 The bud penetrates the metanephric tissue

 The bud dilates, forming the primitive renal pelvis, and splits
into cranial and caudal portions, the future major calyces.

 Each calyx forms 2 new buds while penetrating the

metanephric tissue.

 These buds continue to subdivide until 12 or more generations

of tubules have formed
 The tubules of the 2nd order enlarge and absorb
those of the 3rd and 4th generations, forming the
minor calyces of the renal pelvis.

 Collecting tubules of the 5th and successive

generations elongate considerably and converge on
the minor calyx forming the renal pyramid

 The ureteric bud gives rise to the ureter, the renal

pelvis, the major and minor calyces, and
approximately 1 to 3 million collecting tubules.
Excretory System
 Newly formed collecting tubule is covered at its distal end by
ametanephric tissue cap
 Cells of the tissue cap form small vesicles, the renal vesicles, which
in turn give rise to small S-shaped tubules

 Capillaries grow into the pocket at one end of the S and

differentiate  glomeruli.
 These tubules + glomeruli form nephrons/excretory unit

 The proximal end of each nephron forms Bowman’s capsule.

 Continuous lengthening of the excretory tubule results in formation of

the 
proximal convoluted tubule, loop of Henle, and distal convoluted
tubule
 the kidney develops from two sources:
(1) metanephric mesoderm, which provides excretory
units
(2) the ureteric bud, which gives rise to the collecting
system
 Nephrons are formed until birth
 Urine production begins early in gestation, soon after
differentiation of the glomerular capillaries, which
start to form by the 10th week.
Molecular Regulation of Kidney
 Epithelium of the ureteric bud from the mesonephros interacts
with mesenchyme of the metanephric blastema.

 The mesenchyme express WT1, a transcription factor that

makes this tissue competent to respond to induction by the
ureteric bud.

 WT1  regulates production of glialderived neurotrophic

factor (GDNF) and hepatocyte growth factor (HGF, or scatter
factor) by the mesenchyme, and these proteinsstimulate
branching and growth of the ureteric
 buds
 The tyrosine kinase receptors RET(for GDNF), and
MET(for HGF) are synthesized by the epithelium of
the ureteric buds.

 The buds induce the mesenchyme via fibroblast

growth factor 2 (FGF2) and bone morphogenetic
protein 7 (BMP7)

Function : Growth factors block apoptosis & stimulate

proliferation in the metanephric mesenchyme while
maintaining production of WT1
 Conversion of mesenchyme to epithelium for
nephron formation (mediated by the uretric buds
through expression WNT9B &WNT6UPREGULATE
PAX2 & WNT4 (in metanephric mesenchyme )
 PAX2 promotes formation of tubule
 WNT 4causes the condensed mesenchyme to
epithelialize & form tubules.
 Fibronectin, collagen I, and collagen III are
replaced with laminin and type IV collagen,
characteristic of an epithelial basal lamina

 In addition, the cell adhesion molecules syndecan

and E-cadherin, which are essential for
condensation of the mesenchyme into an
epithelium, are synthesized.
Positition of the kidney
 Kidneyinitially in the pelvic region ,later shift to
more cranial position in the abdomen .

 Ascent of the kidney is caused??by diminution of body

curvature & by growth of the body in the lumbar &
sacral regions

 The metanephros receives its arterial supply from a

pelvic branch of the aorta.
 During its ascent to the abdominal level it is
vascularized by arteries that originate from the aorta
Function of the kidney
the definitive kidney formed from the metanephros
become functional near 12th week
urine is passed into the amniotic cavity & mixes with
the amniotic fluid the fluid is swallowed by the fetus
& recycles through the kidney

: during fetal life,the kidneys are not responsible for

excretion of waste product (placenta serves this
function)
Bladder & Urethra
 Saat mnggu ke 4-7 perkembangankloaka terbagi mnjadi
bag anterior (urogenital sinus ) & posterior (anal canal).
 Septum urorectal merupakan lapisan dari mesoderm antara
kanal anal primitive & sinus urogenital.
 Ujung dari septum akan membentuk perineal body

 3 bagian dari sinus urogenital :

a) Bagian atas dan terbesar:urinary bladder
 Pd awalnya urinary bladder nyambung the allantois ,tetapi
saat lumen pd allantois mengalami obliterasi ,trdpt urachus
(thick fibrous cord) yg mnghubungkan apex dari bladder
dgn umbilicus
 Pd org dewasa ,membentuk ligamentum umbilical
mediana
b) Kanal sempit :bagian pelvic dari sinus urogenital
pd laki2 :membentuk prostat & bag membranosa
urethra
c) Bagian terakhir adalah phallic part dari urogenital
sinus
bagian ini datar dari 1 sisi ke sisi lain & saat
tuberkulum genital sdh trbentuk ,bagian ini akan
tertarik ke arah ventral
 Saat differensiasi kloaka ,bag kaudal dari duktus
mesonephric diabsorbsi kedlm dinding kandung
kemih.
 Ureter berkembang dari duktus mesonephric
 Karena posisi ginjal smakin naik orifisium dari
ureter bergerak kranial.
 Ductus mesonephric bergerak saling berdekatan u/
msk kedalam prostathic uretra ( pd laki laki akan
membentuk duktus ejakulatorius )
 Pada akhir mnggu ke 3 epitelium dari prostatic
urethra mulai berproliferasi & berpenetrasi ke
sekitar mesenkim.
 Pada laki laki membentuk kelenjar prostat
 Pada perempuan bagian kranial uretra
membentuk kelenjar urethral dan paraurethral
Embriology of the Genital System
 Gonads appear as a pair of longitudinal ridges ,the
genital/gonadal ridges (formed by proliferation of the epithelium &
condensation of mesenchyem)
 Primordial germ cells originate inepiblast migrate by 3rd
week reside among endoderm cells in the wall of yolk sacby 4th
week ,migrate to the primitive gonads at the beginning of the 5th
week invading genital ridges in the 6th week

 If fail to reach the ridges ,the gonads do not develop

 the primordial germ cells have an inductive influence on

development of the gonad into ovary or testis
 Before & during arrival of primordial germ cells the epithelial of
the genital ridge proliferates form PRIMITIVE SEX CORDS (gonad
is known as INDIFFERENT GONAD)
Testis
 If the embryo is genetically male, the primordial germ cells carry an
XY sex chromosome complex

 The primitive sex cords continue to proliferate and penetrate deep

into the medulla to form the testis or medullary cords.

 During further development, a dense layer of fi brous connective

tissue, the tunica albuginea, separates the testis cords from the
surface epithelium

 By the eighth week of gestation, Leydig cells begin production of

testosterone and the testis is able to infl uence sexual differentiation
of the genital ducts and external genitalia.
 Testis cords remain solid until puberty, when they
acquire a lumen forming the seminiferous tubules

 Once tubulus seminiferus are canalized join the

rete testis tubules enter ductuli
efferent(remaining part of the excretory tubules of
the mesonephric system)(link the rete testis &
wolffian duct)become ductus deferens
Ovary
1) In female embryos with an XX sex chromosome complement and no
Y chromosome, primitive sex cords dissociate into irregular cell
clusters.

2) Later, they disappear and are replaced by a vascular stroma that

forms the ovarian medulla
3) The surface epithelium of the female gonad continues to proliferate
4) 7th weekgive rise to 2nd generation of cords, cortical cords,
which penetrate the underlying mesenchyme.
5) In the third month, these cords split into isolated cell clusters.
6) Cells in these clusters continue to proliferate and begin to surround
each oogonium with a layer of epithelial cells called follicular
cells.
7) The oogonia and follicular cells constitute a primordial follicle
 Initially, both male and female embryos have two
pairs of genital ducts: mesonephric (wolffi an)
ducts and paramesonephric (müllerian) ducts.
Externa Genitalia in Female
 Estrogens stimulate development of the external
genitalia of the female.
 The genital tubercle elongates only slightly forms
the clitoris ,urethral folds do not fuse ( as in male
)but develop into the labio minora
 Urogenital groove is open and forms the vestibule
Anatomi Ginjal ,Traktus
Urinaris,Genitalia
REN (GINJAL )
 Ginjal berbentuk :oval
 Berfungsi mengeluarkan air,garam,dan hasil buangan
metabolisme protein yg ber> dari darah saat mmbawa zat
gizi & zat kimia ke darah

 REN terletak retroperitoneal pd dinding abdomen

posterior
1 pd sisi columna vertebralis setinggi vertebra T12-L3
Ren dextra biasanya trletak sdikit di inferor ren sinistra
 REN berwarna cokelat kemerahan & memiliki ukuran
panjang sekitar 10 cm,lebar 5 cm dan tebal 2,5 cm
 Di superior: ginjal berhubungan dengan diafragma
,yg memisahkan dari cavitas pleuralis & costa 12
 Di inferior permukaan posterior ginjal :berhubungan
dgn musculus quadratus lumborum

 Nervus & P.darah subscostalis & Nervus

ilioinguinalis ,iliohypogastricus turun scara
diagonal mnyilang prmukaan posterior ginjal
 Sblh anterior Ren dextrahepar,duodenum,colon ascenden
 Ren dextra dipisahkan dari hepar recessus hepatorenalis
 Ren sinistra berhub dgn gaster ,lien ,pancreas,jejunum & colon
descendens.

 Batas medial konkaf setiap ginjal :celah vertikal (hilum

renal)(dimana arteri renalis msk & vena renalis serta pelvis
renalis mninggalkan sinus renalis )

 Di hilum vena renalis ada di anterior arteri renalis (trletak di

anterior pelvis renalis
 Hilum Renalejln msk ke ruang dlm ginjal ,sinus renalis,yg diisi o/
pelvis renalis,calices,pembuluh & saraf srta lemak.

 Tepi lateral stiap ginjal berbentuk konveks

 Tepi medial konkaf dimana trletak sinus renalis & pelvis renalis

 Pelvis renalis :ekspansi ujung superior ureter yg rata & berbentuk

seperti terowongan.
 Apeks pelvis renali lanjut mnjadi ureter

 Pelvis renalis menerima 2/3 calices renales majores msing2 mbagi

2 /3 calices renalis minores.
 Stiap calices minores diidentasi papilla renalis,apeks pyramides (dri
sini urin dieksresi)
Ureter

 Mrupakan duktus muskular (panjang 25-30 cm) dgn lumen

smpti yg membwa urin dari renvesica urinaria
 Ureter berjalan di inferior dr apeks pelvis renalis brjalan
pd pelvic brim (tepi pelvis) pd bifurkasio arteri ilaca
communis

 Berjalan dispanjang dinding lateral pelvis dan masuk VU

 Bag abdominal ureter: menempel dgn peritoneum parietal
& trletak retroperitoneal
 Ureter dpt berkonstriksi di 3 tempat
 Pd taut ureter & pelvis renalis
 Dimana ureter menyilang tepi apertura pelvis superior
 Selama pasase melalui dinding vesica urinaria
 Cabang arteri:berasal dari arteri renalis ,ada jg yg
dari arteri testicularis /arteri ovarica ,aorta
abdominalis & arteri iliaca communis.

 Vena yg mendrainase bag abdominal ureter

bermuara ke dlm vena renalis & gonadal
(testicularis/ovarica)
 Pmbuluh limfatik brgabung dengan pembuluh
pngumpul di ginjal /berjalan ke :
 Nodi lumbales dekstri/sinistri (cavales /aortici)
 Nodi iliaci communes
Anatomi permukaan ren & ureter

 Hilum renale sinistra trletak di dkat planum

transpyloricum (5cm dr planum medianum)
 Di posterior ,bag sup ginjal trletak di sblh dalam
costa XI dan XII
 Tinggi ginjal berubah slama respirasi ,ginjal
bergerak 2-3 cm dgn arah vertikal slama gerakan
diafragma
Pembuluh darah & Persarafan Ginjal
 Arteri renalis & Vena Renalis
 Arteri renalis asal dari area stinggi discus IV diantara
vertebra L1 dan L2.
 Arteri renalis dekstra yg lbh pnjang berjalan di posterior
IVC

 Setiap arteri trbagi didkat hilum mnjadi arteri segmental

(End artery )
 Segmen superior (apikal):diperdarahi o/Arteri segmenti
superioris (apikal)
 Segmen anterosuperior & anteroinferior diperdarahi o/ arteri
segmenti anterosuperior & segmenti anteroinferior
 Arteri ini berasal dari cabang anterior arteri renalis
  Arteria segmenti posterioris berasal dari lanjutan cabang
posterior arteri renalis ,mmprdarahi sgmen posterior ginjal .

 Bbrp vena renalismndrainase stiap ginjal &

mnyatummbentuk vena renalis sinistra dan dekstra
 Vena renalis dekstra & sinistra trletak di anterior arteri
renalis dekstra dan sinistra.

 Vena renalis sinistra lbh panjang  mnerima vena

suprarenalis sinistra ,vena gonadal
(testicularis/ovarica)sinistra& vena lumbalis
ascendenkmudian berjalan di anterior aorta

 Tiap vena renalis bermuara ke dlm IVC

 Limfatik & Saraf

 Pembuluh limfatik renalis  Persarafan ginjal asalny dri

mngikuti vena renalis dn
bermuara ke dlm nodi
lumbales dextri dan sinistri
(cavales dan aortici )
 Pmbuluh limfatik dri bag sup
ureter bs gabung dgn
pmbuluh limfatik dr ginjal
/berjalan langsung ke nodi
lymphatici.
 Pmbuluh limfatik dr bag
tngah ureter muara ke
nodi iliaci communis
 Pmbuluh inferior nodi iliaci
communis ,externa & interni
pleksus renalis (trdiri dari serat
simpatis & parasimpatis)
 Plexus renalis dipersarafi o/
serat serat dr nervus splanchnicus
abdominopelvicus
 Persarafan bag abdominal
ureter:pleksus hypogastricus
superior,aorta abdominalis &
renalis
Viscera Pelvis
 Meliputi vesica urinaria & sbagian ureter,sistem reproduksi & bag distal sal
pencernaan( rectum)
 Organ urinari pelvis
 Ureter (mngalirkan urin ke ginjal)
 Vesica urinaria (mnyimpan urin smentara)
 Urethra (mengalirkan urin dari VU ke luar)

 Ureter ada di retroperitoneal ,sparuh superior ada di abdomen dan

separuh inferior ada di pelvis
 Saat mnyilang bifurcatio arteri iliaca communis / awal arteri iliaca externa
ureter berjalan pd tepi pelvis tinggalin abdomenmsk ke pelvis minor

 Ujung inferior ureter dikelilingi o/ pleksus venosus vesicalis

 Urin dibwa ke bwh ureter dgn kontraksi peristaltik (dlm interval 12-20 mnt)
Suplai arteri ureter
cabang dari arteri ovarica,iliaca communis & iliaca
interna memanjang & mnyuplai bag pelvis ureter ,yg
beranastomsis spanjang ureter u/ mmbntuk suplai
darah terus menerus.

Arteri paling konstan yg mmprdarahi pars terminalis

ureter pd perempuan: cbang arteri uterina
Sumber cbang pd laki laki: arteria vesicalis inferior
Drainase Venosa& Inervasi pd ureter
Limfatik pd ureter
vena dari ureter persarafan ureter
mnyertai arteri berasal dari
limfe mendrainase dr pleksus otonom yg
sup ke inf ke nodi berdekatan.
lymphatici iliaci
communes dan
lumbalis & nodi
lymphatici iliaci
externi dan interni
Vesica Urinaria
 Suatu cekungan berongga dgn dinding muskular kuat.
 Vesica urinari mrupakan reservoar temporer u/ urin dan memiliki ukuran,bentuk
,posisi ,hub yg berbeda2 berdasar isi.

 Bila kosongVU ada di pelvis minor (sbag trletak di sup dan sbag di posterior os
pubis )
 VU dipisahkan dr tlg2 o/ spatium retropubicum (Retzius ) & trletak di inferior
peritoneum
(trletak pd os pubis & symphisis pubis di anterior)
(dasar pelvis: di posterior )

 VU relatif bebas di dlm jar berlemak subkutan ekstraperiotenal (kecuali

u/collumnya )trtahan o/ ligamentum lateral vesicae & arcus tendineus fascia
pelvis
Trutama komponen anterior nya : pd laki laki: ligamentum puboprostaticum ,pd
perempuan:ligamentum pubocesicale
 VU yg kosong pd org dewasa trletak hampir sluruhny dlm
pelvis minro
 Jika terisi,vesica msk pelvis major & naik pd jaringan
berlemak ekstraperiotenal dinding abdomen anterior.

 Trdpt 4 permukaan vesica ( superior,2

inferolateral,posterior)tmpak saat mlihat vesica kosong
 Apex vesicamnjuk ke arah superior symphisis pubis jika vescia
kosong
 Fundus vesicatrbntuk o/ dinding posterior
 Corpus vesicabag utama vesica antara apex dan fundus
 Fundus permukaan inferolateral brtemu di inferior pd collum
vesicae
 Tiap sisi os pubis & fascia yg melapisi m.levator ani &
obturatorius internus sup berhub dgn prmukaan
inferolateral vesica

 Pd laki2 fundus dipisahkan dr rectum o/ septum

rectovesicale fascial, & glandula seminalis ,ampulla
ductus deferentis (di bag lateral)

 Pd perempuan,fundus berhub dgn?dinding anterior sup

pd vagina
 Dinding VU??M.detrusor
 Collum vesica lakilakiserat otot mmbentuk sphincter
urethralis interna (Fungsi: berkontraksi selama
ejakulasi u/ mncegah ejakulasi retrograd serat otot
berlanjut dgn jar fibromuskular prostat

 Ostium Ureteris dilingkari o/ lengkung otot

detrusor yg mengencang bila vesica berkontraksi
(mncegah refluks urin ke dlm ureter)
 Suplai arterial pd vesica
arteri utam yg mmprdarahi VU adlh cbang arteri iliaca
interna
Arteri vesicalis superior :mmprdarahi bag anterosuperior
vesica
Pd laki2arteri vesicalis inferior mmprdarahi fundus
& collum vesicae

Pd perempuanarteri vaginalis mngirim cbang kcil ke

bag posteroinferior VU

Arteri obturatoria & glutea inferior

Inervasi vesica
Serat simpatis dibw dari medulla spinalis ke pleksus
vesicalis (trutama melalui pleksus dan nervus
hypogastricus )
serat parasimpatis dr medulla spinalis dibw o/n
splanchnicus pelvicus & plexus hypogastricus inf
 Organ Genital interna Laki2
 Organ genital interna meliputi testis ,epididimis ,ductus deferens ,glandula
seminalis ,ductus ejaculatorius ,prostat & glandula bulbourethralis
Ductus Deferens
Kelanjutan ductus pd epididimis
pnya dinding muskular tebal & lumen kecil
awal dari cauda epididimis
naik di posterior testis (sblh medial epididimis)
mnembus dinding abdomen anterior mellaui canalis inguinalis
brjalan di spanjang dinding lateral pelvis
berakhir dgn bergabung pd ductus glandula seminalis u/ membentuk ductus ejaculatorius

Ductus menyilang di superior ureter dkat sudut posterolateral vesica u/ mncai fundus vesica

Di bag posterior vesicaductus deferens awalny trletak di superior glandula seminalis ttp turun di
medial ureter ductus deferen membesar membentuk ampulla ductus deferen

Arteri ductus deferensarteria ductus deferentis berasal dri arteri vesicali s superior &
beranastomosis dgn arteri testicularis
Glandula Seminalis
suatu struktur memanjang yg trletak diantara fundus vesicae & rectum
kelenjar yg trletak oblik di bag sup prostat & tdk mnyimpan sperma
mensekresi cairan alkali kental yg mengandung fruktosa (smber energi sperma) &
zat koagulatif yg bercampur dgn sperma ktika msk ke dlm ductus ejaculatorius &
uretra

Ujung sup :dilapisi peritoneum & trletak di posterior ureter

Ujung inf: dkat dgn rectum & dipisahkan oleh septum rectovesicale

Ductus deferen+ ductus pd glandula seminalis ductus ejaculatorius

suplai arteri pd glandula seminalisareri ke glandula seminalis berasal dr arteri
rectalis media & arteria vesicalis inferior
 Ductus Ejaculatorius
kluar dkat collum vesicae& berjalan berdekatan ktika lewat bag anteroinferior
melalui bag posterior prostat
Ductus ejaculatorius brtemuuntuk bermuara pd colliculus seminalis

Suplai arterial ductus ejaculatorius: arteri ductus deferentis ,biasanya cabang arteri
vesicalis superior

Prostat
glandula accesorius pling besar pd laki2
bag glandular menyusun skitar 2/3 prosta ,1/3 : fibromuskular
prostat mengelilingi pars prostatica urethrae
adanya capsula fibrosa prostat padat dan neurovaskular
prostat dikelilingi oleh lapisan viseral fascia pelvis membentuk selubung
prostatik fibrosa yg tipis brlanjut di anterolateral dgn lig puboprostaticum
 Lobus prostat dpt dibagi mnjadi:
 Isthmus prostat trletak di anterior urethra ,isthmus bersifat
fibromuskular
 Lobus inferoposterior (posterior) trletak di posterior uretra & di inf
ductus ejaculatorius
 Lobus prostatatae dexter et sinistermmbentuk bag utama prostat
 Lobus medius trletak di antara urethra & ductus ejaculatorius &
berdekatan dgn collum vesicae
 Cairan yg keluar dari prostat mnambah 20% vol semen

 Suplai Arteri Prostat Arteri pd prostat mrupakan cabang

utama arteri iliaca interna
(Terutama: arteri vesicalis inferior,arteria rectalis media &
Pudenda interna
Glandula Bulbourethralis (kelenjar Cowper)
trletak posterolaterla trhdp pars intermedia
urethra
Ductus glandula bulbourethralis berjalan melalui
membran pernei dengan pars intermedia urethrae
& brmuara mlalui apertura kdlm bag proks urethra
spongiosa pd bulbus penis
LO2
MM Histologi Ginjal ,Traktus Urinarius ,Genitalia
laki2 dn prempuan
 Kidney: Cortex, Medulla, Pyramid, and
Minor Calyx
The kidney is subdivided into an outer darker-staining cortex and an inner lighter-staining
medulla.
1) Externally, the cortex  covered with a dense, irregular connective tissue renal capsule.
2) The cortex contains: both distal and proximal convoluted tubules (4, 11), glomeruli (2),
and medullary rays (3).
 Present also in the cortex are the interlobular arteries (12) and interlobular
veins (13).

The medullary rays (3) are formed by the straight portions of nephrons, blood
vessels, and collecting tubules that join in the medulla to form the larger collecting
ducts (6).

The medullary rays do not extend to the kidney capsule (1) because of the
subcapsular convoluted tubules (10).

 The medulla comprises the renal pyramids. The base of each pyramid (5) is adjacent to the
cortex and its apex forms the pointed renal papilla (7) that projects into the surrounding,
funnellike structure,
 the minor calyx (16), which represents the dilated portion of the ureter. The area cribrosa
(9) is pierced by small holes, which are the openings of the collecting ducts (6) into the
minor calyx (16).
 The tip of the renal papilla (7) is usually covered with a simple columnar
epithelium (8).
 As the columnar epithelium of the renal papilla (7) reflects onto the outer wall of
the minor calyx (16), it becomes a transitional epithelium (16).

 A thin layer of connective tissue and smooth muscle (not illustrated) under this
epithelium then merges with the connective tissue of the renal sinus (15).

 Present in the renal sinus (15) are branches of the renal artery and vein called
the interlobar artery (17) and the interlobar vein (18).

 The interlobar vessels (17, 18) enter the kidney and arch over the base of the
pyramid (5) at the corticomedullary junction as the arcuate artery and vein (14).

 The arcuate vessels (14) give rise to smaller, interlobular arteries (12) and
interlobular veins (13) that pass radially into the kidney cortex and give rise to the
afferent glomerular arteries that give rise to the capillaries of the glomeruli (3).
 The renal corpuscles (5, 9) consist  glomerulus (5a) and the glomerular
(Bowman’s) capsule (5b).

 The glomerulus (5a) is a tuft of capillaries that is formed from the afferent
glomerular arteriole (11), and is supported by fine connective tissue and
surrounded by the glomerular capsule (5b).

 Visceral layer (9a) of the glomerular capsule (5b) surrounds the glomerular
capillaries with modified epithelial cells called podocytes (9a)

 At vascular pole (8) of the renal corpuscle (9), the epithelium of the visceral layer
(9a) reflects to form the simple squamous parietal layer (9b) of the glomerular
capsule (5b).

 The space between the visceral layer (9a) and the parietal layer (9b) of the renal
corpuscle (9) is the capsular space (10).
 2 types of convoluted tubulesThese are the proximal convoluted tubules (1)
and distal convoluted tubules (2, 4).
 The convoluted tubules are the initial and terminal segments of the nephron.

 The proximal convoluted tubules (1) are longer than the distal convoluted tubules (2,
4) and aremore numerous in the cortex.
 exhibit a small, uneven lumen
 a single layer of cuboidal cells with eosinophilic, granular cytoplasm.
 A brush border (microvilli) lines the cells

 The medullary rays include the following three types of tubules: straight
(descending) segments of the proximal tubules (14), straight (ascending)
segments of the distal tubules (6), and the collecting tubules (12).

 The medulla contains only straight portions of the tubules and the segments of the
loop of Henle (thick and thin descending segments, and thin and thick ascending
segments). The thin segments of the loops of Henle (15) are lined by simple
squamous epithelium and resemble the capillaries (13).
 At the vascular pole, modified epithelioid cells with cytoplasmic
granules replace the smooth muscle cells in the tunica media of the
afferent glomerular arteriole (12). These cells are the
juxtaglomerular cells (4).

 In the adjacent distal convoluted tubule, the cells that border the
juxtaglomerular cells (4) are narrow and more columnar.

 This area of darker, more compact cell arrangement is called the

macula densa (5). The juxtaglomerular cells (4) in the afferent
glomerular arteriole (12) and the macula densa (5) cells in the distal
convoluted tubule form the juxtaglomerular apparatus.
Kidney Medulla (Papillary Region )
 The papilla in the kidney faces the minor calyx and
contains the terminal portions of the collecting tubules,
now called the papillary ducts (3).

 The papillary ducts (3) exhibit large diameters and wide

lumina, and are lined by tall, pale-staining columnar cells.

 Also present in the papilla are the: straight (ascending)

segments of the distal tubules (7, 10)& the straight
(descending) segments of the proximal tubules (1, 6,
11) Interspersed among the ascending (7, 10) and
descending straight tubules (1, 6, 11) are the transverse
sections of the thin segments of the loop of Henle (5, 8)
Ureter
 Undistended lumen of the ureter (4) exhibits numerous longitudinal mucosal
folds formed by the muscular contractions.
 The wall of the ureter consists of : mucosa,muscularis, and adventitia.
 The ureter mucosa consists of : transitional epithelium (7) and a wide lamina
propria (5).
 The transitional epithelium has several cell layers, the outermost layer characterized by
large cuboidal cells. The intermediate cells are polyhedral in shape, whereas the basal cells
are low columnar or cuboidal.

 The lamina propria (5) contains :fibroelastic connective tissue, which is denser with
more fibroblasts under the epithelium and looser near the muscularis.

 In the upper ureter, the muscularis consists of two muscle layers, an inner longitudinal
smooth muscle layer (3) and a middle circular smooth muscle layer (2), An
additional third outer longitudinal layer of smooth muscle is found in the lower third
of the ureter near the bladder

 The adventitia (9) blends with the surrounding fibroelastic connective tissue and
adipose tissue (1, 10), which contain numerous arterioles (6), venules (8), and
small nerves.
Urinary Bladder
 The bladder has a thick muscular wall.
 In the wall are found: 3 loosely arranged layers of smooth muscle, the inner
longitudinal, middle circular, and outer longitudinal layers.
 The three layers are arranged in anastomosing smooth muscle bundles (1)
between which is found the interstitial connective tissue (2).
 The interstitial connective tissue (2) merges with the connective tissue of the serosa
(3).

 Mesothelium (3b) covers the connective tissue of serosa (3a) and is the
outermost layer.
 Serosa (3) lines the superior surface of the bladder,whereas its inferior surface is
covered by the connective tissue adventitia, which merges with the connective tissue
of adjacent structures.

 The mucosa of an empty bladder exhibits numerous mucosal folds (5) that
disappear during bladder distension. The transitional epithelium (6) is thicker
than in the ureter and consists of about six layers of cells. The lamina propria (7),
inferior to the epithelium, is wider than in the ureters.
LO 3
MM Fisiologi Ginjal
REABSORPSI TUBULUS
Steps of transepithelial transport
 Sekresi aldosteron ditingkatkan o/
1) Pengaktifan sistem renin-angiotensin-aldosteron oleh faktor
yang brkaitan dengan penurunan Na+ & tekanan darah.
2) Stimulasi langsung korteks adrenal o/ peningkatan
konsentrasi K+ plasma.

Angiotensin selain dapat merangsang efek aldosteron,

dpt juga u/ mendorong prtumbuhan zona glomerulosa.

3) Hormon adrenokortikotropik (ACTH) dri hipofisis

anteriormendorong sekresi kortisol bkn aldosteron –
 Di tubulus proksimal dan ansa Henle Terjadi
reabsorpis Na+ yg terfiltrasi dgn persentase tetap
(Berapapun beban Na+ )(jumlah total Na+ DI cairan
Tubuh)

 Di tubulus Distal Reabsorpsi persentase kecil Nat+

yg terfiltrasi berada dibwh kontrol hormon
Aldosteron merangsang reabsorpsi
Na+ di tubulus distal & koligentes
 Reabsorpsi Na+ yang terfiltrasi terjadi di tubulus
proksimal dan ansa Henle.
 Di bag tubulusreabsorpsi Na+ yang terfiltrasi ada
dibwh kontrol hormon.
 Tingkat reabsorpsi berbanding terbalik dengan jumlah
Na+ ditubuh.
 Jika Na+ terlalu bnyaksedikit yang direabsorspi
 Jika Na+ kurangmaka seluruh Na+ direabsorpsi
(menghemat Na+ )

 Jumlah Na+ di tubuh tercermin dalam vol CES.

 Jika jumlah Na+ diatas normalaktivitas osmotik CES
meningkat ( maka ke> Na+ akan menahan H20)
meningkatkan vol plasma.
 Jika Na+ dibwah normal aktivitas osmotik CES berkurang
jumlah H20 yang ditahan rendahvol CES berkurang
 Pengaktifan sistem renin-angiotensin
aldosteron
 Sistem yang terlibat dalam regulasi Na+  renin-
angiotensin-aldosteron (SRAA).
 Sel granular aparatus jukstaglomerulusmengeluarkan
hormon enzimatik renin ke dalam darah (sbg respon
terhadap penurunan NaCl/vol CES/pe tekanan darah).

3 masukan berikut ke sel granular meningkatkan sekresi

renin:
 Sel granular berfungsi sbg baroreseptor intrarenal,(sel ini
peka t’rhadap perubahan tekanan di arteriol aferen)dpt
mendeteksi pe tekanan darahkeluarin banyak renin.
 Sel makula densa dibag tubulus aparatus jukstaglomerulus  peka
terhadap NaCl yang melewatinya lewat lumen tubulus.
sbg respon trhadap penurunan NaCl sel makula densamemicu sel
granular keluarin >>renin

 Sel granular disarafi o/sistem saraf simpatis.

saat T.d turun refleks baroreseptor meningkatkan aktivitas
simpatismerangsang sel granularkeluarin >> renin

Sinyal yang terkait u/meningkatkan sekresi reninperlu

u/meningkatkan vol plasma meningkatkan tekanan arteri.

Peningkatan sekresi reninpeningkatan reabsorpsi Na+oleh

tubulus distal & koligentes.
Cl- secara pasif akan mengikuti Na+

Manfaat retensi NaClretensi tersebut mendorong retensi H20

Membantu memulihkan vol plasma.
 Stelah renin disekresike darahrenin bekerja u/
mengaktifkan angiotensinogen angiotensin I.
Angiotensinogen (protein plasma yang disintesis o/
hati & selalu ada di plasma dalam konsentrasi .

 Melewati paru angiotensin I diubah jadi angiotensin II

o/ angiotensin-converting enzyme (ACE) (banyak di
kapiler paru)
Angiotensin II perangsang utama sekresi hormon
aldosteron dari korteks adrenal.

 Aldosteron meningkatkan reabsorpsi Na+ o/tubulus

distal & koligentes(mendorong penyisipan sal Na+ ke
dalam membran luminal & penambahan pembawa Na+
K+ ATPase ke dalam membran basolateral sel tubulus
dan koligentes
 Lalu terjadinya peningkatan fluks pasif Na+ msk ke
tubulus dr lumen & peningkatan reabsorbsi Na+
(peningkatan pemompaan Na+ keluar sel ke dlm
plasma) disertai Cl-

 SRAA  mendorong retensi garam menyebabkan

retensi H20 & peningkatan t.darah arteri.

 Melalui umpan balik -  faktor yang memicu

pelepasan renin dihilangkan (penurunan t.darah
,penurunan vol plasma)

 Angiotensin II selain mrangsang sekresi aldosteron

merupakan :
 Konstriktor poten arteriol sistemik
 Secara langsung meningkatkan t.darah dengan meningkatan
resistensi perifer
 Merangsang rasa haus (naiknya kebutuhan cairan)
 Merangsang vasopressin
 Jika jumlah Na+,vol CES & plasma,t.darah arteri >dri
normal  sekresi renin terhambat.
Angiotensinogen tdk diaktifkan mnjadi angiotensin I
dan II sekresi aldosteron tdk terangsang tidak
terjadi reabsorpsi Na+akan keluar bersama urin
pengeluaran terus dapat dengan cpt mengeluarkan
ke> Na+ dri tubuh .

Jika tdk ada aldosteron ,garam yang bsa diekskreskan/hari

adlh 20 gram.

 Pd Sekresi aldosteron maks,semua na+ yg terfiltrasi

direabsorpsi ekskresi garam di urin 0
REGULATION OF ALDOSTERON
SECRETION
Peptida Natriuretik Atrium ( PNA)
 PNA sistem pembuang Na+ dan pnurun tekanan darah.
 Jantung dpt mnghasilkan PNA yg disimpan di granula dalam
sel otot atrium jantuung khusus

 PNA dibebaskan dari atrium jika jantung secara mekanis

teregang o/ pningkatan vol plasma krn pningkatan volume
CESterjadi krn retensi NaCl dan H20 tekanan darah
arteri naik

 PNA
 mendorong natriuresis & diuresis
 Menurunkan vol plasma
 Mempengaruhi sistem kardiovaskular untuk menurunkan tekanan
darah
 Kerja utama PNAmenghambat scara langsung reabsorpsi Na+ di
bag distal nerfron shingga eksresi Na+ mningkat di urin.

 PNA  dpt mningkatkan eksresi Na+ di urin dgn mnghambat 2 thap

SRAA
 Pna menghambat sekresi renin o/ ginjal & bekerja pd korteks adrenal
u/ mnghambat sekresi aldosteron

 Mendorong natriuresis & diuresis dgn meningkatkan GFR (melalui dilatasi

arteriol aferen ,mningkatkan t.d kapiler glomerulus & melemaskan sel
mesangium glomerulus agar terjadi peningkatan Kf

 ANP scara lgsg mnurunkan t.darah dgn mnurunkan curah jantung

& resistensi vaskular perifer (dgn menghambat aktivitas simpatis
& p.d)
Glukosa & Asam Amino
 Bahan ini seluruhnya akan direabsorpsi kembali ke darah
o/mekanisme yg dependen energi & dependen Na+ di tubulus
proksimal .

 Reabsorpsi terjadi cpt agar mencegah hilangnya nutrien organik

pnting dari tubuh.
 Glukosa dan asam amino direabsorpsi sampai konsentrasi di cairan
tubulus hampir 0

 Glukosa & Asam Amino dipindahkan o/transpor aktif sekunder

 Pd proses ini  pmbwa kotranspor khusus yg hanya trdpt di tubulus

proksimal memindahkan Na+ dan molekul organik spesifik dr lumen
ke dlm sel .
 Gradien konsentrasi Na+ lumen sel yg dipertahankan
o/ pompa Na+ K+ basolateral (yg memerlukan
energi) mnjalankan sistem kotranspor & mnarik molekul
organik melawan gradien konsentrasi tnpa pengeluaran
energi langsung

 Krn proses keseluruhan reabsorpsi glukosa & asam

amino brgantung pd pemakaian energi (dianggap
direabsorpsi scara aktif tp secara tidak secara lgsg)

 Transport aktif sekunder prlu Na+ didlm lumen ,tnpa

Na ,pmbawa kotranspor tdk bsa kerja.
 Stlh diangkut ke tubulus glukosa & asam amino
berdifusi secara pasif mnuruni gradien
konsentrasi mnembus membran basolateral u/ msk
ke dlm plasma
 Bahan yg direabsorpsi scara aktif akan ikatan dgn pmbawa ( dimembran
plasma yg memindahkannya mnembus membran)

 Pembawa sifatnya spesifik u/ jenis bahan (cth :pmbawa kotranspor glukosa

tdk dpt pindahin AA)

 Jmlh dri pembawa yg ad di sel mlapisi tubulus terbatas trdpt btas atas
jmlh bahan trtentu yg bsa secara aktif dipindahkan

 Laju reabsorpsi maks:saat pmbwa spesifik tdk lagi dpt menangani bahan
tambahan pd saat itu

 Transpor maksimal = maksimum tubulus (Tm)

Bahan yg udh melebihi Tm nya tdk akan direabsorpsi
Glukosa
 Konsentrasi glukosa plasma normal : 100 mg glukosa/100 ml
plasma
 Glukosa di glomerulus terfiltrasi bebas,jd pd saat lewat kapsul
Bowman dgn konsentrasi sma dgn di plasma.

 Trdpt 100 mg glukosa u/ stiap 100 ml plasma yg difiltrasi.

 125 ml plasma yg difiltrasi scara normal stiap mnit ,125 mg glukosa

yg akan lewat ke kapsul Bowman

 Jumlah stiap bahan yg difiltrasi per menit :jumlah terfiltrasi

 Jumlah filtrasi: konsentrasi plasma bahan x GFR
 Jumlah filtrasi glukosa : 100 mg/100 ml x 125 ml/mnt : 125 mg /mnt
Maksimum Tubulus u/ Glukosa
 Tm u/ glukosa : sekitar 375 mg/mnt (mekanisme pngangkut glukosa
mampu scara aktif mereabsorpsi smpai 375 mg glukosa/mnt )

 Pd konsentrasi glukosa glukosa normal:100mg/100ml ,125 mg

glukosa yg tersaring /mnt dpt cpt direabsorpsi o/ mekanisme
pengangkut glukosa.shingga tdk ditemukan glukosa pd urin

 Jika glukosa >> terfiltrasi /menit dibanding yg dpt direabsorpsi krn

Tm trlampaui jmlh direabsorpsi maks dan ke>>glukosa akan ada
dlm filtrat u/ diekrsikan

 Jdi konsentrasi glukosa plasma hrs 300mg/100ml baru ditemukan

glukosa di urin
Ambang ginjal untuk glukosa
 Renal Threshold:konsentrasi plasma dimana Tm
suatu bahan tcapai dan bahan sdh mulai muncul di
urin

 Tm rerata:375 mg/mnt dan GFR 125ml/mnt

 Renal threshold untuk glukosa: 300 mg/ml
 Diatas Tm,reabsorpsi ttp pd laju maks & tiap
pningkatan jmlh yg difiltrasi menyebabkan
pningkatan jmlh yg diekskresikan
 Cth:
 Pd konsentrasi glukosa plasma 400mg/100 ml

Jmlh glukosa yg difiltrasi ??500mg/mnt

375 mg/mnt diantaranya direabsorpsi (senilai Tm)

Sisanya ?? 125 mg/mnt diekskresi di urin

 Ginjal tdk mmpengaruhi konsentrasi glukosa plasma
dlm kisaran nilai yg lebar
 Krn Tm u/ glukosa jauh diatas jumlah normal yg
difiltrasi mka ginjal biasanya akan nahan smua
glukosa supaya tdk kehilangan di urin

 Ginjal tdk mengatur glukosa krn ginjal gk bsa

mempertahankan glukosa pd konsentrasi plasma
trtentu
Fosfat
 Ginjal tdk scara lgsg brperan dlm pngaturan bnyak elektrolit (misal
fosfat(P04-) dan kalsium (Ca2+) krn ambang ginjal u/ inorganik sma
dgn konsentrasi plasma normalny

 Pmbawa transpor u/ elektrolit ada di tubulus proksimal

 Cth:makanan bnyak akan fosfat ,ttp krn tubulus dpt mereabsorpsi

hingga jmlh yg setara dgn konsentrasi fosfat di plasma (tdk
lbh)kelebihan fosfat dpt dibuang ke urinkonsentrasi plasma ke
normal

 Smakin >> fosfat yg dimakan smakin bnyak jg yg dieksresikan

 Reabsorpsi fosfat dan kalsium jg dipengaruhi oleh hormon

 Hormon paratiroid dpt mengubah ambang ginjal u/ fosfat dan kalsium
Reabsorpsi aktif Na+ mnyebabkan
reabsorpsi pasif Cl,H20 dan urea
 Reabsorpsi klorida
ion klorida yg bermuatan (-) direabsorpsi scara pasif mnuruni gradien listrik
(muncul krn reabsorpsi aktif ion na+ yg bermuatan (+)

Jmlh klorida yg direabsorpsi ditentukan o/ laju reabsorpsi aktif Na+ & tdk
dikontrol lgsg oleh ginjal

Reabsorpsi Air
Air direabsorpsi scara pasif di sluruh panjang tubulus krn H20 scara osmosis
mngikuti Na+ yg direab aktif.
Dari H20 yg terfiltrasi , 65%-117 liter sehari direabsorpsi scara pasif (akhir
tubulus proks)

15 % dari H20 yg difiltrasi ,direabsorpsi di ansa henle

 Total 80% dari H20 yg difiltrasi ini direabsorpsi di tubulus proksimal dan
ansa henle (brpapun jmlh & tdk dikontrol oleh ginjal
 Sisa 20% direabsorpsi dlm jmlh bervariasi di tubulus
distal
 Jmlh yg direabsorpsi di tubulus distal & koligentes
berada dibwh kontrol hormon

 Slama reabsorpsi ,H20 melewati akuaporin/sal air

(trbentuk o/ protein membran plasma spesifik di
tubulus)
 Akuaporin di tubulus proksimal slalu terbuka sgt
permeabel terhadap H20
 Akuaporin di bagian distal nefron diatur oleh hormon
vasopressin shingga reabsorpsi H20 berubah2
 Gaya utama pendorong reabsorpsi H20 di tubulus
prokskompartemen hipertonisitas di ruang lateral antara
sel tubulus yg tercipta krn pompa basolateral yg aktif
mengeluarkan Na+konsentrasi Na+ di cairan tubulus dan
sel tubulus mnurun & diruang lateral konsentrasiny naik.

 Gradien osmotik memicu aliran netto pasif H20 dari

lumen ke ruang lateral (mnembus sel/mngalir melalui taut
erat yg krg prmeabel)

 Terjadilah akumulasi cairan diruang lateral mningkatnya

tekanan hidrostatik menarik H20 keluar dr ruang lateral
ke caira interstisium kapiler peritubulus
 Air dpt scara osmosis ikut zat terlarut lain (misal glukosa)
 Tekanan osmotik koloid plasma lbh> di kapiler peritubulus
 Konsentrasi protein plasma ,yg menentukan tkanan
osmotik koloid plasma,mningkat didarah yg msk ke
kapiler peritubulus krn filtrasi ekstensif H20 di kapiler
glomerulus.

 Protein plasma yg tertinggal di glomerulus trkonsentrasi

dlm vol H20 plasma yg lbh sdikitterjadi pningkatan
tekanan osmotik koloid plasma pd darah yg blm trfiltrasi
mnuju ke kapiler peritubulus
Reabsorpsi Urea
 Reabsorpsi pasif urea scara tdk lgsg berkaitan dgn reabsorpsi aktif
Na+
 Urea :suatu produk sisa dr pemecahan protein
 Reabsorpsi H20 yg brlgsg cara osmosis di tubulus proksimal
sekunder trhdp reabsorpsi aktif Na+ mnghasilkan gradien
konsentrasi u/ urea (mndorong reabsorpsi pasif )

 Terjadi reabsorpsi H20 yg besar di tubulus proksimal mngurangi

filrat mnjadi 44 ml /mnt di luman akhir tubulus proksimal (awal
filtrat: 125 ml/mnt)

 Urea trmsk bahan yg sdh terfiltrasi tp blm direabsorpsi

 Cairan yg ada di tubulus smakin pekat krn H20 direabsorpsi, yg
lain tertinggal
 Konsentrasi urea diplasma yg msk ke kapiler peritubulus
dgn konsentrasi urea saat difiltrasi konsentrasiny identik

 Jmlh urea yg ada dlm 125 ml cairan di awal tubulus proks

terkonsentrasi hingga 3x lipat dlm 44ml cairan di akhir
tubulus konsentrasi urea di cairan tubulus lbh besar dr yg
dikapiler skitartrbentuk gradien konsentrasi scara pasif
difusi urea dari lumen tubulus ke kapiler peritubulus

 Hnya 50% dari urea yg trfiltrasi di reabsorpsi scara pasif

(krn dinding tubulus proksimal krg permeabel)
 FIGURE 14-20 Passive reabsorption of urea at the
end of
 the proximal tubule. (a) In Bowman’s capsule and at
the beginningof the proximal tubule, urea is at the
same concentration as in the plasma and surrounding
interstitial fl uid. (b) By the end of the proximal tubule,
65% of the original fi ltrate has been reabsorbed,
concentrating the fi ltered urea in the remaining fi
ltrate. This establishes a concentration gradient favoring
passive reabsorption of urea.
Produk sisa yg tdk diperlukan
Produk –produk sisa lainn yg difiltrasi
fenol dan kreatinin jg terkonsentrasi didlm cairan tubulus
sewaktu H20 mninggalkan filtrat u/ msk ke plasma(ttp
bahan ini tidak direabsorpsi spt urea)

Molekul urea krn bahan sisa yg terkecil (satu2 ny

zat sisa scara pasif direabsorpsi

bahan lain tdk dpt mninggalkan lumen mnuruni gradien

konsentrasinya untuk scara pasif direabsorpsi (krn tdk bsa
nembus dinding tubulus)diekskresikan di urin dlm
konsentrasi tinggi
Sekresi Tubulus
Sekresi Ion Hidrogen
 Sekresi H+ ginjal sgt penting dlm mngatur
keseimbangan asam basa di tubuh
 Ion Hidrogen yg disekresikan ke dlm cairan tubulus
dieliminasi dr tubuh lewat urin
 Ion hidrogen dpt disekresikan o/tubulus proksimal,distal
/koligentes dgn tingkat sekresi keasaman cairan tubuh.

 Ktika cairan tubuh trlalu asam maka sekresi H+

mningkat
 Saat sekresi H+ berkrg jika konsentrasi H+ di cairan
tubuh trlalu rendah
Sekresi ion kalium dikontrol oleh
aldosteron
 Ion kalium secara aktif direabsorpsi ditubulus proksimal &
secara aktif disekresikan di tubulus distal & koligentes.

 K+yang difiltrasi hmpir seluruhnya direabsorpsi ditubulus

proksimal maka sbagian besar K+ di urin berasal dari
sekresi K+ dibag distal nefron.

 Selama deplesi K+sekresi k+ dibag distal nefron ber-

smpai min shingga hanya sebag dri K+ yang terfiltrasi lolos
dari reabsorpsi di tubulus proksimal akan dieksresikan di
urin,dgn cara ini K+ yang seharusnya keluar di urin ditahan
di tubuh
Mekanisme sekresi K+
 Sekresi ion kalium di tubulus distal &
koligentesdigabungkan dgn reabsorpsi oleh
pompa Na+ K+ basolateral dependen energi.

 Konsentrasi K+ intrasel yang meningkatmendorong

perpindahan netto K+ dari sel ke dalam lumen
tubulus.(perpindahan menembus membran luminal
brlangsung pasif )(krn adanya gradien konsentrasi)

 Pompa basolateral mendorong perpindahan pasif

K+ keluar plasma kapiler peritubulus cairan
interstisium.Ion kalium lalu dipompa ke dalam sel
(secara pasif berpindah ke dalam lumen).
Kontrol sekresi K+
 Faktor yang dpt mengubah laju sekresi K+ 
aldosteron.
 Hormon ini merangsang sekresi K+ o/sel tubulus diakhir
nefron dan meningkatkan reabsorpsi Na+ oleh sel ini.

 Pningkatan konsentrasi K+ plasma merangsang

korteks adrenal u/meningkatkan pengeluaran
aldosteron mendorong sekresi & eksresi kelebihan k+
diurin.
 Pnurunan konsentrasi K+ plasmapenurunan sekresi
aldosteron & penurunan sekresi k+ginjal
Efek sekresi H+pada sekresi K+
 Faktor lain yang dpt scara tdk sengaja mengubah
tingkat sekresi K+Status asam basa tubuh.

 Pompa basolateral di bag distal nefrondpt

mensekresikan K+ / H+ untuk dipertukarkan dgn Na+
yang direabsorpsi.

 Secara normal,ginjal akan mensekresikan K+ tp kalau

cairan tubuh terlalu asam & sekresi H+ ditingkatkan
sbg kompensasisekresi K+ berkurang .
Pnting dlm mengatur konsentrasi K+
Plasma
 Kalium : pnting dalam aktivitas listrik membran
jaringan peka rangsang.
 Pningkatan & pnurnan konsentrasi K+ plasma (CES)
dpt mngubah gradien konsentrasi K+ iontrasel
trhdp ekstrasel
 Pningkatan konsentrasi K+ Ces mnyebabkan
penurunan potensial istirahat dan peningkatan
eksitabilitas (khususnya otot jantung)
 Kepekaan ber>>> dpt menyebabkan pningkatan
kecepatan jantung aritmia jantung
Sekresi kation & anion organik
 Tubulus proksimal :mngandung 2 jenis pembawa sekretorik khusus :sekresi
anion organik & sekresi untuk sekresi kation organik

Fungsi sistem sekresi ion organik

a) Dgn mnambahkan sjenis ion organik ke jmlh yg msk ke cairan
tubulus ,jalur sekresi organik ini mmpermudah ekskresi bahan
berbagai pembawa pesan kimiawi yg trdpt didarah spt
prostaglandin,histamin,dan norepinefrin

b) Ion organik krg larut dlm air ,supaya bisa diangkut dalam
darah,ion harsu terikat ke protein plasma
Sekresi tubulus mempermudah eliminasi ion-ion organik yg tdk dpt
difiltrasi melalui urin
c)Sistem sekresi ion organik tubulus proksimal
berperan dlm eliminasi bnyak.Snyawa asing dari
tubuh.Sistem ini dpt keluarin berbagai ion organik
dlm jmlh besar

yg diproduksi secara endogen /ion organik asing

yg bsa msk ke cairan tubuh
sifat non selektif memungkinkan sistem sekresi ion
organik mempercepat pembuangan bnyak bahan
kimia (trmsk zat aditif makanan,polutan
lingkungan),obat ,pestisida
LO 4
ANAMNESA,PF dn Pp ,KIE
PALPATION
 Although kidneys are not usually palpable
 Detecting an enlarged kidney may prove to be very
important.
Palpation of The left kidney
 Move to the patient’s left side.

 Place your right hand behind the patient just below

and parallel to the 12th rib, with your fingertips just
reaching the costovertebral angle.
 Lift, trying to displace the kidney anteriorly. Place your
left hand gently in the left upper quadrant, lateral and
parallel to the rectus muscle. Ask the patient to take a
deep breath.
 At the peak of inspiration, press your left hand firmly
and deeply into the left upper quadrant, just below the
costal margin, and try to “capture” the kidney between
your two hands.
 Ask the patient to breathe out and then to stop
breathing briefly.
 Slowly release the pressure of your left hand, feeling at
the same time for the kidney to slide back into its
expiratory position.
 If the kidney is palpable, describe its size, contour, and
any tenderness.
 Palpation of the Right Kidney.
 To capture the right kidney, return to the patient’s right
side. Use your left hand to lift from in back, and your
right hand to feel deep in the left upper quadrant.
Proceed as before.
 A normal right kidney may be palpable, especially in
thin, well-relaxed women.

 It may or may not be slightly tender. The patient is

usually aware of a capture and release.
 Occasionally, a right kidney is located more anteriorly
than usual and then must be distinguished from the liver.

 The edge of the liver, if palpable, tends to be sharper

and to extend farther medially and laterally. It cannot
be captured. The lower pole of the kidney is rounded.
 Causes of kidney enlargement include
hydronephrosis, cysts, and tumors. Bilateral
enlargement suggests polycystic disease.

 Pain with pressure or fist percussion suggests

pyelonephritis, but may also have a musculoskeletal
cause.
 ASSESING KIDNEY TENDERNESS
 You may note tenderness when examining the
abdomen, but also search for it at each
costovertebral angle.
 Pressure from your fingertips may be enough
to elicit tenderness, but if not, use fist
percussion.

 Place the ball of one hand in the

costovertebral angle and strike it with the
ulnar surface of your fist. Use enough force to
cause a perceptible but painless jar or thud in
a normal person.

 Pain with pressure or fist percussion suggests

pyelonephritis, but may also have a
musculoskeletal cause.
 Bladder
 The bladder normally cannot be examined unless it is
distended above the symphysis pubis.
 On palpation, the dome of the distended bladder feels
smooth and round.
 Check for tenderness.
 Use percussion to check for dullness and to determine how
high the bladder rises above the symphysis pubis

 Bladder distention from outlet obstruction due to urethral

stricture, prostatic hyperplasia; also from medications and
neurologic disorders such as stroke, multiple sclerosis.

 Suprapubic tenderness in bladder infection

PP
Urinalisis
 Parameter Fisik Urin
 Warna  normal pucat-kuning tua tergantung kadar urokrom,keadaan
patologis dpt mngubah warna.Urin merah disebabkan
Hb,mioglobin/pengaruh obat rifampisin.Warna hijau:dpt karena zat klinis
eksogen (biru metilen)/infeksi pseudomonas,warna oranye/jinggapigmen
empedu.Jika keruh bsa karena fosfat /leukosituria & bakteri (abnormal)
 Turbiditas normal transparan ,urin keruh karena hematuria,infeksi dan
kontaminasi
 Baupnyakit bau yg khas :bau keton,maple syrup diseaseisofloric
acidemia
 Densitas relatif
 Berat jenis: diukur pakai urinometer ,mudah dilakukan,butuh urin 25cc
,dipengaruhi oleh suhu,urin,protein,glukosa dan kontras media .nilai
normal:1010-1030
 Refraktometri: mudh dilakukan dan hnya butuh 1cc urin
 Osmolalitas :temperatur dan protein tdk mempengaruhi (beda dgn bj)
,osmolalitas normal : 50-1200m0sm/l (pnting mnandakan konsentrasi urin)(kasus
batu ginjal /kelainan elektrolit (prlu diperiksa u//diagnosis
 Diptik:memakai indikator prubahan warna pd diptik
 Parameter kimia
 pH:tes memakai dipstik,pd pH<5,5 atau >7,5 akurasinya kurang
dan hrs memakai ph meter,hasilnya dipengaruhi ph sistemik
 Hb:dlm kondisi normal tdk dijumpai,jika ada curiga
hemolisis/mioglobinuria
 glukosa:dgn dipstik untuk menilai reabsorpsi glukosa dan bahan
lain (tes ini sgt sensitif dan dpt dilanjutkan dgn kadar glukosa urin
scara kuantitatif dgn metode enzimatik
 Protein:normal proteinuria tdk > dari 150 mg/hari untuk dewasa
 Pd kondisi patologis proteinuria dpt dibedakan
 Proteinuria glomerulus: terjadi pada pnyakit glomerulus krn gg permeabilitas
protein (albumin,globulin)
 Protein tubular :ini trjadi pd penyakit tubulus dan interstisium dan
disebabakan gangguan reabsorpsi protein berta molekul ringan
(mikroglobulin,b2 mikroglobulin,retinal binding protein \
  Proteinuria overload: ini disebabkan peningkatan protein BM
rendah melebihi kapasitas reabosorpsi tubulus (bence jones
protein,lisosom,mioglobin)
 Proteinuria benigna:protein trmasuk proteinuria krn demam
,ortostatik atau kerja fisik
 Proteinuria biasanya dites memakai dipstik dan cukup
sensitif trhdp albumin.
 Untuk protein bence joneshrs pakai teknik presipitasi
dgn asam sulfa salisil,asam triklorasetik/pemanasan
dan bufer acid sodium acetat.
 Metode dipstiksemikuantitatif dgn nilai 0-4+

(jika ingin telilt untuk nilai protein kuantitatif bs digunakan

metode turbimetri)
 Jjmlh protein kuantitatif 24 jam diekspresikan sbg
g/L ,g/24 jam per 1,73 m2
 Cara lain :mnghitung rasio protein kreatinin (dipakai
urin random dan single)

 Analisis kualitatif proteinuria dilakukan scara

elketroforesa asetat selulos /agarose/memakai SDS-
PAGEDgn metode ini dpt diketahui selektifitas
proteinuria (krn dpt membedakan jenis dri protein
:beta2 mikroglobulin,albumin,IgG,kadang dpt
mengetahui respon terapi dan prognosis
 Leukosit esterase
 Tes dipstik ini berdasarkan aktivitas esterase indoksil yg
dihasilkan oleh neutrofil,granulosit dan makrofag &
memberi nilai+ jika pling sedikit 4 leukosit
 Nitrit
 Dasar tes:adanya bakteri yg dpt mengubah nitrat jadi nitrit
melalui enzim reduktase itrat
 Enzim ini bnyak pd bakteri Pseudomonas,Staphylococcus
albus dan enteroccocus
 Sblm tes dilakukan,pasien yg ingin melalkukan tes hrs diet
dgn kaya nitrat (sayuran)
 Tes ini mmpnyai sensitivitas rendah (20-80%)dan
spesifisitas 90%
 Keton
 Mnunjukan adanya asa, asetoasetat dan aseton
 Positif di urin pnyakit asidosis
diabetik,puasa,muntah/olahraga berlebih
KIE
KIE
 Minum cukup air
 Hindari terlalu banyak minum kopi dan the
DAFTAR PUSTAKA
 Bates,B .Bates’Guide to Physical Examination& History Taking.8th
Ed.New York:Lippincott.2007
 Moore KL,Clinically Oriented Anatomy ,5th ed,Baltimore,Lippincott
William & Wilkins.
 Netter,FH,Atlas of Human Anatomy,2nd ed.Canada :Icon Learning
System.
 Sherwood,S.Human Physiology.7th
edition,Brooks/Cole,Belmont,USA,2010
 Difiore
 Mescher,AL.Junquiera’s Basic Histology:Text and Atlas,12th ed .New
York:McGraw-Hill,2010
 Sudoyo AW,Setiyohadi B,Alwi I,dkk.Ed.Buku Ajar Ilmu Penyakit
Dalam Jilid II.Edisi 5.Interna Publishing,Jakarta,2009.