1. Anatomi, histologi dan fisiologi dari ginjal?

Anatomy of the Kidneys

Location
The kidneys are a pair of organs found along the posterior muscular wall of
the abdominal cavity. The left kidney is located slightly more superior than
the right kidney due to the larger size of the liver on the right side of the
body. Unlike the other abdominal organs, the kidneys lie behind the
peritoneum that lines the abdominal cavity and are thus considered to be
retroperitoneal organs. The ribs and muscles of the back protect the kidneys
from external damage. Adipose tissue known as perirenal fat surrounds the
kidneys and acts as protective padding.
Structure
The kidneys are bean-shaped with the convex side of each organ located
laterally and the concave side medial. The indentation on the concave side of
the kidney, known as the renal hilus, provides a space for the renal artery,
renal vein, and ureter to enter the kidney.
A thin layer of fibrous connective tissue forms the renal capsule surrounding
each kidney. The renal capsule provides a stiff outer shell to maintain the
shape of the soft inner tissues.

Deep to the renal capsule is the soft, dense, vascular renal cortex. Seven
cone-shaped renal pyramids form the renal medulla deep to the renal cortex.
The renal pyramidsare aligned with their bases facing outward toward the
renal cortex and their apexes point inward toward the center of the kidney.
Each apex connects to a minor calyx, a small hollow tube that collects urine.
The minor calyces merge to form 3 larger major calyces, which further merge
to form the hollow renal pelvis at the center of the kidney. The renal pelvis
exits the kidney at the renal hilus, where urine drains into the ureter.

Blood Supply
1. The renal arteries branch directly from the abdominal aorta and enter the
kidneys through the renal hilus.
2. Inside our kidneys, the renal arteries diverge into the smaller afferent
arterioles of the kidneys.
3. Each afferent arteriole carries blood into the renal cortex, where it separates
into a bundle of capillaries known as a glomerulus.
4. From the glomerulus, the blood recollects into smaller efferent arterioles that
descend into the renal medulla.
5. The efferent arterioles separate into the peritubular capillaries that surround
the renal tubules.
6. Next, the peritubular capillaries merge to form veins that merge again to
form the large renal vein.
7. Finally, the renal vein exits the kidney and joins with the inferior vena cava,
which carries blood back to the heart
The Nephron
Each kidney contains around 1 million individual nephrons, the kidneys’
microscopic functional units that filter blood to produce urine. The nephron is
made of 2 main parts: the renal corpuscle and the renal tubule.
 Responsible for filtering the blood, our renal corpuscle is formed by the
capillaries of the glomerulus and the glomerular capsule (also known as
Bowman’s capsule). The glomerulus is a bundled network of capillaries that
increases the surface area of blood in contact the blood vessel walls.
Surrounding the glomerulus is the glomerular capsule, a cup-shaped double
layer of simple squamous epithelium with a hollow space between the layers.
Special epithelial cells known as podocytes form the layer of the glomerular
capsule surrounding the capillaries of the glomerulus. Podocytes work with
the endothelium of the capillaries to form a thin filter to separate urine from
blood passing through the glomerulus. The outer layer of the glomerular
capsule holds the urine separated from the blood within the capsule. At the
far end of the glomerular capsule, opposite the glomerulus, is the mouth of
the renal tubule.
A series of tubes called the renal tubule concentrate urine and recover non-
waste solutes from the urine. The renal tubule carries urine from the
glomerular capsule to the renal pelvis.

1. The curvy first section of the renal tubule is known as the proximal
convoluted tubule. The tubule cells that line the proximal convoluted tubule
reabsorb much of the water and nutrients initially filtered into the urine.
2. Urine next passes through the loop of Henle, a long straight tubule that
carries urine into the renal medulla before making a hairpin turn and
returning to the renal cortex.
3. Following the loop of Henle is the distal convoluted tubule.
4. Finally, urine from the distal convoluted tubules of several nephrons enters
the collecting duct, which carries the concentrated urine through the renal
medulla and into the renal pelvis.
5. From the renal pelvis urine from many collecting ducts combines and flows
out of the kidneys and into the ureters.
Physiology of the Kidneys
Excretion of Wastes
The primary function of the kidneys is the excretion of waste products
resulting from protein metabolism and muscle contraction.
The liver metabolizes dietary proteins to produce energy and produces toxic
ammonia as a waste product. The liver is able to convert most of this
ammonia into uric acid and urea, which are less toxic to the body. Meanwhile,
the muscles of our body use creatine as an energy source and, in the process,
produce the waste product creatinine. Ammonia, uric acid, urea, and
creatinine all accumulate in the body over time and need to be removed from
circulation to maintain homeostasis.
The glomerulus in the kidneys filter all four of these waste products out of the
bloodstream, allowing us to excrete them out of our bodies in urine. Around
50% of the urea found in the blood is reabsorbed by the tubule cells of the
nephron and returned to the blood supply. Urea in the blood helps to
concentrate other more toxic waste products in urine by maintaining the
osmotic balance between urine and blood in the renal medulla.

Filtration, Reabsorption, and Secretion

1. The kidneys filter blood as it passes through the capillaries that form the
glomerulus. Blood pressure forces most of the blood plasma through the
 lining of the capillaries and into the glomerular capsule. Blood cells are too
large to pass through the capillary lining and so remain within the capillaries
along with some residual plasma. The filtered plasma, now known as tubular
fluid, begins to flow out of the glomerular capsule and into the proximal
convoluted tubule.
2. At the same time, the concentrated blood that remains inside the capillaries
of the glomerulus moves into the efferent arterioles and on to the peritubular
capillaries surrounding the proximal convoluted tubule. Epithelial cells lining
the tubule actively reabsorb valuable molecules of glucose, amino acids, and
ions from the filtrate and deposit them back into the blood. These cells also
absorb any waste products remaining in the blood (such as ammonia and
creatinine) and secrete these chemicals into the filtrate. While these solutes
are being exchanged, osmotic pressure pushes water from the dilute,
hypotonic filtrate back into the concentrated, hypertonic blood.
3. From the proximal convoluted tubule, the tubular fluid next enters the loop of
Henle, where water and ions are reabsorbed. The descending limb of the loop
of Henle is permeable to water and carries the filtrate deep into the medulla
of the kidney. Tissues in the medulla surrounding the tubule contain a high
concentration of ions and very little water compared to the filtrate. Osmotic
pressure between the hypotonic filtrate and hypertonic medullary cells pushes
water out of the filtrate and into the cells. The cells of the medulla return this
water to the blood flowing through nearby capillaries.
4. Filtrate next passes through the ascending limb of the loop of Henle as it exits
the medulla. The tissues surrounding the ascending limb are not permeable to
water but are permeable to ions. The filtrate is very concentrated after
passing through the descending limb, so ions easily diffuse out of the filtrate
and into the cells lining the ascending limb. These ions are returned to the
blood flowing through nearby capillaries.
5. Tubular fluid exiting the loop of Henle next passes through the distal
convoluted tubule and the collecting duct of the nephron. These tubules
continue to reabsorb small amounts of water and ions that are still left in the
filtrate. The tissues surrounding the collecting duct actively absorb excess
potassium and hydrogen ions from the nearby capillaries and secrete these
excess ions as waste into the filtrate.
6. When filtrate reaches the end of the collecting duct, almost all of the valuable
nutrients, ions, and water have been returned to the blood supply while waste
products and a small amount of water are left to form urine. The urine exits
the collecting duct and joins with urine from other collecting ducts in the renal
pelvis.
Water Homeostasis
The kidneys are able to control the volume of water in the body by
changing the reabsorption of water by the tubules of the nephron. Under
normal conditions, the tubule cells of the nephron tubules reabsorb (via
osmosis) nearly all of the water that is filtered into urine by the glomerulus.
Water reabsorption leads to very concentrated urine and the conservation of
water in the body. The hormones antidiuretic hormone (ADH) and aldosterone
both increase the reabsorption of water until almost 100% of the water
filtered by the nephron is returned to the blood. ADH stimulates the formation
of water channel proteins in the collecting ducts of the nephrons that permit
water to pass from urine into the tubule cells and on to the blood.
 Aldosterone functions by increasing the reabsorption of Na+ and Cl- ions,
causing more water to move into the blood via osmosis.

In situations where there is too much water present in the blood,

our heart secretes the hormone atrial natriuretic peptide (ANP) in order to
increase the excretion of Na+ and Cl- ions. Increased concentration of Na+
and Cl- in urine draws water into the urine via osmosis, increasing the volume
of urine produced.
Acid/Base Homeostasis
The kidneys regulate the pH level of the blood by controlling the excretion of
hydrogen ions (H+) and bicarbonate ions (HCO3-). Hydrogen ions accumulate
when proteins are metabolized in the liver and when carbon dioxide in the
blood reacts with water to form carbonic acid (H2CO3). Carbonic acid is a
weak acid that partially dissociates in water to form hydrogen ions and
bicarbonate ions. Both ions are filtered out of the blood in the glomerulus of
the kidney, but the tubule cells lining the nephron selectively reabsorb
bicarbonate ions while leaving hydrogen ions as a waste product in urine. The
tubule cells may also actively secrete additional hydrogen ions into the urine
when the blood becomes extremely acidic.
The reabsorbed bicarbonate ions enter the bloodstream where they can
neutralize hydrogen ions by forming new molecules of carbonic acid. Carbonic
acid passing through the capillaries of the lungs dissociates into carbon
dioxide and water, allowing us to exhale the carbon dioxide.
Electrolyte Homeostasis
The kidneys maintain the homeostasis of important electrolytes by controlling
their excretion into urine.
 Sodium (Na+): Sodium is a vital electrolyte for muscle function, neuron
function, blood pressure regulation, and blood volume regulation. Over 99%
of the sodium ions passing through the kidneys are reabsorbed into the blood
from tubular filtrate. Most of the reabsorption of sodium takes place in the
proximal convoluted tubule and ascending loop of Henle.
 Potassium (K+): Just like sodium, potassium is a vital electrolyte for muscle
function, neuron function, and blood volume regulation. Unlike sodium,
however, only about 60 to 80% of the potassium ions passing through the
kidneys are reabsorbed. Most of the reabsorption of potassium occurs in the
proximal convoluted tubule and ascending loop of Henle.
 Chloride (Cl-): Chloride is the most important anion (negatively charged ion)
in the body. Chloride is vital to the regulation of factors such as pH and
cellular fluid balance and helps to establish the electrical potential of neurons
and muscle cells. The proximal convoluted tubule and ascending loop of Henle
reabsorb about 90% of the chloride ions filtered by the kidneys.
 Calcium (Ca2+): Calcium is not only one of the most important minerals in
the body that composes the bones and teeth, but is also a vital electrolyte.
Functioning as an electrolyte, calcium is essential for the contraction of
muscle tissue, the release of neurotransmitters by neurons, and the
stimulation of cardiac muscle tissue in the heart. The proximal convoluted
tubule and the ascending loop of Henle reabsorb most of the calcium in
tubular filtrate into the blood. Parathyroid hormone increases the
reabsorption of calcium in the kidneys when blood calcium levels become too
low.
 Magnesium (Mg2+): Magnesium ion is an essential electrolyte for the proper
function of enzymes that work with phosphate compounds like ATP, DNA, and
RNA. The proximal convoluted tubule and loop of Henle reabsorb most of the
magnesium that passes through the kidney.
Blood Pressure Homeostasis
The kidneys help to control blood pressure in the body by regulating the
excretion of sodium ions and water and by producing the enzyme renin.
Because blood is mostly made of water, an increased volume of water in the
body results in an increase in the volume of blood in the blood vessels.
Increased blood volume means that the heart has to pump harder than usual
to push blood into vessels that are crowded with excess blood. Thus,
increased blood volume leads to increased blood pressure. On the other hand,
when the body is dehydrated, the volume of blood and blood pressure
decrease.
The kidneys are able to control blood pressure by either reabsorbing water to
maintain blood pressure or by allowing more water than usual to be excreted
into urine and thus reduce blood volume and pressure. Sodium ions in the
body help to manage the body’s osmotic pressure by drawing water towards
areas of high sodium concentration. To lower blood pressure, the kidneys can
excrete extra sodium ions that draw water out of the body with them.
Conversely, the kidneys may reabsorb additional sodium ions to help retain
water in the body.

Finally, the kidneys produce the enzyme renin to prevent the body’s blood
pressure from becoming too low. The kidneys rely on a certain amount of
blood pressure to force blood plasma through the capillaries in the
glomerulus. If blood pressure becomes too low, cells of the kidneys release
renin into the blood. Renin starts a complex process that results in the
release of the hormone aldosterone by the adrenal glands. Aldosterone
stimulates the cells of the kidney to increase their reabsorption of sodium and
water to maintain blood volume and pressure.

Hormones
The kidneys maintain a small but important endocrine function by producing
the hormones calcitriol and erythropoietin.
 Calcitriol is the active form of vitamin D in the body. Tubule cells of the
proximal convoluted tubule produce calcitriol from inactive vitamin D
molecules. At that point, calcitriol travels from the kidneys through the
bloodstream to the intestines, where it increases the absorption of calcium
from food in the intestinal lumen.
 Erythropoietin (EPO) is a hormone produced by cells of the peritubular
capillaries in response to hypoxia (a low level of oxygen in the blood). EPO
stimulates the cells of red bone marrow to increase their output of red blood
cells. Oxygen levels in the blood increase as more red blood cells mature and
enter the bloodstream. Once oxygen levels return to normal, the cells of the
peritubular capillaries stop producing EPO.
Several hormones produced elsewhere in the body help to control the
function of the kidneys.

 Antidiuretic hormone (ADH), also known as vasopressin, is a hormone

produced by neurosecretory cells in the brain’s hypothalamus. These cells
extend into the posterior pituitary, which stores and releases ADH. ADH
 production is stimulated by a decrease in blood volume and increased blood
osmolarity. ADH helps the body retain water by increasing the number of
water channels in the cells of the collecting ducts of the kidneys. These water
channels allow water remaining in urine to be reabsorbed into the blood,
resulting in extremely concentrated urine.
 Angiotensin II is a hormone made in the liver and activated by the enzymes
renin and angiotensin-converting enzyme. Once activated, angiotensin II
increases the reabsorption of sodium and chloride ions in the proximal
convoluted tubule, leading to an increased reabsorption of water as well.
 Aldosterone is a hormone produced in the adrenal cortex in response to
Angiotensin II. Aldosterone binds to target cells in the walls of the nephron’s
collecting ducts. These cells reabsorb additional sodium and chloride ions that
would have been excreted as urine. The target cells also remove potassium
ions from the blood and excrete it into urine.
 Atrial natriuretic peptide (ANP) is a hormone produced by cardiac muscle cells
in the atria of the heart. These cells produce ANP in response to high levels of
sodium in the blood or increased blood pressure. In the kidneys, ANP
increases the glomerular filtration rate so that more blood plasma is forced
into the glomerular capsule and into the renal tubules. ANP also removes
some solutes from the cells of the renal medulla, making the loop of Henle
less efficient in reabsorbing water and ions from the filtrate. The net result of
ANP is that more sodium and water end up being excreted into urine, blood
volume decreases, and blood pressure decreases as well.

http://www.innerbody.com/image_urinov/dige05-new.html#full-description

HISTOLOGI
Korteks dan medula
Korteks  korpuskel renalis. Fungsi : filtrasi
Medula  tubulus (ansa henle, distal). Fungsi : reabsorbsi

FISIOLOGI
- Pengaturan keseimbangan elektrolit dan air
- Pengaturan konsentrasi osmolalitas air dan elektrolit
- Pengaturan keseimbangan asam dan basa
- Sekresi hormon
- Pengaturan tekanan arteri

2. Bagaimana mekanisme pembentukan urin secara fisiologis?

Arteriol membawa darah  masuk ke ginjal  filtrasi di glumerulus (glukosa,
air, sodium, klorisa, ion bikarbonat) duktus kontortus proximal  reabsorbsi
(pasif) jadi urin primer ansa henle descenden  lapisan tipis ansa henle 
ansa henle ascenden tubulus kontortus distal  reabsorbsi aktif  tubulus
kolektivus (aktivasi ADH untuk reabsorbsi air dan aldosteron untuk reabsorbsi
Na) ureter

Filtrasi tergantung besar molekul dan muatan (postitif lebih mudah di filtrasi)

Ada 3 proses : filtrasi, reabsorbsi, augmentasi

 Tubulus Tubulus
1 Proksimal 4 Distal
N Nutri H
HC a H entsK N HC
- + -
O a O

H N K H
+ + +
H

KORT
EKS
Filtr 2Lengkung
asi Henle
H2O
Salts (NaCl and N
others) H a
–
HCO3 MED N
H
+ ULA a
Urea Tubulu
Glucose; amino 3Lengkung
Henle s5

K Ur
e ea
Active N H
transport a
Passive MED
transport
ULA

The filtration process that occurs within the kidneys is accomplished through a process of
filtration barriers. The fluid that enters into the glomerular capsule is referred to as the
filtrate. The fluid is known as filtrate or ultrafiltrate because it is formed under the hydrostatic
pressure of the blood. The force that favors the filtration is opposed by a counterforce that is
developed by the hydrostatic pressure of fluid within the glomerular capsule. The greater
osmotic colloid pressure of plasma promotes the osmotic return of filtered water. Glomerular
capillaries are extremely permeable and have an extensive surface area, thus the net filtration
pressure produces a very large volume of filtrate. The glomerular filtration rate (GFR) is the
volume of filtrate produced by both kidneys per minute. Vasoconstriction or dilation of
afferent arterioles affects the rate of blood flow to the glomerulus and thus affects the GFR.
Sympathetic Nerve activities (such as those that occur during the fight or flight response and
exercise) stimulate constriction of the afferent arterioles and help to preserve blood volume
and divert blood to the muscles and heart. When the blood pressure undergoes changes, the
GFR remains relatively constant despite these changes in the mean arterial pressure. This is
accomplished thanks to the kidneys’ ability to maintain a relatively constant GFR in the face
of fluctuating blood pressures, which is referred to as renal autoregulation. (1)

Filtrate becomes modified as it passes through the different segments of the nephron tubules
before becoming the urine. The first potential filtration barrier is the capillary fenestrae, but
these pores are too large to exclude any plasma molecule from the filtrate. The second
potential barrier is the glomerular basement membrane. The glomerular basement membrane
is a layer of glycoproteins lying immediately outside of the capillary endothelium. The filtrate
must pass through the inner (visceral) layer of the glomerular capsule, where the third
potential filtration barrier is then located. The third potential filtration barrier is composed of
cells that are called podocytes. Podocytes are shaped somewhat like an octopus with a bulbous
cell body and several thick arms. Each arm of the podocytes has thousands of cytoplasmic
extensions that are known as pedicels, or foot processes; the pedicles interdigitate as they
wrap around the glomerular capillaries. The narrow slits (slit diaphragms) between the
adjacent pedicles provide passageways through which the filtered molecules must pass in
order to enter into the interior of the glomerular filtrate. All of the dissolved plasma solutes
pass easily through the three potential filtration barriers in order to enter into the interior of
the glomerular capsule. Plasma proteins are mostly excluded from the filtrate because of their
large size and negative net charges. The slit diaphragm is a major barrier to the passage of
these plasma proteins into the filtrate. (1) Small amounts of albumin (a major plasma protein)
may pass through into the filtrate, but less than one percent of it is excreted in the urine
because it is either reabsorbed or transported across the cells of the proximal tubule into the
surrounding blood. (1)

When the direct effect of sympathetic stimulation is unavailable, the effect of systemic blood
pressure on the GFR remains relatively constant despite the changes in the mean arterial
pressure within a range of 70-180 mmHg (when the normal is 100 mmHg). The ability of the
kidneys to maintain this relatively constant GFR in the situation of fluctuating blood
pressures is referred to as the renal autoregulation. During renal autoregulation, afferent
arterioles dilate when the mean arterial pressure falls toward 70 mmHg and then constrict
when the mean arterial pressure rises above the normal (100 mmHg). The flow of blood to the
glomeruli and GFR can remain relatively constant within the autoregulatory range of blood
pressure values thanks to this regulatory aspect of the kidney. When there is an increased
arterial pressure that causes a rise in the GFR, an increased delivery of NaCl and H2O to the
distal tubule results. When this happens, a sensor group of specialized cells located in the
thick portion of the ascending limb where contact is made with the afferent and efferent
arterioles in the renal cortex in the tubuloglomerular feedback reaction called the macula
densa sends a chemical signal causing the constriction of the afferent arteriole. This response
then works to protect the late distal tubule and cortical collecting duct from becoming
overloaded. (1)
The filtration process that occurs within the kidneys is accomplished through a process of
filtration barriers. The fluid that enters into the glomerular capsule is referred to as the
filtrate. The fluid is known as filtrate or ultrafiltrate because it is formed under the hydrostatic
pressure of the blood. The force that favors the filtration is opposed by a counterforce that is
developed by the hydrostatic pressure of fluid within the glomerular capsule. The greater
osmotic colloid pressure of plasma promotes the osmotic return of filtered water. Glomerular
capillaries are extremely permeable and have an extensive surface area, thus the net filtration
pressure produces a very large volume of filtrate. The glomerular filtration rate (GFR) is the
volume of filtrate produced by both kidneys per minute. Vasoconstriction or dilation of
afferent arterioles affects the rate of blood flow to the glomerulus and thus affects the GFR.
Sympathetic Nerve activities (such as those that occur during the fight or flight response and
exercise) stimulate constriction of the afferent arterioles and help to preserve blood volume
and divert blood to the muscles and heart. When the blood pressure undergoes changes, the
GFR remains relatively constant despite these changes in the mean arterial pressure. This is
accomplished thanks to the kidneys’ ability to maintain a relatively constant GFR in the face
of fluctuating blood pressures, which is referred to as renal autoregulation. (1)

Filtrate becomes modified as it passes through the different segments of the nephron tubules
before becoming the urine. The first potential filtration barrier is the capillary fenestrae, but
these pores are too large to exclude any plasma molecule from the filtrate. The second
potential barrier is the glomerular basement membrane. The glomerular basement membrane
is a layer of glycoproteins lying immediately outside of the capillary endothelium. The filtrate
must pass through the inner (visceral) layer of the glomerular capsule, where the third
potential filtration barrier is then located. The third potential filtration barrier is composed of
cells that are called podocytes. Podocytes are shaped somewhat like an octopus with a bulbous
cell body and several thick arms. Each arm of the podocytes has thousands of cytoplasmic
extensions that are known as pedicels, or foot processes; the pedicles interdigitate as they
wrap around the glomerular capillaries. The narrow slits (slit diaphragms) between the
adjacent pedicles provide passageways through which the filtered molecules must pass in
order to enter into the interior of the glomerular filtrate. All of the dissolved plasma solutes
pass easily through the three potential filtration barriers in order to enter into the interior of
the glomerular capsule. Plasma proteins are mostly excluded from the filtrate because of their
large size and negative net charges. The slit diaphragm is a major barrier to the passage of
these plasma proteins into the filtrate. (1) Small amounts of albumin (a major plasma protein)
may pass through into the filtrate, but less than one percent of it is excreted in the urine
because it is either reabsorbed or transported across the cells of the proximal tubule into the
surrounding blood. (1)
When the direct effect of sympathetic stimulation is unavailable, the effect of systemic blood
pressure on the GFR remains relatively constant despite the changes in the mean arterial
pressure within a range of 70-180 mmHg (when the normal is 100 mmHg). The ability of the
kidneys to maintain this relatively constant GFR in the situation of fluctuating blood
pressures is referred to as the renal autoregulation. During renal autoregulation, afferent
arterioles dilate when the mean arterial pressure falls toward 70 mmHg and then constrict
when the mean arterial pressure rises above the normal (100 mmHg). The flow of blood to the
glomeruli and GFR can remain relatively constant within the autoregulatory range of blood
pressure values thanks to this regulatory aspect of the kidney. When there is an increased
arterial pressure that causes a rise in the GFR, an increased delivery of NaCl and H2O to the
distal tubule results. When this happens, a sensor group of specialized cells located in the
thick portion of the ascending limb where contact is made with the afferent and efferent
arterioles in the renal cortex in the tubuloglomerular feedback reaction called the macula
densa sends a chemical signal causing the constriction of the afferent arteriole. This response
then works to protect the late distal tubule and cortical collecting duct from becoming
overloaded. (1)

http://human-physiology---ashley-vg.wikispaces.com/Urology
3. Bagaimana patogenesis bengkak?
reaksi antibodi dan antigen  glumerulonefritis  GMB (glumerulus Membran
Basalis) permeabilitas meningkat  kebocoran (protein hanya lewat tidak di
filtrasi)  tidak diikuti pembentukan albumin lagi  albumin turun  tekanan
onkotik menurun  ekstravasasi cairan dalam vaskuler ke intersisial 
osmoreseptor di jaringan merangsang sekresi vasopresin dan aldosteron 
bengkak

vol darah di vaskuler menurun  low pressure baroreseptor  mengeluarkan

vasopresin dan aldosteron  retensi Na dan air  peningkatan pembentukan
cairan di ginjal tapi tidak diikuti oleh pembentukan albumin
4. Mengapa ditemukan keluhan bengkak pada kedua kelopak mata dan 3 bulan
kemudian bengkak hampir seluruh tubuh?
vol darah di vaskuler menurun  low pressure baroreseptor  mengeluarkan
vasopresin dan aldosteron  retensi Na dan air  peningkatan pembentukan
cairan di ginjal tapi tidak diikuti oleh pembentukan albumin

fungsi albumin : mempertahankan cairan agar tetap di PD

albumin : protein utama yang diekskresikan dalam urin
hipoalbuminemia : katabolisme protein tp tidak diimbangi pembentukan
albumin

di kelopak mata memiliki jaringan ikat yang paling longgar di tubuh

5. Faktor yang menyebabkan orang ini sakit ginjal apa saja (etiologi)?
- Primer
o Lesi minimal
o Lesi membranosa
o Glumerulonefritis proliferatif
o Vokal segmental
- Sekunder
o Infeksi
o Keganasan
o Efek obat dan toksin
o Dll
 Infeksi
 Inflamasi

6. Hubungan pemberian obat dan pengurangan keluhan penderita? Jenis dan

contoh obat?
Diuretik  meningkatkan proses diuresis
Klasifikasi :
- Diuretik osmotik
- Diuretik kuat  ansa henle epitel tebal
- Diuretik tiazid

Pembentukan albumin di hepar meningkat  hiperlipidemia

7. Hubungan didapatkannya TD 130/85 mmHg dengan keluhan (gejala klinis) ?

kategori JNC VII !!
vol darah meningkat  CO tetap  rusaknya ginjal meningkatkan resistensi
dinding PD  tekanan darah meningkat
 http://www.nhlbi.nih.gov/files/docs/guidelines/express.pdf

8. Klasifikasi glumerulonefritis?
- Primer
o Lesi minimal
o Lesi membranosa
o Glumerulonefritis proliferatif
o Vokal segmental
- Sekunder
o Infeksi
o Keganasan
o Efek obat dan toksin
o Dll

9. Patofisiologi dari keluhan pasien (glumerulonefritis) ?

Infeksi di glumerulus  streptokokus punya protein m yang bersifat destruktif
glumerulus dan mengubah antibody di glumerulus memakan protein sendiri
(bersifat mimikri)  reaksi antigen – antibody  hipoalbumin  peningkatan
GMB  ekstravasasi cairan  edem

10. Patogenesis dan imunopatogenesis glumerulonefritis ??

The different forms of glomerulonephritis and nephrotic syndrome probably
represent differences in the nature, extent, and specific cause of immune-
mediated renal damage A number of cytokines in particular TGF 1 (growth
factor 1 and platelet derived growth factor (PDGF) are synthesized by mesangial
cells, inciting an inflammatory reaction in some forms of glomerular disease.

Acute glomerulonephritis
Postinfectious acute glomerulonephritis is due to immune attack in the infecting
organism in which there is a cross-reactivity between antigen of the infecting
organisma (eg. Group of A beta hemolytic streptococci) and a host antigen. The
result is deposition of immune complexes and complement in glomerullar
capillaries and the magnesium

Rapidly progressive glomerulonephritis

Whereas the natural history of most cases of acute glomerulonephritis inculdes
resolution of the underlying renal disease, some case display often abruptly a
form of renal disease that rapidly progresses to chronic renal failure over a
period of weeks to months. Still unknown why this happens. Gaps and focals
discontinue in the glomerular basement memberane.

Chronic Glomerulonephritis
Celullar proliferation, either in the mesangium or in the capillary, is a
pathological hallmark. THE OTHERS ARE NOTABLE FOR OBLITERATION OF
GLOMERULI (sclerosing chronic glomerulonephritis, which include both focal
and diffuse subsets) and yet other display irregular subepithelial proteinaceous
deposits with uniform involvement of individual glomeruli (membranous
glumerulonephritis).

Pathophysiology of Disease
Stephen J.McPhee, Viswanath R.Lingappa, WF Ganong.

Secara garis besar dua mekanisme terjadinya GN yaitu circulating immune

complex dan terbentuknya deposit kompleks imun secara in-situ.
Antigen (Ag) yang berperan pada pembentukan deposit in-situ dapat
berasal dari komponen membran basal glomerulus (MBG) sendiri (fixed a
tigen) atau substansi dari luaryang terjebak pada glomerulus (planted-
antigen).
 Mekanisme pertama apabila Ag dari luar memicu terbentuknya
antibodi (Ab) spesifik, kemudian membentuk kompleks imun Ag-
Ab yang ikut dalam sirkulasi. Kompleks imun akan mengaktivasi
sistem komplemen yang kemudian berikatan dengan kompleks
Ag-Ab. Kompleks imun yang mengalir dalam sirkulasi akan
terjebak pada glomerulus dan mengendap di sub-endotel dan
mesangium. Aktivasi sistem komplemen akan terus berjalan
setelah terjadi pengendapan kompleks imun.
 Mekanisme kedua apabila Ab secara langsung berikatan dengan Ag
yang merupakan komponen glomerulus. Alternatif lain apabila Ag
 non-glomerulus yang bersifat kation terjebak pada bagian anionik
glomerulus, diikuti pengendapan Ab dan aktivasi komplemen
secara lokal. Selain kedua mekanisme tersebut GN dapat dimediasi
oleh imunitas selular (cell-mediated immunity). Studi
eksperimental membuktikan bahwa sel T dapat berperan langsung
terhadap timbulnya proteinuria dan terbentuknya kresen pada GN
kresentik.
IPD
KERUSAKAN GLOMERULUS PADA GN
Tidak langsung disebabkan oleh endapan komplek imun.
Kerusakannya dipengaruhi oleh : proses inflamasi, sel inflamasi, mediator
inflamasi, komplemen, proses imun, terbentuknya Ag-Ab, lokasi endapan,
komposisi, jumlah endapan dan Ab.
Prosesnya dapat melibatkan :
a. sistem komplemen dan sel infamasi
b. sistem komplemen, tanpa sel inflamasi
c. sel inflamasi,tanpa sistem komplemen
d. akibat langsung imunitas seluler melalui sel T yang tersensitasi.
Pada sebagian GN : disebabkan oleh endapan kompleks imun  proses
inflamasi glomerulus  proliferasi sel.
Sedangkan pada : GN non proliferatif dan skleroting (GN
Membranosa/GNMN) / Glomerulosklerosis fokal segmental (GSFS) 
tidak melibatkan sel inflamasi.

PROSES INFLAMASI PADA KERUSAKAN GLOMERULUS

Penyebab kerusakan : endapan kompleks imun  proses inflamasi.
Proses inflamasi di pengaruhi oleh : sel inflamasi, molekul adhesi dan
kemokin (efek kemotaktik : menarik sel inflamasi dari darah ke jaringan).
Tahap proses inflamasi :
a. melekatnya sel inflamasi pada endotel. Yang di perantarai oleh
molekul adkesi L, E, P (leukosit, endotel, trombosit)
b. endotel melepaskan CD13 dan PECAM1 (platelet endotelial cell adhesi
molecule1)  aktivasi sel inflamasi
c. reaksi di atas menyebabkan perlekatan sel inflamasi dan endotel
semakin kuat. Perlekatan ini di mediasi oleh VLA-4 (very late
antigen4) pada permukaan sel inflamasi dan VCAM1 pada endotel
yang teraktivasi.
d. Ikatan LFA1 (limfoisit function asociated antigen1) pada permukaan
sel inflamasi dan ICAM1 (intracelular cell adhesion molecule) pada sel
ondotel  sel endotel mempercepat perlekatan.
Kemotaktik meningkat  inflamasi bertambah berat.

Ilmu penyakit Dalam, FKUI

Proses GNAPS dimulai ketika kuman streptokokus sebagai antigen masuk
kedalam tubuh penderita,yang rentan, kemudian tubuh memberikan respon
dengan membentuk antibodi. Bagian mana dari kuman streptokokus yang
bersifat antigen masih belum diketahui. Beberapa penelitian pada model
binatang dan penderita GNAPS menduga yang bersifat antigenik adalah: M
protein, endostreptosin, cationic protein, Exo-toxin B, nephritis plasmin-binding
protein dan streptokinase.3 Kemungkinan besar lebih dari satu antigen yang
terlibat dalam proses ini, barangkali pada stadium jejas ginjal yang berbeda
dimungkinkan akibat antigen M protein dan streptokinase.3,

Mekanisme terjadinya jejas renal pada GNAPS

GNAPS adalah suatu penyakit imunologik akibat reaksi antigen-antibodi yang

terjadi dalam sirkulasi atau in situ dalam glomerulus.8,9 Mekanisme terjadinya
inflamasi yang mengakibatkan terjadinya jejas renal didahului oleh proses
sebagai berikut:

1. Terbentuknya plasmin sebagai akibat pemecahan plasminogen oleh

streptokinase yang akan menaktivasi reaksi kaskade komplemen.
2. Terperangkapnya kompleks Ag-Ab yang sudah terbentuk sebelumnya
kedalam glomerulus.
3. Antibodi antistreptokokus yang telah terbentuk sebelumnya berikatan dengan
molekul tiruan (molecul mimicry) dari protein renal yang menyerupai Ag
Streptokokus (jaringan glomerulus yang normal yang bersifat autoantigen).

Proses terjadinya jejas renal pada GNAPS diterangkan pada gambar dibawah ini:
Gambar . Mekanisme imunopatogenik GNAPS

DIAGNOSIS DAN PENATALAKSANAAN GLOMERULONEFRITIS AKUT *

Dedi Rachmadi
Bagian Ilmu Kesehatan Anak
FK. UNPAD-RS. Dr. Hasan Sadikin Bandung
 11. Hasil pemeriksaan laborat urin rutin yang dilakukan? Harga normal ??

12. Apakah maksud proteinuria +++?

The filtration of albumin and nonalbumin proteins across the abnormal glomerular capillary
wall (GCW) exposes mesangial and tubular cells to these proteins. Albumin and nonalbumin
proteins are normally reabsorbed from the glomerular filtrate in the proximal convoluted
tubule (PCT).

Heavy proteinuria may exceed the capacity of lysosomes in the PCT cells to metabolize
reabsorbed protein, and toxic enzymes may leak into the cells and the surrounding renal
interstitium[1] as a consequence of lysosomal degranulation. Whether the nephrotoxic protein
is albumin, nonalbumin protein, or both remains unclear.

Other proteins, such as transferrin, complement components, and low-density lipoproteins

(LDLs), also appear to be directly toxic to tubular cells. In addition, lipoproteins appear to be
toxic to mesangial cells and may contribute to the development of glomerular sclerosis.

A consequence of protein-mediated cytotoxicity is the production of chemokines and

cytokines that initiate an inflammatory response and ultimately lead to sclerosis and fibrosis.

13. Hubungan proteinuria dengan diagnosis glumerulonefritis?

 - Peradangan pada glumerulus  dinding kapiler rusak  yang bermuatan
negatif jadi mudah untuk difiltrasi  proteinuria
- Kelainan epitel tubulus  gangguan reabsorbsi di tubulus
- Perubahan hemodinamik (cnth : olahraga, makanan (?), dll)

14. Apa DD pasien ini? Dibikin kolom ! (definisi, etiologi, patogenesis, patofisiologi,
gejala klinis, terapi, pemeriksaan penunjang)

GLOMERULONEFRITIS
DEFINISI
Penyakit yang sering dijumpai dalam praktik klinik sehari – hari
dan merupakan penyebab penting PGTA (penyakit ginjal tahap
akhir)
IPD Jilid 1 FK UI
Sindrom paling agresif dari GN akut dan memiliki ciri perburukan
cepat ke arah agagl ginjal terminal dalam beberapa hari atau
minggu, kecuali bila diterapi dengan tepat. Jarang ditemukan.
Kapita selekta KD jilid I edisi III
KLASIFIKASI
Berdasarkan histopatologinya:
 GN lesi minimal identik SN=nefrosis lupoid
 Glomerulosklerosis fokal dan segmental (GSFS)gejala SN: proteinuria
massif, hipertensi, hematuri
 GN membranosa (GNMN)
 GN proliferative proliferasi sel mesangial dan infiltrasi leukosit,
infiltrasi makrofag penebalan MBG.
IPD
ETIOLOGI
Glomerulonefritis proliferatif primer
Sindrom goodpasture
Vaskulitis (granulomatosis wegener, poliarteritis, purpura Henoch
schonlein)
SLE
Mikroangiopati trombotik (sindrom uremia hemolitik, purpura
trombositopenia trombotik)
Kapita selekta KD jilid I edisi III
PATOFISIOLOGI
proses imunologik diatur oleh berbagai faktor imunogenetik yang
menentukan bagaimana individu merespon suatu kejadian.ada 2
mekanisme :
a. circulating imune complex
 Apabila Ag dari luar memicu terbentuknya antibodi spesifik 
kemudian membentuk kompleks imun Ag-Ab yang ikut dalam
sirkulasi  kompleks imun akan mengaktivasi sistem komplemen
yang akan berikatan dengan kompleks Ag-Ab  kompleks imun
yang mengalir dalam sirkulasi akan terjebak pada glomerulus dan
mengendap di subendotel glomerulus  menyebabkan kerusakan
glomerulus  dapat terjadi inflamasi
b. terbentuknya deposit kompleks imun secara in situ
Apabila Ab berikatan secara langsung dengan Ag yang merupakan
komponen glomerulus. Kerusakan glomerulus tidak hanya
disebabkan oleh endapan kompleks imun tapi jua karena proses
inflamasi, sel inflamasi, mediator inflamasi, komplemen yang
berperan pada kerusakan glomerulus
IPD Jilid 1 FK UI
MANISFESTASI KLINIS
Gejala umunya hematuria berat, oliguria berat, dan nyeri pinggang.
Kecurigaan terutama bila ditemukan :
Sindrom nefritik akut pada orang dewasa
Hematuria mikroskopik yang berat pada sindrom nefritik akut
Proteinuria berat pada sindrom nefritik akut
Oliguria berat atau anuria
Penurunan laju filtrasi glomerolus
Adanya penyakit sistemik
Kapita selekta KD jilid I edisi III
DIAGNOSIS
Mencari informasi riwayar GN dalam keluarga, penggunaan obat antiinflamasi
non-steroid, preparat emas organik, heroin, imunosupresif seperi sikloporin
dan riwayat infeksi streptokokus endokarditis atau virus.

Diagnosis ditegakkan berdasarkan gejala dan hasil pemeriksaan laboratorium.

GN ditandai dengan proteinuria, hematuria, penurunan fungsi ginjal dan
perubahan ekskresi garam dengan akibat edema, kongesti aliran darah dan
hipertensi.

Px lab:
 Px urin
 Biopsi ginjal
 Gula darah
 Serum albumin
  Profil lemak
 Fungsi ginjal
 Px serologi seperti ASTO, C3, C4, ANA
IPD
DD
PENATALAKSANAAN
Pertukaran plasma
pertukaran plasma secara intensif, biasanya menukar 4 liter
plasma pasien dengan albumin atau cairan plasma protein setiap
hari selama 1 – 2 minggu, diikuti dengan penurunan bertahap
dalam frekuensi, dikombinasi dengan imunosupresi dan terapi
antitrombotik (biasanya prednisolon 1 mg/kg/BB/hari,
siklosfosfamid 1,5 – 2,5 mg/kg/BB/hari dan dipiridamol 400
mg/hari). Dengan terapi ini, biasanya hanya pasien dengan anuria
lengkap yang tidak mengalami perbaikan fungsi ginjal
Terapi steroid pulsasi
Diberikan metilprednisolon secara intravena dengan pulsasi
berupa 1 g/hari selama 3 hari atau 30 mg/kg/BB setiap hari
kedua untuk tiga dosis dan diulangi 1 minggu kemudian bila
responnya tidak baik
Kapita selekta KD jilid I edisi III
PROGNOSIS
o 80 % sembuh, diatasi pengobatan yg sesuai
o 10 % mjd kronik
o 10 % berakibat fatal
http://www.klinikmedis.com/archive/artikel/
KOMPLIKASI

SINDROM NEFROTIK
DEFINISI
Penyakit yang tiba – tiba muncul pada anak – anak biasanya berupa
oliguria dengan urin berwarna gelap atau kental akibat proteinuria
berat
Kapita selekta KD jilid I edisi III
KLASIFIKASI

SN bawaan
Diturunkan sebagai resesif autosomal atau karena reaksi maternofetal.
Resisten terhadap semua pengobatan. Gejalanya adalah edema pada masa
neonatus. Prognosis buruk dan biasanya penderita meninggal dalam bulan-
bulan pertama kehidupannya.
2. SN sekunder
Disebabkan oleh:
a. Malaria kuartana atau parasit lainnya.
b. Penyakit kolagen seperti lupus eritematosus diseminata,
purpura anafilaktoid.
c. Glomerulonefritis akut atau glomerulonefritis kronis, trombosis
vena renalis.
d. Bahan kimia seperti trimetadion, paradion, penisilamin, garam
emas, sengatan lebah, air raksa.
e. Amiloidosis, penyakit sel sabit, hiperprolinemia, nefritis
membranoproliferatif
f. hipokomplementemik.

3. SN idiopatik (tidak diketahui penyebabnya)

Berdasarkan histopatologi yang tampak pada biopsi ginjal dengan
pemeriksaan mikroskop biasa dan mikroskop electron, Churg dan kawan-
kawan membagi dalam 4 golongan, yaitu :
a. Kelainan minimal
Dengan mikroskop biasa glomerulus tampak normal, sedangkan
dengan mikroskop electron tampak foot processus sel epitel berpadu.
Dengan cara imunofluoresensi ternyata tidak terdapat IgG pada
dinding kapiler glomerulus. Golongan ini lebih banyak terdapat pada
anak daripada orang dewasa. Prognosis lebih baik dibandingkan
dengan golongan lain.
b. Nefropati membranosa
Semua glomerulus menunjukan penebalan dinding kapiler yang
tersebar tanpa proliferasi sel. Tidak sering ditemukan pada anak.
Prognosis kurang baik.
c. Glomerulonefritis proliferatif
*Glomerulonefritis proliferatif eksudatif difus
Terdapat proliferasi sel mesangial dan infiltasi sel polimorfonukleus.
Pembengkakkan sitoplasma endotel yang menyebabkan kapiler
tersumbat. Kelainan ini sering ditemukan pada nefritis yang timbul
setelah infeksi dengan Streptococcus yang berjalan progresif dan pada
 SN.prognosis jarang baik, tetapi kadang-kadang terdapat penyembuhan
setelah pengobatan yang lama.
d. Glomerulosklerosis fokal segmental
Pada kelainan ini yang mencolok sklerosis glomerulus. Sering ditandai
dengan atrofi tubulus. Prognosis buruk.
Sindroma nefrotik bisa terjadi akibat berbagai glomerulopati atau penyakit
menahun yang luas.
Sejumlah obat-obatan yang merupakan racun bagi ginjal juga bisa
menyebabkan sindroma nefrotik, demikian juga halnya dengan pemakaian
heroin intravena.

Sindroma nefrotik bisa berhubungan dengan kepekaan tertentu.

Beberapa jenis sindroma nefrotik sifatnya diturunkan.

Sindroma nefrotik yang berhubungan dengan infeksi HIV (human

immunodeficiency virus, penyebab AIDS) paling banyak terjadi pada orang
kulit hitam yang menderita infeksi ini.
Sindroma nefrotik berkembang menjadi gagal ginjal total dalam waktu 3-4
bulan.
http://www.klinikmedis.com/archive/artikel/art_SN.pdf
Penyebab umum SN:
Kelainan primer glomerulus:
- GN membranosa/GNMN: MBG rusak krn akibat endapan kompleks
imun di sub epitel
- GN membranoproliferatif/GNMP
- GN sklerosis fokal/GSF: permeabilitas MBG naik sel epitel
visceral glomerulus terlepas dari MBG, shg berkurangnya heparin
sulfat proteoglikan menyebabkan muatan – MBG menurun, albumin
dpt lolos mll urin. (Saringan dari filtrasinya jadi lebih
gedepermeabilitas naik, jadi albumn lolos)
- Nefropati IgA
- Penyakit lesi minimal
- GN proliferative
Kelainan sekunder:
- Herediter-familial: DM, sickle cell
- Autoimun: LE, RA
- Infeksi: post infeksi, GN, endokarditis
- Drug: NSAID, heroin, emas, kaptopril,penisilamin
- Neoplasma: limfoma, leukemia, MM
Buku Internoid Tosca Enterpris
ETIOLOGI
Pada anak2 :
Glomerulonefritis kelainan minimal (sebagaian besar)
Glomerulonefritis fokal dan segmental
Glomerulonefritis membranoproliferatif
Glomerulonefritis pascastreptokok
Pada dewasa :
Glomerulonefritis primer (sebagian besar tidak diketahui
sebabnya) Glomerulonefritis membranosa
Glomerulonefritis kelainan minimal
Glomerulonefritis membranoproliferatif
Glomerulonefritis pascastreptokok
Glomerulonefritis sekunder
SLE (lupus erotematosus sistemik)
Obat (emas, penisilamin, kaptopril, antiinflamasi nonsteroid)
neoplasma (kanker payudara, kolon, bronkus)
penyakit sistemik yang mempengaruhi glomerolus (diabetes,
amlioidosis)
Kapita selekta KD jilid I edisi III
PATOFISIOLOGI
Kerusakan dinding kapiler glomerolus  peningkatan permeabilitas
membran glomerolus terhadap protein plasma  protein lolos dari
plasma  protein masik filtrat glomerolus  proteinuria 
hipoalbuminemia dan terbaliknya rasio albumin globulin 
penurunan tekanan osmotik  odem generalisata  cairan keluar
dari pembuluh darah  masuk ke dalam jaringan  volume plasma
menurun  filtrasi berkurang  sekresi kompensatorik aldosteron +
penurunan GFR dan penurunan sekresi peptida natriuretrik 
mendorong retensi garam dan air penimbunan cairan dalam jumlah
besar  odem anasarka
Patologi robin kumar jilid 2
Peningkatan permeabilitas membran glomerolus  proteinuria 
sebagian besar albumin melampaui sintesis hepar 
hipoalbuminemia  retensi garam dan air
Kapita selekta KD jilid I edisi III
MANISFESTASI KLINIS
Edema generalisata terutama jelas pada kaki namun dapat
ditemukan edem muka, asites, dan efusi pleura
Hiperlipidemia, umumnya ditemukan hiperkolesterolemia
Hiperkoagulabilitas, yang akan meningkatkan risiko trombosis
vena dan arteri
Proteinuria > 3,5 g/hari pada dewasa atau 0,05 g/kg BB/hari pada
anak2
Hipoalbuminemia < 30 g/l
Kapita selekta KD jilid I edisi III

DIAGNOSIS
DD
PENATALAKSANAAN
Tentukan penyebabnya (biopsi ginjal pada seluruh orang dewasa)
Edema
Dianjurkan untuk tirah baring dan memakai stoking yang menekan
terutama untuk pasien lanjut usia. Hati – hati dalam pemberian
diuretik, karena adanya proteinuria berat dapat menyebabkan gagal
ginjal atau hipovolemik. Harus diperhatikan dan dicatat
keseimbangan cairan pasien, biasanya diusahakan penurunan berat
badan dan cairan 0,5 – 1 kg/hari. Dilakukan pengawasan terhadap
kalium plasma, natrium plasma, kreatinin, dan ureum. Bila perlu
diberi tambahan kalium. Diuretik yang biasanya diberikan adalah
diuretik ringan seperti thiazid atau furosemid dosis rendah, dosisnya
dapat ditingkatkan sesuai kebutuhan. Garam dalam diet dan cairan
dibatasi bila perlu. Pemberian albumin iv hanya diperlukan pada
kasus – kasus refrakter terutama bila terjadi kekurangan volume
intravaskular atau oliguria
Memperbaiki nutrisi
Dianjurkan pemberian makanan tinggi kalori dan rendah garam.
Manfaat diet tinggi protein tidak jelas dan mungkin tidak sesuai
karena adanya gagal ginjal, biasanya cukup dengan protein 50 – 60
g/hari ditambah kehilangan dari urin
Mencegah infeksi
Biasanya diberikan antibiotik profilaksis untuk menghindari infeksi,
terutama terhadap pneumokok
Pertimbangan obat antikoagulasi
Dilakukan pada pasien dengan sindrom nefrotik berat, kecuali bila
terdapat kontraindikasi. Terapi (biasanya warfarin) dipertahankan
sampai penyakitnya sembuh
Penatalaksaan penyebabnya
 Pada orang dewasa, tidak perlu seperti pada anak2 dimana dilakukan
terapi steroid sebagai bagian dari penegakan diagnosis, kelainan
minimal hanya menjadi penyebab pada 10 – 20 % kasus. Terapi
disesuaikan dengan diagnosis dan penyebab yang mendasarinya
Kapita selekta KD jilid I edisi III
PROGNOSIS
KOMPLIKASI
Gagal ginjal akut
Trombosis
Infeksi
Malnutrisi
Kapita selekta KD jilid I edisi III

Beda atau sama antara sindroma nefrotik dan nefritis sindrom???

15. Pemeriksaan penunjang lain?

- Darah rutin (LED)  EDTA. Yang perlu sel lengkap pakai EDTA, selain itu
pakai beku.
- Tes fungsi ginjal (kreatinin ureum, )

Laboratory studies
To determine whether patients have transient proteinuria, perform the following:

 Urinalysis and microscopic examination on at least 3 separate occasions

 Albumin-to-creatinine or protein-to-creatinine ratio in random urine sample[7, 8]
 Urinalysis on early morning sample, before patients are involved in physical
activity
To determine whether patients have orthostatic proteinuria, perform the following:

 Urine microscopy
 Split urine collection - Daytime (7 am to 11 pm) and overnight (11 pm to 7
am)
To determine whether proteinuria may be glomerular in origin, perform the following:

 Urine microscopy
 Urine collection (24 h) for quantification of albumin (or protein) excretion
andcreatinine clearance
 Serum creatinine, albumin, cholesterol (see HDL cholesterol and LDL
cholesterol), and blood glucose determinations
 Autoantibody determinations, if indicated - If indicated; including antinuclear
antibodies (ANAs), anti-DNA antibodies, complement levels, and
cryoglobulins
 Hepatitis B, hepatitis C, and HIV serologies - If indicated
 Urine and plasma protein electrophoresis - If indicated
Imaging studies
Imaging studies in proteinuria can include the following:

 Renal ultrasonography scan - If glomerular disease is being considered

 http://emedicine.medscape.com/article/238158-workup

Creatinine is critically important in assessing renal function because it has several interesting
properties. In blood, it is a marker of glomerular filtration rate; in urine, it can remove the need
for 24-hour collections for many analytes or be used as a quality assurance tool to assess the
accuracy of a 24-hour collection.

The reference ranges for serum creatinine and urine creatinine are listed below.

Serum creatinine
 Adult males: 0.5–1.2 mg/dL*
 Adult females: 0.4 – 1.1 mg/dL*
 Children (up to 12 years of age): 0.0–0.7 mg/dL
*The reference interval varies with race, ethnicity, and gender. As a result, one should look at
the calculated eGFR (estimated glomerular filtration rate), as reported from the measured
serum creatinine, to assess renal function. The GFR can also be calculated from the
creatinine clearance (see below).

Table 1. Glomerular Filtration Rate[1] (Open Table in a new window)

Mean GFR

Age (Years)
(mL/min/1.73 m2)

20-29 116

30-39 107

40-49 99

50-59 93

60-69 85

70+ 75

Urine creatinine [2]

 Adult males: 20-25 mg/kg/day (roughly 1575 mg/day for a 70-kg male)
 Adult females: 15-20 mg/kg/day (roughly 1050 mg/day for a 60-kg female)