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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.
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.
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
Filtrasi tergantung besar molekul dan muatan (postitif lebih mudah di filtrasi)
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
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
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
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
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.
Proses terjadinya jejas renal pada GNAPS diterangkan pada gambar dibawah ini:
Gambar . Mekanisme imunopatogenik GNAPS
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.
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.
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.
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
Laboratory studies
To determine whether patients have transient 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:
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).
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
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)