1.

Histologi system urinary

The outer parietal layer of a
glomerular capsule consists of a
simple squamous epithelium
supported externally by a basal
lamina. At the tubular pole, this
epithelium changes to the simple
cuboidal epithelium that
continues and forms the proximal
tubule.

The visceral layer of a renal corpuscle consists of unusual

stellate epithelial cells called podocytes (Figures 19–5c, d),
which together with the capillary endothelial cells compose
the apparatus for renal filtration. From the cell body of each
podocyte several primary processes extend and curve
around a length of glomerular capillary. Each primary
process gives rise to many parallel, interdigitating
secondary processesor pedicels (L. pedicellus, little foot;
Figures 19–5c, d). The pedicels cover much of the capillary
surface, in direct contact with the basal lamina (Figures 19–
5c and 19–6).

In addition to capillary endothelial cells and podocytes,

renal corpuscles also contain mesangial cells (Gr. mesos,
in the midst + angion, vessel), most of which resemble
vascular pericytes in having contractile properties and
producing components of An external lamina. Mesangial
cells are difficult to distinguish in routine sections from
podocytes , but often stain more darkly. They and their
surrounding matrix comprise the mesangium (Figure 19–
7), which fills interstices between capillaries that lack
podocytes. Functions of the mesangium include the following:
■ Physical support of capillaries within the glomerulus;
■ Adjusted contractions in response to blood pressure changes, which help maintain an optimal
filtration rate;
■ Phagocytosis of protein aggregates adhering to the glomerular filter, including antibody-antigen
complexes abundant in many pathological conditions; and
■ Secretion of several cytokines, prostaglandins, and other factors important for immune defense and
repair in the glomerulus.
 Conversely, organic anions and cations not filtered in the renal corpuscle (because of the
polyanions in the filter or binding to plasma proteins) may be released in the peritubular
capillaries, taken up by the cells of the proximal tubules and undergo secretion into the filtrate
Table 19–1). Organic anion and cation transporters allow the kidneys to dispose of such
substances at a higher rate than by glomerular filtration alone. Because these molecules include
important substances (such as bile salts, creatinine, etc) and many antibiotics and other drugs,
this process of tubular secretion is of great pharmacologic importance as a key Mechanism of
Drug clearance.
The cells of the proximal tubules have central nuclei and very acidophilic cytoplasm
Figures 19–8 and 19–9) because of the abundant mitochondria. The cell apex has very many long
microvilli that form a prominent brush border in the lumen that facilitates reabsorption (Figures
19–8 through 19–10). Because the cells are large, each transverse section of a PCT typically
contains only three to five nuclei. In routine histologic preparations, the long brush border may
be disorganized and give the lumens a fuzz-filled appearance. Peritubular capillaries are abundant
in the sparse surrounding connective tissue interstitium, which fills only about 10% of the cortex

Besides their
major roles in
reabsorption and
secretion, cells of the
proximal tubule also
perform hydroxylation
of vitamin D and
release to the
capillaries. Moreover,
fibroblastic interstitial
cells in cortical areas
near the proximal
tubules produce
erythropoietin, the
growth factor secreted
in response to a
prolonged decrease in
local oxygen
concentration.
 The loops of Henle and surrounding interstitial connective tissue are involved in further adjusting the
salt content of the filtrate. Cuboidal cells of the loops’ TALs actively transport sodium and chloride ions
out of the tubule against a concentration gradient into the hyaluronate-rich interstitium, making that
compartment hyperosmotic. This causes water to be withdrawn passively from the thin descending part
of the loop, thus concentrating the filtrate. The thin ascending limbs reabsorb sodium chloride (NaCl) but
are impermeable to water. The countercurrent flow of the filtrate (descending, then immediately
ascending) in the two parallel thin limbs establishes a gradient of osmolarity in the interstitium of the
medullary pyramids, an effect that is “multiplied” at deeper levels in the medulla. Countercurrent blood
flow in the descending and ascending loops of the vasa recta helps maintain the hyperosmotic
interstitium. The interstitial osmolarity at the pyramid tips is about four times that of the blood.
 The ascending limb of the nephron is straight as it enters the cortex and forms the macula densa, and
then becomes tortuous as the distal convoluted tubule (DCT) (see Figure 19–2). Much less tubular
reabsorption occurs here than in the proximal tubule. The simple cuboidal cells of the distal tubules differ
from those of the proximal tubules in being smaller and having no brush border and more empty lumens
(Figure 19–9). Because distal tubule cells are flatter and smaller than those of the proximal tubule, more
nuclei are typically seen in sections of distal tubules than in those of proximal tubules (Figure 19–8). Cells
of the DCT also have fewer mitochondria than cells of proximal tubules, making them less acidophilic
(Figure 19–9). The rate of Na absorption here is regulated by aldosterone from the adrenal glands.

Where the initial, straight part of the distal

tubule contacts the arterioles at the vascular pole
of the renal corpuscle of its parent nephron, its
cells become more columnar and closely packed,
forming the macula densa (L. thicker spot). This is
part of a specialized sensory structure, the
juxtaglomerular apparatus (JGA) that utilizes
feedback mechanisms to regulate glomerular
blood flow and keep the rate of glomerular
filtration relatively constant. The JGA is shown in
Figures 19–5 and 19–12. Cells of the macula densa
typically have apical nuclei, basal Golgi
complexes, and a more elaborate and varied
system of ion channels and transporters. Adjacent
to the macula densa, the tunica media of the
afferent arteriole is also modified. The smooth
muscle cells are modified as juxtaglomerular
granular (JG) cells, with a secretory phenotype
including more rounded nuclei, rough ER, Golgi
complexes, and zymogen granules with renin
(Figures 19–5 and 19–12). Also at the vascular
pole are lacis cells (Fr. lacis, lacework), which are
extraglomerular mesangial cells that have many
of the same supportive, contractile and defensive
functions as these cells inside the glomerulus.

Basic functions of the JGA in the

autoregulation of the GFR and in controlling blood
pressure include the following activities. Elevated
arterial pressure increases glomerular capillary
blood pressure, which increases the GFR. Higher
GFR leads to higher luminal concentrations of Na+
and Cl- in the TAL of the nephron, which are
monitored by cells of the macula densa. Increased ion levels in the lumen cause these cells to release
ATP, adenosine, and other vasoactive compounds that trigger contraction of the afferent arteriole, which
lowers glomerular pressure and decreases the GFR. This lowers tubular ion concentrations, which turns
off the release of vasoconstrictors from the macula densa.

Decreased arterial pressure leads to increased autonomic stimulation to the JGA as a result of
baroreceptor function, including local baroreceptors in the afferent arteriole, possibly the JG cells
themselves. This causes the JG cells to release renin, an aspartyl protease, into the blood. There renin
cleaves the plasma protein angiotensinogen into the inactive decapeptide angiotensin I. Angiotensin-
converting enzyme (ACE) on lung capillaries clips this further to angiotensin II, a potent vasoconstrictor
that directly raises systemic blood pressure and stimulates the adrenals to secrete aldosterone.
Aldosterone promotes Na and water reabsorption in the distal convoluted and connecting tubules, which
raises bloodvolume to help increase blood pressure. The return of normal blood pressure turns off
secretion of renin by JG cells.

Ultrastructurally the principal cells can be seen to have

basal membrane infoldings, consistent with their role in ion
transport, and a primary cilium among the microvilli. The
medullary collecting ducts are the final site of water
reabsorption from the filtrate. Principal cells are particularly
rich in aquaporins, the integral membrane pore proteins that
function as specific channels for water molecules, but here
most aquaporins are sequestered in membranous
cytoplasmic vesicles.

Antidiuretic hormone (ADH), released from the pituitary

gland as the body becomes dehydrated, makes collecting
ducts more permeable to water and increases the rate at
which water molecules are pulled osmotically from the
filtrate.

Scattered among the principal cells are variably darker

intercalated cells, or IC cells, with more abundant
mitochondria and projecting apical folds. Intercalated cells, a
few of which also occur in the DCTs, help maintain acid-base
balance by secreting either H+ or HCO3-
Urine is transported by the ureters from the renal pelvis to the urinary bladder where it is stored until
emptying by micturition via the urethra. The calyces, renal pelvis, ureter, and bladder have somewhat
similar histologic structure, with the walls becoming gradually thicker closer to the bladder. The mucosa
of these organs is lined by the unique stratified transitional epithelium or urothelium. Cells of this
epithelium are organized as three layers:

■ A single layer of small basal cells resting on a very thin basement membrane;
■ An intermediate region containing from one to several layers of more columnar cells; and
■ A superficial layer of very large, bulbous cells called umbrella cells that are occasionally bi- or
multinucleated and are highly differentiated to protect underlying cells against the cytotoxic effects of
hypertonic urine.

Most of the apical surface consists of asymmetric unit membranes in which regions of the outer lipid
layer appear ultrastructurally to be twice as thick as the inner leaflet. These regions are composed of lipid
rafts containing mostly integral membrane proteins called uroplakins that assemble into paracrystalline
arrays of stiffened plaques 16 nm in diameter. These membranous plaques are impermeable to water
and protect cytoplasm and underlying cells from the hyperosmotic effects of urine.
Urothelium is surrounded by a folded lamina propria and submucosa, followed by a dense sheath of
interwoven smooth muscle layers and adventitia (Figures 19–16 and 19–17). Urine is moved from the
renal pelvises to the bladder by peristaltic contractions of the ureters. The bladder’s lamina propria and
dense irregular connective tissue of the submucosa are highly vascularized. The bladder in an average
adult can hold 400 to 600 mL of urine, with the urge to empty appearing at about 150 to 200 mL. The
muscularis consists of three poorly delineated layers, collectively called the detrusor muscle, which
contract to empty the bladder (Figure 19–17). Three muscular layers are seen most distinctly at the neck
of the bladder near the urethra (Figure 19–17). The ureters pass through the wall of the bladder obliquely,
forming a valve that prevents the backflow of urine into the ureters as the bladder fills. All the urinary
passages are covered externally by an adventitial layer, except for the upper part of the bladder that is
covered by serous peritoneum.
The urethra is a tube that carries the urine from the bladder to the exterior (Figure 19–18). The urethral
mucosa has prominent longitudinal folds, giving it a distinctive appearance in cross section. In men, the
two ducts for sperm transport during ejaculation join the urethra at the prostate gland (see Chapter 21).
The male urethra is longer and consists of three segments:
- The prostatic urethra, 3 to 4 cm long, extends through the prostate gland and is lined by urothelium.
- The membranous urethra, a short segment, passes through an external sphincter of striated muscle and
is lined by stratified columnar and pseudostratified epithelium.
- The spongy urethra, about 15 cm in length, is enclosed within erectile tissue of the penis (see Chapter
21) and is lined by stratified columnar and pseudostratified columnar epithelium (Figure19–18), with
stratified squamous epithelium distally.

In women, the urethra is exclusively a urinary organ. The female urethra is a 4- to 5-cm-long tube, lined
initially with transitional epithelium, then by stratified squamous epithelium and Some areas of
pseudostratified columnar epithelium. The middle part of the female urethra is surrounded by the
external striated muscle sphincter.

Sumber :
Mescher A.L. 2013. Junqueira’s Basic Histology TEXT AND ATLAS THIRTEENTH EDITION. McGrawHill : New
York

2. Mekanisme pembentukan urin

Normally functioning kidneys produce a large volume of dilute urine when fluid intake is high, and a small
volume of concentrated urine when fluid intake is low or fluid loss is large. ADH controls whether dilute
urine or concentrated urine is formed. In the absence of ADH, urine is very dilute. However, a high level
of ADH stimulates reabsorption of more water into blood, producing a concentrated urine.

Glomerular Filtration

1. Fluid that enters the capsular space is glomerular filtrate.

2. The filtration membrane consists of the glomerular endothelium, basal lamina, and filtration
slits between pedicels of podocytes.
3. Most substances in blood plasma easily pass through the glomerular filter. However, blood cells
and most proteins normally are not filtered.
4. Glomerular filtrate amounts to up to 180 liters of fluid per day. This large amount of fluid is
filtered because the filter is porous and thin, the glomerular capillaries are long, and the capillary
blood pressure is high.
5. Glomerular blood hydrostatic pressure (GBHP) promotes filtration; capsular hydrostatic
pressure (CHP) and blood colloid osmotic pressure (BCOP) oppose filtration. Net filtration
pressure (NFP) = GBHP - CHP - BCOP. NFP is about 10 mmHg.
6. Glomerular filtration rate (GFR) is the amount of filtrate formed in both kidneys per minute; it
is normally 105–125 mL/min.
7. Glomerular filtration rate depends on renal autoregulation, neural regulation, and hormonal
regulation.

Tubular Reabsorption and Tubular Secretion

1. Tubular reabsorption is a selective process that reclaims materials from tubular fluid and
returns them to the bloodstream. Reabsorbed substances include water, glucose, amino acids,
urea, and ions, such as sodium, chloride, potassium, bicarbonate, and phosphate
2. Some substances not needed by the body are removed from the blood and discharged into the
urine via tubular secretion. Included are ions (K+,H+, and NH4+), urea, creatinine, and certain drugs.
3. Reabsorption routes include both paracellular (between tubule cells) and transcellular (across
tubule cells) routes.
4. The maximum amount of a substance that can be reabsorbed perunit time is called the
transport maximum (Tm).
5. About 90% of water reabsorption is obligatory; it occurs via osmosis, together with
reabsorption of solutes, and is not hormonally regulated. The remaining 10% is facultative water
reabsorption, which varies according to body needs and is regulated by ADH.
6. Na+ ions are reabsorbed throughout the basolateral membrane via primary active transport.
7. In the proximal convoluted tubule, sodium ions are reabsorbed through the apical membranes
via Na+–glucose symporters and Na+/H+ antiporters; water is reabsorbed via osmosis; Cl-
,K+,Ca2+,Mg2+, and urea are reabsorbed via passive diffusion; and NH3 and NH4+ are secreted.
8. The loop of Henle reabsorbs 20–30% of the filtered Na+, K+,Ca2+,and HCO3-; 35% of the filtered
Cl-; and 15% of the filtered water.
9. The distal convoluted tubule reabsorbs sodium and chloride ions via Na+–Cl- symporters.
10. In the collecting duct, principal cells reabsorb Na and secrete
K ; intercalated cells reabsorb K and HCO3 and secrete H+.
+ -

11. Angiotensin II, aldosterone, antidiuretic hormone, atrial natriuretic peptide, and parathyroid
hormone regulate solute and water reabsorption
 Sumber :
Tortora G.J & Derrickson B. 2009. PRINCIPLES OF ANATOMY AND PHYSYIOLOGY Twelfth Edition.
Jon Wiley & Sons, Inc : Hoboken

3. Patomekanisme gejala scenario

The classic presentation in patients with acute pyelonephritis is as follows:
 Fever - This is not always present, but when it is, it is not unusual for the temperature to exceed
103°F (39.4°C)
 Costovertebral angle pain - Pain may be mild, moderate, or severe; flank or costovertebral angle
tenderness is most commonly unilateral over the involved kidney, although bilateral discomfort
may be present
 Nausea and/or vomiting - These vary in frequency and intensity, from absent to severe; anorexia
is common in patients with acute pyelonephritis
Gross hematuria (hemorrhagic cystitis), unusual in males with pyelonephritis, occurs in 30-40%
of females, most often young women, with the disorder.
Symptoms of acute pyelonephritis usually develop over hours or over the course of a day but
may not occur at the same time. If the patient is male, elderly, or a child or has had symptoms
for more than 7 days, the infection should be considered complicated until proven otherwise.
The classic manifestations of acute pyelonephritis observed in adults are often absent in
children, particularly neonates and infants. In children aged 2 years or younger, the most
common signs and symptoms of urinary tract infection (UTI) are as follows:
 Failure to thrive
 Feeding difficulty
 Fever
 Vomiting
 Elderly patients may present with typical manifestations of pyelonephritis, or they may
experience the following:
 Fever
 Mental status change
 Decompensation in another organ system
 Generalized deterioration

Sumber :
Fulop T. 2016 Acute Pyelonephritis. Viewed 24 Januari 2017. From <
http://emedicine.medscape.com/article/245559-overview >

4. Diagnosis DD scenario
Sign and symptom Pyelonephritis akut Pyelonephritis urolithiasis Cystisis (Female)
kronis
Demam 39.4oC + disertai menggigil

Nyeri berkemih 40% kasus + + +

Volume urin kurang +

Nyeri pinggang bawah + (disertai

komplikasi)
Pegal-pegal

Nyeri costovertebral + + + +
angle
Leukositosis +

Eritrosituria/hematuria + + +

Leukosituria

Nitrat urinalisis +25% +25% +25%

Leukosit cast

Riwayat nyeri + + +
suprapubic
Riwayat Diabetes (komplikasi)
Melitus
Riwayat hipertensi + +

Lainnya Nausea & vomit, Nausea & vomit , Positif batu, tanda Malaise, pyuria,
anorexia, lethargy, pyuria, radang proteinuria
perubahan status azotemia,
mental, susah
makan, pyuria,
bacteriuria, NGAL +
 Sumber :
Lohr J.W. 2015. Chronic Pyelonephritis. Viewed 24 Januari 2017. From <
http://emedicine.medscape.com/article/245464-overview >
Fulop T. 2016 Acute Pyelonephritis. Viewed 24 Januari 2017. From <
http://emedicine.medscape.com/article/245559-overview >
Syakh S.M. 2016. Pediatric Urolithiasis. Viewed 24 januari 2017. From <
http://emedicine.medscape.com/article/983884-overview >
Brusch J.L. 2016. Cystisis in Females. Viewed 24 januari 2017. From <
http://emedicine.medscape.com/article/233101-overview >

5. Macam-macam penyakit ISK yang temasuk golongan 4A pada SKDI

Sumber :
http://www.kki.go.id/assets/data/arsip/SKDI_Perkonsil,_11_maret_13.pdf

6. Manajemen pada diagnosis

Terapi ditujukan untuk mencegah terjadinya kerusakan ginjal yang lebih parah dan memperbaiki
kondisi pasien, yaitu berupa terapi suportif dan pemberian antibiotika. Antibiotika yang
dipergunakan pada keadaan ini adalah yang bersifat bakterisidal, dan berspektrum luas, yang
secara farmakologis mampu mengadakan penetrasi ke jaringan ginjal dan kadarnya didalam urine
cukup tinggi. Golongan obat-obat ni adalah: aminoglikosida yang dikombinasikan dengan
aminopenisilin (ampisilin atau amoksisilin), aminopenisilin dikombinasi dengan asam klavulanat
atau sulbaktam, karboksipenisilin, sefalosporin, atau fluoroquinolone.

Sumber :
Kee, Joyce Le Fever. 2010. Pedoman Pemeriksaan Laboratorium dan Diagnostik. EGC : Jakarta.

7. Gejala ISK atas dan ISK bawah

ISK Bawah
 Sumber :
Kuo H.C. 2014. Differential Diagnosis of Male Lower Urinary Tract Symptoms Suggestive of Benign
Prostatic Hyperplasia and Non-Benign Prostatic Hyperplasia. Viewed on 25 Januari
2017. From < http://www.tcs.org.tw/issue/folder/1_1suppl/1-1-suppl-3-6.pdf >

ISK Atas
 Sumber :

Gibson Kim & Toscano Joseph . 2012. Urinary

Tract Infection Update. Vol.9 no.2. viewed on 25
January 2017. From <
http://www.aapsus.org/wp-
content/uploads/uti82.pdf >

Infeksi Saluran Kemih bagian atas (ISKA)

Infeksi saluran kemih atas terdiri dari pielonefritis dan pielitis. Istilah pielonefritis lebih sering
dipakai dari pada pielitis, karena infeksi pielum (pielitis) yang berdiri sendiri tidak pernah
ditemukan di klinik. Sedang pada Pielonefritis sendiri terbagi menjadi pielonefritis akut (PNA)
dan pielonefritis kronik (PNK).
Pielonefritis akut (PNA) adalah radang akut dari ginjal, ditandai oleh terjadinya peradangan
jaringan interstitial (primer) dan sekunder jika mengenai tubulus dan akhirnya dapat mengenai
kapiler glomerulus, yang disertai dengan manifestasi klinik juga adanya bakteriuria tanpa
ditemukan kelainan radiologik.
Pielonefritis Kronik (PNK) adalah kelainan jaringan interstitial (primer) dan sekunder yang
mengenai tubulus dan glomerulus, mempunyai hubungan dengan infeksi bakteri (immediate
atau late effect) dengan atau tanpa adanya bakteriuria juga selalu disertai kelainan-kelainan
radiologik. PNK yang tidak disertai bakteriuria disebut PNK fase inaktif. Tetapi dengan adanya
bakteriuria yang ditemukan pada seorang penderita bukan lantas merupakan suatu pielonefritis
kronik fase aktif; Bakteriuria tersebut dapat juga berasal dari saluran kemih bagian bawah yang
tidak memberikan keluhan. Untuk itu untuk menegakkan diagnosis PNK harus mempunyai dua
kriteria yakni pertama adanya bukti kelainan-kelainan fisiologis dan anatomi dan yang kedua
adalah kelainan-kelainan tersebut mempunyai hubungan dengan infeksi bakteri. Dari semua
faktor predisposisi ISK, nefrolithiasis dan refluks vesiko-ureter lebih memegang peranan penting
dalam patogenesis PNK.
Infeksi Saluran Kemih bagian Bawah (ISKB)
Infeksi saluran kemih bawah terdiri dari sistitis, prostatitisdan epidimitis, uretritis, serta sindrom
uretra. Presentasi klinis ISKB tergantung dari jenis kelamin.Pada perempuan biasanya berupa
sistitis dan sindrom uretra akut, sedangkan pada laki-laki berupa sistitis, prostatitis, epidimitis,
dan uretritis
 Sistitis terbagi menjadi sistitis akut dan sistitis kronik. Sistitis akut adalah radang selaput mukosa
kandung kemih (vesika urinaria) yang timbulnya mendadak, biasanya ringan dan sembuh
spontan (self-limited disease) atau dapat juga berat jika disertai dengan penyulit ISKA
(pielonefritis akut). Sistitis akut termasuk ISK tipe sederhana (uncomplicated type). Sebaliknya
sistitis akut yang sering kambuh (recurrent urinary tract infection) termasuk ISK tipe
berkomplikasi (complicated type), ISK jenis ini perlu perhatian khusus dalam
penatalaksanaannya. Sistitis kronik adalah radang kandung kemih yang menyerang berulang-
ulang (recurrent attack of cystitis) dan dapat menyebabkan kelainan-kelainan atau penyulit dari
saluran kemih bagian atas dan ginjal. Sistitis kronik merupakan ISKB tipe berkomplikasi, dan
memerlukan pemeriksaan lanjutan untuk mencari faktor predisposisi.
Sindrom Uretra Akut (SUA) adalah presentasi klinis sistitis tanpa ditemukan mikroorganisme
(steril), sering dinamakan sistitis abakterialis karena mikroorganisme penyebab tidak dapat
diisolasi. Penelitian terkini menunjukkan bahwa SUA disebabkan oleh mikroorganisme
anaerobik.

Sumber :
Purnomo, Basuki B. 2009. Dasar-dasar urologi edisi kedua. FK Univ. Brawijaya : Malang.

8. Patomekanisme hasil lab

Leukocytosis (loo_-ko¯-si¯-TO¯-sis), an increase in the number of WBCs above 10,000/_L, is a normal,
protective response to stresses such as invading microbes, strenuous exercise, anesthesia, and surgery.
The skin and mucous membranes of the body are continuously exposed to microbes and their toxins.
Some of these microbes can invade deeper tissues to cause disease. Once pathogens enter the body, the
general function of white blood cells is to combat them by phagocytosis or immune responses. To
accomplish these tasks, many WBCs leave the bloodstream and collect at sites of pathogen invasion or
inflammation. Once granular leukocytes and monocytes leave the bloodstream to fight injury or infection,
they never return to it. Lymphocytes, on the other hand, continually recirculate—from blood to interstitial
spaces of tissues to lymphatic fluid and back to blood. Only 2% of the total lymphocyte population is
circulating in the blood at any given time; the rest are in lymphatic fluid and organs such as the skin, lungs,
lymph nodes, and spleen.

Sumber :
Tortora G.J & Derrickson B. 2009. PRINCIPLES OF ANATOMY AND PHYSYIOLOGY Twelfth Edition.
Jon Wiley & Sons, Inc : Hoboken

The erythrocyte sedimentation rate (ESR) determination is a commonly performed laboratory test
with a time-honored role.

Sedimentation of red cells in this system is affected by forces both for and against sedimentation. The
forces resisting sedimentation are the negative charge on the red cell surface (causing red cells to repel
each other (zeta potential)), the up flow of plasma displaced by falling red cells, and the rigidity of red
cells. The forces accelerating sedimentation are anemia and plasma proteins. Plasma proteins bind to red
cell membranes thereby reducing the zeta potential thus allowing rouleaux formation to occur. The
degree to which proteins reduce the zeta potential can be rated on a scale of 1-10: fibrinogen 10, beta-
globulin 5, alpha globulin 2, gamma globulin 2, and albumin 1.

Any condition that elevates fibrinogen (e.g., pregnancy, diabetes mellitus, end-stage renal failure,
heart disease, collagen vascular diseases, malignancy) may also elevate the ESR. Anemia and macrocytosis
increase the ESR. In anemia, with the hematocrit reduced, the velocity of the upward flow of plasma is
altered so that red blood cell aggregates fall faster. Macrocytic red cells with a smaller surface-to-volume
ratio also settle more rapidly. A decreased ESR is associated with a number of blood diseases in which red
blood cells have an irregular or smaller shape that causes slower settling.

Sumber :

Hameed M.A & Waqas Sobia. 2016. Physiological Basis and Clinical Utility of Erythrocyte
Sedimentation Rate. Vol 22 no 2. Viewed 24 Januari 2016. From <
http://www.pjms.com.pk/issues/aprjun06/article/cme.html >

Hematuria

Sumber :

Sudoyono et al. 2014. Buku Ajar Ilmu Pentakit Dalam Edisi 6 jilid 1. InternaPublishing : Jakarta