CHAPTER I

BACKGROUND

Obstructive uropathy is one of the most urgent clinical entities that both
nephrologists and urologist have to diagnose.1 Epidemiologically, obstructive
uropathy accounts for 10% of the causes of acute renal failure and 4% of the cases
of chronic end stage renal failure.2 It is classified on the basis of several criteria,
including the degree, duration, site of obstruction and whether it is bilateral or not.
The degree of obstruction refers to whether the obstruction of the urine flow is
partial or complete. Regarding the duration of the obstruction, obstructive
uropathy is categorized in acute and chronic. Acute obstruction occurs for short
period of time and therefore renal parenchyma lesions are mostly reversible, while
chronic obstruction, after several weeks, causes permanent damage. In cases of
chronic obstruction, the term obstructive nephropathy is also used.

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 CHAPTER II
LITERATURE REVIEW

2.1 Anatomy of Urinary Tract

Figure 2.1 Urinary Tract (Smith and Tanagho's Urology, 2013)

KIDNEY
External Anatomy
The paired kidneys are reddish, bean-shaped organs located just above the
waist between the peritoneum and the posterior wall of the abdomen. Kidneys are
retroperitoneal because their position is posterior to the peritoneum of the
abdominal cavity. Kidneys are located between the levels of vertebrae TXII and
LIII. The kidneys lie along the border of the psoas muscle and therefore obliquely

2
placed. The postion of the liver causes the right kidney to be lower than the left. A
typical adult kidney is 10-12 cm long, 5-7 cm wide and 3 cm thick and weighs
about 150 g each.

Figure 2.2 Gross Anatomy of Right Kidney, Anterior View (Tortora's Principle of
Human Anatomy and Physiology 12th Ed, 2009)

The concave medial border of each kidney faces the vertebral column.
Near the center of the concave border is an indentation called renal hilum, through
which the ureter emerges from the kidney along with the blood vessels and
nerves. Three layers of tissue surround each kidney. The deep layer is the renal
capsule, the middle layer is the adipose capsule that is known as perirenal fat, the
superficial layer is the renal fascia which is another thin layer that anchors the
kidney to the surrounding structures and to the abdominal wall.

Internal Anatomy

There are two distinct region in the internal anatomy of the kidney. A
superficial, light red are called the renal cortex and a deep, darker reddish-brown
inner region called the renal medulla.
The renal cortex is divided into two parts, the outer cortical zone and inner
juxtamedullary zone. The portions of renal cortex that extend between renal
pyramids are called renal column.
The renal medulla consists of several cone-shaped renal pyramids. The
base of renal pyramids (wider end) faces the renal cortex and the apex (narrower
end) of renal pyramids called renal papilla point towards the renal hilum.
Together renal cortex and renal pyramids of the renal medullae constitute
the parenchyma (functional portion) of the kidney. Within the parenchyma, the

3
functional units of the kidney, is called nephron. Nephrons are microscopic
structures in the kidney in the amount of 1 million nephrons in one kidney. One
unit of nephron is composed of a tubule that has both secretory and excretory
function. The secretory portion (renal corpuscle and secretory tubule) is
contained largely within the renal cortex. The excretory portion (collecting tubule)
lies in the medulla.
Urine formed by the nephrons drained into papillary ducts, which extend
through the renal papilla of the pyramids. The papillary ducts drain into cuplike
structures called minor and major calyces. Each kidney has 8 to 18 minor calyces
and 2 or 3 major calyces, urine drains into single larege cavity called the renal
pelvis and the out through ureter to the urinary bladder.

Figure 2.3 Internal Anatomy of Kidney, Frontal Section (Tortora's Principle of

Human Anatomy and Physiology 12th Ed, 2009)

Blood supply of the kidney

Usually there is one renal artery, a branch of the aorta that enters the hilum
of the kidney between the pelvis, which normally lies posteriorly. It may branch
before it reaches the kidney and two or more separates arteries may be noted.

4
 A. Posterior branch of renal artery and its
distribution to the central segment of the
posterior surface of the kidney
B. Branches of the anterior division of the
renal artery supplying the entire anterior
surface of the kidney as well as the upper and
lower poles at both surfaces
C. Lateral convex margin of the kidney.
Brodel's line which is 1 cm from the convex
margin, is the bloodless plane demarcated by
the distribution of the posterior branch of the
renal artery

Figure 2.4 Anterior and Posterior Branches of Renal Artery (Smith and
Tanagho's Urology, 2013)

The renal artery divides into anterior and posterior branches. The posterior
branch supplies the midsegment of the posterior surface. The anterior branch
supplies both upper and lower poles as well as the entire anterior surface. The
renal arteries are all end arteries.
The renal artery further divides into interlobar arteries which travel in the
renal column and then arch along the base of the pyramids (arcuate arteries).
These arteries then divide as interlobular arteries. From these vessels, smaller
(afferent) branches pass to the glomeruli. From the glomerular tuft, efferent
arterioles pass to the tubules in the stroma.
The renal veins are paired with arteries, but any of them will drain the
entire kidney if the others are tied off.
Although the renal artery and vein are usually the sole blood vessels of the
kidney, accessory renal vessels are common and may be of clinical importance if
they are so placed to compress he ureter, in which case hydronephrosis may occur.

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 Figure 2.5 Blood Suply of the Kidney, Frontal Section (Tortora's Principle of Human
Anatomy and Physiology 12th Ed, 2009)

Nerve Supply of The Kidney

Many renal nerves originate in the renal ganglion and pass through the
renal plexus into the kidneys along with the renal arteries. Renal nerves are part of
the sympathetic division of the autonomic nervous system. Most are vasomotor
nerves that regulate the flow of blood through the kidney by causing
vasodilatation or vasoconstriction of renal arterioles.

RENAL PELVIS AND URETER

Anatomy
Renal Pelvis, the pelvis may be entirely intrarenal or partly intrarenal and
partly extrarenal. Interomedially, it tapers to join the ureter.
Ureter, adult ureter is about 30 cm long, varying in direct relation to the
height of the individual. Areas that stones are often impacted: 1. Ureteropelvic
junction, 2. Where the ureter crosses over the illiac vessels and 3. Where it
courses through the bladder wall. On their course downward, the ureters lie on the
psoas muscles, pass medially to the sacroiliac joints and the swing laterally near
the ischial spines before passing medially to penetrate the base of bladder. In

6
females, the uterine arteries are closely related to the juxtavesical portion. The
ureters are covered by the posterior peritoneum.
Blood supply
Renal pelvis and upper ureters derive their blood supply from the renal
arteries. The midureter is fed by the internal spermatic (or in woman ovarian
arteries). The lower portion of ureter is served by branches from the common
iliac, internal iliac (hypogastric) and vesical arteries. The veins of renal pelvis and
ureters are paired with the arteries.
Lymphatics
The lymphatic vessel of upper portion of ureter as well as those from
pelvis enter the lumbar lymph nodes. The lymphatic vessel of midureter portion
pass to the internal (hypogastric) and common iliac lymph nodes. The lymphatic
vessel of lower portion of the ureter empty to the vesical and hypogastric lymph
nodes.

BLADDER
Bladder is a hollow muscular organ that serves as reservoir for urine. The
adult bladder normally has the capacity of 400-500 ml.
Anatomy
When empty, the adult bladder lies behind the pubic symphysis and is
largely a pelvic organ. When it is full, it rises until above the symphysis and can
be readily be palpated and percussed. When overdistended (in acute or chronic
urinary retention), may cause the bulging in the lower abdomen.
The ureters enter the bladder posteroinferiorly. The internal sphincter or
bladder neck is not true circular sphincter but a thickening formed by interlaced
and converging muscle fibers of the detrusor as they pass distally to become
smooth musculature of the urethra.
Blood Supply
The bladder supplied by the superior, middle and inferior vesical arteries
which arise from the anterior trunk of the internal iliac artery and by smaller
branches from the obturator and inferior gluteal arteries. In females, the uterine

7
 and vaginal arteries also send branches to the bladder. Rich plexus of the veins
ultimately empties into the internal iliac veins.
Nerve supply
The bladder receives symphatetic and parasymphatetic inneravation. The
sensory afferent of the bladder originates from both subepithelial nerve endings
and nerve fibers between the detrusor muscles bundles.
Lymphatics
The lymphatics of the bladder drain into the vesical, external iliac, internal
iliac and common iliac lymph nodes.

2.2 Definition
Obstructive uropathy refers to the functional or anatomic obstruction of
urinary flow at any level of the urinary tract. Obstructive nephropathy is present
when the obstruction causes functional or anatomic renal damage.3

2.3 Epidemiology
The prevalence of urinary tract obstruction is best estimated from autopsy
series. In a series of 59,064 autopsies performed on individuals ranging from
neonates to geriatric subjects, hydronephrosis was reported in 3.1%. There were
no gender differences in this series until the age of 20 years. However,
hydronephrosis was more prevalent in women in the 20- to 60-year interval. The
latter was attributed to pregnancy and development of gynecologic malignancies.
It was more prevalent in males after age 60 years, because of prostatic diseases.
Hydronephrosis has been reported to be present in 2% to 2.5% of children
subjected to autopsy. It is somewhat more prevalent in boys, and the majority of
cases were in subjects younger than 1 year. The aforementioned prevalences are
most likely an underestimate of obstructive events, because temporary bouts of
obstruction such as those induced by prior pregnancy or stone episodes were not
captured3.
There are no new data regarding the prevalence and incidence of
obstructive uropathy. However, there are new data on ureteropelvic junction
obstruction and ureterocele that may permit certain inferences. Based on the

8
 United States published andcoded data on ureteropelvic junction obstruction
generated by the Healthcare Cost and Utilization Project (HCUP) and Kids
Inpatient Database (KID), the number of inpatient hospitalizations for
ureteropelvic junction have decreased from 1.1 per 100,000 in 1994 to 0.8 per
100,000 in 2000. Although this may be influenced by a shift to more outpatient
procedures or observational management, it could also be due to a decreasing
incidence of this problem. However, this has not been demonstrated for those
afflicted with ureterocele where the rates have been stable over this interval3.

2.4 Etiology
In adult life, the acquired type of obstruction is the most common cause in
urinary obstruction and stasis. Acquired obstruction are numerous and maybe
primary in the urinary tract or secondary to retroperitoneal lesions that invade or
compress the urinary passages. The common causes of acquired urinary tract
obstruction are:
1. Urethral stricture secondary to infection or injury
2. Benign prostatic hyperplasia or cancer of the prostate
3. Vesical tumor involving bladder neck or urethral orifices
4. Local extension of cancer of the prostate or cervix into the base of the
bladder and occlude the ureters
5. Compression of the ureters at the pelvic brim by metastatic nodes from
cancer of the prostate or cervix
6. ureteral stone
7. Retroperitoneal fibrosis or malignant tumor
8. Pregnancy.

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 RENAL URETER BLADDER and URETHRA

Congenital Congenital Congenital

- Renal Cyst - Ureterocele - Posterior Urethral Valve
- Phimosis
Neoplastic Neoplastic
- Wilms Tumor - Primary Carcinoma Neoplastic
- Prostate Carcinoma
Inflammatory Inflammatory
- Tuberculosis - Tuberculosis Inflammatory
-Echinococcus infection - Schostosomiasis - Prostatitis

Metabolic Miscellanous Miscellanous

- Calculi - Trauma - Neurogenic Bladder
- Aortic Aneurysm - Benign Prostatic Hypertrophy
Miscellanous - Retroperitoneal Fibrosis
- Trauma
- Renal Artery Aneurysm

Figure 2.6 Possible Etiology of Obstructive Uropathy (Campbell-Walsh

Urology, 2012)

2.5 Classification
It is classified on the basis of several criteria, including the degree,
duration, site of obstruction and whether it is bilateral or not. The degree of
obstruction refers to whether the obstruction of the urine flow is partial or
complete. Regarding the duration of the obstruction, obstructive uropathy is
categorized in acute and chronic. Acute obstruction occurs for short period of time
and therefore renal parenchyma lesions are mostly reversible, while chronic
obstruction, after several weeks, causes permanent damage3.

2.6 Pathophysiology
Both obstrutive disorder and neuropathic disorder of the vesical have the
same effects on the urinary tract. We can understand these changes in the best way
by considering 1. the effects on the lower urinary tract (distal to the bladder neck)
of severe external urinary meatal stricture, 2. the effects on the mid tract (bladder)
of benign prostate hyperplasia and 3. the effects on the upper tract (ureter and
kidney) of benign prostate hyperplasia.

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1. Lower tract (example: urethral stricture)
Hydrostatic pressure proximal to the obstruction causes dilatation of the
urethra. The wall of urethra may become thin and diverticulum may form. If the
urine becomes infected, urinary extravasation may occur and periurethral abscess
can result. The prostatic ducts may become widely dilated.

2. Mid tract (example: Benign Prostatic Hyperplasia)

In brief explanation, the earlier stages as still in the compensatory phase,
the muscle wall of the bladder becomes hypertrophied and thickened. With
decompensation, it becomes less contractile and weakened in time.

Compensation stages
To balance the increasing outlet resistance, the muscle wall of the bladder
becomes hypertrophied and thickened. Its thickness may double or triple. With
this compensation, complete emptying of the bladder is still possible.
Secondary infection can be happened in this phase, oedema of the
submucosa may occur, which may be infiltrated with plasma cells, lymphocytes
and polymorphonuclear cells.

Figure 2.7. Changes in the bladder wall developing from urinary obstruction (Smith and Tanagho's
Urology, 2013)

Explanation Upper left: normal bladder and prostate. Upper Right: Obstructing prostate causing
trabeculation, cellulae formation and hypertrophy of interureteric ridge. Bottom: Marked
trabeculation (hypertrophy) of the vesical musculature; diverticulum displacing the ureter.

The picture above showed us what we can see during cystoscopy, surgery
or autopsy in the person with middle urinary tract obstruction.

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 Trabeculation of the bladder wall: Normal bladder wall is quiet smooth, but
with hypertrophied condition, muscle bundles with deposit of interstitial
collage fibers become taut and give a coarsely interwoven appearance to the
mucosal surface that commonly called as trabeculation. The trigonal muscle
hypertrophied their smooth muscle in respond to obstruction, the ridge of this
muscle become prominent.
Cellules: normal intravesical pressure is about 30 cm H2O at the beginning of
micturition. When the pressure got two until four times higher it still can be
reached by the hypertrophied bladder in its attempt to force urine past the
obstruction. This pressure tends to push mucosa between the superficial
muscle bundles, causing the formation of small pockets or cellules.
Diverticula: it is originate from cellules. If cellules force their way through the
musculature of the bladder wall, they become saccules, then actual diverticula.
Diverticula have no muscles wall and therefore unable to expel their contents
into the bladder efficiently. If infection occurs, surgical procedure to remove
the diverticula is needed.
Mucosa: when the acute infection occurs, the mucosa of bladder wall become
reddened and edematous and can lead to vesicourethral reflux in the presence
of a "borderline" junction.

Decompensation Stage
Its varies greatly amongst individual. Decompensation of the dextrusor
muscle may occur in the face of progressive outlet obstruction, resulting in the
presence of residual urine after voiding. The amount may range up to 500 ml or
more.

3. Upper tract
Ureter

In the early stages of obstruction, intravesical pressure is normal while the

bladder fills and is increased only during voiding. The pressure is not transmitted
to the ureters and renal pelves because of the competence of the ureterovesical
"valves". But, owing to trigonal hypertrophy and to the resultant increase in

12
resistance to urine flow across the terminal ureter, there is progressive back
pressure on the ureter and kidney, resulting in ureteral dilatation and
hydronephrosis. Later, with the phase of decompensation accompanied by residual
urine, there is an added stretch effect on the already hypertrophied trigone that
increases the resistance to flow at the lower end of the ureter and induces further
hydroureteronephrosis. With decompensation of the ureterotrigonal complex, the
valvelike action may be lost, vesicoureteral reflux occurs, and the increased
intravesical pressure is transmitted directly to the renal pelvis, aggravating the
degree of hydroureteronephrosis.
Secondary to the back pressure resulting from reflux or from obstruction
by the hypertrophied and stretched trigone or by a ureteral stone, the ureteral
musculature thickens in its attempt to push the urine downward by increased
peristaltic activity (stage of compensation). This causes elongation and some
tortuosity of the ureter. At times, this change becomes marked, and bands of
fibrous tissue develop. On contraction, the bands further angulate the ureter,
causing secondary ureteral obstruction. Under these circumstances, removal of the
obstruction below may not prevent the kidney from undergoing progressive
obstruction due to the secondary ureteral obstruction.

Figure 2.7 Early Stage Figure 2.8 Later Stage

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 At the end, if the cause of the obstruction still remain, because of the
increasing pressure, the ureteral wall becomes attenuated and therefore loses its
contractile power (decompensation phase). Dilatation may be so extreme that the
ureter can resemble the bowel.

Kidney

The pressure within the renal pelvis is normally close to zero. When this
pressure increases because of obstruction or reflux, the pelvis and calyces dilate.
The degree of hydronephrosis that develops depends on the duration, degree, and
site of the obstruction. The higher the obstruction, the greater the effect on the
kidney. If the renal pelvis is entirely intrarenal and the obstruction is at the
ureteropelvic junction, all the pressure will be exerted on the parenchyma. If the
renal pelvis is extrarenal, only part of the pressure produced by a ureteropelvic
stenosis is exerted on the parenchyma; this is because the extrarenal renal pelvis is
embedded in fat and dilates more readily, thus "decompressing" the calyces.

Figure 2.9 Intrarenal Pelvis Figure 2.10 Extrarenal Pelvis

2.7 Diagnosis
The differentiation between acute or chronic obstruction is purely clinical.
Chronic obstruction is usually asymptomatic. When the obstruction is bilateral,
patients may present with uremia. Most acute obstructive uropathies, on the other

14
hand, are associated with significant pain or the abrupt diminution of urine flow.
The severity of the pain depends on the rate of distention more than the amount of
dilation of the renal capsule.5 Patients describe a colic pain in the flank that
increases with consumption of large amounts of fluid or following diuretic
administration. Anuria frequently occurs in acute obstruction and less frequently
in chronic situations. Sometimes, in unilateral obstruction or partial bilateral
obstruction, the patient may notice significant increases in urinary output
independent of fluid intake related to the damaged kidneys inability to
concentrate urine.3
The clinician needs to obtain a detailed history about the type and duration
of symptoms, hematuria, lower urinary tract symptoms, previous urinary tract
infections (UTIs), history of stone disease, family history of prostate or pelvic
cancer, and urinary output patterns. The presence of infection should always be
considered as it may require emergent drainage.
Examination may reveal volume overload.5 There may be a palpable
abdominal mass with or without costovertebral tenderness, related to
hydronephrosis. Hydronephrosis that causes the kidney to expand enough to
become palpable usually is related to a chronic condition. The bladder may be
palpable secondary to obstruction low in the urinary tract. Women presenting with
suspected urinary obstruction should always receive a complete pelvic
examination, and both genders receive a rectal examination.3 In pregnant females,
symptoms of frequency, dysuria, nausea, vomiting or back pain may be present
even in a normal pregnancy. So, urological management is required only in
pregnancy hydronephrosis complicated by strong flank pains or urolithiasis or
pyelonephritis.7

Laboratory
Urinalysis results may be normal in both acute and chronic obstructions.
Albuminuria may be absent but is commonly present in the range of less than 1.5
g/24 hours reflecting the increased glomerular permeability during urinary
retention. Even sparse albuminuria indicates glomerular dysfunction.
Microglobulin alpha-1, a low molecular weight protein, is an indicator of tubular

15
dysfunction. Normally, nearly all microglobulin alpha-1 filtered by the glomerulus
is reabsorbed by the proximal tubule.6 With renal calculus or tumour involvement,
microscopic hematuria is possible, but gross hematuria is unlikely.8 Chronic
obstruction leads to renal tubule damage, and the urinary chemistry findings are
similar to those in intrinsic renal failure. These findings include urinary sodium
greater than 20 mEq/L, fractional excretion of sodium (FE Na) greater than 1%,
urine to plasma creatinine ratio of less than 20 and urine osmolality less than 350
mOsm/kg H2O.3 With acute obstruction the urinary chemistry values are similar
to those in prerenal azotemia. These findings include urinary sodium less than 20
mEq/L, FE Na less than 1%, urine to plasma creatinine ratio of greater than 30
and urine osmolality greater than 500 mOsm/kg H2O. Microscopic evaluation of
the urine may reveal erythrocytes,
leukocytes, and bacteria. Blood tests include complete blood counts, hematocrit,
haemoglobin, serum electrolytes (Na+, Cl-, K+, HCO3-, Ca++, HPO
4-, Mg++), creatinine, blood urea nitrogen (BUN), uric acid, albumin and ABG.3
The WBC count assesses for possible inflammation or infection secondary to
obstruction or neoplasm as a cause of the obstruction. The hematocrit is important
to assess for anaemia related to chronic renal insufficiency.8 Patients with
increasing serum creatinine without significant proteinuria, and trace to moderate
numbers of red blood cells in the urine should immediately be suspected of having
an obstruction.5

Radiological Evaluation
Ultrasonography has become one of the most important tools for assessing
urinary tract obstruction because it is rapid, low-cost, safe and sensitive. It is the
diagnostic modality of choice in pregnancy. The test is 98% sensitive for detecting
hydronephrosis, but the specificity is 78%.9 Though operator-dependent,
ultrasound detects the type and level of the lesion, shows hydronephrosis, can
indicate pyonephrosis (echoes within the collecting system) and tells the thickness
of the renal parenchyma as an indicator of the duration and severity of
obstruction. Since up to 22% cases of hydronephrosis are not obstructive, there is
room for error.9 Dilation without obstruction may be seen in vesicoureteral reflux,

16
chronic massive diuresis, extrarenal pelvis, calyceal diverticula, congenital
megacalyces and ileal conduits. Obstruction without dilation may be seen in
intrarenal crystals, nephrocalcinosis, staghorn calculi and retroperitonealn
obstruction.

Figure 2.11 USG

A supine radiograph [KUB] of the abdomen can reveal radio-opaque

urinary tract calculi as the cause of obstructive uropathy. However, alone it does
not prove the calculi to be the cause of obstruction, it misses out radiolucent
calculi and radio-opacity due to any other cause can be mistaken for the urinary
calculi.

Figure 2.12

Intravenous urogram (IVU) has been the gold standard for the detection of
ureteral obstruction. The significant difference in IVU compared with
ultrasonography is that the IVU shows both increased anatomic detail and
functional attributes of the urinary system. It tells about the exact site of

17
obstruction, its cause, the degree of hydronephrosis, the status of renal
parenchyma, guides the best treatment option, and also helps in deciding the best
surgical approach for a particular patient. However, in view of nephrotoxicity of
the contrast material, the usefulness of the test for patients already suspected of
having obstructive nephropathy is questionable.9 Also, poor renal function may
render the test useless because of non-excretion of contrast. In general, a serum
creatinine level of less than 2 mg% is needed. Another dilemma with IVU is the
significant time requirement, up to several hours, for performing serial delayed
films. Still, IVU remains the most widely used imaging modality to guide the
management of patients of obstructed kidney, because of its low cost and easy
availability. A kidney which is non-visualized on IVU (absence of both
nephrogram and pyelogram even on delayed films taken after 24-72 hours) should
be assessed with a renal scan before labelling it as a non-functioning kidney
(single kidney GFR which is not sufficient to take care of body wastes). A kidney
may be non-visualized on IVU because of renal agenesis, post-nephrectomy, poor
function with or without obstruction, or even in the presence of normal function
during renal colic leading to renal artery spasm.

Figure 2.13

Non-contrast computerized tomography (CT) scan is an effective imaging

tool for acute renal obstruction. With spiral scanners, images can be performed
effectively without contrast media, take only 5 to 10 minutes to perform, and cost
about the same as IVPs. In terms of benefits, the CT equals the accuracy of the

18
IVP in determining the presence of obstruction, but surpasses the IVP in detecting
the specific cause of the obstruction. Various signs of obstruction on spiral CT
include hydroureter, perinephric stranding, hydronephrosis, periureteral oedema
and renal swelling. However, a non-contrast CT does not indicate function of the
kidneys.

Figure 2.14

MRI gives no added advantage over CT scan. In addition it does not

visualise the stone. However, it correctly identifies the point of obstruction and the
noncalculous causes of obstruction. MR excretory urography is a promising
technique which affords equivalent functional and additional anatomical
information to isotope renography. It is more accurate than Doppler ultrasound in
the assessment of ureteric obstruction in pregnancy and is not associated with any
risk of exposure to radiation, unlike IVU or renal scan.
Nuclear renography is a useful, noninvasive test for evaluating patients
with suspected obstruction. It provides a functional assessment without
exposure to iodinated contrast material. Radiopharmaceuticals for renography
are selected on the basis of the function to be studied. The glomerular agent
technetium (Tc) 99m DTPA and the tubular agent 99mTc-MAG3 are most
commonly used in the evaluation of obstruction. 99mTc-MAG3 has a high renal
extraction rate, associated with rapid clearance, lower radiation dose, and tubular
secretion. 99mTc-MAG3 has a 55% renal uptake in contrast with a 20% renal
uptake associated with 99mTc-DTPA (Tremel et al, 1996). All
radiopharmaceutical tracers are administered intravenously, and their uptake and
subsequent clearance can then be evaluated and quantitated scintigraphically.
From these data, relative renal function can be calculated. Obstruction can be

19
 assessed by measuring the clearance curves, either from a visual assessment of the
pattern or from calculation of the half-time (time at which 50% of the
radiopharmaceutical is eliminated from the collecting system). By convention, a
half-time less than 10 minutes is considered normal, greater than 20 minutes is
considered obstructed, and between 10 and 20 minutes is equivocal. Tracer
clearance can be spuriously delayed because of renal insufficiency and the
presence of vesicoureteral reflux, and some have suggested that renal immaturity
in neonates may generate false-positive studies.3

2.8 Complications
Stagnation of urine leads to infection, which then may spread throughout
the entire urinary system. Once established, infection is difficult and at times
impossible to eradicate even after the obstruction has been relieved.
Often, the invading organisms are urea splitting (Proteus, staphylococci),
which causes the urine to become alkaline. Calcium salts precipitate and form
bladder or kidney stones more easily in alkaline urine. If both kidneys are
affected, the result may be renal insufficiency. Secondary infection increases renal
damage.
Pyonephrosis is the end stage of a severely infected and obstructed kidney.
The kidney is functionless and filled with thick pus. At times, a plain film of the
abdomen may show an air urogram caused by gas liberated by infecting
organisms.

2.9 Therapy
Pain Management
Obstructive uropathy pain is due to the increase of the pressure within the
collecting system and due to ureteral wall/ renal capsule distention. Five classes of
drugs are used to treat pain associated with acute renal colic, namely, nonsteroidal
anti-inflammatory drugs (NSAIDs), narcotic analgesics, calcium channel
blockers, corticosteroids, and 1 blockers. NSAIDs and narcotic analgesics are
now most commonly used. Cochrane meta-analysis studies have demonstrated the
effectiveness of both agents but suggest that NSAIDs are preferred. Other

20
investigators have demonstrated the superiority of NSAID. The present level of
evidence supports the role of NSAIDs as first-line drugs for the management of
renal colic presenting to the emergency department, with narcotics being reserved
as second-line drugs. The choice of pain management should be based on the
patients clinical profile. NSAIDs should not be used in patients with renal
insufficiency, because this could be exacerbated by the induced reduction in RBF.3

Relief of Obstruction
1. Lower tract obstruction (distal to the bladder
With patients in whom secondary renal or ureterovesical damage (reflux in
the latter) is minimal or nonexistent, correction of the obstruction is
sufficient. If significant reflux is demonstrated and does not subside
spontaneously after relief of obstruction, surgical repair may be needed.
Repair becomes imperative if there is considerable hydronephrosis in addition
to reflux. Preliminary drainage of the bladder by an indwelling catheter or
other means of diversion (eg, loop ureterostomy) is indicated in order to
preserve and improve renal function. If, after a few months of drainage, reflux
persists, the incompetent ureterovesical junction should be surgically
repaired. Persistent obstruction from prostatic enlargement of urethral
stricture may also require surgical intervention.
2. Upper tract obstruction (above the bladder)
If tortuous, kinked, dilated, or atonic ureters have developed secondary to
lower tract obstruction (so that they are themselves obstructive), vesical
drainage will not protect the kidneys from further damage; the urine proximal
to the obstruction must be diverted by nephrostomy or ureterostomy. The
kidneys then may regain some function. Over a period of many months, the
ureter may become less tortuous and less dilated; its obstructive areas may
open up. If radiopaque material instilled into thenephrostomy tube passes
readily to the bladder, it may be possible to remove the nephrostomy tube. If
obstruction or reflux persists, surgical repair is indicated. Permanent urinary
diversion (eg, ureteroileal conduit) may be necessary. If one kidney has been
irreversibly damaged, as measured by kidney function tests, urography,
sonography, CT scan, or scintigraphy, nephrectomy may be necessary.

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 Eradication of Infection
Once the obstruction is removed, every effort should be made to eradicate
infection. If the infection has been severe and prolonged, antibiotics may fail to
sterilize the urinary tract

2.10 Prognosis
Early diagnosis of the cause of obstructive uropathy is crucial for the
prognosis of the disease. No simple statement can be made about the prognosis in
this group of patients. The outcome depends on the cause, site, degree, and
duration of the obstruction. The prognosis is also definitely influenced by
complicating infection, particularly if the infection has been present for a long
time. If renal function is fair to good, if the obstruction or other causes of stasis
can be corrected, and if complicating infection can therefore be eradicated, the
prognosis is generally excellent.

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 CHAPTER III

1. Obstructive uropathy refers to the functional or anatomic obstruction of

urinary flow at any level of the urinary tract.
2. Obstructive uropathy can occur in all ages. There were no gender
differences until the age of 20 years. However, hydronephrosis was more
prevalent in women in the 20- to 60-year interval. It was more prevalent in
males after age 60 years.
3. The best way to understand the patophysiology of obstructive uropathy is
by determining the possibility where is the obstruction occur (lower tract,
middle tract, and upper tract).
4. The outcome o the patiens depends on the cause, site, degree, and duration
of the obstruction.

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