HYDRONEPHROSIS

Hydronephrosis (hydronephrotic degeneration, hydronephrotic atrophy) is a

permanent progression of dilation of the pelvico-caliceal system, followed by the
atrophy and dysfunction of the renal parenchyma, caused by the urine passage
disorder.
Ethiology and pathogenesis. Hydronephrosis develops owing to construction
of the pelvic-urethral system, high coming out of the ureter, construction of the
ureter by blood vessels, embrional fascicles, abdominal adhesions, etc.
Depending on the reason of development, are differed:
a) Hydronephrosis caused by the obstacle of the pelvic-urethral segment;
b) Obstacle within the ureter;
c) Obstacle at the lower ureter;
d) Neurogenic disorders.
The pressure within the renal pelvis is normally close to zero. When this
pressure increases because of obstruction or reflux, the pelvis and calices dilate. The
degree of hydronephrosis that develops depends upon the duration, degree, and site
of the obstruction. The higher the obstruction, the greater the effect upon the kidney.
If the renal pelvis is entirely intrarenal and the obstruction is at the ureteropelvic
junction, all the pressure will be exerted upon the parenchyma. If the renal pelvis is
extrarenal, only part of the pressure produced by a ureteropelvic stenosis will be
extender on the parenchyma; this is because the extrarenal renal pelvis is embedded
in fat and dilates more readily, thus decompressing the calices.
In the earlier stages, the pelvic musculature undergoes compensatory
hypertrophy in its effort to force urine past the obstruction. Later, however, the
muscle becomes stretched and atonic (decompensated).
The progression of hydronephrotic atrophy is as follows:
1) The earliest changes in the development of hydronephrosis are seen in the
calices. The end of a normal calyx (as seen on urograms) is concave because of the
papilla that projects into it; with increase in intrapelvic pressure, the fornices
1

become blunt and rounded. With persistence of increased intrapelvic pressure, the
papilla becomes flattened, then convex (clubbed) as a result of compression
enhanced by ischemic atrophy. The parenchyma between the calices is affected to a
lesser extent. The changes in the renal parenchyma are due to (1) compression
atrophy from increase in intrapelvic pressure (more accentuated with intrarenal
pelvis) and (2) ischemic atrophy from hemodynamic changes, mainly manifested in
arcuate vessels that run at the base of the pyramids parallel to the kidney outline and
are more vulnerable to compression between the renal capsule and the centrally
increasing intrapelvic pressure.
This spotty atrophy is caused by the nature of the blood supply of the kidney.
The arterioles are end arteries, therefore, ischemic is most marked in the areas
farthest from the interlobular arteries.

As the backpressure increases,

hydronephrosis progresses, with the cells nearest the main arteries exhibiting the
greatest resistance.
This increased pressure is transmitted to the tubules. The tubule become
dilated and the cells will have atrophy from ischemia.
It should be pointed out that a few instances of dilated renal pelvis and calices
are not due to the presence of obstruction. Rarely, the renal cavities are congenitally
capacious and thus simulate hydronephrosis. More commonly, hydronephrosis may
occur in childhood due to the backpressure associated with vesicoureteral reflux. If
the valvular incompetence resolves (and this is common), some degree of the
hydronephrotic changes may persist. These persisting changes may cause the
physician to suspect the presence of obstruction, which may lead to unnecessary
surgery. An isotope renogram or the Whitaker test can be performed to determine
whether organic obstruction is present.
2) Only in unilateral hydronephrosis are the advanced stages of
hydronephrotic atrophy seen. Eventually the kidney is completely destroyed and
appears as a thin-walled sac filled with clear fluid (water and electrolytes) or pus.
If obstruction is unilateral, the increases intrarenal pressure will cause some
suppression of renal function on that side. The closer the intrapelvic pressure
2

approaches the glomerular filtration pressure (6-12 mm Hg), the less urine can be
secreted. Glomerular filtration rate and renal plasma flow are reduced, concentrating
power is gradually lost, and the urea: creatinine concentration ratio of urine from the
hydronephrotic kidney is lower than that of urine from the normal kidney.
Classification.

Hydronephrosis is primary or congenital, that develops

because of congenital obstacle of the ureter.

Secondary hydronephrosis arises as a complication of any other disease
(urinary stones of kidney or ureter, pedunculitis, tumors of kidney).
Hydronephrotic atrophy may be uni- or bilateral, aseptic and infected, opened,
closed and intermitted.
There are 3 stages of the disease. The 1 st stage reflects pyeloectasy (dilation
just of the renal kidney with a moderate dysfunction).
II prehydronephrosis (hydrocalicosis the broadening of the renal pelvis
and calices, thinning of the parenchyma with expressed dysfunction.
III stage hydronephrotic atrophy, atonic of the renal pelvis. This stage means
degeneration of kidney into great hollowed sack with fluid, volume up to 2 and
more.
The renal tissue preserves as a slim strip along the conveyed surface, semilunar in shape. The number of nephrones is sharply decreased, glomeruli are
deformed. Cells of the nephrones tubes are vacuolated, granular and liquid
degeneration is present, even necrobiosis and necrosis can be formed. Capsules of
the glomeruli are thickened due to collagen fibrosis (sclerosis).
Micro- and macroarchitectonics of the kidney is rather degenerated;
compensative hyperemia is typical for the first stage. It is followed by lengthening
and narrowing of the vessels, ischemia. Dystrophy of the nervous system is
observed.
If one kidney is damaged due to hydronephrotic atrophy, the second one is
enlarged in result of compensative adopting process to provide homeostasis.
Infecting leads to terminal damage of the kidney.

Clinical signs.

There are no specific symptoms of hydronephrosis. Aseptic

unilateral hydronephrotic atrophy is continuously asymptomate.

Course of the disease is circulating. The intensity of signs depends on the
stage of urinary tract constriction presence, activity of the infection, etc. The pain in
loin is frequent. Its intensity depends on stage of structure of the urinary tract and
infection activity. It may be dull, intermitting, renal colic, permanent, ache.
Renal colic is observed in case of initial hydronephrotic atrophy; dull pain and
feeling of swelling appears while cumulating of urine within the kidney. The kidney
is palpable, enlarged and painful while renal colic attacks.
If colic is cupped off, ache is still present for some time, but kidney isnt
palpable. This intermittent filling of kidney with the urine and its emptying may
occur without pain, especially in children. Parents may notice swelling of the loin,
that disappears. Ache often is followed by hematuria, fever. Therefore, hematuria
may be the only sign of hydronephrosis.
Renal concrements cause activation of hydronephrosis clinical signs, progress
of atrophy and sclerosis. Stone forms due to urine congestion and retardation of its
passage.
Rather significant hydronephrosis, especially in children, may defigurate the
abdomen. The kidney may be palpated as a large, mobile cyst, lying lower than
common location. It is elastically resistant, with smooth surface, painful.
Frequent complication is acute or chronic pyelonephritis. Hydronephrosis,
that is complicated with pyelonephritis, manifests in acute pain, fever, nausea,
vomiting, sometimes elevation of the blood pressure rate.
The significant hydronephrosis may be ruptured because of trauma.
Diagnosis.
Laboratory findings. Anemia may be found secondary to chronic infection or
in advanced bilateral hydronephrosis (stage of uremia). Leukocytosis is to be
expected in the acute stage of infection. Little if any elevation of the white blood
count accompanies the chronic stage. Large amounts of protein are usually not found
in the obstructive uropathies. Casts are not common from hydronephrotic kidneys.
4

Microscopic hematuria may indicate renal or vesical infection, tumor, or stone. Pus
cells and bacteria may or may not be present.
In the presence of unilateral hydronephrosis, results of the PSP test will be
normal because of the contrlateral renal hypertrophy. Suppression of PSP excretion
indicates bilateral renal damage, residual urine (vesical or bilateral ureterorenal), or
vesicoureteral reflux.
In the presence of significant bilateral hydronephrosis, urine flow through the
renal tubules will be slow. Thus, urea is significantly reabsorbed but creatinine is
not. Biochemical analyses therefore reveals urea: creatinine ratio will be above the
normal 10:1.
X-ray findings. A plain film of the abdomen mayshow enlargement of renal
shadows, calcific bodies suggesting ureteral or renal stone, or tumor metastases to
the bones of the spine or pelvis. Metastases in the spine may be the cause of spinal
cord damage (neuropathic bladder); if they are osteoblastic, they are almost certainly
from cancer of the prostate.
Excretory urograms will reveal almost the entire story unless renal function is
severely impaired. They are more informative when obstruction is present because
the radiopaque material is retained. These urograms will demonstrate the degree of
dilatation of the pelvis, calices, and ureters. The point of ureteral stenosis will be
revealed. Segmental dilatation of the lower end of a ureter implies the possibility of
vesicoureteral reflux, which can be revealed by cystography. The cystogramm may
show trabeculation as an irregularity of the vesical outline and may show
diverticula. Vesical tumors, nonopaque stones, and large intravesical prostatic lobes
may cause radiolucent shadows. A film taken immediately after voiding will show
residual urine. Few tests that are as simple and inexpensive give the physician so
much information.
Retrograde cystography shows changes of the bladder wall caused by distal
obstruction (trabeculation, diverticula) or demonstrate the obstructive lesion itself
(enlarged prostate, posterior urethral valves, cancer of the bladder). If the
ureterovesical valves are incompetent, ureteropyelograms will be obtained by reflux.
5

Retrograde urograms may show better detail than the excretory type, but care
must be taken not to over distend the passages with too much opaque fluid; small
hydronephrosis can be made to look quite large. The degree of ureteral or
ureterovesical obstruction can be judged by the degree of delay of drainage of the
radiopaque fluid instilled.
CT scanning and sonography can also help determine the extent of dilatation
and parenchymal atrophy.
Isotope scanning. In the presence of obstruction, the radioisotope renogram
may show depression of the vascular and secretors phases and a rising rather than a
falling excretory phase due to retention of the radiopaque urine in the renal pelvis.
The I activity recorded on the gamma camera will show that the isotope is
poorly taken up, slowly transported through the parenchyma, and accumulated in the
renal pelvis.
Instrumental examination. Exploration of the urethra with a catheter or other
instrument is a valuable diagnostic measure. A stricture or tumor may block passage.
Spasm of the external sphincter may make passage difficult. Passage of the catheter
immediately after voiding allows estimation of the amount of residual urine in the
bladder. Residual urine is common in bladder neck obstruction (enlarged prostate),
cystocele, and neurogenic (neuropathic) bladder. Residual urine is usually absent
with urethral stricture, even though the urinary stream may be markedly impaired.
Measurement of vesical tone by means of cystometry is helpful in diagnosing
neurogenic bladder and in differentiating between bladder neck obstruction and
vesical atony.
Inspection of the urethra and bladder by means of cystoscopy and
panendoscopy may reveal the primary obstructive agent. Catheters may be passed to
the renal pelvis and urine specimens obtained. The function of each kidney may be
measured and retrograde ureteropyelograms can be made.
Interventional uroradiology. If there is doubt about the presence of true
obstruction, either the Whitaker test or an isotope renogram can be done. However,
Whitaker and Buxton-Thomas (1984) have shown that neither test is without error.
6

Differential Diagnosis.
A thorough examination usually leaves no doubt about the diagnosis. The
differential diagnosis under these circumstances is rarely difficult. If seemingly
simple infection does not respond to medical therapy or if infection recurs,
obstruction or vesicoureteral reflux is the probable cause, and complete study of the
urinary tract is indicated.
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.
Treatment.
Relief of obstruction. Treatment of the main causes of obstruction and stasis
(benign prostatic hyperplasia, cancer of the prostate, neurogenic bladder, ureteral
stone, posterior ureteral valves, and ureteral stenosis) is described in detail
elsewhere in this book.
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 (e.g., loop ureterostomy) is indicated
7

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.
Upper tract obstruction (above the bladder) If tortuous, kicked, 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 the nephrostomy 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 (e.g., 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.
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.
Operations are plastic and restoring, depending on the reason of
hydronephrosis, presence of secondary changes in pelvico-caliceal system. If there is
external compression ureterolyse, shift of the vessels or resection of the pelvicoureteral segment is performed with forming of new pelvico-ureteral anastomosis.
The lateral anastomose of ureter and renal pelvis without resection of the
pelvico-ureteral segment is used in case of high coming out of ureter.
Nephrectomy is indicated in case of complete hydronephrotic atrophy.

Prognosis
No simple statement can be made about the prognosis in this group of
patients. The outcome depends upon the cause, site, degree, and duration of the
8

obstruction. The prognosis is also definitely influenced by complicating infection,

particularly if it 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 then be eradicated, the prognosis is
generally excellent.
Ureterohydronephrosis.
Ureterohydronephrosis is the dilation of the ureter, renal pelvis and calyces
with gradual renal function failure and parenchymal atrophy. The primary
(congenital) hydronephrosis (while construction of the ureter orifice, ureterocele etc)
and secondary (acquired) urolithiasis, traumatic injury, etc are differed. It may be
uni- and bilateral.
Clinical findings.
There are 5 stages of the ureterohydronephrosis, owing to pelvic obstruction
development:
Hypotonia and dilation of pelvic part of ureter;
Hypotonia of the ureter, its inability for peristalsis, renal excretory
dysfunction;
Hypotonia of renal pelvis, calices, ureter, secreting-excretory renal
dysfunction;
Hypotonia and evacuative dysfunction of the upper urinary tract;
Atrophy of renal parenchyma.
Ureterohydronephrosis may course without any signs. The main signs are
ache of various intensity, enlarging of the kidney, microhematuria and leukocyturia
when infecting.
Diagnosis is made on the research that is similar to hydronephrosis.
Treatment is surgical. Removal of the obstacle (ureterolyse, ureterolithotomy,
suturing of the ureterocele etc), resection of the ureter with anastomosing end-to-end
by means of ureterocystoneostomia (direct or non-direct) is performed.

Nephrectomy is reasonable in case of atrophy of parenchyma. Prognosis is good if

the operative measures are made in time.

NEPHROPTOSIS
Nephroptosis (kidney prolapsus) is the pathological state, at which a kidney is
displaced far outside its physiology mobility. Mostly it goes down vertically.
Ethiology and pathogenesis.
A characteristic feature of kidney is mobility of three kinds:
1) Respiratory which is connected with the respiratory motions of thorax and
front abdominal wall (their amplitude is from 1,5 to 3-5 cm.);
2) Static, that is shown in transition man from horizontal in the vertical
position or vice versa (amplitude 1-2 cm.);
3) Palpation, that is determined by distance, on which it is possible to move
(downward and more medial) a kidney at palpation (makes 3-5 sm). If the kidney
mobility exceeds mentioned parameters, it is considered pathological (nephroptosis).
In the origin of pathological kidney prolapsus numerous factors of
physiologic-anatomical and mechanical, congenital and acquired nature takes part. A
leading part in the origin of nephroptosis is taken by the changes of fixing kidney
vehicle in combination with action of factors of environment. The fixing kidney
vehicle consists of definite anatomic parts: ligaments, vessels, fatty kidney capsule,
and kidney fascia. Kidney state depends on the anatomic terms, that are forms and
depths of kidney bed, intraperitoneal pressure. To the pathological factors which
promote changes of connection kidney vehicle and form circumstances for the
development of nephroptosis, belong: contagious diseases that lower mesenchim
activity, traumas (high falling, jumps on the legs), unfavorable job conditions
(specifically, lasting standing on legs, vibration), rapid losing flash, frequent child
birth, decreasing muscle tone of front abdominal wall. Sometimes nephroptosis can
be one of the splanchnoptosis manifestations. Nephroptosis exists mainly at women
10

(1:20) by age 25-40 years. It is explained by the constitutional features of their

organism: a pelvis at women is wider, than at men; paravertabral recesses isnt so
deep, especially from the right side, more opened downward and wider in this place.
As a result of pregnancy and births the tone of front abdominal wall sometimes goes
down.
At the pathological terms the kidney can considerably go down and take place
in the different departments of stomach, in the epigastrical area, in the small pelvis.
The right-side nephroptosis exists 5-6 times frequent than the left-side one. It is
explained by the lower position of right kidney and stronger connection vehicle of
left one. A bilateral prolapsus is marked in 15 % cases of this anomaly. Nephroptosis
can be mobile and fixed. Kidney can circle around longitudinal and transversal axis.
While circling around longitudinal axis lateral kidney edge becomes a front or even
inner, and medial back or vise versa. While circling around the transversal axis,
upper kidney tip lean back and lower moves forward (kidney retrowersio or vise
versa). Upper kidney tip can move forward, and lower backward (kidney
anteversio).
Symtomatology and clinical motion.
Nephroptosis is distinguished to have 4 stages. At 1stage the lower kidney tip
can be palpated, II - all kidney is palpated, III - the kidney goes down in pelvis and
freely moves in all sides, IV - comes (rotary press) back around the longitudinal or
transversal axis.
As far as the prolapsus and rotary press of kidney its vessels stretch and are
twisted at the sharp turn of trunk. The diameter of kidney artery diminishes in the
1,5-2 times, and a length is multiplied in the 2-3 times and more. It results in the
considerable violation of kidney hemodynamic and urodynamics, lymph drainage
from her. The narrowing and tension of artery causes kidney ischemia of bud, and
overawing of vain - venous hypertension. The violation of outflow of blood and
lymph assists development of pyelonephritis, and at the bilateral pathology kidney
insufficiency. In case of prolapsus kidney is usually mobile and when the body takes
horizontal position, kidney takes its usual (physiological) state. Its a mobile
11

nephroptosis. If around the kidney appears comissures process, it is fixed in

pathologic position. Its fixed nephroptosis, which can cause, especially at fixed bend
of ureter, spreading calices-pelvis system (pieloectopia, hydronephros), at the
violation of urine outlaw from the kidney stones creation.
In 1 stage kidney prolapsus is not accompanied by the clinical symptoms.
With the increase of kidney displacement nephroptosis shows itself with symptomcomplex, which is predetermined both by the kidney prolapsus, and by the
pathological process, that arises up in her. A sick usually complain of the periodic
dull pain in the lumbar area, that increases in case of the physical loading, rapid step,
raising heavy things. In the horizontal position of patient the pain disappears.
As far as growth of kidney (that is in II stages of nephroptosis) displacement
the pain appears on all stomach, which spreads in the back area. It is a result of
tightening of nervous branches of hills renalis and its bed. A short, attack pain
(kidney colic) can be observed in sick on nephroptosis during the kidney cycling
around its limb. Hematuria, erythrocyturia, and proteinuria often accompany a
paroxysm of pain.
In III stages of nephroptosis pain becomes permanent, that considerably
lowers a capacity of a sick. In 13 % of sick on nephroptosis moderate hypertension,
caused by violations of hemodynamic exists also.
The progress of disease results in appearance of new symptoms kidney
colic, hematuria, leukocyturia, pyuria, loss of appetite, headache, promoted
fatigability, violation of functions of bowels, periodic rise of body temperature.
These

symptoms

testify

to

the

joining

complications

pyelonephritis,

hydronephrosis, fornix bleeding, arterial hypertension. Functional kidney state at the

1 and 2 stages of nephroptosis, as a rule, is not changed. At the 3 stage the
decreasing of kidneys function is connected with different diseases that complicate
nephroptosis.
A diagnostics is based on the complaints of sick, anamnesis data, palpation
and roentgenologic research in the horizontal and vertical position of the sick. The
basic method of examination is see urography. It allows setting a displacement
12

degree and functional ability of the pathologically mobile kidney. At the kidney turn
around axis shade of its bowl on pyelogram is narrow, bowls are shortened.
Sometimes bowls are covered by the bowl shade, and then are contours its
inexpressive or are not quite determined. At nephroptosis the bends and wrings of
ureters are often exposed, wring of, above which an expansion of them and also
calices-pelvis system of kidneys is determined.
Radiometry renography and the scanning allow defining the position and
function of dropped and contrlateral kidneys. Kidney arteriography, which is
executed in the horizontal and vertical position of sick, allows to expose not only
displacement of kidney, but also changes of proper kidney artery (length, diameter,
corner ofsplitting). In the case of nephroptosis stenosis of kidney artery that exposed
in the vertical position of sick disappears in horizontal one. First of all differential
diagnostics of nephroptosis carries out with kidney dystonia. In this case see
urography in the horizontal and vertical position of sick and aortography is
executed. In case of kidney dystopy ureter is shortened, arteries move away from
aorta lower than normally.
Nephroptosis can be display of splanchnoptosis. For this exposure go to
research of digestion organs. In case of differentiation of nephroptosis with tumor,
basic diagnostic method there is aortography.
Treatment
The medical treatment of a sick on nephroptosis can be conservative and
surgical. A conservative medical treatment is expedient at 1 stage of disease. It
consists of the setting spasmolytic and anti-inflammatory medications, carrying a
special corset, implementation of complex of physical exercises for the
strengthening muscles of front abdominal wall. In case of complication of
nephroptosis (often pleasing chronic pyelonephritis, strong pain, that deprives sick
capacity) surgical medical treatment id demanded. It is possible to divide a method
of the kidney (nephropexy) fixing on three groups: autoplastic:
a) Using kidney capsule;
b) Strengthening of a fascias vagina of kidney;
13

c) Fixing by fasciae and by the muscular shred;

d) Fixing by the skin shred; alloplastic; combinatined (with the removal of
occlusion of kidney artery, pyelolythotomy and etc.).
At one time the Fedorov and Rivoir methods were widespread.
The most physiological operation of the fixing a dropped kidney there is
nephropexia after Rivoir in the Pitel-Lopatcin modification. After lumbotomia and
kidney nuking, longitudinal shred of m. psoas on the leg as thick as 1.2-2 sm., as
long as 15-20 sm. Its lower tip is pushed into a tunnel under the fibrous capsule of
lower kidney part and is fixed by stitches to the capsule. Exactly by this process a
new ligament, that holds the kidney in normal position with preservation of its
physiological mobility.
In the postoperative period a patient is concluded in bed on two weeks with a
bit heaved up lower edge.
At children the fascioplication after the Horash method is the effective
method of nephropexia. A prognosis in case of timely medical treatment is
favorable.
References:
1. Donald R. Smith, M.D. General Urology, 11-th edition, 1984.
2. O.F.Vozianov, O.V.Lyulko. Urinology.- Kyiv: Vischa shkola, 1993.
3. Urinology edited by N.A.Lopatkin, Moscow, 1982.
4. Scientific Foundations of Urology. Third Edition 1990. Edited by Geoffrey
D. Chisholm and William R. Fair, MD. Heinemann Medical Books, Oxford.
5. Urinary Tract Infection and Inflamation / Jackson E. Fowler, JR. MD. Year
Book Medical Publishers, Chicago 1989.
6. Platts M. M., Williams J. M. Renal function in patients with unilateral
hydronephrosis // Brit. Med. J.- 1973.- V. 2., N 5367.- P. 1243-1247.
7. Szoroly V., Pinter J. Pyeloplastic surgery in the presence of suppurative
pyelonephritis // Int. Urol. Nephrol.- 1985.- V. 17, N 1.- P. 15-21.

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8. Pellegrini F., Rizzo M. Some intrastructural aspects of human pathological

pelviureteric junction in idiopathic hydronephrosis // J. Submicrosc. Cytol.- 1982.V. 14, N.4.- P.697-709.
9. Shokeir A. A., Provoost A. P., Nijman R. I. Recoverability of renal function
after relief of chronic partial upper urinary tract obstruction // B. J. U. International.1999.- V. 83.- P. 11-17.
10. Wilcox D., Mouriduand P. Management of megaureter in children // Eur.
Urol.- 1998.- V. 34.- P. 73-78.

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