# 13 - 331 Urinary Tract Obstruction

## 331 Urinary Tract Obstruction

Calcium Phosphate 
Calcium phosphate stones share risk factors 
with calcium oxalate stones, including higher concentrations of urine 
calcium and lower concentrations of urine citrate, but additional fac­
tors deserve attention. Higher urine phosphate levels and higher urine 
pH (typically ≥6.5) are associated with an increased likelihood of cal­
cium phosphate stone formation. Calcium phosphate stones are more 
common in patients with distal renal tubular acidosis and primary 
hyperparathyroidism.
There are no randomized trials on which to base preventive recom­
mendations for calcium phosphate stone formers, so the interventions 
are focused on modification of the recognized risk factors. Thiazide 
diuretics (with sodium restriction) may be used to reduce urine cal­
cium, as described above for calcium oxalate stones. In patients with 
low urine citrate levels, alkali supplements (e.g., potassium citrate or 
bicarbonate) may be used to increase urine citrate. However, the urine 
pH of these patients should be monitored initially because supple­
mental alkali can raise urine pH, thereby potentially increasing the 
risk of stone formation. Because these patients tend to have a urinary 
acidification defect, reducing the urine pH is not an option. Reduction 
of dietary phosphate may be beneficial by reducing urine phosphate 
excretion.
Uric Acid 
The two main risk factors for uric acid stones are per­
sistently low urine pH and higher uric acid excretion. Urine pH is the 
predominant influence on uric acid solubility; therefore, the mainstay 
of prevention of uric acid stone formation entails increasing urine pH. 
Alkalinizing the urine can be achieved by increasing the intake of foods 
rich in alkali (e.g., fruits and vegetables) and reducing the intake of 
foods that produce acid (e.g., animal flesh). If necessary, supplementa­
tion with bicarbonate or citrate salts (preferably potassium-based) can 
be used to reach the recommended pH goal of 6.5 throughout the day 
and night.
Urine uric acid excretion is determined by uric acid generation. 
Uric acid is the end product of purine metabolism; thus, reduced 
consumption of purine-containing foods can lower urine uric acid 
excretion. It is noteworthy that the serum uric acid level is dependent 
on the fractional excretion of uric acid and, therefore, does not provide 
information on urine uric acid excretion. For example, an individual 
with high uric acid generation and concurrent high fractional excre­
tion of uric acid will have high urine uric acid excretion with a normal 
(or even low) serum uric acid level. If alkalinization of the urine alone 
is not successful and if dietary modifications do not reduce urine uric 
acid sufficiently, then the addition of a xanthine oxidase inhibitor, such 
as allopurinol or febuxostat, can reduce urine uric acid excretion by 
40–50%.
Cystine 
Cystine excretion is not easily modified. Long-term dietary 
cystine restriction is not feasible and is unlikely to be successful; thus, 
the focus for cystine stone prevention is on increasing cystine solu­
bility. This goal may be achieved by treatment with medication that 
covalently binds to cystine (tiopronin or penicillamine) and a medica­
tion that raises urine pH. Tiopronin is the preferred choice owing to its 
better adverse event profile. The preferred alkalinizing agent to achieve 
a urine pH of 7.5 is potassium citrate or bicarbonate as sodium salts 
may increase cystine excretion. As with all stone types, and especially 
in patients with cystinuria, maintaining a high urine volume is an 
essential component of the preventive regimen.
Struvite 
Struvite stones, also known as infection stones or triplephosphate stones, form only when the upper urinary tract is infected 
with urease-producing bacteria such as Proteus mirabilis, Klebsiella 
pneumoniae, or Providencia species. Urease produced by these bacteria 
hydrolyzes urea and may elevate the urine pH to a supraphysiologic 
level (>8.0). Struvite stones may grow quickly and fill the renal pelvis 
(staghorn calculi).
Struvite stones require complete removal by a urologist. New stone 
formation can be avoided by the prevention of UTIs. In patients 
with recurrent upper UTIs (e.g., some individuals with surgically 
altered urinary drainage or spinal cord injury), the urease inhibitor 

acetohydroxamic acid can be considered; however, this agent should 
be used with caution because of potential side effects.

■
■LONG-TERM FOLLOW-UP
In general, the preventive regimens described above do not cure the 
underlying pathophysiologic process. Thus, these recommendations 
typically need to be followed for the patient’s lifetime, and it is essential 
to tailor recommendations in a way that is acceptable to the patient. 
Because the memory of the acute stone event fades and patients often 
return to old habits (e.g., insufficient fluid intake), long-term followup, including repeat 24-h urine collections typically annually, is impor­
tant to ensure that the preventive regimen has been implemented and 
has resulted in the desired reduction in the risk of new stone formation.
Follow-up imaging should be planned thoughtfully. Many patients 
with recurrent episodes of renal colic that lead to emergency room 
visits often undergo repeat CT studies. While CT does provide the 
best information, the radiation dose is higher than that with plain 
abdominal radiography (KUB). Small stones may be missed by KUB, 
and ultrasound has a limited ability to determine the size and num­
ber of stones. Minimizing radiation exposure should be a goal of the 
long-term follow-up plan and must be balanced against the gain in 
diagnostic information.
CHAPTER 331
■
■FURTHER READING
Coe FL: The physiology of kidney stone prevention: A narrative for 
patients and physicians. Available at https://bpb-us-w2.wpmucdn.com/
voices.uchicago.edu/dist/c/3637/files/2022/10/KIDNEY-STONES_Pathogenesis-and-Prevention.pdf.  Accessed November 2, 2023.
Coe FL, Worcester EM, Evan AP, Lingeman JE (eds): Kidney Stones: 
Urinary Tract Obstruction
Medical and Surgical Management, 2nd ed. New Dehli, Jaypee Brothers 
Medical Publishing, 2019.
European Association of Urology Guidelines on Urolithiasis. Available 
at https://d56bochluxqnz.cloudfront.net/documents/full-guideline/EAUGuidelines-on-Urolithiasis-2023.pdf. Accessed November 22, 2023.
Pearle MS et al: Medical management of kidney stones: AUA guide­
line. J Urol 192:316, 2014.
Julian L. Seifter

Urinary Tract Obstruction
Obstruction to the flow of urine, with attendant stasis and elevation 
in urinary tract pressure, impairs renal and urinary conduit functions 
and is a common cause of acute and chronic kidney disease (obstruc­
tive nephropathy). Early recognition and prompt treatment of urinary 
tract obstruction (UTO) can prevent or reverse devastating effects on 
kidney structure and function, and decrease susceptibility to hyperten­
sion, infection, and stone formation. Chronic obstruction may lead to 
permanent loss of renal mass (renal atrophy) and excretory capability. 
Because obstructive disease may be secondary to serious underlying 
inflammatory, vascular, or malignant disease, familiarity with clinical 
findings, appropriate diagnostic testing, and the therapeutic approach 
is of great importance to the clinician.
Recent developments have advanced our knowledge of fetal and 
genetic causes of lower urinary tract obstruction (LUTO) and chronic 
anomalies of the kidneys and urinary tracts (CAKUT), the rubric 
for a cluster of developmental uropathies associated with cysts and 
obstruction. In the last few years, studies in mice, zebrafish, and plu­
ripotent stem cells (kidney organoids) have identified possible genetic 
mutations implicated in cases of CAKUT producing low nephron 
number, including duplications and deletions (copy number vari­
ants) and familial candidate genes (HFN1β, PAX2, SIX1, GATA3, and

many others). Given that there is no nephrogenesis in humans after 
birth, obstructive disease manifesting in early or middle adulthood 
may in fact have origins in a decreased number of nephrons during 
fetal development. Fetal LUTO, if untreated, often results in pulmo­
nary hypoplasia and death in infancy; kidney failure may be a more 
long-term outcome. Since amniotic fluid is produced by fetal inges­
tion of urine, LUTO should be suspected when the mother develops 
oligohydramnios or anhydramnios. Improvements in second-trimester 
diagnosis and treatment with vesicoamniotic shunting have improved 
neonatal survival.

One of the most significant concerns in renal medicine is progres­
sion to a chronically fibrotic failing kidney. To date, there has been 
no demonstration of reversal of scarring, but many investigations 
are underway to find antifibrosis drugs, including those that address 
fibrosis in genetic diseases that lead to obstructive nephropathy. Many 
mechanisms contribute to this progression, including inflammatory 
responses, hemodynamic consequences of the declining number of 
healthy nephrons, and compression of normal nephrons by cysts in 
genetic diseases such as autosomal dominant polycystic kidney disease 
(ADPKD), where a gene mutation in polycystin causes proliferation of 
cystic masses. In ADPKD, primary cilia of tubule epithelial cells have 
been implicated in the development of cysts, resulting in inflamma­
tory processes and cell death. Polycystic disease is one of several such 
ciliopathies that ultimately lead to fibrosis.
PART 9
Disorders of the Kidney and Urinary Tract
■
■ETIOLOGY
Obstruction to urine flow can result from intrinsic or extrinsic mechan­
ical blockade as well as from functional defects not associated with fixed 
occlusion of the urinary drainage system. Mechanical obstruction can 
occur at any level of the urinary tract, from within the renal tubules or 
the renal calyces to the external urethral meatus (obstructive uropa­
thy). Normal points of narrowing, such as the ureteropelvic and ure­
terovesical junctions, bladder neck, and urethral meatus, are common 
sites of obstruction. When lower UTO is above the level of the bladder, 
unilateral dilatation of the ureter (hydroureter) and renal pyelocalyceal 
system (hydronephrosis) occurs; lesions at or below the level of the 
bladder cause bilateral involvement.
Common forms of obstruction are listed in Table 331-1. Childhood 
causes include congenital malformations, such as narrowing of the ure­
teropelvic junction (UPJ) and abnormal insertion of the ureter into the 
bladder, the most common cause. Vesicoureteral reflux in the absence 
of urinary tract infection or bladder neck obstruction often resolves 
with age. Reinsertion of the ureter into the bladder is indicated if reflux 
is severe and unlikely to improve spontaneously, if renal function dete­
riorates, or if urinary tract infections recur despite chronic antimicro­
bial therapy. Vesicoureteral reflux may cause prenatal hydronephrosis 
and, if severe, can lead to recurrent urinary infections, hypertension, 
and renal scarring in childhood. Posterior urethral valves are the most 
common cause of bilateral hydronephrosis in boys. In adults, UTO 
has usually been attributed to acquired defects. Pelvic tumors, calculi, 
and urethral stricture predominate. Ligation of, or injury to, the ureter 
during pelvic or colonic surgery can lead to hydronephrosis, which, 
if unilateral, may remain undetected. Obstructive uropathy may also 
result from extrinsic neoplastic (carcinoma of cervix or colon) or 
inflammatory disorders. Lymphomas, particularly follicular, and pel­
vic or colonic neoplasms with retroperitoneal involvement are causes 
of ureteral obstruction. As many as 50% of men aged >40 years may 
have lower urinary tract symptoms associated with benign prostatic 
hypertrophy, but these symptoms may occur without bladder outlet 
obstruction. Regardless of the primary cause, the chronic kidney dis­
ease that results may be exacerbated by a secondary contributor like 
diabetes mellitus, hypertension, kidney stones, infection, and meta­
bolic disturbances.
Functional impairment of urine flow occurs when voiding is altered 
by abnormal pontine or sacral centers of micturition control. It may be 
asymptomatic or associated with lower urinary tract symptoms such 
as frequency, urgency, and postmicturition incontinence, nocturia, 
straining to void, slow stream, hesitancy, or a feeling of incomplete 
emptying. A history should be sought for trauma, back injury, surgery, 

TABLE 331-1  Common Mechanical Causes of Urinary Tract 
Obstruction
URETER
BLADDER OUTLET
URETHRA
Congenital
Ureteropelvic junction 
narrowing or obstruction
Ureterovesical junction 
narrowing or obstruction 
and reflux
Ureterocele
Retrocaval ureter
Bladder neck obstruction
Ureterocele
Posterior urethral valves
Anterior urethral valves
Stricture
Meatal stenosis
Phimosis
Acquired Intrinsic Defects
Calculi
Inflammation
Infection
Trauma
Sloughed papillae
Tumor
Blood clots
Benign prostatic 
hyperplasia
Cancer of prostate
Cancer of bladder
Calculi
Diabetic neuropathy
Spinal cord disease
Anticholinergic drugs 
and α-adrenergic 
agonists
Stricture
Tumor
Calculi
Trauma
Phimosis
Acquired Extrinsic Defects
Pregnant uterus
Retroperitoneal fibrosis
Aortic aneurysm
Uterine leiomyomata
Carcinoma of uterus, 
prostate, bladder, colon, 
rectum
Lymphoma
Pelvic inflammatory 
disease, endometriosis
Accidental surgical 
ligation
Carcinoma of cervix, 
colon
Trauma
Trauma
diabetes mellitus, neurologic or psychiatric conditions, and medica­
tions. Causes include neurogenic bladder, often with adynamic ureter, 
and vesicoureteral reflux. Reflux in children may result in severe uni­
lateral or bilateral hydroureter and hydronephrosis. Overflow urinary 
incontinence combined with sudden-onset fecal incontinence, severe 
lower back pain, and saddle anesthesia, requires emergency evalua­
tion for possible cauda equina syndrome. Urinary retention may be 
the consequence of α-adrenergic and anticholinergic agents, as well as 
opiates. Hydronephrosis in pregnancy is due to relaxational effects of 
progesterone on smooth muscle of the renal pelvis, as well as ureteral 
compression by the enlarged uterus, more often on the right side.
Diagnostic tools to identify anatomic obstruction include urinary 
flow measurements and a postvoid residual measurement. Bladder vol­
ume may be readily assessed by bedside ultrasound. Cystourethroscopy 
and urodynamic studies may be reserved for the symptomatic patient 
to assess the filling phase (cystometry), pressure-volume relation­
ship of the bladder, bladder compliance, and capacity. Pressure-flow 
analysis evaluates bladder contractility and bladder outlet resistance 
during voiding. Bladder obstruction is characterized by high pressures 
in women, whereas in men, a diagnosis of bladder outlet obstruction is 
based on flow rate and voiding pressures. A voiding cystourethrogram 
may be useful in evaluating incomplete emptying and bladder neck and 
urethral pathology.
■
■CLINICAL FEATURES AND PATHOPHYSIOLOGY
The pathophysiology and clinical features of UTO are summarized 
in Table 331-2. Flank pain, the symptom that most commonly leads 
to medical attention, is due to distention of the collecting system or 
renal capsule. Pain severity is influenced more by the rate at which 
distention develops than by the degree of distention. Acute supravesical

TABLE 331-2  Pathophysiology of Bilateral Ureteral Obstruction
HEMODYNAMIC 
EFFECTS
TUBULE EFFECTS
CLINICAL FEATURES
Acute
Pain (capsule distention)
Azotemia, oliguria, or 
anuria
↑ Renal blood flow
↓ GFR
↓ Medullary blood flow
↑ Vasodilator 
prostaglandins, nitric 
oxide
↑ Ureteral and tubule 
pressures
↑ Reabsorption of Na+, 
urea, water
Chronic
Azotemia
Hypertension
AVP-insensitive polyuria
Natriuresis
Hyperkalemic, 
hyperchloremic acidosis
↓ Renal blood flow
↓↓ GFR
↑ Vasoconstrictor 
prostaglandins
↑ Renin-angiotensin 
production
↓ Medullary osmolarity
↓ Concentrating ability
Structural damage; 
parenchymal atrophy
↓ Transport functions for 
Na+, K+, H+
Release of Obstruction
Postobstructive diuresis
Potential for volume 
depletion and electrolyte 
imbalance due to losses 
of Na+, K+, PO4
Slow ↑ in GFR (variable)
↓ Tubule pressure
↑ Solute load per 
nephron (urea, NaCl)
Natriuretic factors 
present
2–, Mg2+, 
and water
Abbreviations: AVP, arginine vasopressin; GFR, glomerular filtration rate.
obstruction, as from a stone lodged in a ureter (Chap. 330), is associ­
ated with excruciating, sometimes intermittent, pain, known as renal 
colic. This pain often radiates to the lower abdomen, testes, or labia. 
By contrast, more insidious causes of obstruction, such as chronic nar­
rowing of the UPJ, may produce little or no pain and yet result in total 
destruction of the affected kidney. Flank pain that occurs only with 
micturition is pathognomonic of vesicoureteral reflux.
Obstruction of urine flow results in an increase in hydrostatic pres­
sures proximal to the site of obstruction. It is this buildup of pressure 
that leads to the accompanying pain, the distention of the collecting 
system in the kidney, and elevated intratubular pressures that initiate 
tubular dysfunction. In the first days of obstruction, the dilatation 
of the poorly compliant collecting system may be minimal. As the 
increased hydrostatic pressure is expressed in the urinary space of the 
glomeruli, further filtration decreases or stops completely.
Azotemia develops when overall excretory function is impaired, 
often in the setting of bladder outlet obstruction, bilateral renal pelvic 
or ureteric obstruction, or unilateral disease in a patient with a solitary 
functioning kidney. Complete bilateral obstruction should be sus­
pected when acute renal failure is accompanied by anuria. Any patient 
with renal failure otherwise unexplained, or with a history of neph­
rolithiasis, hematuria, diabetes mellitus, prostatic enlargement, pelvic 
surgery, trauma, or tumor should be evaluated for UTO.
In the acute setting, partial, bilateral obstruction may mimic pre­
renal azotemia with a high blood urea nitrogen–to–creatinine ratio, 
concentrated urine, and sodium retention. Renal vascular resistance 
may be increased. However, with more prolonged obstruction, symp­
toms of polyuria and nocturia commonly accompany partial UTO and 
result from loss of medullary hypertonicity with diminished renal con­
centrating ability. Failure to produce urine free of salt (natriuresis) is 
due to downregulation of salt reabsorption in the proximal tubule and 
of transport proteins including the Na+, K+ adenosine triphosphatase 
(ATPase), Na:K:2Cl cotransporter (NKCC2) in the thick ascending 
limb, and the epithelial Na+ channel (ENaC) in collecting duct cells. 
In addition to direct effects on renal transport mechanisms, increased 
prostaglandin E2 (PGE2) (due to induction of cyclooxygenase-2 
[COX-2]), angiotensin II (with its downregulation of Na+ transport­
ers), and atrial or B-type natriuretic peptides (ANP or BNP) due to 
volume expansion in the azotemic patient contribute to decreased 
salt reabsorption along the nephron. Nitric oxide synthases (NOS) 

in ureteral smooth muscle and urothelial tissues have been found to 
oppose the high ureteral pressure in unilateral obstruction.

Dysregulation of aquaporin-2 water channels in the collecting duct 
contributes to the polyuria. The defect usually does not improve with 
administration of vasopressin and is, therefore, a form of acquired 
nephrogenic diabetes insipidus.
Wide fluctuations in urine output in a patient with azotemia should 
always raise the possibility of intermittent or partial UTO. If fluid 
intake is inadequate, severe dehydration and hypernatremia may 
develop. However, as with other causes of poor renal function, excesses 
of salt and water intake may result in edema and hyponatremia.
Partial bilateral UTO often results in acquired distal renal tubular 
acidosis, hyperkalemia, and renal salt wasting. The H+-ATPase, situated 
on the apical membrane of the α-intercalated cells of the collecting 
duct, is critical for distal H+ secretion. The trafficking of intracellular 
H+ pumps from the cytoplasm to the cell membrane is disrupted in 
UTO. The decreased function of the ENaC, in the apical membrane 
of neighboring collecting duct principal cells, contributes to decreased 
Na+ reabsorption (salt wasting) and, therefore, decreased K+ secretion 
via K+ channels. Ammonium (NH+) excretion important to the elimi­
nation of H+ is impaired. These defects in tubule function are often 
accompanied by renal tubulointerstitial damage. Azotemia with hyper­
kalemia and metabolic acidosis should prompt consideration of UTO.
CHAPTER 331
The renal interstitium becomes edematous and infiltrated with 
mononuclear inflammatory cells early in UTO. Later, interstitial fibro­
sis and atrophy of the papillae and medulla occur and precede these 
processes in the cortex. The increase in angiotensin II noted in UTO 
contributes to the inflammatory response and fibroblast accumulation 
through mechanisms involving profibrotic cytokines. With time, this 
process leads to chronic kidney damage.
Urinary Tract Obstruction
UTO must always be considered in patients with urinary tract 
infections or urolithiasis. Urinary stasis encourages the growth of 
organisms. Urea-splitting bacteria are associated with magnesium 
ammonium phosphate (struvite) calculi that may take on a staghorn 
appearance. Hypertension is frequent in acute and subacute unilateral 
obstruction and is usually a consequence of increased release of renin 
by the involved kidney. Chronic kidney disease from bilateral UTO, 
often associated with extracellular volume expansion, may result in 
significant hypertension. Erythrocytosis, an infrequent complication 
of obstructive uropathy, is secondary to increased erythropoietin 
production.
■
■DIAGNOSIS
A history of difficulty in voiding, pain, infection, or change in urinary 
volume is common. Evidence for distention of the kidney or urinary 
bladder can often be obtained by palpation and percussion of the abdo­
men. A careful rectal and genital examination may reveal enlargement 
or nodularity of the prostate, abnormal rectal sphincter tone, or a rectal 
or pelvic mass.
Urinalysis may reveal hematuria, pyuria, and bacteriuria. The urine 
sediment is often normal, even when obstruction leads to marked 
azotemia and extensive structural damage. An abdominal scout film, 
although insensitive, may detect nephrocalcinosis or a radiopaque 
stone. As indicated in Fig. 331-1, if UTO is suspected, a bladder 
catheter should be inserted. Abdominal ultrasonography should be 
performed to evaluate renal and bladder size, as well as pyelocalyceal 
contour. Ultrasonography is ~90% specific and sensitive for detection 
of hydronephrosis. False-positive results are associated with diuresis, 
renal cysts, or the presence of an extrarenal pelvis, a normal congenital 
variant. Congenital UPJ obstruction may be mistaken for renal cystic 
disease. Hydronephrosis may be absent on ultrasound when obstruc­
tion is <48 h in duration or associated with volume contraction, 
staghorn calculi, retroperitoneal fibrosis, or infiltrative renal disease. 
Duplex Doppler ultrasonography may detect an increased resistive 
index in urinary obstruction. The radiodensity of renal stones is mea­
sured in Hounsfield units (HUs). Calcium oxalate and calcium phos­
phate stones may be distinguished from uric acid calculi by their HU 
radiodensities on noncontrast computed tomography (CT) scan, the 
test of choice for acute flank pain.

Unexplained renal failure
Insert bladder catheter
No diuresis: do
ultrasound
Diuresis
Obstruction below
bladder neck
Hydronephrosis
Do CT scan to identify
site and etiology of
obstruction
Urologic
evaluation
Positive or negative
but still high suspicion
PART 9
Disorders of the Kidney and Urinary Tract
Retrograde urography
and ureteral stent
considered
Antegrade urography
and percutaneous
nephrostomy considered
FIGURE 331-1  Diagnostic approach for urinary tract obstruction in unexplained renal failure. CT, computed tomography.
Recent advances in technology have led to alternatives and have 
replaced the once standard intravenous urogram in the further evalu­
ation of UTO. The high-resolution multidetector row CT scan, in 
particular, has the advantages of visualizing the retroperitoneum, as 
well as identifying both intrinsic and extrinsic sites of obstruction. 
Noncontrast CT scans improve visualization of the urinary tract in 
the patient with renal impairment and are safer for patients at risk for 
contrast nephropathy. Magnetic resonance urography is not at this time 
superior to the CT scan, and certain gadolinium agents carry a risk of 
systemic sclerosis in patients with renal insufficiency. Recently, prom­
ising alternatives to gadolinium have emerged, including iron-based 
contrast and inhalation of xenon gas, although thus far, gadolinium 
produces the clearest images and most-established safety. CT scanning 
may define the site of obstruction, identify and characterize kidney 
stones, and demonstrate dilatation of the calyces, renal pelvis, and 
ureter above the obstruction. The ureter may be tortuous in chronic 
obstruction. Though radionuclide scans give less anatomic detail than 
CT scans, they are able to give differential renal function. In the case 
of asymmetric renal function, the clinician may decide on a preferable 
kidney to decompress in the case of bilateral obstruction. Furosemide 
is sometimes given to increase detection with imaging and to distin­
guish functional from anatomic obstruction. The increase in urinary 
flow may bring out the pain of an acute obstructive process.
To facilitate visualization of a suspected lesion in a ureter or renal 
pelvis, retrograde or antegrade urography should be attempted. These 
procedures do not carry risk of contrast-induced acute kidney injury 
in patients with renal insufficiency. The retrograde approach involves 
catheterization of the involved ureter under cystoscopic control, 
whereas the antegrade technique necessitates percutaneous placement 
of a catheter into the renal pelvis. Although the antegrade approach 
may provide immediate decompression of a unilateral obstructing 
lesion, many urologists initially attempt the retrograde approach unless 
the catheterization is unsuccessful.
Voiding cystourethrography is of value in the diagnosis of vesico­
ureteral reflux and bladder neck and urethral obstructions. Postvoiding 
films reveal residual urine. Endoscopic visualization by the urologist 
often permits precise identification of lesions involving the urethra, 
prostate, bladder, and ureteral orifices.

No
hydronephrosis
High suspicion
Low suspicion
No further workup
for obstruction
Negative
TREATMENT
Urinary Tract Obstruction
UTO complicated by infection requires immediate relief of obstruc­
tion to prevent development of generalized sepsis and progressive 
renal damage. Sepsis necessitates prompt urologic intervention. 
Drainage may be achieved by nephrostomy, ureterostomy, or ure­
teral, urethral, or suprapubic catheterization. Prolonged antibiotic 
treatment may be necessary. Chronic or recurrent infections in a 
poorly functioning obstructed kidney may necessitate nephrec­
tomy. When infection is not present, surgery is often delayed until 
acid-base, fluid, and electrolyte status is restored. Nevertheless, 
the site of obstruction should be ascertained as soon as feasible. 
Elective relief of obstruction is usually recommended in patients 
with urinary retention, recurrent urinary tract infections, persis­
tent pain, or progressive loss of renal function. Benign prostatic 
hypertrophy may be treated medically with α-adrenergic block­
ers and 5α-reductase inhibitors. Renal colic may be treated with 
anti-inflammatory medication as edema often contributes to an 
obstructing ureteral stone, and α-adrenergic blockers may also be of 
benefit. The clinician should be aware of the risk of intraoperative 
floppy iris syndrome associated with cataract surgery in patients 
taking α-adrenergic blockers. Use of nonsteroidal anti-inflamma­
tory medication must take into account the potential for renal 
harm, and opiates in patients with decreased renal function may be 
dangerous and should be used with caution. Functional obstruction 
secondary to neurogenic bladder may be decreased with the combi­
nation of frequent voiding and cholinergic drugs.
■
■PROGNOSIS
With relief of obstruction, the prognosis regarding return of renal func­
tion depends largely on whether irreversible renal damage has occurred. 
When obstruction is not relieved, the course will depend mainly on 
whether the obstruction is complete or incomplete and bilateral or uni­
lateral, as well as whether or not urinary tract infection is also present. 
Complete obstruction with infection can lead to total destruction of 
the kidney within days. Partial return of glomerular filtration rate may

follow relief of complete obstruction of 1 and 2 weeks’ duration, but after 
8 weeks of obstruction, recovery is unlikely. In the absence of definitive 
evidence of irreversibility, every effort should be made to decompress 
the obstruction in the hope of restoring renal function at least partially. 
A renal radionuclide scan, performed after a prolonged period of decom­
pression, may be used to predict the reversibility of renal dysfunction.
■
■POSTOBSTRUCTIVE DIURESIS
Relief of bilateral, but not unilateral, complete obstruction commonly 
results in polyuria, which may be massive. The urine is usually hypo­
tonic and may contain large amounts of sodium chloride, potassium, 
phosphate, and magnesium. The natriuresis is due in part to the correc­
tion of extracellular volume expansion, the increase in natriuretic fac­
tors accumulated during the period of renal failure, and depressed salt 
and water reabsorption when urine flow is reestablished. The retained 
urea is excreted with improved glomerular filtration rate, resulting in 
an osmotic diuresis that increases the urine volume of electrolyte-free 
water. Electrolyte-free water excretion (hypotonic urine) is recognized 
as being present when the sum of the urinary concentrations of sodium 
and potassium is lower than the serum sodium concentration. Precipi­
tating factors include suppression of antidiuretic hormone at arterial 
baroreceptor sites, elevation of natriuretic peptides, or nephrogenic 
diabetes insipidus due to obstructive tubular injury. In the majority of 
patients, this diuresis results in the appropriate excretion of the excesses 
of retained salt and water. When extracellular volume and composition 
return to normal, the diuresis usually abates spontaneously. Occasion­
ally, iatrogenic expansion of extracellular volume is responsible for, or 
sustains, the diuresis observed in the postobstructive period. Replace­
ment with intravenous fluids in amounts less than urinary losses usu­
ally prevents this complication. More aggressive fluid management is 
required in the setting of hypovolemia, hypotension, or disturbances in 
serum electrolyte concentrations.
The loss of electrolyte-free water with urea may result in hyper­
natremia. Measured urinary output and serum and urine sodium, 
potassium, and osmolal concentrations should guide the use of 

appropriate intravenous replacement. Often replacement with 0.45% 
saline is required because of the likelihood of appropriately matching 
urine electrolyte concentrations. Relief of obstruction may be followed 
by urinary salt and water losses severe enough to provoke profound 
dehydration and vascular collapse. In these patients, decreased tubule 
reabsorptive capacity is probably responsible for the marked diuresis. 
Appropriate therapy in such patients includes intravenous administra­
tion of salt-containing solutions to replace sodium and volume deficits.

■
■FURTHER READING
Capone V et al: Definition, diagnosis and management of fetal lower 
urinary tract obstruction: Consensus of the Erknet Cakut-Obstructive 
Uropathy Work Group. Nature Rev Urol 19:295, 2022.
Frokiaer J: Urinary tract obstruction, in Brenner and Rector’s The 
Kidney, 10th ed, Skorecki K et al (eds). Philadelphia, W.B. Saunders 
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