INTRODUCTION — Urinary tract obstruction (UTO) occurs due to blockage of urine flow along the urinary tract and generally manifests as hydronephrosis on imaging. UTO may be acute or chronic, partial or complete, and unilateral or bilateral. Kidney function impairment from UTO, if present, is readily reversible if the obstruction is promptly corrected. Uncorrected UTO can lead to progressive kidney function impairment and end-stage kidney disease.
This topic will review UTO and hydronephrosis in adults. Other related issues are discussed elsewhere:
●Hydronephrosis in infants and children (see "Congenital ureteropelvic junction obstruction" and "Primary megaureter in infants and children" and "Clinical presentation and diagnosis of posterior urethral valves" and "Fetal hydronephrosis: Etiology and prenatal management")
●Management of UTO with ureteral stents (see "Placement and management of indwelling ureteral stents")
●Findings related to UTO on imaging (see "Radiologic assessment of kidney disease")
EPIDEMIOLOGY — The incidence of UTO causing acute kidney injury (AKI) is not known with certainty. In a survey-based study of over two million hospitalized adults from mainland China, UTO was identified as the cause of AKI among 12 percent of patients . In another study of 381 critically ill older adults (>80 years of age), UTO was the cause of AKI among 22 percent of patients .
While there are no extensive epidemiologic data, in our combined clinical experience, the incidence of UTO varies considerably by the patient population. As an example, compared with adults, children more commonly have UTO as a cause of urinary tract symptoms or kidney function impairment (due to congenital abnormalities). UTO is more common among males compared with females, particularly as males age, due to prostatic enlargement .
Overall, UTO is not a common cause of kidney failure in adults, but the likelihood of UTO being discovered as an underlying etiology depends upon the clinical setting and the relative risks of other contributing causes. As an example, UTO is an important cause of kidney function impairment in patients with cancer, particularly among those with bulky abdominal malignancies. UTO is a rare cause of hospital-acquired AKI but is more common in the outpatient setting .
ETIOLOGY — UTO can occur anywhere along the urinary tract (figure 1). Each renal papilla secretes urine into a minor calyx and the infundibula of the minor calyces converge into two or three major calyces (figure 2). The major calyces coalesce to form the renal pelvis and, eventually, the proximal ureter.
Each ureter travels inferiorly in the retroperitoneum, passing posterior to the bladder and inserting into the base of the bladder. The urethra originates at the bladder neck, just inferior to the ureteral orifices. The urethra in males is surrounded by the prostate gland (figure 1) .
The causes of UTO vary, in part, based upon the site of the obstruction (table 1). The obstruction at each of the sites can result from intrinsic blockage (eg, stones) or extrinsic compression (eg, pelvic tumors):
●Obstruction within the kidney causes dilation of individual calyces or caliectasis (image 1). Potential causes of intrarenal obstruction include kidney stones, sequelae of current or prior infection, urothelial carcinoma, blood clots, and sloughed papillae. Tuberculosis is a rare cause of intrarenal obstruction; it is mainly a disease diagnosed in countries with a high prevalence of tuberculosis. (See "Malignancies of the renal pelvis and ureter", section on 'Clinical presentation' and "Urogenital tuberculosis", section on 'Renal and urologic tuberculosis' and "Overview of traumatic and iatrogenic ureteral injury", section on 'Clinical presentations' and "Overview of traumatic upper genitourinary tract injuries in adults", section on 'Clinical features and diagnosis' and "Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis", section on 'Symptomatic stones'.)
●Obstruction at (image 2) or distal to the renal pelvis (ie, at the level of the ureter) causes diffuse caliectasis or hydronephrosis. Ureteral obstruction may result from causes such as stones, urothelial carcinoma, thrombi, tumors, or retroperitoneal fibrosis. Obstruction of an indwelling ureteral stent can lead to recurrent hydronephrosis. In women, uterine, cervical, or ovarian cancer can cause unilateral or bilateral obstruction. (See "Overview of traumatic and iatrogenic ureteral injury", section on 'Clinical presentations' and "Clinical manifestations and diagnosis of retroperitoneal fibrosis", section on 'Clinical features' and "Malignancies of the renal pelvis and ureter", section on 'Clinical manifestations' and "Endometriosis of the bladder and ureter" and "Candida infections of the bladder and kidneys".)
●Obstruction distal to the ureters can result from pathologies of the bladder and urethra. Bladder tumors can obstruct one or both ureters or ureteral orifices. The most common causes of bilateral ureteral obstruction include bladder outlet obstruction (from prostatic enlargement or posterior urethral valves) and neurogenic bladder (image 3). (See "Clinical presentation and diagnosis of posterior urethral valves" and "Management of posterior urethral valves" and "Non-urothelial bladder cancer", section on 'Clinical presentation' and "Clinical presentation, diagnosis, and staging of bladder cancer", section on 'Voiding symptoms' and "Clinical manifestations and diagnostic evaluation of benign prostatic hyperplasia", section on 'Complications'.)
The causes of UTO also vary with the age of the patient. Anatomic causes (including urethral valves or stricture and stenosis at the ureterovesical or ureteropelvic junction) account for the majority of cases in children. By comparison, stones are most common in young adults, while prostatic hypertrophy or carcinoma, retroperitoneal or pelvic neoplasms, and stones are the primary causes in older patients [6,7].
Often, the clinical setting and past medical history of the patient will strongly suggest the likely cause of the obstruction. (See "Clinical presentation, diagnosis, and staging of bladder cancer", section on 'Initial evaluation' and "Malignancies of the renal pelvis and ureter", section on 'Diagnosis'.)
PATHOPHYSIOLOGY — The histopathologic damage to the kidney parenchyma from a complete UTO, however short in duration, can be evident even in the absence of functional glomerular filtration rate (GFR) impairment. As an example, in an experimental study of rats that had complete unilateral ureteral obstruction for 24 hours, approximately 15 percent of obstructed nephrons were nonfunctional as late as 60 days after relief of obstruction, a presumed reflection of irreversible injury . Despite this nephron loss, the GFR returned to normal because of hypertrophy and hyperfiltration in the remaining functional nephrons. It is likely that a similar process of compensatory hypertrophy occurs in human obstruction as noted in other disease processes (eg, lupus nephritis) .
The mechanism by which UTO leads to irreversible kidney injury and atrophy is incompletely understood. Following the onset of obstruction, there is an increase in pressure proximal to the obstruction due to continued glomerular filtration and generation of urine ; this rise in pressure and collection of urine leads to dilation of the collecting system. The elevated pressure is eventually transmitted back to the proximal tubule counteracting the normal intraglomerular pressure gradient that drives glomerular filtration, thereby lowering the GFR. Over time, the rise in intratubular pressure induces secondary renal vasoconstriction and often a marked reduction in glomerular blood flow [10,11]. Such vasoconstriction is regulated locally by the individual obstructed nephrons and is mediated, in part, by the release of angiotensin II and thromboxanes [10,12,13]. This vasoconstriction within obstructed nonfunctioning nephrons may be a physiologic adaptation to help shunt blood away from them .
The net effect is that there is chronic reduction in GFR due primarily to the decrease in kidney perfusion, which ultimately lowers the elevated intratubular pressures toward normal [10,14,15]. The importance of increased intrarenal pressure is supported by findings in obstructed animals in whom the tubular dysfunction can be reduced by renal decapsulation, which limits the rise in pressure .
The tubular injury from UTO may be mediated initially by the increase in intratubular pressure and later by atrophy resulting from ischemia and/or inflammation [10,17]. The obstructed kidney appears to release substances that are chemotactic for monocytes and macrophages [10,18,19]. These infiltrating cells can then release transforming growth factor-beta (TGF-beta) and other cytokines, proteases, and oxygen free radicals that may contribute to tubular injury and fibrosis [18,20].
The combination of tubular atrophy and inflammatory cell injury can, over a period of time, lead to irreversible injury and interstitial fibrosis that limits the extent to which kidney function is restored, even when the obstruction is relieved .
CLINICAL FEATURES — The clinical presentation, in particular the presence or absence of pain, depends upon the site of obstruction, the degree of obstruction (ie, partial or complete), and the rapidity with which obstruction develops . Most often, patients who have UTO come to medical attention due to rise in serum creatinine.
Symptoms and signs — The vast majority of patients with UTO not due to stones are asymptomatic on presentation. However, infrequently, patients may have urinary urgency, hypertension, hematuria, changes in urine output, or pain.
Pain as a symptom is frequently absent, even in acute obstruction; when present, it is usually due to the underlying cause rather than the dilation of the urinary tract. Relatively severe pain (renal or ureteral colic) may be seen with acute complete or partial obstruction within a ureter (as with a ureteral stone). Pain is usually absent with external ureteral compression because of the slowly progressive course of the UTO. Urinary retention is also asymptomatic in many patients, although acute urinary retention causes sharp pain in many patients as the bladder fills and cannot be emptied.
Patients can present with or without apparent changes in urinary volume or frequency. Urine output may be quite variable with UTO. It can range from anuria (as in the setting of complete bilateral ureteral or complete urethral obstruction) to oliguria, normal urine volume, or even polyuria. Polyuria in the presence of reduced glomerular filtration rate (GFR) may result from tubular injury, which impairs the ability of the renal tubules to concentrate the urine [11,22,23]. In addition, the patient may incorrectly report polyuria when they have urinary frequency, urgency, or nocturia due to bladder distension and overflow incontinence in the setting of urethral obstruction.
Physical examination findings of UTO are often limited. Among patients with a bladder outlet obstruction, bladder distension can often be detected by percussion of the pelvis and lower abdomen. In severe cases, there may also be abdominal distension. There are no pathognomonic findings associated with obstruction proximal to the bladder (upper tract obstruction), although costovertebral tenderness may be present.
Some patients with UTO can have elevated blood pressure, which may be due to hypervolemia in patients with oligoanuria. Alternatively, elevated blood pressure may result from activation of the renin-angiotensin system due to reflex vasoconstriction of the afferent glomerular capillaries in the obstructed kidney [24,25]. Elevated blood pressure typically resolves with relief of obstruction and restoration of urine flow.
UTO may be associated with urinary tract infection (UTI) of varying severity, including severe UTI with associated sepsis. UTIs associated with UTO are discussed at length separately. (See "Acute complicated urinary tract infection (including pyelonephritis) in adults and adolescents".)
●Increase in serum creatinine – In general, an increase in serum creatinine is unusual among patients with obstruction of one of their two kidneys, unless there is underlying chronic kidney disease. However, bilateral obstruction or unilateral obstruction among patients who have a single kidney or who have preexisting kidney disease will lead to an increase in serum creatinine. Such an increase, often detected incidentally, may be the first indication of obstruction.
●Hematuria, pyuria, and crystalluria – The urinalysis may be relatively normal or reveal only a few white or red cells . Significant hematuria may be present if the UTO is due to a ureteral stone, a sloughed papilla, or an intraluminal malignancy. Crystalluria may suggest a kidney stone and provide a clue to its composition.
●Hyperkalemic renal tubular acidosis – Patients with chronic UTO often have hyperkalemic distal renal tubular acidosis . (See "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance", section on 'Voltage-dependent RTA'.)
Other laboratory tests are generally not helpful in distinguishing obstruction from other causes of kidney disease.
Radiologic findings — The diagnosis of UTO is usually made by imaging. Ultrasound and computed tomography (CT) are the most commonly used modalities. (See 'High suspicion for UTO: Diagnostic testing' below.)
●Classic findings – The hallmarks of UTO are hydronephrosis, the dilation of the collecting system in the kidney, and hydroureter, the dilation of the ureter. With hydronephrosis, the major calyces and renal pelvis are usually dilated; the dilation of the minor calyces occurs later in the course of obstruction. Dilation of the ureter is typically a late finding and is often absent initially.
Patients with a bladder outlet obstruction will also have a dilated bladder visualized by imaging.
On ultrasound, hydronephrosis appears as a hypoechoic fluid accumulation (urine) that displaces the echogenic renal sinus fat in a branching pattern (image 4) . On an unenhanced CT scan, urine has greater attenuation than that of the renal sinus fat but slightly lesser than that of the kidney parenchyma (image 5). On a contrast-enhanced CT scan, the parenchyma appears considerably brighter than the urinary space (image 6) until the scan reaches the excretory phase, at which point the contrast brightens the collecting system. The urinary space will be similarly dilated on magnetic resonance imaging (MRI) scans, with urine being bright on T2-weighted images.
●Assessment of severity – Assessment of the severity of hydronephrosis is usually subjective and does not necessarily correlate with the degree of obstruction, especially in the acute setting. As an example, a patient diagnosed as having "mild hydronephrosis" could have severe UTO.
The assessment of severity can also be affected by timing of the study and urine output of the patient. The urine exits the kidneys in a pulsatile manner by calyceal contraction. Thus, the major calyces may be visible prior to contraction, especially in patients with a high urine output.
In mild hydronephrosis, which can be observed in normal kidneys even in the absence of obstruction, dilation of the minor calyces and proximal ureter is usually absent. In severe hydronephrosis, urine fills most of the renal sinus and there is dilation of the proximal ureter. Assigning a severity grade between mild and severe (ie, moderate) generally does not provide any useful clinical information other than to assess progression or resolution of the hydronephrosis.
●Localizing the site of obstruction – Radiologic tests can usually localize the level of obstruction. Dilation of the proximal ureter on ultrasound (image 7) without a distended bladder or dilated distal ureter indicates obstruction within the ureter, which usually requires further delineation by CT or MRI to help define the cause of the dilatation (image 8). Dilation of the proximal and distal ureter on ultrasound without bladder distension indicates obstruction of the ureteral orifice, usually due to a stone or bladder carcinoma (image 9). In this case, CT will show dilation of the entire ureter.
Bladder outlet obstruction, often caused in males by prostatic enlargement, can be detected as an enlarged postvoid bladder on the dedicated bladder ultrasound or an automated bedside bladder scanner (image 10). A bedside bladder scanner can detect urinary retention but is not used as a standalone modality to identify bladder outlet obstruction. Bladder scanners cannot display images and cannot distinguish a urine-filled bladder from adjacent fluid collections such as ascites or large ovarian cysts.
The pulsatile movement of urine into the bladder (ureteral jets) is readily visualized by Doppler ultrasound and can often be detected by B-mode ultrasonography as well (image 11). Although the presence of jets indicates patency of the ureter, their absence is not definitive proof of ureteral obstruction.
●Other important findings – In addition to the collecting system, imaging may also provide useful information about the kidney parenchyma. Cortical thinning may be noted when UTO is chronic or when UTO occurs in a patient with preexisting chronic kidney disease (CKD) (image 12 and image 13). Severe thinning of the kidney parenchyma indicates longstanding obstruction, relief of which is unlikely to improve kidney function. The most extreme example of this is congenital ureteropelvic obstruction, in which the kidney is recognizable only as a collection of fluid.
Atypical presentations — In some cases, UTO can occur without hydronephrosis, while in other cases, hydronephrosis may be present without UTO.
Obstruction without hydronephrosis — Obstruction with no hydronephrosis can occur early in the course of acute obstruction (usually due to a stone or bladder retention) before urine has accumulated (image 14) or when urine production is reduced for other reasons, such as parenchymal kidney disease [27-30]. Hydronephrosis may also be absent among patients with a partial UTO.
Hydronephrosis without obstruction — Hydronephrosis does not always indicate urinary obstruction. A large diuresis can distend the intrarenal collecting system, giving it the appearance of obstruction [31,32]. The most notable example of this is pregnancy, in which dilation of the collecting system and ureters begins in the first trimester and persists for a few weeks postpartum [33,34]. However, most causes of nonobstructive hydronephrosis will be described radiologically as nonsevere [35,36]; "severe" hydronephrosis does not typically occur in the absence of obstruction, except in patients with congenital arginine vasopressin disorders. (See "Maternal adaptations to pregnancy: Renal and urinary tract physiology" and "Arginine vasopressin resistance (nephrogenic diabetes insipidus): Treatment".)
In addition, hydronephrosis may remain for varying periods of time (including permanent dilation of the collecting system) after resolution of obstruction, particularly if it was chronic.
Overview of the approach — UTO is usually suspected because of symptoms of bladder retention or unexplained kidney failure. Occasionally, hydronephrosis is an incidental finding during imaging for other indications. Our approach to diagnosis is as follows (see 'Approach to imaging' below):
●In a patient with a high clinical suspicion for urinary retention or bladder outlet obstruction, a simple bedside bladder scan and subsequent catheterization, if indicated, is sufficient. (See 'When to have a high suspicion for UTO' below.)
●In a patient with a high clinical suspicion for UTO (eg, known or suspected abdominal or retroperitoneal malignancy, prior urologic surgery), the presence of hydronephrosis (with any imaging modality) confirms the diagnosis of UTO.
●In a patient suspected of having a UTO due to a kidney stone, noncontrast CT is the best initial study to diagnose ureteral obstruction.
●In a patient with unexplained kidney failure, either acute or chronic, ultrasonography is the appropriate initial imaging to exclude UTO as a possible cause of the kidney failure. Absence of hydronephrosis in a patient with a low pretest probability of having obstructive uropathy essentially rules out the possibility of UTO.
●In a patient with low clinical suspicion for UTO who has hydronephrosis detected on imaging (typically as an incidental finding), nonobstructive causes should be considered. (See 'Hydronephrosis without obstruction' above.)
Otherwise, further imaging should be performed. A noncontrast CT scan can usually identify the cause, and if it does not identify the cause, CT urography may be required.
●In the rare patient with a high clinical suspicion but no hydronephrosis on imaging, cystoscopy and retrograde pyelography may be appropriate.
Early diagnosis of UTO is important since most cases can be corrected and a delay in therapy can lead to irreversible kidney injury. (See 'Prognosis' below.)
When to have a high suspicion for UTO — The clinical suspicion for UTO is high among patients who have acute or subacute kidney failure, newly discovered chronic kidney disease, or symptoms potentially related to obstruction, and who also have one or more of the following:
●History of prostatic hypertrophy or prostate cancer, which would raise suspicion for bladder outlet obstruction
●Prior urologic surgery (including prior procedure to relieve UTO)
●Known or suspected abdominal or retroperitoneal malignancy (including metastases from nonabdominal cancer)
●Prior history of nephrolithiasis, or presence of renal colic
●Profuse gross hematuria
●Prior pelvic or retroperitoneal surgery
●New lower abdominal, pelvic, or flank pain or tenderness
●Neurologic disorders affecting the bladder
●An unrevealing evaluation for other causes of kidney function impairment
High suspicion for UTO: Diagnostic testing
Approach to imaging — In patients with suspected UTO, ultrasound of the kidneys is typically the initial test of choice to diagnose or exclude obstruction. A different initial approach is used in patients with suspected urinary retention and a normal serum creatinine (ie, a bladder scan or postvoid bladder catheter should be performed) or in nonpregnant patients with suspected nephrolithiasis (ie, a noncontrast CT should usually be performed rather than an ultrasound). If the initial imaging study (ultrasound or CT) is nondiagnostic and suspicion for UTO remains high, then percutaneous nephrostomy or cystoscopy (with antegrade urography or retrograde pyelography, respectively) should be performed.
●Kidney ultrasound in most patients – A kidney ultrasound is the preferred initial test to diagnose or exclude UTO, unless a stone is suspected. An unenhanced CT scan is indicated in addition to and following the ultrasound when the kidneys cannot be adequately visualized by ultrasound or when ultrasound is unable to identify the cause of ureteral obstruction. (See 'Additional imaging to identify etiology' below.)
Ultrasound is safe and relatively inexpensive, and a negative study essentially excludes a diagnosis of UTO. In three observational studies of patients with suspected UTO, ultrasound revealed hydronephrosis in 97 of 102 kidneys that were confirmed to be obstructed by excretory urography (ie, sensitivity was 95 percent and false-negative rate was 5 percent) [37-39]. However, of the five false-negative ultrasounds, two kidneys were obstructed by staghorn kidney stones and one kidney could not be well visualized because of bowel gas. Excluding those three kidneys from consideration, the false-negative rate of ultrasound to diagnose patients with suspected UTO was 2 percent.
Conversely, ultrasound detected hydronephrosis in 27 of 250 kidneys that were not obstructed (ie, specificity was 89 percent and false-positive rate was 11 percent); these data reflect the fact that hydronephrosis often occurs in the absence of UTO [37-39].
●Patients with suspected urinary retention – Urinary retention can cause UTO and may result from medications, general and epidural anesthesia, mechanical obstruction (eg, urethral stricture, prostatic hypertrophy or inflammation, cystocele, rectocele, pelvic mass), neurologic impairment (eg, spinal injury from trauma or stroke, epidural infection, metastasis), and other causes. It generally manifests with changes in urinary flow; typically, there is a decline or cessation of urinary flow or, rarely, an increase in urinary frequency from overflow incontinence. However, changes in urine output may not occur in chronic cases. Urinary retention can also be associated with acute kidney injury (AKI). Urinary retention is often asymptomatic, even when severe.
Urinary retention can be diagnosed by kidney and bladder ultrasound or by one of the two following methods: bedside bladder scanning (postvoid volume of 300 mL or more is consistent with urinary retention) (image 10 and image 15); and postvoid bladder catheterization (drain volume of 200 mL or more is consistent with retention). Diagnosis of urinary retention is presented in detail separately. (See "Acute urinary retention", section on 'Initial evaluation'.)
●Patients with suspected nephrolithiasis – With the exception of individuals who are pregnant, patients with suspected nephrolithiasis (eg, presenting with flank pain and hematuria) should undergo a noncontrast CT for the diagnosis. An ultrasound is the imaging modality of choice among pregnant patients or if CT is not readily available. The rationale for choosing noncontrast CT rather than ultrasound in nonpregnant patients with suspected nephrolithiasis is discussed elsewhere. (See "Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis", section on 'Diagnostic imaging' and "Kidney stones in adults: Kidney stones during pregnancy", section on 'Diagnosis in pregnancy'.)
●If clinical suspicion for UTO remains high despite nondiagnostic imaging – Occasionally, the initial imaging study (ultrasound or CT) is nondiagnostic. If suspicion of UTO remains high in a patient with nondiagnostic initial imaging, then the next appropriate step is either percutaneous nephrostomy with antegrade urography or cystoscopy with retrograde pyelography .
Nuclear medicine scans are generally not used to diagnose urinary obstruction. While they can be useful in documenting that hydronephrosis is nonobstructive and that there is function in a hydronephrotic kidney, this information can usually be obtained by CT or magnetic resonance (MR) urography.
Patients with in situ stents — Patients with patent ureteral stents who undergo an imaging study with a full bladder may have hydronephrosis. This is because the patients are usually supine and urine can flow from the bladder back into the kidneys. In patients without stents, this is normally prevented by ureteral sphincters. Thus, stent obstruction can only be diagnosed when hydronephrosis is present with an empty bladder; this is usually sufficient for the diagnosis. Of note, it is common for the ureter with the indwelling stent to be dilated, even in the absence of an obstruction.
Patients with a kidney transplant — Obstruction is a much more common cause of AKI in transplanted kidneys compared with native kidneys. The main causes of UTO in the transplanted kidney are ureteral strictures (from trauma or ischemia) [40,41], external compression by lymphoceles or hematomas (image 16), and bladder dysfunction.
Among patients with a kidney transplant, ultrasound is the modality of choice for diagnosis of UTO because ultrasound has a sensitivity of over 90 percent in such patients . Other modalities are rarely necessary since the ureter can usually be visualized in its entirety on ultrasound. As in patients with indwelling stents, the collecting system of a transplanted kidney could be mildly dilated, even in the absence of obstruction [43,44]. However, dilation of minor calyces or the proximal ureter suggests UTO.
Ureteral stent placement is common at the time of transplantation and can be associated with nonobstructive hydronephrosis due to backflow from the bladder. Often, but not always, dilation disappears when the bladder is emptied. However, most ultrasounds are performed for evaluation of acute allograft failure. A mild degree of hydronephrosis rarely, if ever, indicates obstruction as a cause of acute allograft failure . Percutaneous nephrostogram with possible stent placement is usually the next appropriate study when clinically significant ureteral obstruction is diagnosed or suspected.
Patients with chronic hydronephrosis — The diagnostic approach is similar to that for acute hydronephrosis. However, chronic obstruction can lead to atrophy of the kidney, usually apparent as small size and/or thin cortex. In these cases, interventions to relieve the obstruction are unlikely to result in improved kidney function. Nonobstructive hydronephrosis can persist in many patients. If subsequent UTO is suspected (eg, in someone with chronic hydronephrosis who presents with AKI), studies other than ultrasound or noncontrast CT, such as antegrade urography or retrograde pyelography, may be required.
Patients who are pregnant — Dilation of the collecting system and ureters in the absence of obstruction is normal in pregnancy. This begins in the first trimester and persists for a few weeks postpartum [33,34]. Thus, pregnant patients can have nonsevere hydronephrosis as a normal finding. (See "Maternal adaptations to pregnancy: Renal and urinary tract physiology", section on 'Urinary tract'.)
UTO is rare in pregnancy and is almost always due to kidney stones. The details regarding the diagnosis of nephrolithiasis in pregnancy are discussed in detail elsewhere. (See "Kidney stones in adults: Kidney stones during pregnancy", section on 'Diagnosis in pregnancy'.)
Low suspicion for UTO with incidental hydronephrosis — Nonsevere hydronephrosis may be present in the absence of UTO. Incidentally detected mild hydronephrosis in the absence of obstruction is not uncommon. Additional imaging is often not necessary in patients with normal kidney function, particularly when an explanation (eg, high urine output, pregnancy) is readily apparent.
An ultrasound finding of significant hydronephrosis that is surprising (ie, incidental hydronephrosis in someone not believed to have UTO) should be followed by additional testing to exclude true obstruction unless there is a readily apparent explanation for the hydronephrosis (eg, pregnancy, high urine output). (See 'Hydronephrosis without obstruction' above.)
In such cases, ultrasound should be repeated at a later time when it is unlikely to yield a false-positive result (eg, six weeks postpartum, during a period of normal urine output).
However, in the rare cases when there is no apparent explanation for the hydronephrosis from ultrasound and noncontrast CT, percutaneous nephrostomy with antegrade urography or cystoscopy with retrograde pyelography may be required.
ADDITIONAL IMAGING TO IDENTIFY ETIOLOGY — Once hydronephrosis is identified by ultrasound, then additional testing may be necessary to determine whether obstruction is present and to identify the cause, if not already apparent. An unenhanced CT is the next appropriate study to identify ureteral obstruction; it should also be performed when the kidneys cannot be adequately visualized by ultrasound or when the diagnosis of hydronephrosis is uncertain on ultrasound (eg, when hydronephrosis cannot be distinguished from peripelvic cysts or extrarenal pelvis). Retrograde pyelography may be necessary to establish or exclude the diagnosis in some cases, such as when the unenhanced CT is inconclusive and the patient cannot receive intravenous contrast.
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of UTO includes the findings by imaging that can mimic hydronephrosis and the nonobstructive causes of hydronephrosis. Peripelvic cysts (image 17), extrarenal pelvis (image 18), and dilated renal veins can be mistaken for hydronephrosis.
Peripelvic cysts, which are actually dilated lymphatics, can have a branching pattern similar to calyces. However, as opposed to dilated calyces, peripelvic cysts have sinus fat separating the fluid from the kidney parenchyma, and there is no accompanying dilation of the ureter.
An extrarenal pelvis is a focal dilation of the proximal ureter, often with some dilation of the major calyces. However, it can be differentiated from UTO because the minor calyces and the rest of the ureter are not dilated.
Dilated veins usually branch outside the kidney and can be followed to the vena cava. They can also be distinguished by the presence of blood flow on Doppler ultrasound.
Conditions with large diuresis (particularly arginine vasopressin disorders) and pregnancy can result in the appearance of hydronephrosis without the presence of true obstruction (see "Urine output in arginine vasopressin disorders (diabetes insipidus)" and "Maternal adaptations to pregnancy: Renal and urinary tract physiology"). Chronic vesicoureteral reflux (resulting from a congenital abnormality or as a consequence of ureteral reimplantation surgery or urinary diversion such as an ileal loop) can be associated with ureteral and calyceal dilation and can eventually result in cortical thinning as seen in chronic obstruction. This condition is best diagnosed by retrograde pyelography. Likewise, ureteral stents can allow backflow of urine into the kidney and give the appearance of hydronephrosis without presence of an obstruction.
PROGNOSIS — The prognosis of UTO depends upon the severity and duration of the obstruction. Complete UTO that is not resolved promptly or prolonged partial UTO can result in renal tubular atrophy, interstitial fibrosis, and, eventually, irreversible kidney injury [46,47]. However, a nearly complete recovery of glomerular filtration rate (GFR) can be achieved if UTO is relieved within one week, while little or no recovery can be expected after 12 weeks . The degree of recovery from UTO can also depend upon other factors, such as preexisting kidney disease, hypertension, or presence of a concomitant urinary tract infection.
Radionuclide scanning and kidney ultrasound have been used to predict the likelihood of functional recovery. Adverse prognostic findings indicative of severe and potentially irreversible disease include total nonvisualization of the obstructed kidney on radionuclide scan and marked cortical atrophy on ultrasound.
If kidney function recovers, most of the recovery occurs in the first 7 to 10 days after relief of the obstruction [47,48]. However, some patients with severe kidney function impairment may require dialysis for a period of weeks after the obstruction is relieved until there is sufficient improvement to discontinue dialysis . Such patients rarely experience complete recovery of their kidney function.
In addition to the persistent reduction in GFR, tubular function may also be impaired by chronic partial obstruction. This may be manifested by polyuria due to decreased concentrating ability from a reduction in the number of water channels and mild sodium wasting due to failure of normal salt-reabsorbing mechanisms. In addition to polyuria, patients may also have distal renal tubular acidosis [10,11,23,26]. (See "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance", section on 'Voltage-dependent RTA'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute kidney injury in adults".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Hydronephrosis in adults (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Overview – Urinary tract obstruction (UTO) occurs due to blockage of urine flow along the urinary tract and generally manifests as hydronephrosis on imaging. UTO may be acute or chronic, partial or complete, and unilateral or bilateral. Kidney function impairment from UTO, if present, is readily reversible if the obstruction is promptly corrected. Uncorrected UTO can lead to progressive kidney function impairment and end-stage kidney disease. (See 'Introduction' above.)
●Etiology – UTO can occur anywhere along the urinary tract (figure 1 and figure 2). The causes of UTO vary, in part, based upon the site of the obstruction (table 1). The causes of UTO also vary with the age of the patient. Anatomic causes (including urethral valves or stricture and stenosis at the ureterovesical or ureteropelvic junction) account for the majority of cases in children. By comparison, stones are most common in young adults, while prostatic hypertrophy or carcinoma, retroperitoneal or pelvic neoplasms, and stones are the primary causes in older patients. (See 'Etiology' above.)
●Clinical features – Other than those with stones, most patients with UTO are asymptomatic on presentation. Infrequently, patients may present with urinary urgency, hypertension, hematuria, changes in urine output, or pain. Urine output can vary from anuria (as in the setting of complete bilateral ureteral or complete urethral obstruction) to oliguria, normal urine volume, or even polyuria. An increase in serum creatinine is unusual among patients with obstruction of one of their two kidneys, unless there is underlying chronic kidney disease. However, bilateral obstruction or unilateral obstruction in a patient with a single kidney or preexisting kidney disease will lead to an increase in serum creatinine. (See 'Symptoms and signs' above and 'Laboratory findings' above.)
The radiologic hallmarks of UTO are hydronephrosis and hydroureter. Assessment of the severity of hydronephrosis is usually subjective and does not necessarily correlate with the degree of obstruction, especially in the acute setting. Obstruction with no hydronephrosis can occur early in the course of acute obstruction (usually due to a stone or bladder retention) before urine has accumulated or when urine production is reduced for other reasons, such as parenchymal kidney disease. (See 'Radiologic findings' above.)
●When to suspect UTO – The clinical suspicion for UTO is high among patients who have acute or subacute kidney failure, newly discovered chronic kidney disease, or symptoms potentially related to obstruction, and who also have one or more of the following (see 'When to have a high suspicion for UTO' above):
•Prostatic hypertrophy or prostate cancer
•Prior urologic surgery
•Known or suspected abdominal or retroperitoneal malignancy
•History of nephrolithiasis or presence of renal colic
•Profuse gross hematuria
•Prior pelvic or retroperitoneal surgery
•New lower abdominal, pelvic, or flank pain or tenderness
•Neurologic disorders affecting the bladder
•Unexplained kidney function impairment
●Diagnostic testing – In patients with suspected UTO, ultrasound of the kidneys is typically the initial test of choice to diagnose or exclude obstruction. A different initial approach is used in patients with suspected urinary retention as the cause of obstruction (ie, a bladder scan or postvoid bladder catheter should be performed first) or in nonpregnant patients with suspected nephrolithiasis (ie, noncontrast CT should usually be performed rather than an ultrasound). If the initial imaging study is nondiagnostic and suspicion for UTO remains high, then percutaneous nephrostomy with antegrade urography or cystoscopy with retrograde pyelography should be performed. Special considerations are needed when evaluating patients with in-situ ureteral stents, a kidney allograft, or in pregnant individuals. (See 'Approach to imaging' above.)
Once hydronephrosis is identified by ultrasound, noncontrast CT is typically performed to identify the cause of obstruction (unless the cause is apparent by ultrasound). Noncontrast CT is also performed if the kidneys cannot be adequately visualized by ultrasound or when the diagnosis of hydronephrosis is uncertain on ultrasound. (See 'Additional imaging to identify etiology' above.)
●Incidental hydronephrosis – Nonsevere hydronephrosis may be present in the absence of UTO. An ultrasound finding of hydronephrosis that is surprising (ie, incidental hydronephrosis in someone not believed to have UTO) should be followed by additional testing to exclude true obstruction unless there is a readily apparent explanation for the hydronephrosis (eg, pregnancy, high urine output). (See 'Low suspicion for UTO with incidental hydronephrosis' above.)
●Differential diagnosis – The differential diagnosis of UTO includes the findings by imaging that can mimic hydronephrosis and the nonobstructive causes of hydronephrosis. Peripelvic cysts (image 17), extrarenal pelvis (image 18), and dilated renal veins can be mistaken for hydronephrosis. (See 'Differential diagnosis' above.)
●Prognosis – The prognosis of UTO depends upon the severity and duration of the obstruction. Complete UTO that is not resolved promptly or prolonged partial UTO can result in renal tubular atrophy, interstitial fibrosis, and, eventually, irreversible kidney damage. (See 'Prognosis' above.)
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