INTRODUCTION — Obstruction to urinary flow may occur at any site in the urinary tract. Urinary tract obstruction (UTO) may be acute or chronic, partial or complete, and unilateral or bilateral. UTO is important to recognize since it is readily reversible if quickly corrected. If uncorrected, UTO may predispose to urinary tract infection (UTI) and even severe UTI with associated sepsis and eventually cause end-stage renal disease (ESRD).

This topic reviews the diagnosis of UTO and hydronephrosis in adults. Hydronephrosis in infants and children is discussed elsewhere. (See "Congenital ureteropelvic junction obstruction" and "Primary megaureter in infants and children" and "Clinical presentation and diagnosis of posterior urethral valves".)

UTI that occurs as a result of nephrolithiasis is also discussed elsewhere. (See "Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis".)

EPIDEMIOLOGY — UTO is a common problem but a relatively rare cause of significant acute kidney injury (AKI). While there are no extensive published epidemiologic data, based upon our combined clinical experience, it is clear that the incidence of UTO varies considerably with the patient population. As an example, UTO is more common among children than among adults presenting with urinary tract symptoms or renal failure because of the contribution of congenital abnormalities. UTO is more common among men than women, particularly as men age, due to prostatic enlargement.

Overall, UTO is not a common cause of renal 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 causes of renal failure. UTO is a rare cause of AKI in the hospital setting but is more common in the outpatient setting [1]. UTO is always an important cause of renal failure in patients with cancer.

ETIOLOGY — UTO can occur anywhere along the urinary tract. The anatomy of the genitourinary system is shown in the figures (figure 1 and figure 2). Each renal papilla secretes urine into a minor calyx, with the infundibula of the minor calyces converging into two or three major calyces (figure 1). 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, and, in males, is surrounded by the prostate gland (figure 2) [2].

The causes of UTO vary in part based upon the location of the obstruction (table 1).

●Obstruction within the kidney causes dilatation of individual calyces or caliectasis. Potential causes of intrarenal obstruction include kidney stones, transitional cell carcinoma, blood clots, and sloughed papillae (image 1).

●Obstruction at or distal to the renal pelvis causes diffuse caliectasis or hydronephrosis. Ureteral obstruction may result from stones, transitional cell carcinoma, external compression (tumors, enlarged lymph nodes, retroperitoneal fibrosis), blood clots, and fungus balls. When obstruction has been relieved with a stent, obstruction of the stent can lead to recurrent hydronephrosis.

Bladder tumors can obstruct one or both ureters or ureteral orifices. The most common causes of bilateral obstruction include bladder outlet obstruction (from prostatic enlargement or posterior urethral valves) and neurogenic bladder (image 2). In women, uterine, cervical, or ovarian cancer should be considered when unilateral or bilateral hydronephrosis is detected.

The causes of UTO also vary with the age of the patient. Anatomic abnormalities (including urethral valves or stricture and stenosis at the ureterovesical or ureteropelvic junction) account for the majority of cases in children. In comparison, calculi are most common in young adults, while prostatic hypertrophy or carcinoma, retroperitoneal or pelvic neoplasms, and calculi are the primary causes in older patients [3,4].

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'.)

CLINICAL PRESENTATION

Overview — 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 [3]. Generally, patients present with one of more of the following symptoms and signs:

●Pain

●Change in urine output

●Hypertension

●Hematuria

●Increased serum creatinine

Symptoms and signs — Pain is frequently absent, even in acute obstruction, and, when present, usually results from bladder distension, secondary infection, or obstructing stones or masses. Hydronephrosis alone is almost always asymptomatic, and pain should prompt a consideration of additional diagnoses such as stones, papillary necrosis, or infection.

Relatively severe pain (renal or ureteral colic) may be seen with acute complete obstruction (as with a ureteral calculus). However, with external ureteral compression leading to UTO, pain is usually absent because of the slowly progressive course of obstruction.

A normal urine output does not rule out UTO. Urine output may be quite variable, ranging from anuria with complete bilateral ureteral or complete urethral obstruction to oliguria, normal volume, or even polyuria. Polyuria, even in the presence of reduced glomerular filtration rate (GFR), may result from tubular injury, with impairment of the ability of tubules to retain salt and concentrate the urine [5,6]. In addition, urethral obstruction may lead to bladder distention and overflow incontinence, which may result in frequency, urgency, nocturia, and a sensation of polyuria. (See "Medical treatment of benign prostatic hyperplasia".)

In this setting, an enlarged bladder can often be detected by careful percussion of the pelvis and lower abdomen. In severe cases, there may be abdominal distension.

There are no pathognomonic findings associated with obstruction proximal to the bladder (upper tract obstruction), although costovertebral tenderness may be present.

Patients may be normo- or hypertensive. Hypertension, when present, may be due to retained salt and water in the setting of oligoanuria or due, in some cases, to activation of the renin-angiotensin system. If the hypertension is due to volume retention, it responds promptly to restoration of urine flow. Activation of the renin-angiotensin system may occur because of reflex vasoconstriction of afferent glomerular capillaries in the obstructed kidney; this may be relieved by relief of the obstruction. In unilateral obstruction, renal vein renin studies have shown increased renin release from the obstructed kidney and reduced renin release from the unobstructed kidney [7,8].

UTO may be associated with urinary tract infection (UTI) and, occasionally, severe UTI with associated sepsis. UTI that is associated with obstruction is discussed elsewhere. (See "Acute complicated urinary tract infection (including pyelonephritis) in adults".)

Characteristic laboratory findings

Increased serum creatinine — In general, obstruction of a single kidney, while the contralateral kidney is normal and not obstructed, does not lead to a perceptible increase in creatinine. However, bilateral obstruction or unilateral obstruction in the presence of underlying kidney disease will lead to an increase in creatinine. Such an increase, often detected incidentally, may be the first indication of obstruction.

There are rare reports of unilateral obstruction that is associated with anuria and acute kidney injury (AKI) [9]. Vascular or ureteral spasm mediated by autonomic activation was thought to underlie the loss of function in the nonobstructed kidney in reported cases. However, lesions involving the contralateral kidney, such as acute tubular necrosis (ATN), cannot be excluded.

Hematuria and pyuria — The urinalysis may be relatively normal or reveal only a few white cells or red cells [3]. However, as noted above, significant hematuria may be present, depending on the cause of obstruction.

Hyperkalemic renal tubular acidosis — Patients with chronic obstruction often have a hyperkalemic, distal renal tubular acidosis, possibly due to mineralocorticoid resistance with impaired distal Na resorption and loss of the lumen-negative potential difference due to reduced activities of transporter proteins, such as apical Na/K/2Cl cotransporters, sodium channels, and basolateral Na-K-ATPase [4,10]. (See "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance".)

Other laboratory tests are generally not helpful in distinguishing obstruction from other causes of renal failure.

DIAGNOSIS

Overview — Early diagnosis of UTO is important since most cases can be corrected and a delay in therapy can lead to irreversible renal injury. (See 'Predicting recovery' below.)

The diagnosis of UTO is made by imaging, which should be performed in all patients who present with acute kidney injury (AKI) of unknown cause. Imaging is rarely useful in patients in whom another cause of AKI is likely [1]. Occult UTO should be ruled out by imaging in all patients with chronic kidney disease (CKD).

Ultrasound is the preferred imaging test for most patients since it is safe and relatively inexpensive. However, ultrasound is associated with a high false-positive rate of 26 percent due to the fact that mild hydronephrosis can be present in the absence of obstruction [11,12] . The positive predictive value is 70 percent in patients with a clinical suspicion [11] but can be as low as 6 percent for mild hydronephrosis as an incidental finding [12]. The value of ultrasound is primarily in ruling out obstruction, with a negative predictive value of 98 percent [11].

A bladder ultrasound can also diagnose or exclude urinary retention (image 3). Some clinicians use a bladder ultrasound exclusively to diagnose urinary retention and believe that it completely eliminates the need for diagnostic catheterization. However, other clinicians elect to use bladder catheterization both to diagnose and relieve obstruction. The advantage to using a bladder ultrasound rather than catheterization for diagnosis is that, if negative, a bladder ultrasound eliminates the need for catheterization and the patient discomfort associated with the procedure. However, a bladder ultrasound may not be immediately available in some places, and, in such cases, a straight catheterization will diagnose obstruction and, if obstruction is present, relieve the discomfort associated with a full bladder. A straight catheterization may also allow one to obtain a urine sample, which, by analysis of sediment, may allow the diagnosis of other nonobstructive causes of AKI.

For most patients, computed tomography (CT) is not appropriate as an initial diagnostic test, since it exposes the patient to radiation. However, CT should be the initial study when an obstructing stone is suspected, such as in patients with characteristic symptoms and signs (severe flank pain, nausea, vomiting dysuria, urgency, and gross hematuria) and strong risk factors (prior history or family history of nephrolithiasis) (see "Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis"). Also, CT may be required for patients with autosomal dominant polycystic kidney disease, in whom stones and hydronephrosis can be difficult to detect by sonography.

If an obstructing stone is suspected, a noncontrast CT is preferred. (See "Kidney stones in adults: Diagnosis and acute management of suspected nephrolithiasis".)

In patients who a low pretest probability of UTO, a negative ultrasound is sufficient to exclude a diagnosis of chronic obstruction or to exclude acute obstruction as a cause of renal failure. However, if the clinical suspicion is high, as in a patient with a history of abrupt cessation of urine flow, a negative ultrasound does not rule out UTO. Obstruction may occur without apparent hydronephrosis, for example, early in the course of obstruction or when retroperitoneal processes restrict the ability of the ureters to dilate. CT is indicated after the ultrasound when the kidneys cannot be adequately visualized by ultrasound or to determine cause when the ultrasound suggests ureteral obstruction. In some cases, retrograde urography may be necessary to establish or rule out the diagnosis.

Magnetic resonance imaging (MRI) may be an alternative to CT [13] since it does not expose patients to radiation and has a diagnostic yield similar to CT, whether performed with gadolinium [14] or without [15]. However, stones are poorly visualized by MR. Among patients with moderate to severe renal disease, particularly those requiring dialysis, the administration of gadolinium during MRI has been strongly linked to an often severe disease called nephrogenic systemic fibrosis. As a result, it is recommended that gadolinium-based imaging be avoided, if possible, in patients with an estimated glomerular filtration rate (eGFR) <30 mL/min. Opinion among experts differs as to whether or not one would expose patients with an eGFR of 30 to 60 mL/min to gadolinium. (See "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease".)

Radiographic findings — The hallmark of urinary obstruction is dilatation of the collecting system in one or both kidneys. This is readily apparent on sonograms because the hypoechoic fluid displaces the echogenic sinus fat (image 4) [2]. On CT, the urine has greater attenuation than the sinus fat but only slightly less than the renal parenchyma (image 5). On contrast-enhanced scans, the parenchyma is considerably brighter than the urinary space (image 6) until the excretory phase, when contrast fills the collecting system (image 7). Usually, the minor and major calyces and the renal pelvis are dilated, but dilation of the minor calyces may not be apparent early.

A grading system has been applied to the severity of hydronephrosis [2]. In grade 1, there is minimal separation of the central sinus fat by fluid. In grade 2, the separation of sinus fat by fluid extends out from the central area in a branching, calyceal pattern but not to the parenchyma (ie, there is continuity of the sinus fat). Extension to the parenchyma (or discontinuity of the sinus fat) indicates grade 3 hydronephrosis and generally represents dilatation of the minor calyces.

This grading system is rarely of clinical utility. Grade 1 can occur with significant obstruction, while grade 3 can occur in the absence of obstruction.

In addition to the collecting system, it is important to evaluate the parenchyma since cortical thinning often indicates chronic obstruction (image 8 and image 9). However, acute obstruction in a patient with CKD could have a similar appearance. A paper-thin parenchyma indicates longstanding obstruction, relief of which is unlikely to improve renal function. The most extreme example of this is congenital ureteropelvic obstruction, in which the kidney is recognizable only as a collection of cysts (image 10).

Dilation of the proximal ureter (image 11) without a distended bladder indicates obstruction of the ureter, which can be further delineated by CT scanning (image 12). Dilation of the distal ureter without bladder distension indicates obstruction of the ureteral orifice, usually due to a stone or bladder carcinoma (image 13). Patent ureteral stents can also result in hydronephrosis due to transmission of pressure from the bladder. Thus, stent obstruction can only be diagnosed when hydronephrosis is present with an empty bladder (image 14) . Bladder outlet obstruction is frequently caused by prostatic enlargement, which often can be detected on the bladder sonogram (image 15). The pulsatile movement of urine into the bladder (ureteral jets) can often be detected by B-mode sonography and, particularly, Doppler ultrasound (image 16). However, although the presence of jets indicates patency of the ureter, their absence is not definitive proof of obstruction.

Obstruction with minimal hydronephrosis may be observed in early acute obstruction (usually by a stone) before accumulation of urine occurs (image 17) or when urine production is reduced for other reasons, such as parenchymal renal disease [16-19] or in the setting of retroperitoneal fibrosis, which restricts the ability of the ureters to dilate.

Percutaneous nephrostomy and antegrade urography are not used as initial diagnostic tests, although they are commonly performed after ureteral obstruction is detected in order to relieve the obstruction and may be done to establish a diagnosis of obstruction among patients who are at very high risk for obstruction and who have a nondiagnostic CT or ultrasound [16]. Nuclear medicine scans are not used to diagnose urinary obstruction, although they can be useful in documenting that hydronephrosis is nonobstructive or determining the function of a hydronephrotic kidney. However, this information can usually be obtained by CT or MR urography.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of UTO generally includes all causes of acute or chronic kidney injury (CKD) in the setting of a benign urinalysis and absent proteinuria. (See "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".)

Among patients who present with anuria, the differential diagnosis is much more limited. Although the urine volume can be reduced in any form of renal disease, anuria is most often seen in two conditions: complete bilateral UTO and shock. Other, less common causes of anuria are the hemolytic-uremic syndrome, renal cortical necrosis, bilateral renal arterial obstruction, and crescentic or rapidly progressive glomerulonephritis, particularly anti-glomerular basement membrane (GBM) antibody disease. (See appropriate topic reviews.)

Among patients who present with ultrasound findings of UTO, the differential diagnosis includes peripelvic cysts (image 18 and image 19 and image 20), extrarenal pelvis (image 21), and dilated renal veins. Peripelvic cysts are actually dilated lymphatics within the renal pelvis and can usually be distinguished from hydronephrosis because neither the minor calyces nor the proximal ureter are dilated (image 18). Extrarenal pelvis is a focal dilatation of the proximal ureter, often with some dilatation of the major calyces. However, the minor calyces and the rest of the ureter are not be enlarged. 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.

HYDRONEPHROSIS WITHOUT OBSTRUCTION — Hydronephrosis does not always indicate urinary obstruction. A large diuresis can distend the intrarenal collecting system [20,21], but this rarely produces sizable hydronephrosis, except in the case of nephrogenic diabetes insipidus, particularly congenital disease. (See "Treatment of nephrogenic diabetes insipidus", section on 'Special considerations in hereditary disease'.)

Most other nonobstructive hydronephrosis is only mild or moderate [12,22]. Most notable of these is pregnancy, in which dilatation of the collecting system and ureters begins in the first trimester and persists for a few weeks postpartum [23,24]. (See "Maternal adaptations to pregnancy: Renal and urinary tract physiology".)

URINARY OBSTRUCTION IN TRANSPLANTED KIDNEYS — Obstruction is a much more common cause of acute kidney injury (AKI) in transplanted kidneys compared with native kidneys, and, as opposed to native kidneys, imaging should be performed in most cases of AKI. Ultrasound is the modality of choice for diagnosis, with a sensitivity over 90 percent [25]. Other modalities are rarely indicated since the entire ureter can usually be visualized. The principal causes of UTO in the transplanted kidney are ureteral strictures secondary to trauma or ischemia [26,27], external compression by lymphoceles (image 22), and bladder dysfunction.

Among transplant recipients, the collecting system is frequently visualized and sometimes dilated in the absence of obstruction [28,29]. Often, but not always, dilatation disappears when the bladder is emptied. Mild degrees of hydronephrosis rarely, if ever, indicate obstruction as a cause of acute allograft failure [30]. Ureteral stents are commonly placed during transplantation and must always be considered as a cause of nonobstructive hydronephrosis. As with native kidneys, percutaneous nephrostomy is usually the next appropriate study after ureteral obstruction is diagnosed or suspected.

PROGNOSIS AND RECOVERY OF RENAL FUNCTION — It is clear that complete or prolonged partial UTO can lead to tubular atrophy, interstitial fibrosis, and, eventually, irreversible renal injury [31,32]. The renal prognosis after relief of UTO is dependent upon the severity and duration of the obstruction. With total ureteral obstruction, for example, there is evidence that relatively complete recovery of glomerular filtration rate (GFR) can be achieved if obstruction is relieved within one week, while little or no recovery occurs after 12 weeks [32].

However, measurement of the GFR probably overestimates the true degree of recovery. In a rat model, in which complete unilateral ureteral obstruction was induced for only 24 hours, approximately 15 percent of nephrons were nonfunctional as late as 60 days after release, a presumed reflection of irreversible injury [33]. 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 since it has been demonstrated in other diseases such as lupus nephropathy [34].

The course of partial obstruction is less predictable. It clearly depends on the severity and duration of the obstruction, as well as other potential complicating factors, such as hypertension, infection, or pre-existing renal disease. It is not uncommon, for example, to see an adult who is noted to have moderate or even massive hydronephrosis due to previously unsuspected ureteropelvic junctional obstruction. In this setting, pain may occur only during periods of high fluid intake, when the urine flow rate exceeds the rate at which urine can flow through the obstructed area. Correction of the obstruction may not be necessary if the patient is largely asymptomatic, the plasma creatinine concentration is normal, and there seems to be little or no parenchymal atrophy on renal ultrasonography.

The mechanism by which UTO leads to irreversible renal injury and atrophy is incompletely understood. Following the onset of obstruction, there is an initial increase in pressure proximal to the obstruction due to continued glomerular filtration [35]; this rise in pressure is eventually responsible for the dilatation of the collecting systems that can be detected by renal ultrasonography or computed tomography (CT) scanning.

The elevation in pressure is also transmitted back to the proximal tubule, thereby lowering the GFR by counteracting the high intraglomerular pressure that normally drives glomerular filtration. However, the rise in intratubular pressure induces secondary renal vasoconstriction and an often marked reduction in glomerular blood flow [6,35]. This response is regulated locally by individual obstructed nephrons and is mediated in part by the release of angiotensin II and thromboxanes [35-37]. It can be viewed as an appropriate physiologic adaptation since the increase in local glomerular resistance shunts blood flow away from obstructed nonfunctioning nephrons [36].

The net effect is that the chronic reduction in GFR is due primarily to the decrease in renal perfusion; as a result, the elevated intratubular pressures slowly fall toward normal [35,38]. Studies in which renal pelvic pressures were monitored suggest that a similar process occurs in humans [39].

Thus, the tubular injury that occurs with UTO may be mediated initially by the increase in intratubular pressure and later by atrophy induced by ischemia and/or inflammation [35,40]. The importance of increased intrarenal pressure is supported by findings in obstructed animals that the associated tubular dysfunction can be ameliorated, but not prevented, by renal decapsulation, which limits the rise in pressure [41].

The injury that is independent of pressure may be due both to ischemia and to the influx of inflammatory cells. The obstructed kidney appears to release substances that are chemotactic for monocytes and macrophages [35,42,43]. 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 [42]. Further support for a role for TGF-beta is provided by experimental data suggesting that administration of a TGF-beta inhibitor suppresses fibrosis in obstructive uropathy [44].

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 restoration of renal function when the obstruction is relieved [45].

Predicting recovery — As a result of the unreliability of clinical indices, radionuclide scanning and renal ultrasound have been used in an attempt to predict the likelihood of functional recovery. Adverse prognostic findings thought to be indicative of severe and usually irreversible disease include total nonvisualization on renal scan and marked cortical thinning on ultrasonography.

Most of the functional recovery will usually be seen in the first 7 to 10 days after relief of the obstruction [32,46]. However, some patients with severe renal failure may, after the obstruction is relieved, require dialysis for a period of weeks, until sufficient improvement occurs to allow dialysis to be discontinued [47]. Only partial recovery is seen in this setting, with the plasma creatinine concentration generally stabilizing at a value above 3 mg/dL (264 micromol/L).

In addition to the persistent reduction in GFR, tubular function may also be impaired by chronic obstruction. This may be manifested by polyuria due to decreased concentrating ability (because of decreased expression of water channels), mild sodium wasting, the severity of which is usually limited by the low filtration rate and by distal renal tubular acidosis, with hyperkalemia due to diminished distal hydrogen and potassium secretion [6,35,48,49]. (See "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance".)

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 5^th to 6^th 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 10^th to 12^th 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

●Urinary tract obstruction (UTO) is a readily reversible cause of kidney injury that is important to recognize. If uncorrected, UTO may predispose to urinary tract infection (UTI) and even severe UTI with associated sepsis and eventually cause end-stage renal disease (ESRD). (See 'Introduction' above.)

●UTO can occur anywhere along the urinary tract. The anatomy of the genitourinary system is shown in the figures (figure 1 and figure 2). (See 'Etiology' above.)

●The clinical presentation of UTO depends upon the site of obstruction, the degree of obstruction (ie, partial or complete), and the rapidity with which obstruction develops. Signs and symptoms include pain, a change in urine output, hematuria, and an increased serum creatinine. Hypertension may be present, and, among patients with bladder outlet obstruction, a distended lower abdomen or an apparent abdominal mass may be detected. The urinalysis may show hematuria, but the sediment is generally benign. (See 'Symptoms and signs' above.)

●The diagnosis is made by imaging, and ultrasound is the modality of choice. Imaging should be performed in all patients who present with renal insufficiency of unknown cause but is not necessary in patients in whom another cause of renal failure is apparent. For most patients, a negative ultrasound is sufficient to exclude a diagnosis of obstruction. A computed tomography (CT) is indicated among patients with acute flank pain and suspected nephrolithiasis or among patients in whom visualization of the ureters is required. (See 'Diagnosis' above.)

●Complete or prolonged partial UTO can lead to tubular atrophy and, eventually, irreversible renal injury. The renal prognosis after relief of UTO is dependent upon the severity and duration of the obstruction. (See 'Prognosis and recovery of renal function' above.)