Obstructive uropathy is structural or functional hindrance of normal urine flow, sometimes leading to renal dysfunction (obstructive nephropathy). Symptoms, less likely in chronic obstruction, may include pain radiating to the T11 to T12 dermatomes and abnormal voiding (eg, difficulty voiding, anuria, nocturia, and/or polyuria). Diagnosis is based on results of bladder catheterization, cystourethroscopy, and imaging (eg, ultrasonography, CT, pyelography), depending on the level of obstruction. Treatment, depending on cause, may require prompt drainage, instrumentation, surgery (eg, endoscopy, lithotripsy), hormonal therapy, or a combination of these modalities.
Each year about 2/1000 people in the US are hospitalized for obstructive uropathy. The condition has a bimodal distribution. In childhood, it is due mainly to congenital anomalies of the urinary tract. Incidence then declines until after age 60, when incidence rises, particularly in men because of the increased incidence of benign prostatic hyperplasia (BPH) and prostate cancer. Overall, obstructive uropathy is responsible for about 4% of end-stage renal disease. Hydronephrosis is found at postmortem examination in 2 to 4% of patients.
Many conditions can cause obstructive uropathy, which may be acute or chronic, partial or complete, and unilateral or bilateral (see Table 1: Causes of Obstructive Uropathy).
The most common causes differ by age:
Obstruction may occur at any level, from the renal tubules (casts, crystals) to the external urethral meatus. Proximal to the obstruction, effects may include increased intraluminal pressure, urinary stasis, UTI, or calculus formation (which may also exacerbate or cause obstruction). Obstruction is much more common in males (usually due to BPH—see Benign Prostatic Hyperplasia (BPH)), but acquired and congenital urethral strictures and meatal stenosis occur in both males and females. In females, urethral obstruction may occur secondary to a primary or metastatic tumor or as a result of stricture formation after radiation therapy, surgery, or urologic instrumentation (usually repeated dilation).
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Pathologic findings consist of dilation of the collecting ducts and distal tubules and chronic tubular atrophy with little glomerular damage. Dilation takes 3 days from the onset of obstructive uropathy to develop; before then, the collecting system is relatively noncompliant and less likely to dilate. Obstructive uropathy without dilation can also occur when fibrosis or a retroperitoneal tumor encases the collecting systems, when obstructive uropathy is mild and renal function is not impaired, and in the presence of an intrarenal pelvis.
Obstructive nephropathy is renal dysfunction (renal insufficiency, renal failure, or tubulointerstitial damage) resulting from urinary tract obstruction. The mechanism involves, among many factors, increased intratubular pressure, local ischemia, and, often, UTI. If obstruction is bilateral, nephropathy may result in renal insufficiency. Renal insufficiency may rarely occur when obstruction is unilateral because autonomic-mediated vascular or ureteral spasm may affect the functioning kidney. The time and rate at which irreversible damage to the kidney (or kidneys) develops after obstruction depends on so many factors that it is hard to predict. To prevent irreversible damage, obstruction of the urinary tract should be diagnosed and treated as promptly as possible.
Symptoms and Signs
Symptoms and signs vary with the site, degree, and rapidity of onset of obstructive uropathy.
Pain is common when obstruction acutely distends the bladder, collecting system (ie, the ureter plus the renal calyces), or renal capsule. Upper ureteral or renal pelvic lesions cause flank pain or tenderness, whereas lower ureteral obstruction causes pain that may radiate to the ipsilateral testis or labia. The distribution of kidney and ureteral pain is usually along T11 to T12. Acute complete ureteral obstruction (eg, an obstructing ureteral calculus) may cause severe pain accompanied by nausea and vomiting. A large fluid load (eg, from beer drinking or osmotic diuresis due to an IV contrast agent) causes dilation and pain if urine production increases to a level greater than the flow rate through the area of obstruction. Pain is typically minimal or absent with partial or slowly developing obstructive uropathy (eg, congenital ureteropelvic junction obstruction, pelvic tumor). Hydronephrosis may occasionally cause a palpable flank mass, particularly in massive hydronephrosis of infancy and childhood.
Urine volume does not diminish in unilateral obstruction unless it occurs in the only functioning kidney (solitary kidney). Absolute anuria occurs with complete obstruction at the level of the bladder or urethra. Partial obstruction at that level may cause difficulty voiding or abnormalities of the urine stream. In partial obstruction, urine output is often normal and is rarely increased. Increased urine output with polyuria and nocturia occur if the ensuing nephropathy causes impaired renal concentrating capacity and Na reabsorption. Long-standing nephropathy may also result in hypertension.
Infection complicating obstruction may cause dysuria, pyuria, urinary urgency and frequency, referred kidney and ureteral pain, costovertebral angle tenderness, fever, and, occasionally, septicemia.
Obstructive uropathy should be considered in patients with any of the following:
The history may suggest symptoms of BPH, prior cancer (eg, prostate, kidney, ureteral, bladder, gynecologic, colorectal), or urolithiasis. Because early relief of obstruction usually achieves the best outcome, diagnosis should be as rapid as possible.
Urinalysis and serum chemistries (serum electrolytes, BUN, creatinine) should be done. Other tests are done depending on symptoms and suspected level of obstruction. Infection with urinary obstruction requires immediate evaluation and treatment.
In an asymptomatic patient with long-standing obstructive uropathy, urinalysis may be normal or reveal only a few casts, WBCs, or RBCs. In a patient with acute renal failure who has a normal urinalysis, bilateral obstructive nephropathy should be considered.
If serum chemistries indicate renal insufficiency, obstruction is probably bilateral and severe or complete. Other findings in bilateral obstruction with nephropathy may include hyperkalemia. Hyperkalemia may result from type 1 renal tubular acidosis due to decreased hydrogen ion and K secretion by distal segments of the nephron.
Evaluation of suspected urethral obstruction:
If urine output is diminished or if there is a distended bladder or suprapubic pain, bladder catheterization should be done. If catheterization results in a normal flow of urine or if the catheter is difficult to pass, a urethral obstruction (eg, prostatic enlargement, urethral valve, or urethral stricture) is suspected. In the absence of palpable bladder distention and inability to void, obstruction can be confirmed by bedside ultrasonography to determine bladder volume after voiding; volume of > 50 mL (slightly higher among older adults) suggests obstruction. Patients with such findings should have cystourethroscopy and children should usually have voiding cystourethrography.
Voiding cystourethrography (VCUG) shows nearly all bladder neck and urethral obstructions as well as vesicoureteral reflux, adequately displaying the anatomy and the volume of urine left in the bladder after voiding (postvoiding residual volume). It is most commonly done in children to diagnose anatomic or congenital abnormalities. However, it may be done in adults if a urethral stricture is suspected.
If symptoms of urethral obstruction are absent or if cystourethroscopy and voiding cystourethrography show no obstruction, the site of obstruction is presumed to be at the ureters or proximal to them.
Evaluation of ureteral or more proximal obstruction:
Patients undergo imaging tests to detect the presence and site of obstruction. The choice and sequencing of tests depend on the clinical scenario.
Abdominal ultrasonography is the initial imaging test of choice in most patients without urethral abnormalities because it avoids potential allergic and toxic complications of contrast agents and allows assessment of associated renal parenchymal atrophy. Ultrasonography is aimed at detection of hydronephrosis. However, the false-positive rate is 25% if only minimal criteria (visualization of the collecting systems) are considered in the diagnosis. Also, absence of hydronephrosis (and false-negative results) can occur if obstruction is early (in the first few days) or mild or if retroperitoneal fibrosis or tumor encases the collecting system, preventing dilation of the ureter.
CT (see Computed Tomography) is sensitive for diagnosing obstructive nephropathy and is used when obstruction cannot be shown by ultrasonography or by intravenous urography. Unenhanced helical CT is the modality of choice for obstruction due to ureteral calculi. CT urography done with and without contrast is particularly useful in the evaluation of hematuria. Thinning of the renal parenchyma suggests more chronic obstruction.
Duplex Doppler ultrasonography can usually show unilateral obstructive uropathy in the first few days of acute obstruction before the collecting system dilates by detecting an increased resistive index (a reflection of increased renal vascular resistance) in the affected kidney (see Ultrasonography). This modality is less useful in obesity and in bilateral obstruction, which cannot be distinguished from intrinsic renal disease.
Excretory urography (contrast urography, intravenous pyelography [IVP], intravenous urography [IVU]) has been largely superseded by CT and MRI (with or without contrast). However, when CT cannot identify the level of obstructive uropathy and when acute obstructive uropathy is thought to be caused by calculi, sloughed papillae, or a blood clot, IVU or retrograde pyelography may be indicated.
Antegrade or retrograde pyelography is preferred to studies that involve vascular administration of contrast agents in patients with azotemia. Retrograde studies are done through a cystoscope, whereas antegrade studies require placement of a catheter into the renal pelvis percutaneously. Patients with intermittent obstruction should be studied when they are having symptoms; otherwise, the obstruction may be missed.
Radionuclide scans also require some renal function but can detect obstruction without the use of contrast agents (see Radionuclide Scanning). When a kidney is assessed as nonfunctioning, a radionuclide scan can determine perfusion and identify functional renal parenchyma. Because this test cannot detect specific areas of obstruction, it is mainly used in conjunction with diuresis renography to evaluate hydronephrosis without apparent obstruction.
MRI (see Magnetic Resonance Imaging) can be used when avoiding ionizing radiation is important (eg, in young children or pregnant women). However, it is inferior in accuracy to ultrasonography or CT, particularly in detection of calculi.
Evaluation of hydronephrosis without apparent obstruction:
Testing may be necessary to determine whether back or flank pain is caused by obstruction in patients who have hydronephrosis but no obvious obstruction revealed by other imaging tests. Testing may also be done to detect otherwise unrecognized obstruction in patients with incidentally recognized hydronephrosis.
In diuretic renography, a loop diuretic (eg, furosemide 0.5 mg/kg IV) is given before a radionuclide renal scan. The patient must have sufficient renal function to respond to the diuretic. If obstruction is present, the rate of washout of the radionuclide (or contrast agent) from the time the tracer appears in the renal pelvis is reduced to a half-life of > 20 min (normal is < 15 min). On rare occasions, if the renogram is negative or equivocal but the patient is symptomatic, a perfusion pressure flow study is done via percutaneous insertion of a catheter into the dilated renal pelvis, followed by fluid perfusion into the pelvis at 10 mL/min. The patient is in a prone position. If obstructive uropathy is present, in spite of the marked increase in urine flow, the rate of washout of the radionuclide during renal scanning is delayed, and there will be further dilation of the collecting system and elevation of the renal pelvic pressure to > 22 mm Hg during perfusion. A renogram or perfusion study that causes pain similar to the patient's initial complaint is interpreted as positive. If the perfusion study is negative, the pain probably has a nonrenal cause. False-positive and false-negative results are common for both tests.
Most obstruction can be corrected, but a delay in therapy can lead to irreversible renal damage. How long it takes for nephropathy to develop and how reversible nephropathy is vary depending on the underlying pathology, the presence or absence of UTI, and the degree and duration of the obstruction. In general, acute renal failure due to a ureteral calculus is reversible, with adequate return of renal function. With chronic progressive obstructive uropathy, renal dysfunction may be partially or completely irreversible. Prognosis is worse if UTI remains untreated.
Treatment consists of eliminating the obstruction by surgery, instrumentation (eg, endoscopy, lithotripsy), or drug therapy (eg, hormonal therapy for prostate cancer). Prompt drainage of hydronephrosis is indicated if renal function is compromised, UTI persists, or pain is uncontrollable or persistent. Immediate drainage is indicated if obstruction is accompanied by infection. Lower obstructive uropathy may require catheter or more proximal drainage. Indwelling ureteral catheters can be placed for acute or long-term drainage in selected patients. Temporary drainage using a percutaneous nephrostomy technique may be needed in severe obstructive uropathy, UTI, or calculi. Intensive treatment for UTI and renal failure is imperative.
In the case of hydronephrosis without evident obstruction, surgery should be considered if the patient has pain and a positive diuretic renogram. However, no therapy is necessary in an asymptomatic patient with a negative diuretic renogram or with a positive diuretic renogram but normal renal function.
Last full review/revision March 2014 by Glenn M. Preminger, MD
Content last modified March 2014