Urinary Tract Obstruction

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116 Urinary Tract Obstruction

A patent urinary tract is necessary for optimal kidney function. Under normal circumstances, urine passes unimpeded from the renal pelvises to the tip of the urethra. Obstruction can occur anywhere along this pathway and may lead to both acute and progressive kidney parenchymal damage.

Several definitions may be encountered when considering urinary tract obstruction:

• Obstructive uropathy refers to disorders that interfere with drainage of the urine. Obstructive uropathy can result from pathology within the urinary tract itself (intrinsic obstruction) or from pathology originating outside the urinary tract that causes external compression of the system (extrinsic obstruction). It may be acute or chronic and either partial or complete; the resulting symptom complex typically depends on both the acuity and severity.

• Obstructive nephropathy refers to cases in which obstructive uropathy causes a decline in renal function.

• Hydronephrosis refers to dilatation of the urinary collecting system, with renal parenchymal changes. Typically, however, the term is used to describe any dilatation of the urinary tract, regardless of renal parenchymal involvement. Hydronephrosis is usually, but not exclusively, seen in obstructive disorders. Nonobstructive pathogenesis of hydronephrosis includes vesicoureteral reflux or excessive flow through the collection system, such as with habitual water drinking or diabetes insipidus.

Epidemiology

Urinary tract obstruction is a common disorder. On autopsy, 3.1% of adults have hydronephrosis.¹ Data from the Healthcare Cost and Utilization Project’s National Inpatient Sample (based on ICD-9 codes) indicate that 1.75% of all hospital discharges are complicated by either hydronephrosis or obstruction.² When hydronephrosis is excluded, urinary tract obstruction occurs in approximately 1% of hospital discharges.² Urinary tract obstruction accounts for approximately 10% of community-acquired acute kidney failure³^–⁵ and is a factor in 2.6% of acute kidney failure cases in the intensive care setting.⁶

Etiology

Many disorders may lead to urinary tract obstruction. A useful classification is to first divide causes by the level of obstruction: upper (from the renal pelvis to the ureterovesicular junction) or lower (from the bladder to the urethra) urinary tract. This approach may then be refined into intrinsic versus extrinsic causes.

Congential Causes

Congenital anomalies may result in obstruction at various levels of the urinary tract. This discussion will be limited to congenital ureteropelvic junction obstruction (UPJO), as this is the congenital disorder most likely to present in adulthood.

Congenital UPJO is usually due to disease intrinsic to the urinary tract. Often an adynamic segment of ureter results in failure of peristalsis at the ureteropelvic junction (UPJ).⁷ Ureteral kinks or valves are another intrinsic cause of UPJO. Potential extrinsic causes of UPJO include abnormal rotation of the kidney during development, leading to ureteral compression and entrapment of the ureter by blood vessels, although significant controversy exists regarding the latter.^7,⁸

Patients with UPJO often present with intermittent abdominal or flank pain, sometimes accompanied by nausea and vomiting. Alternatively, patients may present with hematuria or azotemia, or the condition may be uncovered after an imaging study done for an unrelated problem.

The widespread use of maternal prenatal ultrasound has lead to more antenatal diagnosis of UPJO. The diagnosis may be made by ultrasound, intravenous urography, or in equivocal cases, isotope renography (see later imaging section).

Acquired Causes

There are many causes of acquired obstructive uropathy which may affect the urinary tract at any location from the renal tubules to the tip of the urethra. This discussion will consider upper and lower urinary tract obstruction separately, further dividing the causes into intrinsic versus extrinsic.

Upper Urinary Tract Obstruction

Intrinsic Causes

Intrinsic urinary tract obstruction may be due to pathology within the lumen (intraluminal) or within the walls of the collecting system (intramural).

Intraluminal Causes

Obstruction at the level of the renal tubules may be due to crystal-induced disease, uric acid nephropathy (as in the tumor lysis syndrome), or cast nephropathy due to multiple myeloma. Crystal-induced nephropathy has been classically described with sulfadiazine, acyclovir, indinavir, triamterene, and methotrexate.⁹ Newer literature also implicates orlistat¹⁰ and ciprofloxacin.¹¹

Nephrolithiasis is a common cause of upper urinary tract obstruction at the level of the ureter, with the size of the stone determining the likelihood of obstruction. Stones ≤2 mm, 3 mm, 4 to 6 mm and larger than 6 mm will pass spontaneously 97%, 86%, 50%, and 1% of the time, respectively.¹² Typically the obstruction occurs at one of the three narrowest portions of the ureter: the UPJ, the ureterovesicular junction (UVJ), or at the point where the ureter crosses over the pelvic brim. The obstruction is usually, but not always, acute and symptomatic. Neoplasms, blood clots, and sloughed renal papillae are rarer causes of intrinsic obstruction at the level of the ureter.

The causes of intraluminal obstruction at the level of the bladder are similar to those affecting the ureter, with urolithiasis, blood clots, and neoplasms being most common. Worldwide, infection with Schistosoma hematobium with resulting fibrosis is a common cause of bladder obstruction.¹³ Although rare in industrialized nations, it should be suspected in patients from endemic areas such as Africa and the Middle East.

Intramural Causes

Obstruction due to intramural causes is most often seen in the lower urinary tract. Disorders affecting the neuromuscular control of bladder emptying, such as cerebrovascular accidents,¹⁴ spinal cord injury,¹⁵ multiple sclerosis,¹⁶ and diabetic neuropathy¹⁷ may lead to bladder outlet obstruction. Multiple medications, including anticholinergics, opioid analgesics, nonsteroidal antiinflammatory agents, α-adrenoreceptor antagonists, benzodiazepines, and calcium channel blockers have also been associated with urinary retention.¹⁸ Stricture of the urethra may also lead to obstruction.

One potential intramural cause affecting the upper tract is ureteral stricture due to genitourinary tuberculosis.

Extrinsic Compression

Pregnancy is typically associated with right-sided dilation of the renal pelvis, calyx, and ureter. Hormonal mechanisms and mechanical compression from an enlarging uterus and an enlarging ovarian vein plexus have been implicated in these changes.¹⁹ Clinically meaningful obstruction from the gravid uterus is extremely rare.

Malignancies may cause obstruction by several different mechanisms. Local ureteric compression may be seen in metastatic cancers of the cervix, bladder and prostate, as well as with expanding retroperitoneal soft-tissue masses. Alternatively, the ureters may be compressed or encased by metastatic retroperitoneal lymphadenopathy from a distant primary.²⁰

Retroperitoneal fibrosis may lead to obstruction of one or both ureters via inflammation. It is an uncommon disorder, with a reported incidence rate of 1.3 case per million population and a male/female ratio of 3.3 : 1.²¹ Although the majority of these cases are idiopathic (>75%),²² numerous conditions are suspected to cause retroperitoneal fibrosis, including malignancies, medications, infection, trauma, or radiation.²³ Treatment of idiopathic retroperitoneal fibrosis is initially with steroids, but recurrences are common. Case reports describe the use of cyclophosphamide, azathioprine, colchicine, mycophenolate, or tamoxifen for treatment relapses or steroid-resistant disease, although conclusive data are absent.²² Abdominal aortic aneurysms (AAA) may also cause obstruction due to compression of the ureter or via inflammation. A recent series evaluated 999 cases of inflammatory AAA and found preoperative hydronephrosis in 7.4%.²⁴

Extrinsic compression of the lower urinary tract is more common in males. The etiology is usually either benign prostatic hypertrophy or prostate cancer.

The clinician must always bear in mind that hydroureter and/or hydronephrosis may be absent in obstruction due to retroperitoneal processes. Thus, one must maintain a high degree of suspicion and use alternative imaging modalities when considering these disorders.

The etiology of urinary tract obstruction is summarized in Box 116-1.

Box 116-1

Causes of Urinary Tract Obstruction

Extrinsic Causes

Upper urinary tract:

Pregnancy

Malignancy

Retroperitoneal fibrosis

Abdominal aortic aneurysms

Lower urinary tract:

Benign prostatic hypertrophy

Prostate cancer

Clinical Presentation

The clinical presentation of urinary tract obstruction depends on the location, duration, and severity of obstruction and may therefore be quite variable.

Pain

Acute ureteral obstruction often presents with severe flank pain, otherwise known as renal colic. This is usually due to urolithiasis but may be due to other causes of ureteral obstruction (see earlier). Obstruction causes increased intraluminal pressure and spasm of the ureteral muscles, which are responsible for the colicky pain.²⁵ Partial ureteral obstruction may present with a chronic dull pain. Bladder outlet obstruction may lead to distention and subsequent abdominal discomfort.

Changes in Urine Output

One pitfall in the diagnosis of obstruction is the expectation that patients will be anuric. While true of patients with obstruction of all functioning renal mass—complete bilateral ureteral obstruction, complete obstruction of a solitary functioning kidney, or complete obstruction distal to the bladder neck—this is not the case in patients with less severe disease. The degree of urine output does not reliably predict the presence or absence of obstruction; patients may present with normal urine output or even polyuria due to the effects of obstruction on renal salt and water handling (reviewed later).

Lower Urinary Tract Symptoms

Obstruction of the lower urinary tract often presents with some or all of a predictable constellation of symptoms known collectively as lower urinary tract symptoms, or LUTS. LUTS include voiding symptoms (difficulty urinating, incomplete emptying), postmicturition symptoms (post-void dribbling), and storage symptoms (urgency, frequency, hesitancy, incontinence).²⁶ Alternatively, patients with lower urinary tract obstruction may be asymptomatic.

Kidney Dysfunction

If asymptomatic, the initial clue to underlying obstruction may be an elevated creatinine level on a blood sample drawn for an unrelated reason. The fact that urinary tract obstruction may be asymptomatic mandates its inclusion in the differential diagnosis of unexplained kidney failure. If blood work is not obtained during the course of the obstruction, the kidney function may deteriorate such that the first presentation is with uremic symptoms and need for dialysis.

Infection

The urinary retention associated with lower urinary tract obstruction provides an excellent culture medium for bacteria. Patients may present with cystitis, pyelonephritis, or sepsis. An obstructing renal stone may also be a nidus for infection. Recurrent infection should raise suspicion for possible anatomic abnormalities, especially in men. In one study, 25 out of 83 men (30%) with a febrile urinary tract infection (UTI) had anatomic lesions in the lower urinary tract, supporting imaging of the lower tract in men with this presentation.²⁷ More recent data refute this finding in men younger than 45 years old.²⁸

Laboratory Values

There are no laboratory values specific to obstruction. Blood tests may show no abnormalities or may show values consistent with kidney failure, such as elevated blood urea nitrogen, creatinine, potassium, and phosphorus levels and decreased calcium, bicarbonate, and hemoglobin values. The blood tests may also be indicative of a renal tubular acidosis (see later). The urinalysis may be bland or may include red blood cells (in the setting of a stone or malignancy) or white blood cells (in the setting of infection). An experienced observer may also be able to discern crystals in a freshly voided urine. The fractional excretion of sodium (FE_Na) may be less than 1% in acute obstruction, but it is generally greater than 1% when the obstruction is chronic, owing to renal tubular dysfunction.

Imaging in Urinary Tract Obstruction

Various imaging modalities may be used to diagnose obstruction: plain abdominal radiography, ultrasound, CT, intravenous urography, retrograde pyelography, and nuclear scanning. It is important to understand the indications and limitations of each modality.

Plain Abdominal Radiography

Abdominal radiography (kidney, ureter, and bladder [KUB]) is often the first imaging modality preformed in patients with acute flank pain. Although most stones are composed of calcium and should in theory be visible, only 59% of stones are detected on plain film.²⁹ Compared to CT scanning, the sensitivity and specificity of abdominal films were 45% to 59% and 77%, respectively.²⁹ Further, plain films may not always be able to differentiate phleboliths from calculi. This limits the utility of plain abdominal films to the diagnosis of recurrent disease in those with known radioopaque stones.

Ultrasound

Ultrasound (US) is inexpensive, does not expose the patient to radiation, and is typically readily available. Its accuracy in detecting hydronephrosis makes US a good screening tool for obstruction in the patient with unexplained kidney failure, or the patient with suspected lower urinary tract obstruction (Figure 116-1). US has been largely superseded by noncontrast CT in the detection of nephrolithiasis and stone-related obstruction. When CT is used as a reference, US has a sensitivity of 24% and a specificity of 90% for the detection of kidney stones and is likely to miss those less than 3 mm.³⁰ Another disadvantage of US compared to CT is that bowel gas may obscure visualization of the ureters.³¹ Thus despite its ability to detect hydronephrosis, US may be limited in its ability to demonstrate the cause or site of an obstruction. Other conditions such as peripelvic cysts and renal artery aneurysms may mimic hydronephrosis on US.³¹ These conditions are easily distinguished via CT scanning.

Figure 116-1 Typical appearance of a hydronephrotic kidney, showing renal pelvis and calyceal dilatation. Note the increase in kidney length (14.34 cm) compared with normal (~10-11 cm).

Features such as ureteral jets and resistive indices have been previously advocated as useful adjuncts in the diagnosis of obstruction, but evidence as to their utility is lacking. Despite its limitations, US may be the initial imaging modality of choice when radiation is contraindicated, such as in pregnant women and children.

Computed Tomography

The major utility of CT scanning as it relates to urinary tract obstruction is in the evaluation of acute flank pain and suspected nephrolithiasis (Figure 116-2). In this setting, CT offers a sensitivity of 96% and a specificity of 98% for detection of stones.³² The retroperitoneum is also well visualized, making CT ideal to detect retroperitoneal fibrosis or obstruction due to retroperitoneal lymphadenopathy. In addition to defining the anatomy of the collecting system, CT has the added benefit of visualizing other organ systems, thereby providing information regarding other conditions in the differential diagnosis of acute flank pain.

Figure 116-2 Bilateral nephrolithiasis on an unenhanced computed tomography (CT) scan. Note the staghorn appearance on the left.

One concern raised with CT scanning is the high radiation dose administered. Each CT scan is equivalent to approximately 10 KUBs.³³ Recent work has focused on lower-dose radiation protocols. One study found that lower-dose radiation CT scan (equivalent to that of a plain film) had a sensitivity of 97% and a specificity of 96% for the diagnosis of acute renal colic when compared with standard dose. The lower-dose CT was inferior at detecting stones less than 3 mm in size,³⁴ which may impair its ability to diagnose noncollecting system pathology.

Isotope Renography

In conventional renography, radiographic tracers are injected into the patient’s blood stream, and renal uptake and excretion are measured with a scintillation counter (Figure 116-3). This test provides functional information via demonstration of decreased excretion in the obstructed kidney. The sensitivity of the test may be enhanced by administering a loop diuretic prior to the scan. The increased urine flow may unmask an occult obstruction. Isotope renography may be used if obstruction is suspected clinically but hydronephrosis is absent, or to diagnose a nonobstructive cause of hydronephrosis. In this case, excretion will be normal despite the presence of the hydronephrosis. Isotope renography does not provide anatomic information.

Figure 116-3 Renogram showing left-sided obstruction. Note that both kidneys take up the tracer. On the right side, this is followed by an excretion of the tracer, whereas on the left the tracer remains at peak value.

Intravenous Urography

Intravenous urography (IVU), in which the collecting system is imaged after the administration of intravenous (IV) contrast, used to be the study of choice for patients with acute flank pain. The need to administer nephrotoxic IV contrast and the delay in obtaining information render IVU less attractive than a CT scan.³²

Retrograde Pyelography

CT scanning and US have largely superseded retrograde pyelography for the diagnosis of obstruction. Retrograde pyelography may be indicated when obstruction is highly suspected on clinical grounds, the US is negative for hydronephrosis, and the patient is unable to receive IV contrast.¹

Pathophysiology of Obstruction

Urinary tract obstruction may cause intrinsic kidney dysfunction. The most important effects are changes in renal blood flow, increased tubular hydrostatic pressure (as a result of increased ureteral pressure), and development of fibrosis in long-standing obstruction. Specific tubular derangements in sodium, water, potassium, acid, and divalent cation handling occur as well.

Changes in Renal Blood Flow and Tubular Hydrostatic Pressure

Over the last 3 decades, various animal models have demonstrated the pattern of renal blood flow and tubular hydrostatic pressure over time with obstruction. The initial renal response to obstruction follows a triphasic pattern.³⁵ During the first 2 hours of obstruction, there is an initial increase in both renal blood flow and ureteral pressure. This is followed by a brief (2-3 hour) period in which renal blood flow declines due to increased afferent arteriolar resistance, yet ureteral pressures continue to rise. Ultimately the decrease in renal blood flow leads to a decrease in ureteral pressure, with the pressure returning to normal levels by 10 to 12 hours after obstruction.³⁵ Unresolved obstruction will lead to persistent afferent arteriolar constriction and a sustained decrease in both renal blood flow and glomerular filtration rate (GFR).

The mediators of the hemodynamic responses are still under investigation. Prostaglandins may be involved in the initial vasodilation and increased blood flow, as this can be prevented with the prostaglandin inhibitor, indomethacin.³⁶ The subsequent vasoconstriction is thought to be due to a decrease in available nitric oxide resulting from decreased nitric oxide synthetase substrate.³⁵ In support of this theory are animal studies showing that the decrease in renal blood flow and GFR after obstruction may be attenuated with the administration of L-arginine, a nitric oxide precursor.³⁷ The renin-angiotensin system, in particular angiotensin II (AT II), has also been implicated as an important mediator of renal vasoconstriction during obstruction.³⁸ Identification of these mediators may result in future treatment strategies for patients with urinary tract obstruction.

Change in Glomerular Filtration Rate

The change in GFR during obstruction is directly related to changes in tubular hydrostatic pressure and renal blood flow. GFR is determined by the interaction of Starling’s forces between the glomerular capillary and the tubules. In the initial response to obstruction, GFR may decrease due to increasing tubular hydrostatic pressure, although the increased renal blood flow may attenuate this somewhat. Over time, however, the tubular hydrostatic pressure normalizes, and the decrease in renal blood flow becomes the main mechanism for the decreased GFR.

Tubular Atrophy and Fibrosis

As with all long-standing kidney diseases, prolonged obstruction is associated with the development of tubular atrophy and interstitial fibrosis. Fibrosis results from an imbalance between extracellular matrix deposition and degradation. In urinary tract obstruction, there is simultaneous overproduction of profibrotic and underproduction of antifibrotic agents. Prominent among the former is AT II. In addition to its vasoconstrictive properties, AT II also has many profibrotic actions, including up-regulation of several other profibrotic mediators such as transforming growth factor beta-1 (TGF-β₁), tumor necrosis factor alpha (TNF-α), and nuclear factor kappa B (NFκB).³⁹ Conversely, the activities of metalloproteinases and plasminogen activating inhibitor-1, both antifibrotic, are decreased during obstruction.^38,³⁹

The tubular atrophy and loss of renal mass seen with obstruction are mainly due to apoptosis, which may begin as early as 4 days after obstruction.³⁹ Many mediators are involved including, potentially, AT II.³⁹ Given the importance of the renin-angiotensin system in promoting renal injury after obstruction, antagonizing AT II would appear to be a viable strategy to attenuate injury. Although human data are lacking, animal data show benefit, provided the intervention is done after renal development is complete.³⁸

Tubular Function

Tubular responses to unilateral or bilateral obstruction differ, with bilateral obstruction (or unilateral obstruction in a patient with a solitary kidney) being much more severe and having more important clinical implications. The following discussion will be limited to bilateral obstruction. Urinary tract obstruction impairs all aspects of renal tubular function including the ability to transport sodium, potassium, and hydrogen and to regulate urine concentration.

Sodium Reabsorption

Upon release of a bilateral obstruction, sodium excretion increases five to nine times that of normal.⁴⁰ Because the GFR is also decreased due to the obstruction, fractional excretion of sodium may be 20 times higher than normal.⁴⁰ Clinically, this failure of sodium reabsorption may manifest as hypovolemia.

Animal studies have provided some insights as to the mechanisms of the abnormal sodium handling. Sodium reabsorption in the kidney is accomplished by various apical membrane transporters, which are coupled to the basolateral sodium-potassium ATPase. Many of these transporters, including the sodium/proton exchanger, sodium-phosphate cotransporter, sodium-potassium-2 chloride cotransporter, and the thiazide-sensitive cotransporter are down-regulated during and after release of obstruction.⁴¹ Recent studies suggest that the amiloride-sensitive epithelial sodium channel may be down-regulated as well.⁴² In addition to the down-regulation of transporters, up-regulation of atrial natriuretic peptide, a potent stimulus for sodium excretion, has been demonstrated during and after release of bilateral obstruction.⁴³

Renal Water Handling

Several mechanisms render the kidneys unable to either concentrate or dilute urine after release of an obstruction. Both urinary concentration and dilution require function of the sodium transporters. In the case of urinary concentration, the sodium-potassium-2 chloride cotransporter is required to establish the medullary concentration gradient needed for osmotic water movement out of the collecting tubule. Dilution requires removal of solute in both the loop of Henle and distal convoluted tubule via the sodium-potassium-2 chloride cotransporter and the thiazide-sensitive cotransporter, respectively. Osmotic diuresis due to retained solutes may also lead to an inability to conserve water.

In addition to the effects of abnormal sodium reabsorption on water metabolism in the postobstructed kidney, animal data have demonstrated a direct role of antidiuretic hormone in the concentrating defect as well. Many studies have shown a down-regulation of aquaporins in the obstructed kidney,⁴⁴^–⁴⁷ which may persist for weeks, accompanied by a long-term defect in urinary concentration.⁴⁴ Clinically, this inability to conserve water may manifest as nephrogenic diabetes insipidus and hypernatremia.

Acid-Base and Potassium Balance

Obstruction may be associated with an inability to excrete acid. Acid-base balance is accomplished by reclamation of filtered bicarbonate and excretion of acid, either as titratable acidity (buffering of hydrogen ions by phosphates, sulfates, and other buffers) or by ammonium excretion. Clinically, obstructed or postobstruction patients may have a hyperkalemic, hyperchloremic metabolic acidosis. Although this may be due solely to the decreased GFR, some patients have persistent metabolic abnormalities long after the release of obstruction and stabilization of GFR.⁴⁸ Human data reveal several pathophysiologic mechanisms. The majority of patients studied had a distal renal tubular acidosis in which systemic acidosis did not lower the urinary pH below 5.5.⁴⁸ Abnormalities in sodium transport in the distal nephron (see earlier) may render this tubular segment unable to generate the lumen negative transepithelial difference needed for proton excretion—a so-called voltage-dependent defect.⁴⁹ This voltage defect also leads to potassium retention and clinically apparent hyperkalemia. Other patients were able to acidify their urine to a pH of below 5.5. These patients had low plasma levels of aldosterone with subsequent hyperkalemia—a typical type IV renal tubular acidosis (RTA).⁴⁸ The underlying mechanism in this case is decreased ammoniagenesis, most likely due to the hyperkalemia, although the hypoaldosteronism may also contribute.⁴⁹ Patients with a type IV RTA retain the ability to excrete acid (via titratable acidity) and usually have a mild, self-limited acidosis, whereas those with a distal RTA cannot excrete acid, and the resultant acidosis may be severe.

Recent animal studies have demonstrated down-regulation of key renal acid-base transporters in urinary tract obstruction, including the cortical and medullary sodium hydrogen exchanger and several basolateral sodium-bicarbonate transporters.⁵⁰

Postobstructive Diuresis

Release of a bilateral obstruction (or unilateral obstruction of a solitary kidney) may lead to a profound diuresis. Several of the mechanisms have already been described. Defects in sodium and water handling predispose to large urinary losses of both. The osmotic load of retained solutes also contributes. Much of the diuresis is appropriate, however, in that previously retained salt and water must be excreted. Typically, a postobstructive diuresis is mild, transient, and requires no treatment. Often the degree and duration of this diuresis is worsened by overzealous saline administration in the face of a large, but potentially appropriate, urine output.

Clinical manifestations of a postobstructive diuresis which mandate treatment include volume depletion and hypernatremia (which may be managed by administration of isoosmotic and hypoosmotic fluid, respectively). Careful attention to potassium, magnesium, phosphorus, and calcium levels is warranted as well.

Other Tubular Functions

After release of bilateral obstruction, phosphorus excretion rises proportionally to sodium excretion.⁴⁰ This may be mediated by a decrease in the number of proximal sodium phosphate cotransporters.⁴¹ Magnesium excretion also rises, likely from decreased absorption in the thick ascending loop of Henle, due to a decrease in transepithelial voltage difference created by the decreased sodium-potassium-2 chloride cotransporter activity.⁴⁰ Calcium handling after obstruction is unclear and differs depending upon species studied.⁴⁰

Treatment

Management of obstructive uropathy depends on the location, severity, symptomatology, and etiology of obstruction, as well as the presence of concomitant factors such as infection or a decline in kidney function. The clinical scenario guides timing and whether initial management should be conservative or aimed at reestablishing patency of the urinary tract. A chronic asymptomatic partial obstruction does not need emergent release, whereas an acute, complete obstruction accompanied by infection, pain, or evidence of kidney dysfunction does.

Lower tract obstruction may be relieved simply by placing a urethral catheter, with subsequent evaluation by a urologist for definitive treatment. Upper urinary tract obstructions may be managed either with percutaneously inserted nephrostomy tubes or via retrograde (i.e., via cytoscope) ureteral stenting. As is the case with lower tract obstruction, subsequent urologic input for specific therapy for upper tract disease is indicated.

Factors which may cause or exacerbate obstruction, such as constipation or the use of medications associated with urinary retention, should be addressed. Other supportive measures such as antibiotics and IV hydration should be instituted if clinically warranted. The metabolic abnormalities of kidney failure, particularly hyperkalemia, should be addressed. If needed, dialysis should not be withheld while awaiting decompressive therapy.

Should the obstruction be chronic and the kidney deemed nonfunctional, it may be appropriate to proceed with nephrectomy if there is persistent pain or unresolved infection. This decision requires an estimate of the likelihood of recovery of kidney function.

Recovery of Kidney Function

Whether or not an obstructed kidney will regain function is of paramount importance to the clinician and may dictate whether aggressive interventions are indicated, or if the affected kidney should be removed. Unfortunately, data addressing this question, particularly human data, are scant. Currently there are no methods available which reliability predict kidney recovery after relief of an obstruction,⁴⁰ although one recent study found that a GFR of less than 10 mL/min in the obstructed kidney and abnormal renal perfusion (determined via isotope renography) predicted poor recovery in patients with unilateral ureteral occlusion.⁵¹

Animal studies demonstrate that the likelihood of renal recovery diminishes with longer duration of obstruction.⁴⁰ Even with recovery of GFR, there may be ongoing injury and progressive long-term kidney damage after release of obstruction, likely due to interstitial fibrosis associated with prolonged urinary tract obstruction.⁵² In humans, the cutoff point at which renal function is unlikely to return has not been determined, and partial recovery has been seen even after months of obstruction,⁵³ suggesting that all obstructions be relieved and followed by serial determinations of kidney function. If desired, a kidney biopsy may be done to assess the degree of interstitial fibrosis and provide prognostic information.