Urinary tract obstruction is a common problem encountered by nephrologists, urologists, primary care physicians, hospitalists, and emergency medicine physicians. Obstruction can occur at any point in the urinary tract from the kidneys to the urethral meatus. It may develop secondary to calculi, tumors, strictures, anatomic abnormalities, or functional abnormalities.

Functionally, urinary tract obstruction can be divided into upper and lower urinary tract etiologies. The upper tract consists of the kidneys, the ureteropelvic junction (UPJ), ureters, and the ureterovesical junction (UVJ). The lower urinary tract consists of the bladder, the bladder neck, the urethra, the urethral meatus, and, in male patients, the prostatic urethra. Each entity has its own causes of urinary tract obstruction along with its own set of symptoms and treatments to relieve obstruction.

Obstructive uropathy can result in pain, urinary tract infection (UTI), a loss of renal function, sepsis, or death. Thus, suspected cases of urinary tract obstruction merit a consultation with a specialist for an evaluation. Because long-term obstruction can lead to irreversible damage to the function of the nephron, early detection is essential to preserving renal function. The principles of treatment are identification and a relief of the obstruction.

The incidence of hydronephrosis reported by Bell¹ in a series of 32,360 autopsies was 3.8% (3.9% in males, 3.6% in females). The incidence of clinical manifestations of obstructive uropathy prior to death was not reported, and it is likely that hydronephrosis was an incidental autopsy finding in many of these patients. The incidence of hydronephrosis at autopsy is somewhat lower in children than in adults, at 2% in one series of 16,000 autopsies.² Over 80% of children with hydronephrosis at autopsy were less than 1 year old with the balance of childhood cases being distributed uniformly through the childhood years. In women, hydronephrosis is more likely to occur between the ages of 30 to 70 years secondary to pregnancy and gynecologic malignancies. In men, hydronephrosis is most likely to occur after the age of 60 secondary to prostatic obstruction from benign prostatic hyperplasia.³

Urinary tract obstruction impedes the flow of urine from the kidney to the urethral meatus. This obstruction causes distention of the urinary tract proximal to the point of obstruction. This distention is caused by the increase in intraluminal pressure and can result in pain, which may be the first sign of obstruction. Distortion of the urinary tract and renal failure can develop from obstruction. The severity of damage depends on the degree and duration of obstruction. When the urinary tract is obstructed, urinary stasis develops predisposing the patient to acute or chronic renal failure, UTI, sepsis, or death.

The clinical presentation of urinary tract obstruction varies with the location, duration, degree of obstruction, and the patients themselves. A thorough history and physical examination is key in the patient evaluation. An upper urinary tract obstruction (kidney, ureter) can manifest as flank pain, ipsilateral back pain, ipsilateral groin pain, or no pain at all. Nausea and vomiting are also common and usually occur in acute obstruction. Chronic obstruction is usually indolent and may be asymptomatic. When infection is present, the patient may experience fever, chills, and/or dysuria. Hematuria may or may not be present. When a bilateral obstruction or a unilateral obstruction in a solitary kidney is severe and renal failure exists, a uremia can be present in the patient, as well as anuria. Symptoms of uremia can include weakness, peripheral edema, mental status changes, and pallor. If hydronephrosis is severe, the kidney may be palpable on a physical examination, especially in children. In cases that involve an infectious process, costovertebral angle tenderness may indicate pyelonephritis. Pain from an obstruction of a stone in the ureter will manifest as waxing and waning severe pain. During these pain episodes, the patient will often be found rolling around in bed unable to get comfortable. In contrast, a patient with peritonitis would lie very still and not move.

Lower urinary tract obstruction (bladder, urethra) can manifest as voiding dysfunction such as urgency, frequency, nocturia, incontinence, decrease in the force of stream, hesitancy, postvoid dribbling, and a sensation of incomplete emptying. Suprapubic pain or a palpable bladder indicates urinary retention in some cases. An infection may be present, and patients may experience dysuria. Hematuria may be present with or without infection. Gross hematuria may indicate the presence of a tumor; stone; infection; blood clot; bleeding vessel in the kidney, ureter, bladder, prostate, or urethra; or a foreign body present within the lower or upper urinary tract.

A digital rectal examination can reveal prostate enlargement, a normal-sized prostate, or inflammation suggestive of prostatitis. A urethral stricture often requires a cystoscopy for diagnosis. A urethral meatal stenosis is usually apparent on a physical examination. Patients with a urethral stricture may report a history of trauma, instrumentation, radiation to the pelvis, or a sexually transmitted disease. They may also experience a split urinary stream. In women, the presence of a uterine or bladder prolapse can be visualized on a pelvic examination. A urethral diverticulum can also be palpated on a physical examination.

Indications to treat a patient with urinary obstruction include a patient with bilateral complete obstruction; any type of obstruction in a solitary kidney; an obstruction causing fever, infection, or both; or a renal failure needs immediate attention by a trained physician. Patients with pain that is uncontrolled with oral pain medications or persistent nausea and/or vomiting, which causes dehydration, also need immediate medical attention as well as hospital admission.

In addition, patients may also present with sequelae of urinary tract obstruction such as renal cortical atrophy, hydronephrosis, kidney failure, polycythemia, hypertension, bladder or renal calculi, UTI or sepsis, or urinary ascites.

The volume of the unobstructed collecting system of a kidney is between 5 to 10 mL. Once a kidney or ureter becomes obstructed, the proximal collecting system will become dilated. Chronic urinary obstruction can lead to massive dilation. With this dilation, an increase in intraluminal pressure can occur proximal to the obstruction. This pressure and dilation will eventually affect the medulla of the kidney, with increasing pressure in the tubules of the cortex of the kidney causing cortical thinning and atrophy. In children, this can happen at an accelerated rate with minimal dilation or symptoms, so prompt management is required.

Although hydronephrosis is a strong sign of urinary tract obstruction, a renal cortical atrophy of the kidney is what leads to acute and chronic renal failure. Three mechanisms
have been proposed as to why hydronephrosis leads to renal failure. The first is pressure atrophy due to the rise of intraluminal pressure proximal to the obstruction, leading to damage to the cortex of the kidney. The second is an intrarenal reflux, most commonly seen in children with vesicoureteral reflux, which is the reflux of urine into the ureters and kidneys from the bladder during micturition due to insufficient tunnel length of the intravesical portion of the ureters, causing the ureters to be open during a bladder contraction. This reflux can cause damage to both the medulla and cortex of the kidney, especially if the urine is infected.⁴,⁵ The third cause is ischemia due to a lack of renal blood flow. This can be caused by a massive renal pelvis impeding blood flow through the renal hilum. A chronic obstruction also can lead to decreased renal blood flow, which can lead to ischemic atrophy of the kidney.

A UTI can be a serious or even a fatal complication of urinary tract obstruction. The stasis of urine behind the obstruction provides a perfect medium for bacteria to proliferate. The symptoms of a UTI depend on the location and severity of the infection. Acute pyelonephritis will usually present with fever and ipsilateral flank or back pain and costovertebral angle tenderness, whereas acute cystitis or urethritis will present with suprapubic tenderness, dysuria, and increased frequency or urgency.

The main goal of treating a UTI with urinary tract obstruction is to relieve the obstruction if possible and place the patient on empiric antibiotics while the culture is pending. Upper urinary tract obstruction often requires ureteral stenting and, less frequently, nephrostomy tube placement. Lower urinary tract obstruction typically requires Foley catheter placement. The urine culture can be negative if the sample is taken distal to the obstruction. If the patient continues to have fevers 48 hours after appropriate antibiotics are started, the patient should undergo repeat imaging.

Urinary tract calculi are a common cause of obstruction in the upper urinary tract (Fig. 19.1). Ureteral calculi can obstruct the ureter and may require surgical management if medical expulsive therapy is unsuccessful or not advisable. In the absence of infection, conservative management for a patient with a ureteral stone smaller than 5 mm is appropriate as there is a high likelihood of stone passage.³ Ureteral stones larger than 5 mm are unlikely to pass spontaneously and may require earlier surgical intervention.

Complicated upper urinary tract calculi are often struvite (magnesium ammonium phosphate-calcium carbonate) and result from the association of urinary infection with urea-splitting bacteria. The current management of these stones is an aggressive surgical approach. The American Urological Association (AUA) guidelines strongly recommend endoscopic approaches for these stones to remove all stone burden within the collecting system.³ These stones have a natural tendency to reoccur if all stone burden is not removed or if the infection causing the stones is not eradicated.³

In urinary tract obstruction, hypertension may develop for many reasons, including extracellular fluid (ECF) volume expansion, increased renin secretion, or decreased synthesis of prostaglandins. After the relief of bilateral obstruction, volume overload from fluid resuscitation may result in temporary hypertension.

A unilateral urinary tract obstruction (UUO) has been proven as a cause of temporary hypertension. The relief of temporary hypertension and the return of normal renal vein renin levels has been shown with the removal of upper tract unilateral obstruction compared to the obstructed kidney.⁵”⁷ This sequence resembles the hypertension associated with unilateral renal artery stenosis both in rats and humans. Indeed, ureteral occlusion does cause an acute increase in renin release from the obstructed kidney.⁸,⁹

Under normal conditions, the propulsion of urine from the kidney to the bladder under normal conditions is the result of three factors: (1) hydrostatic pressure, (2) ureteral and pelvic peristalsis, and (3) the rate of urine flow.¹⁰,¹¹ The urinary collecting system is lined by a transitional epithelium and surrounded by circular and longitudinal layers of smooth muscle. Action potentials that originate in smooth muscle cells of the minor calyx in the renal pelvis are conducted along the pelvis and down the ureter. The urine enters the pelvis and the proximal ureter in a passive state, but the presence of urine in the ureter causes peristalsis of the ureteral wall. Dilation of the ureter clearly interferes with this process. The nature of normal ureteral peristalsis also prevents retrograde transmission of the pressures generated during coaptation (10 to 25 mm Hg) to the renal pelvis, and renal pelvic pressures seldom rise above 4 mm Hg.¹⁰

After acute obstruction, smooth muscle fibers increase in tension within the urinary tract in response to the increase in pressure by contracting. With persistent obstruction, tension may decrease as the smooth muscle of the ureteric wall contracts with less force, and dilation of the wall continues. With a superimposed urinary infection, as often occurs in chronic obstruction, the loss of muscle tone is even more dramatic and progressive dilation occurs with no further increase or decrease in wall tension.¹²

Evidence shows that even with a completely obstructed kidney, filtration at the level of the glomeruli does not stop. Urine may escape through the walls of the collecting system, known as forniceal extravasation, and can relieve pressure within the collecting system. In addition to renal tubular reabsorption, urine may be reabsorbed directly across the walls of the renal pelvis through the lymphatics (pyelolymphatic reflux) or the renal venous system (pyelovenous reflux). The lymphatic flow from the kidneys is increased markedly during acute and chronic obstruction. This is most likely due to increased pressure within the venous system of the kidney rather than to urine reabsorbed from the renal pelvis. ¹³

The factors determining the fall in GFR during obstructive uropathy have been clarified by micropuncture studies of glomerular dynamics in experimental animals. Changes in intratubular pressure including stop-flow pressure, which represents glomerular filtration pressure, have provided important insight on the pathophysiology of obstructive nephropathy after unilateral (UUO) and bilateral ureteral obstruction (BUO). Glomerular filtration may be expressed by the formula: GFR = K_f(P_GC-[P_T + π_GS]), where K_f is the glomerular ultrafiltration coefficient, P_GC is the glomerular capillary pressure, P_T is the intratubular pressure, and π_GC is the mean oncotic pressure along the glomerular capillary. δP is the difference between P_GC and P_T and represents the pressure gradient across the glomerular capillary wall. An increase in P_T without a concomitant increase in P_GC will result in a decrease in δP, the driving force for filtration.³ Glomerular filtration also depends on the rate of blood flow entering the glomerular capillary. A decrease in glomerular blood flow during obstructive uropathy will decrease GFR because the rate at which capillary oncotic pressure rises is accelerated when a given volume of filtrate is removed from a smaller volume of blood. Both glomerular blood flow and hydrostatic pressure depend on renal vascular resistance, which is largely divided between two resistance segments—the preglomerular segment (afferent arteriole) and the postglomerular segment (efferent glomerular arteriole). Peritubular capillaries may also provide a postglomerular vascular resistance in urinary tract obstruction.

After either a unilateral or bilateral ureteral obstruction, renal blood flow increases significantly (15% to 25%) in the first 1 to 2 hours and is accompanied by an increase in P_T. This decrease in renal vascular resistance immediately after a complete ureteral obstruction is probably secondary to the synthesis and release of vasodilator prostaglandin (PG; see the following paragraphs). With persisting unilateral or bilateral ureteral obstruction, renal blood flow progressively decreases to 40% to 50% of normal levels by 24 hours.¹⁴,¹⁵ GFR is more markedly reduced than renal blood flow; that is, filtration fraction is low, and GFR is 20% to 30% of normal levels in both UUO and BUO obstruction after 24 hours.¹⁶,¹⁷ However, the site of changes in intrarenal vascular resistance and, therefore, the mechanisms responsible for the decrease in GFR differ between UUO and BUO (Table 19.2).

After an acute UUO, there is an immediate increase in intrapelvic and proximal tubular hydrostatic pressure, the severity of which depends on the diuretic state of the animal.¹⁸ Despite this increase in intratubular pressure, the GFR in surface nephrons is about 80% of normal because of an increase in glomerular capillary hydrostatic pressure and glomerular plasma flow secondary to afferent arteriolar dilation and decreased renal vascular resistance.¹⁹ As unilateral obstruction persists, progressive vasoconstriction and a decrease in nephron filtration rate develop within about 4 hours. By 24 hours, surface nephron GFR is 30% of normal because of a decrease in glomerular capillary pressure and plasma flow associated with an increase in renal vascular resistance, presumably at the level of the afferent arteriole.¹⁶ Proximal intratubular pressure is now normal rather than increased as during the first few hours of obstruction.¹⁴,¹⁶,²⁰,²¹,²²

During acute BUO, proximal tubular hydrostatic pressure increases to a higher level than after unilateral obstruction
and, in sharp contrast to unilateral obstruction, intrarenal pressure remains twice the normal level after 24 hours. Renal blood flow changes are similar to unilateral obstruction. ¹⁵,²³,²⁴ The surface nephron GFR after 24 hours is reduced to about 30% of normal levels in BUO as in UUO. However, the decrease in GFR in BUO is because of a persistent increase in proximal tubular hydrostatic pressure, whereas glomerular capillary pressure and plasma flow are normal.¹⁷ The predominant site of increased vascular resistance thus appears to be the efferent arteriole during a bilateral obstruction, compared to the afferent arteriole with a unilateral obstruction.

In addition to increasing renal blood flow for several hours and increasing pressures in the ureter and renal tubules, an acute ureteral obstruction has hemodynamic effects.²⁵ Several effects have been observed and include blunted vasoconstrictor responses and decreased autoregulation of renal blood flow when ureteral pressure exceeds 75 mm Hg. RBF is directly related to arterial pressure, and vasodilator effects may be shifted due to increased levels of renin being released from the obstructed kidney.²⁶,²⁷,²⁸,²⁹,³⁰

During a chronic complete ureteral obstruction, renal blood flow progressively decreases. After 1 day of a complete obstruction, there is a 40% to 50% decrease in renal blood flow to the kidneys. Prolonged UUO is associated with a further decrease in blood flow to 30% at 6 days, 20% at 2 weeks, and 12% at 8 weeks.³¹ The glomerular filtration rate depends on the fluid status of the patient and may not change during a chronic partial obstruction.

At 1 day postrelief of a unilateral obstruction, GFR remains reduced and renal vascular resistance is increased. However, they soon normalize after 1 week.¹⁶,²¹,²² Following the relief of bilateral obstruction for 24 hours, intratubular pressure decreases from elevated levels to normal, but glomerular capillary pressure and plasma flow also decrease because of afferent arteriolar vasoconstriction, resulting in a persistent decrease in GFR.¹⁷,²⁴,²⁷,³²,³³ Afferent arteriolar pressures appear to keep renal blood flow and glomerular filtration similar the first day after relief of the obstruction.

GFR recovery is dependent on both the duration and the severity of the obstruction. Studies in dogs have looked at reversible factors in the recovery of GFR.³⁴,³⁵ The maximum GFR retained after obstruction of 7 days’ duration was about two-thirds of the GFR before obstruction. When the duration of obstruction was 1 month, the GFR returned to only 20% of its original function. In general, the maximal degree of recovery was observed within 2 to 4 weeks after release of the obstruction.³⁴,³⁵

Nephron function after recovery from an obstruction is not uniform throughout the kidney. There is a decrease in the functioning juxtamedullary nephrons in the superficial cortex of rats after 1 day of UUO.²¹ One study showed an 85% recovery of the whole obstructed kidney and 100% function in the contralateral nonobstructed kidney after 2 weeks with a return to normal GFR.³⁶ The single-nephron GFR of functioning superficial and juxtamedullary nephrons was higher postobstruction than in the contralateral normal kidney.

The findings of function recovery after an obstruction have also been observed in humans, but the number of supporting clinical studies is limited to children with congenital lesions. These studies have shown that the earlier the relief of obstruction, the greater return in GFR during follow-up.³⁷,³⁸

Changes in renal hemodynamics and GFR in obstructive nephropathy are of interest because of their clinical significance. Nishikawa et al.³⁹ demonstrated increased PG synthesis in the hydronephrotic isolated perfused kidney, which leads to changes within the kidney on a metabolic and hemodynamic level. Vasodilator and vasoconstrictor PGs have been studied in relation to the functional changes of urinary tract obstruction with respect to renal hemodynamics.

The early hemodynamic consequences of acute ureteral obstruction are blunted or prevented by the inhibition of PG synthesis after indomethacin. This was studied by giving it prior to obstruction, then measuring intraureteral pressure of the affected kidney.⁴⁰ The studies also found decreases in glomerular capillary pressures and proximal tubular pressure with its administration.⁴⁰,⁴¹,⁴²,⁴³,⁴⁴ The increase in RBF beginning immediately after UUO is prevented by indomethacin or meclofenamate and a similar effect is seen on the vasodilatation that follows BUO.⁴⁰,⁴¹,⁴²,⁴³,⁴⁴,⁴⁶,⁴⁷ The impairment of autoregulation that is seen in the kidney with ureteral obstruction is prevented by indomethacin, and normal autoregulation of renal blood flow with changes in arterial pressure is restored in the obstructed kidney.⁴⁴ A recent study in 2010 showed that Cox-2 inhibition led to decreased intrarenal levels of prostaglandins in bilateral ureteral obstruction with concomitant ureteral relaxation and decreased contractility in rats.⁴⁸

Two vasoconstrictors, TXA₂ and Ang II, play a major role in the decrease in renal plasma flow per nephron and the decline in single-nephron GFR seen following ureteral obstruction.⁴⁷ Both TXA₂⁴⁹ and Ang II⁵⁰ are able to contract mesangial cells in culture and reduce the glomerular capillary area available for filtration, which leads to a decrease in GFR. Rats pretreated with angiotensin-converting enzyme (ACE) inhibitors and thromboxane synthesis inhibitors before ureteral obstruction were observed not to show a decline in renal function.⁵¹

Maximal renin secretion into the renal veins has been observed shortly after ureteral obstruction due to afferent arteriole dilatation associated with the aforementioned postobstructive renal hemodynamics.⁵²,⁵³ This secretion has been shown to be completely halted by the preobstruction administration of cyclooxygenase inhibitors, leading to the conclusion that renal cortical prostaglandins may act as a strong stimulus for renin secretion.⁵⁴,⁵⁵

Angiotensin II plays a central role in the modulation of hemodynamic changes following a ureteral obstruction. The preobstruction administration of captopril⁵⁶,⁵⁷ and enalapril⁵⁷ appear to be highly effective in ameliorating the decline in GFR and renal plasma flow in response to a ureteral obstruction.⁵⁶ Rising levels of angiotensin II also can lead to tubulointerstitial fibrosis during an obstruction due to increased levels of tumor necrosis factor alpha (TNF-α) within the first few hours of an obstruction. This cascade of events can lead to tubular cell apoptosis.³

During acute partial UUO, there is a significant decrease in sodium, potassium, and solute excretion with a decrease in urine sodium concentration and an increase in urine osmolality.⁵⁸ This is due to the increase in both sodium and water reabsorption within the tubules during a partial obstruction,⁵⁸ which had first been thought to be due to a decline in GFR seen with obstruction.⁴⁹,⁵⁹ This reverse phenomenon seen with increased blood flow and increased reabsorption of sodium with the juxtaglomerular cortical nephrons is not expected and appears not to be due to renal nerve activity.⁶⁰,⁶¹

During chronic partial obstruction, the gradual decrease in GFR is accompanied by an increase in the fractional excretion of filtered sodium, thus indicating decreased tubular reabsorption. A micropuncture of surface nephrons in chronic partial UUO or of a solitary kidney with a partial obstruction in the rat indicates that the increased fractional excretion of sodium is due to decreased reabsorption in the distal tubule or the collecting duct of the nephron.⁶²

After the relief of chronic partial UUO in humans, there is no increase in absolute sodium and water excretion from the hydronephrotic kidney, although a decreased concentrating ability and an increased fractional excretion of sodium are observed.⁶³ Other factors, such as volume expansion or a further reduction in functioning nephron mass with uremia, are necessary to cause an increase in salt and water excretion (postobstructive diuresis) following the relief of an obstruction.

After the relief of a complete obstruction of both kidneys or a solitary kidney, there is a prolonged diuresis due to massive losses of water, sodium, and other solutes. A single study showed urine output can equal one-half of the GFR, indicating a dramatic decrease in the reabsorptive ability of the nephron.⁶⁴ If not replaced, such losses can lead to severe hypovolemia and life-threatening electrolyte imbalance due to significant losses in sodium and water from an inability to reabsorb them in the nephron.⁶⁵,⁶⁷,⁶⁸,⁶⁹,⁷⁰ However, a brisk diuresis following the relief of a urinary tract obstruction may also be physiologically appropriate or even iatrogenic rather than an indicator of tubular malfunction. The degree of fluid replacement in a given case will depend on the mechanism involved. Salt diuresis due to ECF expansion can lead to hypervolemia and an increase in atrial natriuretic peptide (ANP) levels, stimulating a diuresis after the relief of the obstruction. This can be continued after the relief of an obstruction iatrogenically due to physicians keeping up with urine output during the diuresis with intravenous fluids that maintain a high ECF volume. Another factor could be the amount of retained urea within the bloodstream and nephrons that act as an osmotic diureticlike mannitol,⁶⁵,⁶⁷,⁷¹ leading to natriuresis. Recovery of GFR is dependent on the duration of obstruction and will dictate the length of postobstructive diuresis.⁷²

A well documented feature of obstructive uropathy is the loss of the ability to concentrate urine. One exception is during an acute partial obstruction due to the increase in renal tubular absorption.⁷³ A recent relief of an obstruction or chronic obstruction has been well documented to show a decrease in renal concentration ability.⁷⁴,⁷⁵ Patients with a marked impairment may present with nephrogenic diabetes insipidus and may demonstrate polyuria and persistently hypotonic urine.⁷⁶,⁷⁷,⁷⁸,⁷⁹ Hypernatremia and severe dehydration can develop if fluid intake is not adequate.⁸⁰

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