Chapter 313: Urinary Tract Obstruction

Obstruction to the flow of urine, with attendant stasis and elevation in urinary tract pressure, impairs renal and urinary conduit functions and is a common cause of acute and chronic kidney disease (obstructive nephropathy). Early recognition and prompt treatment of urinary tract obstruction (UTO) can prevent or reverse devastating effects on kidney structure and function, and decrease susceptibility to hypertension, infection, and stone formation. Chronic obstruction may lead to permanent loss of renal mass (renal atrophy) and excretory capability. Since obstructive disease may be secondary to serious underlying inflammatory, vascular, or malignant disease, familiarity with clinical findings, appropriate diagnostic testing, and therapeutic approach is of great importance to the clinician.

Obstruction to urine flow can result from intrinsic or extrinsic mechanical blockade as well as from functional defects not associated with fixed occlusion of the urinary drainage system. Mechanical obstruction can occur at any level of the urinary tract, from within the renal tubules, or the renal calyces to the external urethral meatus (obstructive uropathy). Normal points of narrowing, such as the ureteropelvic and ureterovesical junctions, bladder neck, and urethral meatus, are common sites of obstruction. When lower UTO is above the level of the bladder, unilateral dilatation of the ureter (hydroureter) and renal pyelocalyceal system (hydronephrosis) occurs; lesions at or below the level of the bladder cause bilateral involvement.

Common forms of obstruction are listed in Table 313-1. Childhood causes include congenital malformations, such as narrowing of the ureteropelvic junction (UPJ) and abnormal insertion of the ureter into the bladder, the most common cause. Vesicoureteral reflux in the absence of urinary tract infection or bladder neck obstruction often resolves with age. Reinsertion of the ureter into the bladder is indicated if reflux is severe and unlikely to improve spontaneously, if renal function deteriorates, or if urinary tract infections recur despite chronic antimicrobial therapy. Vesicoureteral reflux may cause prenatal hydronephrosis and, if severe, can lead to recurrent urinary infections, hypertension and renal scarring in childhood. Posterior urethral valves are the most common cause of bilateral hydronephrosis in boys. In adults, UTO is due mainly to acquired defects. Pelvic tumors, calculi, and urethral stricture predominate. Ligation of, or injury to, the ureter during pelvic or colonic surgery can lead to hydronephrosis which, if unilateral, may remain undetected. Obstructive uropathy may also result from extrinsic neoplastic (carcinoma of cervix or colon) or inflammatory disorders. Lymphomas and pelvic or colonic neoplasms with retroperitoneal involvement are causes of ureteral obstruction. As many as 50% of men aged >40 years may have lower urinary tract symptoms associated with benign prostatic hypertrophy, but these symptoms may occur without bladder outlet obstruction.

Functional impairment of urine flow occurs when voiding is altered by abnormal pontine or sacral centers of micturition control. It may be asymptomatic or associated with lower urinary tract symptoms such as frequency, urgency, and postmicturition incontinence, nocturia, straining to void, slow stream, hesitancy, or a feeling of incomplete emptying. A history should be sought for trauma, back injury, surgery, diabetes, neurologic or psychiatric conditions, and medications. Causes include neurogenic bladder, often with adynamic ureter, and vesicoureteral reflux. Reflux in children may result in severe unilateral or bilateral hydroureter and hydronephrosis. Overflow urinary incontinence combined with fecal incontinence may require an urgent evaluation for cauda equina syndrome. Urinary retention may be the consequence of α-adrenergic and anticholinergic agents, as well as opiates. Hydronephrosis in pregnancy is due to relaxational effects of progesterone on smooth muscle of the renal pelvis, as well as ureteral compression by the enlarged uterus, more often on the right side.

Diagnostic tools to identify anatomic obstruction include urinary flow measurements and a postvoid residual. Bladder volume may be readily assessed by bedside ultrasound. Cystourethroscopy and urodynamic studies may be reserved for the symptomatic patient to assess the filling phase (cystometry), pressure-volume relationship of the bladder, bladder compliance, and capacity. Pressure-flow analysis evaluates bladder contractility and bladder outlet resistance during voiding. Bladder obstruction is characterized by high pressures in women, whereas in men, a diagnosis of bladder outlet obstruction is based on flow rate and voiding pressures. A voiding cystourethrogram may be useful in evaluating incomplete emptying and bladder neck and urethral pathology.

The pathophysiology and clinical features of UTO are summarized in Table 313-2. Flank pain, the symptom that most commonly leads to medical attention, is due to distention of the collecting system or renal capsule. Pain severity is influenced more by the rate at which distention develops than by the degree of distention. Acute supravesical obstruction, as from a stone lodged in a ureter (Chap. 312), is associated with excruciating, sometimes intermittent, pain, known as renal colic. This pain often radiates to the lower abdomen, testes, or labia. By contrast, more insidious causes of obstruction, such as chronic narrowing of the UPJ, may produce little or no pain and yet result in total destruction of the affected kidney. Flank pain that occurs only with micturition is pathognomonic of vesicoureteral reflux.

Obstruction of urine flow results in an increase in hydrostatic pressures proximal to the site of obstruction. It is this buildup of pressure that leads to the accompanying pain, the distention of the collecting system in the kidney, and elevated intratubular pressures that initiate tubular dysfunction. In the first days of obstruction, the dilatation of the poorly compliant collecting system may be minimal. As the increased hydrostatic pressure is expressed in the urinary space of the glomeruli, further filtration decreases or stops completely.

Azotemia develops when overall excretory function is impaired, often in the setting of bladder outlet obstruction, bilateral renal pelvic or ureteric obstruction, or unilateral disease in a patient with a solitary functioning kidney. Complete bilateral obstruction should be suspected when acute renal failure is accompanied by anuria. Any patient with renal failure otherwise unexplained, or with a history of nephrolithiasis, hematuria, diabetes mellitus, prostatic enlargement, pelvic surgery, trauma, or tumor should be evaluated for UTO.

In the acute setting, partial, bilateral obstruction may mimic prerenal azotemia with a high blood urea nitrogen-to-creatinine ratio, concentrated urine and sodium retention. Renal vascular resistance may be increased. However, with more prolonged obstruction, symptoms of polyuria and nocturia commonly accompany partial UTO and result from loss of medullary hypertonicity with diminished renal concentrating ability. Failure to produce urine free of salt (natriuresis) is due to downregulation of salt reabsorption in the proximal tubule and of transport proteins including the Na⁺, K⁺ adenosine triphosphatase (ATPase), NaK₂Cl cotransporter (NaK₂Cl) in the thick ascending limb, and the epithelial Na⁺ channel (ENaC) in collecting duct cells. In addition to direct effects on renal transport mechanisms, increased prostaglandin E₂ (PGE₂) (due to induction of cyclooxygenase-2 [COX-2]), angiotensin II (with its downregulation of Na⁺ transporters), and atrial or B-type natriuretic peptides (ANP or BNP) (due to volume expansion in the azotemic patient) contribute to decreased salt reabsorption along the nephron.

Dysregulation of aquaporin-2 water channels in the collecting duct contributes to the polyuria. The defect usually does not improve with administration of vasopressin and is therefore a form of acquired nephrogenic diabetes insipidus.

Wide fluctuations in urine output in a patient with azotemia should always raise the possibility of intermittent or partial UTO. If fluid intake is inadequate, severe dehydration and hypernatremia may develop. However, as with other causes of poor renal function, excesses of salt and water intake may result in edema and hyponatremia.

Partial bilateral UTO often results in acquired distal renal tubular acidosis, hyperkalemia, and renal salt wasting. The H⁺-ATPase, situated on the apical membrane of the intercalated cells of the collecting duct, is critical for distal H⁺ secretion. The trafficking of intracellular H⁺ pumps from the cytoplasm to the cell membrane is disrupted in UTO. The decreased function of the ENaC, in the apical membrane of neighboring collecting duct principal cells, contributes to decreased Na⁺ reabsorption (salt-wasting), and, therefore, decreased K⁺ secretion via K⁺ channels. Ammonium (NH₄ ⁺) excretion important to the elimination of H⁺ is impaired. These defects in tubule function are often accompanied by renal tubulointerstitial damage. Azotemia with hyperkalemia and metabolic acidosis should prompt consideration of UTO.

The renal interstitium becomes edematous and infiltrated with mononuclear inflammatory cells early in UTO. Later, interstitial fibrosis and atrophy of the papillae and medulla occur and precede these processes in the cortex. The increase in angiotensin II noted in UTO contributes to the inflammatory response and fibroblast accumulation through mechanisms involving profibrotic cytokines. With time, this process leads to chronic kidney damage.

UTO must always be considered in patients with urinary tract infections or urolithiasis. Urinary stasis encourages the growth of organisms. Urea-splitting bacteria are associated with magnesium ammonium phosphate (struvite) calculi that may take on a staghorn appearance. Hypertension is frequent in acute and subacute unilateral obstruction and is usually a consequence of increased release of renin by the involved kidney. Chronic kidney disease from bilateral UTO, often associated with extracellular volume expansion, may result in significant hypertension. Erythrocytosis, an infrequent complication of obstructive uropathy, is secondary to increased erythropoietin production.

A history of difficulty in voiding, pain, infection, or change in urinary volume is common. Evidence for distention of the kidney or urinary bladder can often be obtained by palpation and percussion of the abdomen. A careful rectal and genital examination may reveal enlargement or nodularity of the prostate, abnormal rectal sphincter tone, or a rectal or pelvic mass.

Urinalysis may reveal hematuria, pyuria, and bacteriuria. The urine sediment is often normal, even when obstruction leads to marked azotemia and extensive structural damage. An abdominal scout film, although insensitive, may detect nephrocalcinosis or a radiopaque stone. As indicated in Fig. 313-1, if UTO is suspected, a bladder catheter should be inserted. Abdominal ultrasonography should be performed to evaluate renal and bladder size, as well as pyelocalyceal contour. Ultrasonography is ~90% specific and sensitive for detection of hydronephrosis. False-positive results are associated with diuresis, renal cysts, or the presence of an extrarenal pelvis, a normal congenital variant. Congenital UPJ obstruction may be mistaken for renal cystic disease. Hydronephrosis may be absent on ultrasound when obstruction is less than 48 h in duration or associated with volume contraction, staghorn calculi, retroperitoneal fibrosis, or infiltrative renal disease. Duplex Doppler ultrasonography may detect an increased resistive index in urinary obstruction.

Recent advances in technology have led to alternatives and have largely replaced the once standard intravenous urogram in the further evaluation of UTO. The high-resolution multidetector row computed tomography (CT) scan in particular has advantages of visualizing the retroperitoneum, as well as identifying both intrinsic and extrinsic sites of obstruction. Noncontrast CT scans improve visualization of the urinary tract in the patient with renal impairment and are safer for patients at risk for contrast nephropathy. Magnetic resonance urography is a promising technique but, at this time, not superior to the CT scan and carries the risk of certain gadolinium agents in patients with renal insufficiency. CT scanning may define the site of obstruction, identify and characterize kidney stones, and demonstrate dilatation of the calyces, renal pelvis, and ureter above the obstruction. The ureter may be tortuous in chronic obstruction. Radionuclide scans are able to give differential renal function but give less anatomic detail than CT scans. Furosemide is sometimes given to increase detection with imaging, and to distinguish functional from anatomic obstruction. The increase in urinary flow may bring out the pain of an acute obstructive process.

To facilitate visualization of a suspected lesion in a ureter or renal pelvis, retrograde or antegrade urography should be attempted. These procedures do not carry risk of contrast-induced acute kidney injury in patients with renal insufficiency. The retrograde approach involves catheterization of the involved ureter under cystoscopic control, whereas the antegrade technique necessitates percutaneous placement of a catheter into the renal pelvis. Although the antegrade approach may provide immediate decompression of a unilateral obstructing lesion, many urologists initially attempt the retrograde approach unless the catheterization is unsuccessful.

Voiding cystourethrography is of value in the diagnosis of vesicoureteral reflux and bladder neck and urethral obstructions. Postvoiding films reveal residual urine. Endoscopic visualization by the urologist often permits precise identification of lesions involving the urethra, prostate, bladder, and ureteral orifices.

With relief of obstruction, the prognosis regarding return of renal function depends largely on whether irreversible renal damage has occurred. When obstruction is not relieved, the course will depend mainly on whether the obstruction is complete or incomplete and bilateral or unilateral, as well as whether or not urinary tract infection is also present. Complete obstruction with infection can lead to total destruction of the kidney within days. Partial return of glomerular filtration rate may follow relief of complete obstruction of 1 and 2 weeks’ duration, but after 8 weeks of obstruction, recovery is unlikely. In the absence of definitive evidence of irreversibility, every effort should be made to decompress the obstruction in the hope of restoring renal function at least partially. A renal radionuclide scan, performed after a prolonged period of decompression, may be used to predict the reversibility of renal dysfunction.

Relief of bilateral, but not unilateral, complete obstruction commonly results in polyuria, which may be massive. The urine is usually hypotonic and may contain large amounts of sodium chloride, potassium, phosphate, and magnesium. The natriuresis is due in part to the correction of extracellular volume expansion, the increase in natriuretic factors accumulated during the period of renal failure, and depressed salt and water reabsorption when urine flow is reestablished. The retained urea is excreted with improved GFR, resulting in an osmotic diuresis which increases the urine volume of electrolyte-free water. The urinary concentrations of sodium and potassium that when added are less than the serum sodium is evidence of electrolyte free-water excretion. In the majority of patients, this diuresis results in the appropriate excretion of the excesses of retained salt and water. When extracellular volume and composition return to normal, the diuresis usually abates spontaneously. Occasionally, iatrogenic expansion of extracellular volume is responsible for, or sustains, the diuresis observed in the postobstructive period. Replacement with intravenous fluids in amounts less than urinary losses usually prevents this complication. More aggressive fluid management is required in the setting of hypovolemia, hypotension, or disturbances in serum electrolyte concentrations.

The loss of electrolyte-free water with urea may result in hypernatremia. Measured urinary output and serum and urine sodium, potassium and osmolal concentrations should guide the use of appropriate intravenous replacement. Often replacement with 0.45% saline is required. Relief of obstruction may be followed by urinary salt and water losses severe enough to provoke profound dehydration and vascular collapse. In these patients, decreased tubule reabsorptive capacity is probably responsible for the marked diuresis. Appropriate therapy in such patients includes intravenous administration of salt-containing solutions to replace sodium and volume deficits.