Contributors of Campbell-Walsh-Wein, 12th edition
Casey A. Dauw, Stuart J. Wolf, Craig A. Peters, and Kirstan K. Meldrum
Clinical presentation
Upper urinary tract obstruction refers to the blockage of urinary flow from the renal calyces to the level of the ureterovesical junction. It is distinct from lower urinary tract obstruction (i.e., bladder through urethra); however, it can occur secondarily to lower urinary tract obstruction or dysfunction (i.e., urinary retention). Proper functioning of the lower urinary tract should always be considered in the differential.
Upper urinary tract obstruction can have a variable presentation. It can be symptomatic or asymptomatic, acute or chronic, and unilateral or bilateral, and it has a broad differential diagnosis. Obstructive uropathy accounts for approximately 10% of all cases of renal failure. On a population level, hydronephrosis tends to be more prevalent in women ages 20–60 years owing to pregnancy and gynecologic malignancies. After the age of 60 years, men are more likely to have hydronephrosis owing to the presence of prostatic diseases.
The most common presenting symptom associated with acute upper urinary tract obstruction is flank pain owing to stretching of the renal capsule. This can radiate to the lower abdomen, testicles, or labia and can cause severe degrees of discomfort along with nausea and vomiting. Chronic upper urinary tract obstruction, on the other hand, tends to have a milder course and in some cases can be painless.
Upper urinary tract obstruction can be associated with renal functional damage, particularly if left untreated. This is particularly concerning when present in childhood because congenital obstruction can prevent the kidneys from normal development. Acquired obstruction can similarly be determinantal to existing renal function in the mature adult as well.
Hemodynamic changes
Ureteral obstruction can lead to numerous functional changes that affect renal hemodynamics. Such changes depend on whether the obstruction is unilateral or bilateral. There is a triphasic response of renal blood flow in unilateral ureteral obstruction. In phase 1 (initial 2 hours), there is an increase in renal tubular pressure as a result of obstruction, leading to a decrease in glomerular filtration rate (GFR). The renal vasculature attempts to compensate for this decrease in GFR by increasing renal blood flow mediated by the release of vasodilators such as prostaglandin E2 and nitric oxide. During phase 2 (6–24 hours), the ureteral pressure remains elevated, and renal blood flow diminishes. In phase 3 (>24 hours), renal pelvic pressures trend down but remain elevated, and renal blood flow continues to diminish ( Fig. 24.1 ), leading to renal ischemia.
In the case of bilateral ureteral obstruction (or solitary kidney obstruction), there is only a modest initial increase in renal blood flow followed by a more rapid decline, which can exacerbate the potential for renal function damage ( Fig. 24.2 ). This is of clinical importance because timely decompression is of the essence.
Functional changes
Upper urinary tract obstruction can damage the kidneys in several ways. Some of the functional change can be transient and relieved when the pressure is relieved; however, there is also the potential for permanent damage in cases with longstanding obstruction if associated with high pressures. It is likely that the risk of permanent damage to the affected kidney is related to the duration, degree, and severity of obstruction, though this these parameters are poorly defined.
One unique functional sequelae that occurs upon relief of bilateral ureteral obstruction or obstruction in a solitary kidney is postobstructive diuresis. This condition refers to polyuria that occurs as a result or in relation to osmotic diuresis of accumulated solutes, impaired tubular concentrating ability and reabsorption, as well as an increase in production of atrial natriuretic factor (ANP), which stimulates sodium wasting. Although this condition is typically self-limited, it is important to monitor electrolytes and ensure that the patient can self-hydrate to account for the potential of excess fluid losses. This condition is unlikely to occur in the setting of a normal contralateral kidney, which would otherwise be expected to maintain fluid and electrolyte balance.
Diagnosis and testing
Laboratory studies
Urinalysis.
Can provide an estimation of osmolality, evidence of urinary tract infection, insight into stone formation based on crystals that may be present in the urine, and the possible presence of medical renal disease with the presence of protein and/or cellular casts.
Fractional excretion of sodium (FENa).
Can help differentiate between the three types of acute renal injury: prerenal, intrinsic, and postrenal. FENa = (P Cr × U Na ) / (P Na × U Cr ). FENa <1% suggests prerenal causes, >1% suggests intrinsic causes, >4% suggests postrenal causes (i.e., bilateral ureteral obstruction).
Assessment of renal function.
Measurement of GFR is considered the gold standard, though is commonly estimated using serum creatinine levels. Creatinine is a waste product of muscle metabolism and can be influenced by age, muscle mass, and gender. In general, a GFR >90 mL/min/1.73 m 2 is considered normal, between 60 and 90 mL/min/1.73 m 2 is considered a mild decline in renal function, between 30 and 60 mL/min/1.73 m 2 is a moderate decline in renal function, between 15 and 30 mL/min/1.73 m 2 is a severe decline in renal function, and <15 mL/min/1.73 m 2 is considered renal failure.
Imaging studies ( Tables 24.1 and 24.2 )
Renal ultrasonography is considered a first-line modality in the evaluation of suspected upper urinary tract obstruction. Advantages include low cost, widespread availability, and lack of ionizing radiation. The information obtained by ultrasound is primarily anatomic and can provide renal size, cortical thickness, corticomedullary differentiation, and the grade of collecting system dilation (hydronephrosis). Although the presence of hydronephrosis is suggestive of underlying obstruction, it is important to recognize that hydronephrosis is an anatomic finding, not a functional diagnosis, and that hydronephrosis alone does not indicate urinary tract obstruction. The main downside of renal ultrasonography is that it is often unable to visualize the etiology of a potential obstruction, which often is located in the ureter, an area more challenging to confidently image via ultrasonography alone. Duplex Doppler sonography, which allows for identification of arterial waveforms, has been postulated as a tool to help detect urinary obstruction via calculation of a resistive index (peak systolic velocity-end diastolic velocity/peak systolic velocity). In general, a resistive index of 0.70 is considered to be the upper limits of normal in adults; however, a wide variety of factors have been found to influence this measurement, limiting its widespread applicability. Color Doppler ultrasonography has also demonstrated utility in distinguishing obstructive from nonobstructive causes of obstruction by helping identify the presence of a ureteral jet in the bladder.
| MODALITY | MEDIAN SENSITIVITY (%) | MEDIAN SPECIFICITY (%) |
|---|---|---|
| Conventional radiography | 57 | 76 |
| Ultrasound | 61 | 97 |
| Intravenous pyelography | 70 | 95 |
| MRI | 82 | 98.3 |
| CT (not as gold standard) | 98 | 97 |
| TYPE OF EXAM | EFFECTIVE DOSE (MSV) | |
|---|---|---|
| Ultrasound (US) | Abdomen and pelvis US | 0 |
| Magnetic resonance imaging (MRI) | Abdomen and pelvis MRI | 0 |
| Conventional radiography | ||
| KUB | 0.7 | |
| KUB with tomograms | 3.9 | |
| IVU | 3.0 | |
| Computed tomography (CT) | ||
| Noncontrast CT, abdomen and pelvis | 10.0 | |
| Without and with contrast CT, abdomen and pelvis (two-phase) | 15.0 | |
| Without and with contrast CT, abdomen and pelvis (three-phase) | 20.0 | |
| Noncontrast CT, abdomen and pelvis (low-dose protocol) | 3.0 | |
| Ultra-low dose protocol CT | <1.9 |
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