Pathophysiology of Urinary Tract Obstruction

Includes 2015 AUA Update on Management of Post-Obstructive Diuresis

Diagnosis and evaluation

History and physical exam

• Most common symptom with acute obstruction: flank pain; secondary to stretching of the collecting system.
  • In contrast, chronic obstruction of the urinary tract is usually painless and patients may be entirely asymptomatic
• Obstructive uropathy should always be considered in patients with (3):
  1. New-onset hypertension
  2. Renal failure without a history of renal disease, diabetes, or hypertension
  3. Recurrent UTIs

Laboratory

• Fractional excretion of Sodium (FENa)
  • Often used to differentiate among the 3 types of acute renal injury: pre-renal, intrinsic, and post-renal
  • (FENa = (PCr ×UNa)/(PNa ×UCr ))
    • FENa <1% suggests a pre-renal cause of acute renal failure
    • FENa >4% suggests a post-renal cause of acute renal failure

Imaging

Ultrasound

• Hydronephrosis
  • The term hydronephrosis implies dilatation of the renal pelvis and calyces and can occur without obstruction.
    • Significant hydronephrosis can be present in the absence of obstruction (e.g., vesicoureteral reflux)
  • The term obstructive nephropathy should be reserved for the damage to the renal parenchyma that results from an obstruction to the flow of urine anywhere along the urinary tract.
    • Significant obstruction can be present in the absence of severe hydronephrosis (e.g., very early in the course of acute renal obstruction)
      • Standard renal US may appear normal in 50% of patients with acute urinary obstruction
• Resistive index (RI)
  • Definition of RI: (peak systolic velocity–end diastolic velocity)/peak systolic velocity
  • Changes in intrarenal arterial waveforms have been shown to be associated with urinary obstruction
  • RI >0.70 has been suggested as a technique to improve detection of urinary obstruction during US.
    • However, studies investigating RI in the detection of renal obstruction have not found it useful.
• Ureteric jets
  • Color Doppler US can reliably identify ureteric jet dynamics in the bladder
  • Requires good hydration of the patient
  • Limited by the requirement of a normal contralateral collecting system for comparison.

CT

• Can detect most radiolucent stones with the exception of protease inhibitor stones (i.e., indinavir sulfate) and mucoid matrix stones
  • Test characteristics for stone detection:
    • Sensitivity: 96%
    • Specificity and positive predictive value: 100%
• Low-dose CT may be limited in:
  1. Stones < 3 mm
  2. Patient obesity
  3. Impaction at the ureterovesical junction
• Traditional CT urography involves 3 phases using a single IV bolus injection of contrast:
  1. Unenhanced (initial)
  2. Nephrogenic/nephrographic
     • Obtained ≈100-120 seconds after contrast injection
  3. Excretory
     • Obtained ≈3-5 mins after contrast injection to evaluate the urothelium
  • CT urogram/triphasic does not include corticomedullary (30-70 sec) phase
    • Corticomedullary best at looking at veins (renal vein involvement)
    • Nephrogenic best for parenchymal lesions
  • Note: this is different than 2016 AUA Asymptomatic Microscopic Hematuria Guidelines which describe 4 phases: unenhanced, arterial, corticomedullary, and excretory

MRI

• Poor detection of renal and ureteral stones in comparison to CT because stones appear as signal voids on T1- and T2-weighted images
• The MRU measurement of contrast excretion is the renal transit time, which is defined as the time it takes for contrast to pass from the renal cortex to the proximal ureters
  • Interpretation of contrast excretion time
    • ≤4 minutes: normal
    • > 4 and < 8 minutes: equivocal
    • ≥ 8 minutes: obstructed
• MRU has been demonstrated to have an excellent correlation with the renal isotope GFR in the adult and pediatric patients with obstructed kidneys.
• IV gadopentetate-DTPA allows a dynamic, functional assessment of the collecting system that correlates well with diuretic renal scintigraphy, yet provides far greater anatomic detail than nuclear studies.
  • Differential GFR can be assessed with post-imaging processing, and contrast washout can be measured to calculate renal clearance, differentiating dilated systems from obstructed systems

Excretory urography depends on glomerular filtration and renal excretion of iodinated contrast medium; therefore, the utility of excretory urography is limited in patients with renal insufficiency.

• The risk for contrast nephropathy increases with worsening renal function.
• Excretory urography should not be performed in patients with a history of contrast allergy or those in whom radiation exposure is a concern (i.e., pregnancy).

Nuclear renography

• Tracers commonly used in urology (3): MAG3, DTPA, DMSA
  1. MAG3
     • Tracer properties
       • High extraction by the kidneys
         • Renal uptake is 55% compared with 20% uptake by DTPA
       • Rapid clearance
       • Low radiation dose
       • Tubular secretion
     • Preferred radiopharmaceutical in the evaluation of the obstructed collecting system
  2. DTPA
     • Tracer properties
       • Removed almost exclusively by glomerular filtration
         • MAG3 actively secreted by the tubules
     • Preferred radiopharmaceutical in the evaluation of GFR
       • Adequate imaging of the collecting system, however, is GFR-dependent with DTPA and is therefore limited in patients with renal insufficiency and those <6 months of age because of the immaturity of renal function
  3. DMSA
     • Tracer properties
       • Binds to the proximal convoluted tubules in kidney so the excretion pattern of the kidneys cannot be assessed§
       • Best tissue to background activity ratio
     • Preferred radiopharmaceutical in the evaluation of renal Scarring and prediction of renal recovery (superior to DTPA and MAG-3)

Tracer	Clinical question	Clearance	Useful in renal failure
MAG3	Obstruction, differential function, perfusion, effective renal plasma flow	95% secretion, <5% glomerular filtration	Yes
DTPA	Obstruction, differential function, perfusion, filtration (GFR)	>95% glomerular filtration	No (since tracer has to be filtered)
DMSA	Morphology (cortical defects, ectopic or aberrant kidneys) and differential function	60% tubular filtration, some glomerular filtration

§§

• Phases of a nuclear scan (3):
  1. Flow (initial) phase
     • Characterized by rapid renal uptake of the radiopharmaceutical, reflecting renal perfusion
     • Shows renal uptake, background clearance, and abnormal vascular lesions
  2. Renal phase
     • Characterized by a more gradual rise in uptake over time, usually peaking after 2-5 minutes
     • Primarily evaluates renal function
       • Most sensitive indicator of renal dysfunction
     • Urinary obstruction can diminish the rate of uptake of the radiotracer during the second phase and can therefore alter the assessment of differential renal function
  3. Excretory phase
     • Characterized by a gradual decrease in renal counts over time
     • Often augmented by the administration of a diuretic (diuretic renogram) to induce high urine flow and prevent the false positive results that can be caused by urine stasis in a dilated collecting system
       • The diuretic (usually furosemide 0.5 mg/kg) is administered when maximum collecting system activity is visualized.
     • The T1/2 is the time it takes for collecting system activity to decrease by 50% from that at the time of diuretic administration
       • T1/2 < 10 minutes: normal, non-obstructed collecting system
       • T1/2 10-20 minutes: mild to moderate delay, may be a mechanical obstruction
       • T1/2 > 20 minutes: high-grade obstruction
         • The level of obstruction can usually be determined, as can abnormalities such as ureteral duplication
     • Causes of false-positive results (6): High Definition Nuclear Renography Can Deceive
       1. Hepatobiliary excretion if the area of intestinal activity or gallbladder activity is included in the area of study
       2. Dehydration because of the suboptimal response to a diuretic agent
       3. Neonates because of renal immaturity
       4. High-grade Reflux
       5. CKD (poor renal function)
       6. Presence of massive collecting system Dilation with urinary stasis
• Measurement of differential renal function and tracer washout will vary depending on the protocol and radiopharmaceutical used, and care should be taken when interpreting results if comparative studies have been performed using different protocols or radiopharmaceuticals.

Whitaker test

• Involves placement of a percutaneous needle in the collecting system of the kidney and the infusion of contrast at a rate of 10 mL/min. A urodynamic catheter is also placed in the bladder, and intravesical pressures are monitored and subtracted from measured intrapelvic pressures during the infusion. Intrapelvic pressures are noted at the time that contrast is first seen extending passed the ureteropelvic junction and passed the ureterovesical junction.
• Interpretation:
  • Pressure <15 cm H2O considered normal
  • Pressure 15-22cm considered indeterminate
  • Pressure >22 cm H2O suggestive of obstruction

Hemodynamic changes with obstruction

• Renal blood flow is autoregulated primarily by afferent arteriolar tone.

Unilateral ureteral obstruction

• Triphasic pattern of renal blood flow (RBF) and ureteral pressure changes
  1. First phase
     • Initial 1-2 hours
     • Increase in pressure within the renal tubules and a subsequent decrease in GFR.
     • To compensate for this decreased GFR, there is an increase in RBF due to afferent arteriolar vasodilation
       • Several mechanisms for this increase in RBC have been postulated, including vasodilation from prostaglandins, nitric oxide and tubuloglomerular feedback.
         • Administration of either a prostaglandin synthesis inhibitor (NSAID) or a nitric oxide synthase inhibitor has been shown to block the vasodilatory response and should therefore be avoided in the context of urinary obstruction.
         • ACE-inhibitors or angiotensin receptor blockers reduce constriction at the efferent and affarent arteriole, with a stronger effect on efferent.

• • 1. Second phase
       • From 2-5 hours
       • Ureteral[/tubular] pressure remains elevated but RBF begins to decline. As a result, GFR declines
         • The decline in GFR is accompanied by an increase in efferent arteriole resistance
           • Activation of the renin-angiotensin system appears to play a role in the efferent arteriole vasoconstriction along with endothelin and thromboxane A2.
         • Note that SASP 2017 suggests that efferent arteriole constriction does not occur in the second phase of UUO, only the second phase of BUO. However, 2015 AUA Update on post-obstructive diuresis suggests that efferent arteriole constriction occurs in the second phase of both UUO and BUO.
    2. Third phase
       • Both ureteral[/tubular] pressure and RBF flow progressively decline, resulting in a gradual loss in renal function
       • By about 24 hours after obstruction, the pressure has declined to pre-occlusion levels or even less. GFR remains decreased compared to baseline.
         • In addition, there is a shift of blood flow from the outer to inner cortex with UUO that is opposite to that which is seen with BUO.
  • Renin-mediated hypertension sometimes occurs in acute unilateral renal obstruction and may present a clinical picture suggestive of a renovascular etiology; however, angiographic studies can distinguish if the hypertension is due to a vascular lesion.

Bilateral Ureteral Obstruction (BUO) or Obstruction of a Solitary Kidney

• Complete obstruction of urinary flow results in anuria.

1. First phase
   • Similar to UUO, there is an initial increase in RBF with BUO but this response appears to be less pronounced and of shorter duration (≈90 minutes)
2. Second phase
   • Large decrease in RBF. As a result, GFR declines
     • The decline in GFR is accompanied by an increase in efferent arteriole resistance
3. Third phase
   • The collecting system pressure remains elevated for longer than unilateral obstruction and is often still high at 24 hours
     • It is believed that this persistent increased pressure is secondary to afferent arteriolar vasodilation and efferent arteriolar vasoconstriction, which may be caused by the accumulation of atrial natriuretic peptide or other factors associated with complete obstruction.
     • There is a shift of blood flow to the outer renal cortex with BUO, in contrast to the reversed pattern with UUO.
     • During UUO, preglomerular vasodilation is followed by a more prolonged PREglomerular vasoconstriction, and this increase in afferent arteriolar resistance causes a reduction in glomerular capillary pressure that in turn results in decreased intratubular pressure. In contrast, during BUO preglomerular vasodilation is followed by a prolonged POSTglomerular vasoconstriction

Partial ureteral obstruction

• Effects on renal hemodynamics and GFR are variable, depending on the severity and the duration of obstruction. In general, partial obstruction results in decreased RBF and GFR in the ipsilateral kidney

Egress of urine from the kidney

• Although normal flow of urine from the kidney through the urinary tract is compromised with obstruction, urine may still egress from the kidney by two possible mechanisms:
  1. A rupture of the calyceal fornix and subsequent extravasation of urine can occur during acute obstruction
  2. During chronic obstruction, fluid is thought to exit primarily into the renal venous system [pyelovenous backflow]

Effects of obstruction on tubular function

• Normal urine concentrating ability depends on
  1. A hypertonic medullary interstitial gradient
     • Established by active sodium transport out of the tubule and the countercurrent exchange mechanism
  2. Variable permeability of the tubules to water
     • Mediated by aquaporin water channels.
• Mechanisms of nephropathy secondary to obstruction leading to disrupted electrolyte and acid/base balance:
  1. Decreased concentrating ability, due to (3):
     1. Disruption of the medullary hypertonic interstitial gradient leads to a loss of the osmotic driving force for water to move into the interstitium
     2. Decreased sodium transport after release of obstruction, resulting in salt wasting and also contributes to the concentrating defect observed in response to obstruction
     3. BUO leads to a decrease in the expression of aquaporins (1, 2 and 3) that are important in the absorption of water; a decreased expression of aquaporin 1 can persist after 30 days from relief of obstruction
        • Primary cause of persistent concentrating defect after relief of BUO
  2. Impaired urinary acidification, due to:
     • impaired H+ excretion and bicarbonate transport within the tubule
       • The cumulative evidence shows a major acidification defect in the distal nephron. Release of obstruction does not result in bicarbonaturia, indicating that proximal reclamation remains intact. There is a defect in the proximal handling and breakdown of glutamine, which means that a higher proportion of protons are buffered as titratable acid. The best evidence indicates a defect in the expression of H+-ATPase in the collecting duct
  3. BUO prevents excretion of potassium, phosphate and magnesium. In cases of UUO the overall balance of these electrolytes is maintained by compensation from the contralateral kidney.
  4. Urinary dilution is not affected by chronic unilateral ureteral obstruction.

Pathologic changes of obstruction

• The histologic derangements associated with early obstruction are localized primarily to the tubulointerstitial compartment of the kidney and include:
  1. Massive tubular dilation
  2. Progressive tubulointerstitial fibrosis
  3. Inflammatory cell infiltration
     • One of the earliest pathologic findings associated with UUT obstruction
  4. Apoptosis of tubular and interstitial cells
  • The glomerulus is the renal structure that is best preserved in the presence of obstruction.
    • Glomerular changes are the last to occur with hydronephrosis
    • With long-term obstruction, other more distal components of the kidney are destroyed first.
• Long-standing obstruction ultimately results in glomerulosclerosis most likely as a result of chronic inflammation and/or hyperfiltration injury
• Molecular mechanisms of tubulointerstitial fibrosis
  • Tubulointerstitial fibrosis is a major pathologic component of obstructive renal injury and is associated with a significant accumulation of matrix-producing fibroblasts
    • Fibroblasts are derived from (3):
      1. Resident renal fibroblasts
      2. Bone marrow–derived fibroblasts
      3. Phenotypic transformation of renal tubular epithelial cells into matrix-producing fibroblasts (epithelial mesenchymal transition)
  • One of the earliest histologic changes in the obstructed kidney is an increase in inflammatory cell infiltration into the interstitial compartment of the kidney.
  • There is increased expression of TGF-β with obstruction that contributes to an increase in the extracellular matrix of the kidney and promotes inflammation.
• The release of TNF-α, a potent inflammatory cytokine, is stimulated by angiotensin, especially in the first few hours of renal obstruction.
  • TNF-α can upregulate its own expression as well as that of other inflammatory mediators, such as interleukin-1, platelet-activating factor, nitric oxide, eicosanoids, and cell adhesion molecules.
• Caspases are known to mediate apoptotic cell death in obstructed kidneys
• The presence of increased collagen deposition in the renal parenchyma at the time of pyeloplasty and the presence of extensive glomerulosclerosis have both been shown to have a negative impact on recovery of renal function

Clinical impact of renal obstruction

• Hypertension
  • More common in the presence of BUO than UUO.
  • More likely to be reversed after relief of BUO than UUO
• Compensatory renal growth in response to UUO or renal agenesis
  • The development of contralateral renal growth is influenced by age and the degree and duration of obstruction. This adaptive response allows the remaining kidney to ensure homeostasis and compensate for the lack of functioning contralateral renal tissue
  • The increase in renal volume related to compensatory renal growth is primarily a consequence of cellular hypertrophy rather than hyperplasia

Management of renal obstruction

Pain control

• NSAIDs
  • Reduce the pain associated with renal colic by reducing collecting system pressure and distention.
    • Mechanisms of action:
      • Reduces renal blood flow (primary effect)
      • Prevent the downregulation in aquaporin and major sodium channels in the renal tubule.
  • Superior to opioids
    • Associated with a greater reduction in pain scores, less need for “rescue” analgesia, and less emesis than with opioids
  • Should not be used in patients with renal insufficiency
    • Renal dysfunction can be exacerbated by the decrease in RBF induced by NSAIDs
    • Opiods are preferred in patients with renal insufficiency
  • COX-1 inhibitors also should not be used in patients at risk for gastrointestinal bleeding or when optimal platelet function is needed
  • COX-2 inhibitors have been linked to an increased risk for myocardial infarction and stroke as a result of an adverse effect on blood vessels
• Opiods
  • Although opioids have adverse side effects, they still provide excellent analgesia and remain an important tool in the management of the patient with renal colic
• α1-blockers
  • May facilitate stone passage
  • Reduces the requirement for analgesics

Renal drainage

• Ureteral obstruction that is symptomatic, accompanied by fever, complicated by undrained infection, or determined to be high grade, bilateral, or inducing renal failure warrants immediate drainage.
• Urine cultures should be obtained from the obstructed renal unit at the time of relief of obstruction when infection is suspected, and antibiotic therapy should be instituted.
  • If thick purulent fluid is obtained from the kidney at the time of ureteral stenting, a large-diameter stent should be placed
• Both percutaneous nephrostomy tubes and internal stents have been shown to be equally effective in relieving an obstructed collecting system with similar complication rates
  • Advantages of percutaneous nephrostomy tubes (5):
    1. Superior drainage, especially if the fluid is more purulent, due to larger caliber
    2. Ability to irrigate to prevent clogging
    3. Urine output of the kidney can be measured
    4. Excessive ureteral manipulation can be avoided, decreasing the risk for sepsis or rupture
    5. Can be done using US guidance with local anesthesia and conscious sedation, eliminating the need for an anesthesiologist and ionizing radiation exposure
  • Advantages of internal stents (2):
    1. Increased patient comfort
    2. Lower potential risk for bleeding complications; should be considered first for patients that are coagulopathic.
  • Internal stent placement typically requires greater x-ray exposure than percutaneous nephrostomy placement, which may be of concern in pregnant patients, and accelerated stent encrustation in pregnant patients may increase the risk for stent failure.
  • Historically, ureteral stenting has not been very effective for treating patients with extrinsic ureteral obstruction.
    • New metallic stents composed of a unique continuous unfenestrated coil of nonmagnetic alloy have proved to be safe and effective for patients with extrinsic compression of the ureter and offer longer indwelling times (3.5 to 11 months).
• The duration and severity of obstruction has a significant influence on renal functional recovery.
  • In a canine model, recovery of renal function after UUO:
    • 7 days: 100%
    • 14 days: 70%
    • 4 weeks: 30%
    • 6 weeks: 0%
  • More recent studies demonstrate that renal damage can persist despite recovery of renal function.
  • In humans, delayed relief of obstruction (>2 weeks) has been demonstrated to decrease long-term renal function and increase the risk for hypertension
  • Factors that have a positive influence on functional recovery include:
    1. Smaller degree of obstruction
    2. Greater compliance of the collecting system
    3. Presence of pyelolymphatic backflow
    4. Early relief of obstruction
  • Predictors of diminished recovery of renal function
    1. Older age
    2. Decreased renal cortical thickness
• In general, a nephrectomy should be considered for an obstructed kidney that contributes <10% to the patient’s overall renal function.
• After relief of obstruction, patients with BUO or an obstructed solitary kidney should be monitored for the development of post-obstructive diuresis
  • There is a profound diuresis and an increase in sodium excretion after relief of bilateral ureteral obstruction. This is due to ANP and, perhaps reduced sodium transporters. The massive natriuresis enhances excretion of phosphate, potassium, and magnesium.
    • ANP increases GFR by promoting dilation of the afferent arteriole and constriction of the efferent arteriole. It also decreases the sensitivity of tubuloglomerular feedback, inhibits renin release, and increases the ultrafiltration coefficient.

Post-obstructive diuresis (POD)

Definition

Post-obstructive diuresis: a period of significant polyuria (>200 ml/hr) occurring after the relief of urinary tract obstruction

• Note that definition varies based on source

Classification (2)

• Physiological vs. Pathological

• Physiological
  • More common
  • An appropriate diuresis in response to the volume and solute overload
  • Self-limiting and stops when homeostasis is restored
• Pathological
  • Less common
  • An inappropriate diuresis in response to the volume and solute overload
  • Can result in leading to derangements in blood chemistry and/or volume status.
    • For example, a pathological water diuresis can cause hypernatremia and a pathological sodium loss can cause hypovolemia.

Causes

• Will often accompany relief of BUO in the presence of a normal contralateral kidney
  • The accumulation of extracellular volume stimulates the synthesis and release of ANP, which promotes increased GFR and sodium excretion. Decreases in the aquaporin water channels in the kidney further promote the diuresis.
  • COX-2 activity may be increased in the post-obstructive phase and contributes to polyuria, and impaired urine-concentrating ability
  • One study found that predictors of POD were higher serum creatinine, higher serum bicarbonate and urinary retention.
• Not typically observed with relief of UUO, secondary to the presence of a functional contralateral kidney that can maintain fluid balance
  • Fractional excretion of sodium after relief of obstruction is greater in BUO than UUO
    • The natriuresis following relief of BUO is typically greater than that after UUO
• Most patients do not demonstrate a clinically significant POD after relief of urinary tract obstruction
  • Patients at risk for clinically significant POD typically exhibit signs of fluid overload, including (3):
    1. Edema
    2. Congestive heart failure
    3. Hypertension
  • Special consideration should also be given to patients with high urine outputs (>5 to 6 L daily).

Diagnosis and Evaluation

• History and Physical Exam
  • Physical Exam
    • Vital signs and volume status
• Labs (3):
  1. Serum electrolytes
  2. Creatinine/Blood urea nitrogen
  3. Urinalysis (including osmolality)
• Urine osmolality
  • Can indicate if the diuresis is more of a water or solute/osmotic diuresis.
    • Water diuresis is defined by a lower urine osmolality (often <150 mOsm/kg).
    • Urine osmolality of 150-300 mOsm/kg indicates mixed diuresis
    • Urine osmolality of 300-500 mOsm/kg is usually a solute/osmotic diuresis
  • During the obstruction, water retention can lead to expansion of the extracellular volume that leads to water diuresis as the extracellular volume is restored.

Management

• Continuous urinary drainage
  • Intermittent or gradual drainage is no longer recommended
    • Intermittent or gradual drainage of an obstructed bladder was thought to potentially decrease the rates of hematuria and hypotension. However, with quick drainage the rates of hematuria are generally low and not severe, while the decrease in blood pressure represents a normalization of the pressure without cardiovascular compromise.
• In patients with normal mental status, no evidence of fluid overload, normal electrolytes, and normal renal function
  • Regular monitoring of (3):
    1. Orthostatic vital signs
    2. Electrolytes
    3. Urine output
  • Free access to oral fluids
    • Generally, patients with a normal mental status should not be given IV fluids because this may prolong the period of diuresis
• In patients with evidence of a pathological post-obstructive diuresis
  • More frequent monitoring of vital signs, urine output, electrolytes (every 12 hours or more often if necessary), and urine osmolality
    • Patient can become hypovolemic as a result of excess water loss, and electrolyte abnormalities may develop as result of salt or potassium wasting
  • Patients should continue to have free access to oral fluids.
• Patients with poor cognitive function [or signs of dehydration] should be given IV fluids, although at a rate below maintenance.
  • The type of fluid used depends on the volume and sodium status (from AUA update):
    • Normal volume status (normal blood pressure):
      • Fluid replacement with free water (oral or IV) should be considered if there is a water diuresis (suggested by hypernatremia and a low urine osmolality).
        • Caution should always be taken to avoid correcting sodium alterations too rapidly.
    • Hypovolemia (low blood pressure)
      • 0.9% saline is usually the fluid of choice
      • If the volume deficit is not severe, 0.45% saline can also be used (particularly if hypernatremia is present) to provide sodium and water to help the kidneys maintain homeostasis.
    • Sometimes it is recommended that urine output be replaced with 0.5 ml fluid per 1 ml urine. While this may help prevent hypovolemia, it can also propagate the diuresis if the fluid replacement is inappropriately high for the patient.
    • Hypokalemia can occur and lead to life threatening arrhythmias if severe. As a result, potassium should be replaced aggressively, particularly if renal function is improving. Other electrolyte abnormalities should be corrected as well.
  • The urine is usually isosthenuric initially, and IV fluid replacement with 0.45% saline administration at a rate lower (50-75%) than the hourly urine output is recommended; 0.9% normal saline and Lactated Ringer have no role in post-obstructive diuresis and should not be given [SASP contradicts AUA Update]

Questions

1. What are the phases of a renal scan? Which is the most sensitive indicator of renal dysfunction?
2. Which nuclear scan is preferred to assess renal scarring? Obstruction? GFR?
3. What T1/2 on a nuclear scan is considered non-obstructed vs. obstructed?
4. What are reasons for a false-positive renal scan?
5. What are limitations of a low-dose CT scan?
6. What are the phases of a renal scan?
7. Describe the changes that occur in renal blood flow, ureteral pressure, and GFR in unilateral and bilateral urinary obstruction
8. What are advantages of a nephrostomy tube of ureteral stent?
9. What is the definition of post-obstructive diuresis? What mechanisms contribute to its occurrence?

Answers

1. What are the phases of a renal scan? Which is the most sensitive indicator of renal dysfunction?
   1. Flow (initial), renal, excretion
   2. Renal
2. Which nuclear scan is preferred to assess renal scarring? Obstruction? GFR?
3. What T1/2 on a nuclear scan is considered non-obstructed vs. obstructed?
4. What are reasons for a false-positive renal scan?
5. What are limitations of a low-dose CT scan?
6. What are the phases of a renal scan?
7. Describe the changes that occur in renal blood flow, ureteral pressure, and GFR in unilateral and bilateral urinary obstruction
8. What are advantages of a nephrostomy tube of ureteral stent?
   1. Superior drainage, especially if the fluid is more purulent, due to larger caliber
   2. Tubes can be irrigated to prevent clogging
   3. Urine output of the kidney can be measured
   4. Excessive ureteral manipulation can be avoided, decreasing the risk for sepsis or rupture
   5. Can be done using US guidance with local anesthesia and conscious sedation, eliminating the need for an anesthesiologist and ionizing radiation exposure
9. What is the definition of post-obstructive diuresis? What mechanisms contribute to its occurrence?

References

• Wein AJ, Kavoussi LR, Partin AW, Peters CA (eds): CAMPBELL-WALSH UROLOGY, ed 11. Philadelphia, Elsevier, 2015, chap 48