Urinary Tract Obstruction

Principles & Management of Obstruction

Obstruction damages the kidney through a predictable sequence of haemodynamic, tubular, and fibrotic changes. This tab covers the diagnosis of obstruction, the haemodynamic response to unilateral versus bilateral obstruction, the effects on tubular function and renal architecture, and the management of drainage, recovery, and post-obstructive diuresis.

Diagnosis and Evaluation

• History — the most common symptom of acute obstruction is flank pain (from collecting-system stretch), whereas chronic obstruction is usually painless. Always consider obstructive uropathy with new-onset hypertension, unexplained renal failure, or recurrent UTIs.
• Labs — the fractional excretion of sodium (FENa = (PCr × UNa)/(PNa × UCr)) distinguishes the cause of acute kidney injury: FENa <1% suggests pre-renal and FENa >4% suggests post-renal failure.

Ultrasound

Hydronephrosis (dilatation of the pelvis and calyces) does not equal obstruction — it can occur without it (e.g. reflux), and significant obstruction can exist without hydronephrosis (early acute obstruction). Obstructive nephropathy is the parenchymal damage that results from obstruction. Standard US may appear normal in 50% of acute obstruction. A resistive index >0.70 was proposed to improve detection but has not proven useful; colour-Doppler ureteric jets can be assessed with good hydration and a normal contralateral system.

CT

CT detects most radiolucent stones except protease-inhibitor (indinavir) and mucoid-matrix stones — sensitivity 96%, specificity/PPV 100%. Low-dose CT is limited by stones <3 mm, obesity, and UVJ impaction. CT urography uses three phases (unenhanced, nephrographic at ~100–120 s, and excretory at ~3–5 min) and omits the corticomedullary phase (the corticomedullary phase is best for veins/renal-vein involvement; the nephrographic phase is best for parenchymal lesions). (The 2016 AUA microhematuria guideline describes a 4-phase protocol — unenhanced, arterial, corticomedullary, excretory.)

MRI

MRI is poor for stones (signal voids). The renal transit time (cortex → proximal ureter) interprets as ≤4 min normal, >4–<8 min equivocal, ≥8 min obstructed, and gadolinium MR urography gives dynamic functional assessment correlating with diuretic scintigraphy. (Excretory urography depends on GFR — limited in renal insufficiency, contraindicated in contrast allergy or pregnancy.)

Nuclear Renography

Tracer	Clinical question	Clearance	Use in renal failure
MAG3	Obstruction, differential function, perfusion	~95% tubular secretion, <5% filtration	Yes
DTPA	Obstruction, differential function, GFR	>95% glomerular filtration	No (must be filtered)
DMSA	Morphology (cortical scars), differential function	Binds proximal tubules	—

MAG3 is preferred for the obstructed collecting system, DTPA for GFR, and DMSA for renal scarring and recovery prediction. The scan has three phases — flow (perfusion), renal (function; the most sensitive indicator of dysfunction, peaking at 2–5 min), and excretory (a diuretic renogram uses furosemide 0.5 mg/kg). The washout T½ is <10 min in a normal/non-obstructed system, 10–20 min indeterminate, and >20 min high-grade obstruction. False positives (mnemonic: Hepatobiliary, Dehydration, Neonates, Reflux, CKD, Dilation) include hepatobiliary/gallbladder activity, dehydration, neonatal renal immaturity, high-grade reflux, poor renal function, and a massively dilated system with stasis.

Whitaker Test

A percutaneous needle infuses contrast into the collecting system at 10 mL/min while subtracting intravesical pressure: <15 cm H₂O is normal, 15–22 indeterminate, and >22 cm H₂O suggests obstruction.

Hemodynamic Changes

Renal blood flow (RBF) is autoregulated mainly by afferent arteriolar tone.

• Unilateral ureteral obstruction (UUO) — triphasic: Phase 1 (1–2 h) — rising tubular pressure and falling GFR, with a compensatory rise in RBF from afferent vasodilation (prostaglandins, nitric oxide, tubuloglomerular feedback) — so NSAIDs and NOS inhibitors should be avoided as they block this response. Phase 2 (2–5 h) — pressure stays high but RBF and GFR decline, with efferent vasoconstriction (renin-angiotensin, endothelin, thromboxane A2). Phase 3 — both pressure and RBF fall (pressure returns to baseline by ~24 h while GFR stays low), with a flow shift from outer to inner cortex. UUO produces preglomerular vasodilation then prolonged pre-glomerular vasoconstriction.
• Bilateral obstruction (BUO) / solitary kidney — complete obstruction causes anuria. The initial RBF rise is smaller and shorter (~90 min); RBF then drops markedly with efferent vasoconstriction, and the collecting-system pressure stays elevated longer (often high at 24 h) from afferent vasodilation and efferent vasoconstriction (ANP). Flow shifts to the outer cortex, and BUO produces prolonged post-glomerular vasoconstriction.
• Partial obstruction — variable, but generally reduces ipsilateral RBF and GFR.

Urine can still egress despite obstruction — by calyceal fornix rupture/extravasation (acute) or pyelovenous backflow (chronic).

Effects on Tubular Function

Obstruction disrupts electrolyte and acid-base balance:

• Decreased concentrating ability — from disruption of the medullary hypertonic gradient, reduced sodium transport after relief (salt wasting), and (in BUO) downregulation of aquaporins 1–3; reduced aquaporin-1 can persist >30 days and is the primary cause of the persistent concentrating defect after BUO relief.
• Impaired urinary acidification — a distal-nephron defect, best explained by reduced H⁺-ATPase in the collecting duct (proximal bicarbonate reclamation stays intact).
• BUO prevents excretion of potassium, phosphate, and magnesium (UUO is compensated by the contralateral kidney); urinary dilution is unaffected by chronic UUO.

Pathologic Changes

Early injury is tubulointerstitial — massive tubular dilation, progressive tubulointerstitial fibrosis, inflammatory infiltration (one of the earliest findings), and apoptosis. The glomerulus is best preserved (glomerular changes occur last; long-standing obstruction eventually causes glomerulosclerosis). Matrix-producing fibroblasts arise from resident renal fibroblasts, bone-marrow-derived cells, and epithelial-mesenchymal transition; TGF-β and angiotensin-stimulated TNF-α drive the fibrosis and inflammation. Increased collagen and glomerulosclerosis at pyeloplasty predict poorer functional recovery.

Clinical Impact

• Hypertension is more common with BUO than UUO and more likely to reverse after BUO relief.
• Compensatory renal growth (after UUO or agenesis) is primarily hypertrophy, not hyperplasia.

Management

• Pain control — NSAIDs reduce colic by lowering collecting-system pressure (mainly via reduced RBF) and are superior to opioids (better pain scores, less rescue analgesia, less emesis), but are avoided in renal insufficiency (opioids preferred there) and in GI-bleed risk (COX-1) or cardiovascular risk (COX-2 → MI/stroke). α1-blockers aid stone passage and reduce analgesic need.
• Drainage — obstruction that is symptomatic, febrile, infected, high-grade, bilateral, or causing renal failure needs immediate drainage; obtain a urine culture from the obstructed unit. Percutaneous nephrostomy and internal stents are equally effective with similar complication rates. Nephrostomy advantages: superior (larger-caliber) drainage of purulent fluid, irrigation, measurable urine output, less ureteral manipulation (less sepsis/rupture), and US-guided placement under local anaesthesia. Stent advantages: greater comfort and lower bleeding risk (preferred if coagulopathic), though stent placement needs more radiation and encrusts faster in pregnancy. Standard stents work poorly for extrinsic obstruction (newer metallic coil stents do better).
• Recovery — depends on duration and severity (a canine model showed 100% recovery at 7 days, 70% at 14, 30% at 4 weeks, 0% at 6 weeks); in humans, relief delayed beyond 2 weeks reduces long-term function and raises hypertension risk. Consider nephrectomy for a kidney contributing <10% of total function. After relief of BUO or a solitary obstructed kidney, monitor for post-obstructive diuresis (driven by ANP, which raises GFR by dilating the afferent and constricting the efferent arteriole).

Post-Obstructive Diuresis

POD is significant polyuria (>200 mL/hr) after relief of obstruction. It is physiological (more common — an appropriate, self-limiting response to volume/solute overload) or pathological (an inappropriate diuresis causing derangements — e.g. a water diuresis causing hypernatremia, or sodium loss causing hypovolemia).

• It typically follows BUO relief, not UUO (the functional contralateral kidney maintains balance), and the FENa after relief is greater in BUO. Most patients have no clinically significant POD; those at risk show fluid overload (edema, CHF, hypertension) or very high output (>5–6 L/day).
• Diagnosis — assess volume status; check serum electrolytes, creatinine/BUN, and urine osmolality (water diuresis <150 mOsm/kg, mixed 150–300, solute/osmotic 300–500).
• Management — use continuous drainage (intermittent/gradual is no longer recommended). With normal mentation, electrolytes, and renal function: monitor orthostatic vitals, electrolytes, and output with free oral fluids and no IV fluids (which prolong the diuresis). With a pathological POD: monitor more frequently (≥q12h), and give IV fluids only for poor cognition or dehydration, below maintenance — free water for a water diuresis with hypernatremia, 0.9% saline for hypovolemia (or 0.45% if the deficit is mild), correcting sodium slowly and replacing potassium aggressively.

Ureteropelvic Junction Obstruction

UPJO is restriction of urine flow from the renal pelvis to the proximal ureter. Most cases are congenital (often presenting later in life), and neonatal UPJO is usually detected on maternal-fetal ultrasound. This tab covers its etiology, evaluation, and the full range of management — from observation through endopyelotomy to pyeloplasty.

Etiology

UPJO is classed as congenital/primary vs acquired/secondary and intrinsic vs extrinsic.

• Congenital (mnemonic SHAVA): true ureteral Stricture; High insertion (more common with renal ectopia/fusion); Aberrant (crossing) vessels — which lower endopyelotomy success; Kinks or Valves from mucosal/muscular infoldings; and an Aperistaltic segment. In newborns/infants UPJO is usually an intrinsic narrowing (an interruption of the UPJ circular muscle with altered collagen, causing functional discontinuity and poor pelvic emptying); in childhood/adolescence it is often extrinsic, from an accessory lower-pole vessel crossing anterior to the UPJ.
• Acquired (mnemonic CRIBS): Cancer, Reflux (VUR causing elongation/tortuosity/kinking), Ischemia or post-inflammatory/postoperative scarring, Benign lesions (e.g. fibroepithelial polyps), and Stones.
• Associated congenital anomalies include contralateral UPJO (most common), renal dysplasia, multicystic dysplastic kidney, renal agenesis, horseshoe kidney, VUR, and ectopic or duplex kidneys.
• Intermittent UPJO presents as Dietl's crisis — intermittent abdominal pain with nausea/vomiting after high fluid intake. A Lasix renogram may be falsely negative, so compare a renal ultrasound taken during pain to a symptom-free baseline; increased hydronephrosis when symptomatic is diagnostic, and pyeloplasty is curative.

Diagnosis and Evaluation

• Symptoms — periodic loin pain (typically after diuresis), vomiting, recurrent pyelonephritis, fever, and uncommonly an abdominal mass or haematuria.
• Labs — serum creatinine for baseline function.
• Imaging — CT/MR urography for anatomy, plus nuclear diuretic renography (MAG3, especially in children; DTPA in adults) for differential function and obstruction. Kidneys with <15% differential function are generally non-salvageable in adults (some sources use <10%); if salvageability is unclear, place a temporary stent or nephrostomy and repeat the function study.

Management

Indications for intervention (mirroring stone-plus-hypertension): symptoms, stones, infection, renal dysfunction, and causal hypertension. An asymptomatic patient with indeterminate significance can be observed with serial renal scans. Active options are decompression (stent/nephrostomy), endourologic procedures, pyeloplasty, and ureterocalicostomy.

Endourologic Procedures

Balloon dilation and endopyelotomy are less invasive with shorter recovery but carry a higher failure rate than pyeloplasty (percutaneous endopyelotomy succeeds in ~85–90%). Success depends on the degree of hydronephrosis, ipsilateral function, calculi, and crossing vessels — whereas pyeloplasty suits almost any anatomy; moderate-to-severe hydronephrosis most predicts endopyelotomy failure. Transplant-related obstruction is well suited to endoscopic management.

• Contraindications to endopyelotomy: >2 cm of obstruction, untreated UTI, and untreated coagulopathy.
• Approaches — retrograde ureteroscopic (no percutaneous access; direct visualisation) or percutaneous antegrade (allows simultaneous treatment of pyelocalyceal stones). The full-thickness incision is made laterally (devoid of crossing vessels) with an endopyelotome, holmium laser, or cutting balloon, and a stent is left across the incision to heal.
• Follow-up — avoid strenuous activity for 8–10 days; after stent removal, reassess at 1 month with diuretic renography, and follow for 2–3 years (late failures still occur at 36 months). Adverse events: early bleeding, urinary leak, and hydropneumothorax (higher with upper-pole access); late recurrent obstruction.

Pyeloplasty

The anastomosis must be widely patent, watertight, tension-free, healed over a stent, and funnel-shaped for dependent drainage. Absolute contraindications are untreated UTI, uncorrected coagulopathy, and cardiopulmonary unfitness. The transperitoneal laparoscopic/robotic approach is most widely used.

• Dismembered pyeloplasty (Anderson-Hynes) is preferred — universally applicable, it reduces a redundant pelvis, straightens a tortuous ureter, and is the only method that allows transposition of the UPJ relative to crossing vessels (and complete excision of the abnormal UPJ). It is less suited to long/multiple proximal strictures (where a spiral flap helps) or a small intrarenal pelvis.
• Non-dismembered pyeloplasty — the Foley Y-V-plasty repairs a high ureteral insertion, and flap techniques (Culp) are unsuitable with crossing vessels. External drainage is essential to prevent urinoma, suture-line disruption, and sepsis.
• Postoperative care — remove the Foley at 24–36 h and the drain before discharge; if drainage increases after Foley removal, replace it for 7 days. The ureteral stent is removed at 4–6 weeks, with follow-up diuretic renography. Late complications: persistent urinary leak (usually resolves, but a clot needs early drainage — a nephrostomy in children) and recurrent obstruction (most laparoscopic failures occur within 2 years; managed by repeat pyeloplasty or endoscopy).

Ureterocalicostomy

Indicated for UPJO or a proximal stricture with a small intrarenal pelvis, to provide dependent drainage in rotational anomalies (e.g. horseshoe kidney), or as a salvage after failed pyeloplasty. In general, an open/laparoscopic approach is used after failed endourologic treatment, and an endourologic approach after failed open repair.

Ureteric Stricture Disease

Evaluating and treating ureteral strictures is essential to preserve renal function and exclude malignancy. This tab covers the causes, work-up, and the full ladder of management — decompression, endourologic incision, and reconstruction (with the defect length each repair can bridge) — plus ureteroenteric anastomotic strictures.

Etiology

• Benign (mnemonic SIIRRII-PUF): Stones; endoscopic Instrumentation; Infection (tuberculosis); Renal-ablation injury; Radiation; Ischemia (trauma, surgical dissection); Idiopathic; and PeriUreteral Fibrosis (from abdominal aortic aneurysm or endometriosis).
  • Endometriosis causes cyclic flank pain, dysuria, urgency, haematuria, and recurrent UTIs, though most ureteral obstruction is asymptomatic. Mild obstruction with good function may respond to hormonal therapy (GnRH agonist or medroxyprogesterone/danazol); severe obstruction needs surgery ± hysterectomy/BSO.
  • Hysterectomy accounts for >50% of iatrogenic ureteral injuries — the ureter is most often occluded at the broad ligament and at the vaginal cuff/bladder trigone.
• Malignant — intrinsic (e.g. urothelial carcinoma) or extrinsic (e.g. cervical cancer).

Diagnosis and Evaluation

Flank pain is the usual symptom; check serum creatinine for baseline function. CT can identify obstruction, and an antegrade/retrograde pyelogram, CT urography, or diagnostic ureteroscopy defines the stricture's location and length. Assess differential function before treatment — endourologic therapy requires ≥25% function of the ipsilateral moiety (some sources 20%) for a reasonable success rate.

Management

Three tiers: decompression, endourologic procedures, and surgical repair.

Decompression

A ureteral stent works acutely for most intrinsic strictures, but extrinsic compression eventually needs percutaneous drainage or surgery; tandem (parallel) stents help in extrinsic obstruction. Stenting reduces ureteral contractility, and there is no clear consensus on metallic stents.

Endourologic Procedures

Best for strictures <2 cm with no prior intervention; the main contraindication is a stricture >2 cm (dilation alone usually fails).

• Balloon dilation — success 50–76% with unfavourable long-term outcomes; best for iatrogenic, non-anastomotic strictures (85% vs 50% for anastomotic). A stent is left 2–4 weeks, with diuretic renography ~1 month after removal.
• Endoureterotomy — incise lower strictures anteromedially (away from the iliac vessels) and upper strictures laterally/posterolaterally, using a cold knife, cutting electrode, or holmium laser.

Surgical Repair

The repair is chosen by the length and location of the defect:

Repair	Defect bridged	Key point
Ureteroureterostomy	2–3 cm	End-to-end, upper/mid ureter; tension-free (success >90%)
Ureteroneocystostomy	4–5 cm	Distal ureter; add psoas hitch/Boari if not tension-free
Psoas hitch	6–10 cm (some 5–8)	Lower ureter; fix bladder to psoas above the iliac vessels
Boari flap	10–15 cm	Tubularised bladder pedicle; flap length:base ≤ 3:1
Renal descensus	5–8 cm	Mobilise the kidney inferiorly (up to ~8 cm extra)

• Ureteroureterostomy suits short upper/mid defects; tension causes stricture, so lower strictures are better managed by ureteroneocystostomy. Ureterocalicostomy (ureteral stump sewn end-to-side into a calyx) is reserved for profound pelvis/UPJ damage.
• Ureteroneocystostomy may be intravesical, extravesical, or combined, tunnelled or not — refluxing vs anti-refluxing anastomosis shows no significant difference in renal function or stenosis (though a possible pyelonephritis risk in adults is unclear).
• Psoas hitch is preferred over ureteroureterostomy for lower-ureteral injuries (better blood supply); advantages over the Boari flap are simplicity, less vascular compromise, and fewer voiding problems; it is contraindicated with a small contracted bladder. The femoral nerve is most likely injured (also watch the genitofemoral nerve); contralateral superior-vesical-artery division adds bladder mobility.
• Transureteroureterostomy (TUU) transposes the injured ureter across the midline (through a tunnel under the sigmoid mesentery, proximal to the IMA) into the contralateral ureter — usually a delayed procedure. Absolute contraindication: insufficient donor length; relative: nephrolithiasis, urothelial malignancy, retroperitoneal fibrosis, chronic pyelonephritis, or abdominopelvic radiation (any process risking both ureters). A preoperative VCUG must exclude recipient reflux. Because it risks converting a unilateral injury into a bilateral one, ileal interposition or ureteroureterostomy with renal mobilisation are preferred.
• Ileal ureter substitution uses ileum for very long defects (not in the acute setting); contraindications are renal insufficiency (creatinine >2 mg/dL), inflammatory bowel disease, radiation enteritis, and bladder dysfunction/outlet obstruction. Use a segment ≥15 cm from the ileocecal valve; complications include metabolic abnormalities and malignancy (endoscopic surveillance from postoperative year 3). Other options are the Monti tube or appendix; autotransplantation is the final option before nephrectomy.

For the full operative technique of ureteroureterostomy, ureteroneocystostomy, and the psoas hitch, see the Ureteral Reconstruction procedure page.

Ureteroenteric Anastomotic Stricture

Strictures occur in 3–25% after continent diversion, most within 2 years. Risk rises with the dissection technique, bowel segment, anastomosis type, and side — higher on the left (the left ureter passes under the sigmoid mesentery and may angulate at the IMA); a refluxing anastomosis lowers the stricture risk and is preferred for continent reservoirs. Chronic non-obstructive hydronephrosis is common, so a fall in function or loss of reflux on loopogram should prompt diuretic renography. Endourologic management (long-term patency ~50%) is used first, reserving surgery for failures and strictures >1 cm; antegrade access is preferred (unlike de novo ureteral strictures). Endourologic success is far lower for left-sided strictures (19% vs 41% right) and for strictures >1 cm (6% vs 50%) — favouring primary repair on the left.

Retrocaval Ureter

A retrocaval (circumcaval) ureter passes behind the IVC, producing a characteristic S-shaped/"fish-hook" course and right-sided obstruction. It results from persistence of the posterior cardinal vein (which normally regresses, with the subcardinal vein becoming the infrarenal IVC). (The source cross-references the pediatric ureteral-anomalies chapter; the embryologic cause is added here from standard teaching.)

Retroperitoneal Fibrosis

Retroperitoneal fibrosis (RPF) is an inflammatory, fibrotic process that compresses the retroperitoneal structures, including the ureters. The mass typically centres on the distal aorta at L4–L5 and wraps around the ureters, causing hydronephrosis by extrinsic compression or by interfering with ureteral peristalsis.

Background and Etiology

• Idiopathic (70%) — associated with chronic aortitis.
• Identifiable cause (30%) — most notably medications: methysergide (and other ergot alkaloids), β-blockers, and phenacetin.

The pathogenesis is unknown but appears autoimmune.

Diagnosis and Evaluation

Symptoms and signs are usually non-specific. Labs may show an elevated ESR and CRP, moderate leukocytosis, anaemia, and variable renal insufficiency with electrolyte abnormalities. Although most patients with malignant RPF have a prior cancer history, a thorough work-up for occult malignancy is essential — the most common malignancy in RPF is lymphoma.

Management

• Decompression — patients with hydronephrosis and uraemia need emergent decompression by nephrostomy or stent. Stent placement is usually straightforward in RPF and allows retrograde pyelography and internal drainage; a nephrostomy is favoured in the critically ill patient with electrolyte derangement and little urine output. Monitor for post-obstructive diuresis afterward.
• Medications — steroids are the primary medical therapy, and patients with active inflammation (raised ESR/CRP/leukocytosis or active inflammation on biopsy) respond best. Immunosuppressants (azathioprine, mycophenolate, cyclosporine, cyclophosphamide, colchicine) are reserved for steroid failure — relapse during steroid taper is as high as 50%. Other agents include medroxyprogesterone, progesterone, and particularly tamoxifen.
• Ureterolysis — performed open or laparoscopically. Because the process is generally bilateral (even when hydronephrosis appears unilateral), bilateral ureterolysis is usually required, with the ureters protected by intraperitonealisation or omental wrapping; if ureterolysis is not feasible, renal autotransplantation is an option.