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.
Self-Test
1. What are the phases of a renal scan, and which is the most sensitive indicator of renal dysfunction? Flow (initial), renal, and excretory phases — the renal phase is the most sensitive.
2. Which nuclear tracer is preferred for renal scarring, for obstruction, and for GFR? Scarring → DMSA; obstruction → MAG3; GFR → DTPA.
3. What T½ on a diuretic renogram indicates a non-obstructed versus an obstructed system? <10 min is non-obstructed; >20 min is high-grade obstruction (10–20 min is indeterminate).
4. What causes a false-positive renal scan? Hepatobiliary activity, dehydration, neonatal immaturity, high-grade reflux, poor renal function (CKD), and a massively dilated collecting system with stasis.
5. What are the limitations of low-dose CT? Stones <3 mm, patient obesity, and impaction at the ureterovesical junction.
6. Describe the RBF, ureteral pressure, and GFR changes in unilateral versus bilateral obstruction. UUO: an initial rise in tubular pressure with a compensatory rise in RBF, then falling RBF/GFR with efferent vasoconstriction, then a decline of both (pressure to baseline by 24 h). BUO: a smaller/shorter RBF rise, a large RBF/GFR fall, and a collecting-system pressure that stays elevated past 24 h.
7. What are the advantages of a nephrostomy tube over a ureteral stent? Superior large-caliber drainage of purulent fluid, the ability to irrigate, measurable renal urine output, avoidance of ureteral manipulation, and US-guided placement under local anaesthesia.
8. What is post-obstructive diuresis, and what mechanisms contribute to it? Polyuria (>200 mL/hr) after relief of obstruction, driven by accumulated ANP, reduced sodium transporters, downregulated aquaporins, and increased COX-2 activity.