Urinary Tract Obstruction

Lecture given:


Define the term hydronephrosis and provide a differential diagnosis


  • Uremia: clinical signs and symptoms seen as a result of renal failure (fluid overload, hyperkalemia, impaired mentation, pericarditis, etc)
    • azotemia: elevation of BUN
  • Obstructive uropathy: reversible or irreversible renal dysfunction due to effects of impaired urine drainage
  • Hydronephrosis: dilation of the renal pelvis and calyces (not the same as obstruction)

Hydronephrosis :

  • Can occur with or without obstruction (e.g. vesico-ureteral reflux, megaureter)
  • Identify by ultrasound, intravenous pyelogram, CT

List the potential causes of obstructive renal failure

  • Congenital - e.g. uretheral pelvic junction obstruction by blood vessel compressing; or due to aperistaltic segment
    • Horseshoe kidneys are prone to UPJ and stones
  • Acquired
  • Benign or Malignant
  • Calyceal
  • Renal pelvis
  • Ureteral (unilateral or bilateral)
    • Renal colic: classically described pain associated with acute ureteral obstruction due to an obstructing stone
      • Very severe
      • Persistent with waves of increasing pain
      • Unilateral, begins in flank area and may radiate into the scrotum or labial areas (dermatones T12-L2 "Loin to groin" pain)
      • 85% of stones will show up on xray
  • Bladder outlet
    • Urinary retention: inability to void urine; can be acute (painful) or chronic (not painful)
    • Most commonly seen in bladder outlet obstructure due to BPH
    • Can also occur due to prostate cancer, urethral strictures, neurogenic causes
    • Obstructure can cause stones and frequent UTIs
  • Intrinsic or extrinsic

Outline the principles of treating obstructive renal failure and post obstructive diuresis

Urinary tract obstruction

  • Pathophysiology - Ischemic event causes the renal injury
    • results initially in increase in collecting system pressures (from 6-7 to 50-70mmHg)
    • renal blood flow (RBF) initially increase due to pre-glomerular vasodilation to maintain GFR
    • Persistent elevation in RBF causes shunting of blood to the vasa recta, causing a washout of the countercurrent exchange gradient in the renal medulla. Ability to concentrate urine is lost
    • After 6 hours of obstructure, RBC drops below baseline level due to pre-glomerular vasoconstriction, and ureteral pressures fall
    • Reduced blood flow produces cellular atrophy (tubular damage)
    • It will take 4-6 weeks before long term damage occurs, if there is no infection

Renal impairment

  • Pathophysiology
    • First derangement is the loss of renal concentrating ability
    • Inability to excrete K, and maximally acidifying the urine
    • Glomerular function is spared until late
    • Eventually, all renal functions (including endocrine) are affected

Factors influencing severity of renal dysfunction

  • Degree: Complete or partial obstruction
  • Time: >6 weeks of complete obstruction results in irreversible loss of renal function
  • 50% or 100%: Unilateral or bilateral
  • Infection: Will accelerate nephron loss

Major sequelae

  • Loss of renal function
  • UTI/sepsis (urine stasis leading to ecoli growth, abx ineffective)
  • Stones (stasis, infection)


  • Clinical features
    • Flank pain/renal colic (Loin to Groin)
    • Urinary retention/overflow incontinence
    • Anuria/Oliguira
    • Uremia
    • Stones
    • Recurrent UTI
  • Lab investigations
    • Elevated BUN & Cr (bilateral ureteral or bladder outlet obstruction)
    • Abnormal urinary indices (higher Na than in prerenal or renal causes of AKI)
  • Imaging
    • Ultrasound: often used to screen
    • IVP: CI if SeCr > 200
    • Retrograde pyelogram
    • Lasix renogram (distinguish dilation from physiologically significant obstruction)


  • Supportive care: acid-base, electrolyte balance, dialysis PRN
  • Temporizing measures to relieve source of obstruction
    • Bypass the cause of obstruction
    • Catheter (for bladder outlet obstruction)
    • Stent or nephrostomy tube (renal or ureteral obstruction)
  • Definitive treatment
    • Remove the cause
    • BPH - TURP, drugs
    • Stone - ESWL (Extracorporeal shock wave lithotripsy), ureteroscopy, percutaneous stone removal

Post obstructive diuresis

  • following relief of complete bilateral ureteral or bladder outlet obstruction
  • Large volume diuresis
  • Usually mild and self-limiting, but may be life threatening
  • Causes:
    • Impaired Na reabsorption/urinary concentrating ability, retention of urea and water. Upon relieving obstruction, diuresis of excess urea and water, and continued loss of electrolytes and water until concentrating mechanism is regained
    • Nephrogenic diabetes insipidus (rare) when DCT doesn't respond to ADH, lead to salt losing nephropathy (water and salt wasting). Very rapid hypovolemia and electrolyte disturbances
    • Wash out concentration gradient of the loop of henle by the vasa recta
    • Patient is at first volume overloaded, and will try to get rid of water on relief
  • Management:
    • Hourly monitoring of urine output
    • frequent vital signs (esp postural BP - sensitive for picking up dehydration)
    • daily weight
    • check serum lytes, esp K
    • UO may exceed 150cc/h, but most patients able to replenish losses by drinking
    • if UO>200cc/h, or if patient not capable of drinking, IV fluid is necessary (IV NS 50% of previous hour UO +/- K)


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