Urinary Tract Obstruction

Urinary tract obstruction (UTO) refers to the blockage of the urinary tract, which can occur anywhere in the urinary tract. Urinary tract obstruction can be acute or chronic, partial or complete, and unilateral or bilateral. Urinary tract obstruction can cause acute or chronic kidney disease. The etiology of UTO depends on where the UTO occurs in the urinary tract and includes kidney stones, transitional cell carcinoma, blood clots, and external compression. Clinical presentation depends on the location, degree, and acuteness of the obstruction. Symptoms can include pain, change in urine output, hypertension, hematuria, and increased serum creatinine. Diagnosis is made by imaging, with ultrasound being the preferred initial modality. The mainstay of treatment is to relieve the cause of obstruction with a nephrostomy tube, ureteral stent, or catheterization. Renal function prognosis after the UTO is relieved is dependent on the severity and duration of the obstruction.

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Overview

Epidemiology

  • No specific epidemiological data
  • More common than generally expected
  • Rare cause of acute kidney injury (AKI)
  • More common in children than adults, in patients presenting with urinary tract symptoms or kidney failure (due to congenital abnormalities)
  • More common in men than women (especially due to benign prostatic hyperplasia (BPH) as men age)
  • More common cause of AKI in outpatient setting than in the hospital setting

Etiology

Etiology can be congenital, acquired, or functional. Urinary tract obstruction can occur anywhere along the urinary tract:

  • Obstruction within the kidney causes dilation of specific affected calyces or caliectasis. 
  • Obstruction at or distal to the renal pelvis causes diffuse caliectasis or hydronephrosis.
Table: Etiologies of urinary tract obstruction
RenalBladder inletBladder outletUrethra
Congenital
  • Polycystic kidney disease
  • Peripelvic cyst
  • Ureteropelvic junction narrowing or obstruction (UPJO)
  • Vesicouterine reflux
  • Ureterocele
  • Retrocaval ureter
  • Bladder neck obstruction
  • Ureterocele
  • Posterior urethral valves
  • Anterior urethral valves
  • Stricture
  • Phimosis
  • Meatal stenosis
Acquired intrinsic defects
  • Calculi
  • Inflammation
  • Infection
  • Trauma
  • Sloughed papillae
  • Tumor
  • Blood clots
  • Benign prostatic hyperplasia
  • Cancer of prostate or bladder
  • Calculi
  • Diabetic nephropathy
  • Spinal cord disease
  • Calculi
  • Stricture
  • Tumor
  • Trauma
  • Phimosis
Acquired extrinsic defects
  • Pregnant uterus
  • Retroperitoneal fibrosis
  • Aortic aneurysm
  • Uterine leiomyomata
  • Carcinoma of uterus, prostate, bladder, colon, or rectum
  • Lymphoma
  • Pelvic inflammatory disease
  • Endometriosis
  • Accidental surgical ligation
  • Carcinoma of cervix
  • Carcinoma of colon
Trauma
Functional defects
  • Neurogenic bladder
  • Anticholinergic drugs
  • α-adrenergic antagonists
  • Diabetic nephropathy
  • Detrusor-sphincter dyssynergia
  • Dysfunctional voiding
  • External sphincter pseudodyssynergia
  • Multiple sclerosis
  • Parkinson disease

Pathophysiology

  • Obstruction induces apoptosis of the renal tubular cells: Glomerular cells are resistant to obstruction-related apoptosis. 
  • Renal tubular cell apoptosis is mediated via caspases (generated from cytokine release and inflammatory responses) 
  • Prolonged obstructive processes induce tubulointerstitial fibrosis and inflammation: accumulates extracellular matrix and promotes fibrosis 
  • Postobstructive diuresis: 
    • Physiologic phenomenon seen after acute release of bilateral obstruction 
    • Urine flow increases by about 3–10-fold.
    • Possible mechanisms:
      • Impaired sodium reabsorption due to tubular damage 
      • Impaired urine-concentrating ability
      • Solute diuresis with excretion of retained urea 
      • Increased circulating natriuretic factor (ANP)
Table: Effects of urinary tract obstruction (UTO) on glomerular filtration and renal blood flow
Hemodynamic effectsTubule effects
Acute obstruction
  • ↑ Renal blood flow
  • ↓ GFR
  • ↓ Medullary blood flow
  • ↑ Vasodilator prostaglandins and nitric oxide
  • ↑ Ureteral and tubule pressures
  • ↑ Reabsorption of urea, water, and sodium
Chronic obstruction
  • ↓ Renal blood flow
  • ↓↓ GFR
  • ↑ Renin-angiotensin production
  • ↑ Vasoconstrictor prostaglandins
  • ↓ Medullary osmolarity
  • ↓ Concentrating ability
  • ↓ Transport functions of sodium, potassium, hydrogen
  • Structural damage
  • Parenchymal atrophy
Release of obstructionSlow ↑ in GFR, which is variable
  • Natriuretic factors are present.
  • ↓ Tubule pressure
  • ↓ Solute load per nephron (e.g., urea, sodium chloride)

Clinical Presentation

Clinical presentation depends on the location, degree, and how quickly the obstruction develops.

Symptoms can include:

  • Pain:
    • Often absent
    • If present, is usually the result of bladder distention, secondary infection, or obstructing stone/mass
    • Associated with rate at which the distension develops
    • Often affects the flank or suprapubic region
  • Change in urine output:
    • Azotemia
    • Polyuria
    • Nocturia  
  • Hypertension
  • Hematuria

Classic laboratory findings:

  • Elevated serum creatinine
  • Urinalysis with red cells or white cells 
  • Hyperkalemic renal tubular acidosis: 
    • Mostly found in patients with chronic obstruction
    • Likely from mineralocorticoid resistance impairing distal sodium reabsorption

Diagnosis

  • Take a thorough history and physical:
    • Elicit any prior GU surgical history. 
    • Palpate for costovertebral angle tenderness. 
    • General abdominal exam assessing for suprapubic tenderness 
  • Urinalysis and culture: 
    • Hematuria: 
      • Gross 
      • Microscopic with > 3 RBCs per high power field 
    • Pyuria: WBCs in urine 
    • Bacteriuria: may reveal gross bacteria in urine specimen 
  • Labs: may reveal ↑ creatinine 
  • Gold standard is imaging: 
    • Hallmark finding is dilatation of the collecting system in 1 or both kidneys.
    • Ultrasound is the preferred imaging modality:
      • Advantage of no ionizing radiation 
      • Inexpensive 
      • Identifies hydronephrosis, but is not a functional test 
    • CT scan:
      • Provides superior anatomic information 
      • Ability to have contrasted images with both nephrographic and excretory phases 
      • Excretory phases allow for delayed contrast images to identify the level of obstruction 
      • Risks include: contrast nephropathy and ionizing radiation exposure 
    • Can use voiding cystourethrography to diagnose vesicoureteral reflux or bladder neck and urethral obstructions
Ultrasound of fetal bladder obstruction

Fetal ultrasound revealing urinary tract obstruction (UTO) with classic keyhole sign (B: bladder, U: urethra)

Image: “Ultrasound of fetal bladder obstruction” by St. David’s Women’s Center of Texas, Austin Maternal-Fetal Medicine, 12200 Renfert Way, G-3, Austin, Austin, TX 78758 USA. License: CC BY 4.0

Management

Treatment

Mainstay of treatment is to relieve the cause of obstruction.

  • UTO complicated by infection requires immediate relief of the obstruction to prevent sepsis and renal damage.
  • Drainage may be achieved by nephrostomy tube, ureterostomy, ureteral stent placement, or bladder catheterization.
  • Decompression of the urinary system is combined with antibiosis for sepsis-related obstruction. 
  • Benign prostatic hyperplasia can be treated with α-adrenergic blockers or 5α-reductase inhibitors. When associated with severe infection and bladder outlet obstruction, urethral catheterization is indicated.

Prognosis

After relief of obstruction:

  • Renal prognosis depends on:
    • If irreversible renal damage has occurred
    • Severity and duration of obstruction
  • Most functional recovery is seen 7–10 days
  • Some patients with severe renal failure may require dialysis.

With unrelieved obstruction:

  • Clinical course depends on whether the obstruction is complete, partial, or bilateral. 
  • Complete obstruction that is complicated by infection can lead to complete renal destruction within days.
  • Partial recovery of renal function can be seen after 1–2 weeks of complete obstruction.
  • After 8 weeks of complete obstruction, recovery is unlikely.

References

  1. Dmochowski R. R. Bladder outlet obstruction: etiology and evaluation. Reviews in Urology. 2005; 7 (Supplement 6): S3–S13.
  2. Kumar V, Abbas AK, Aster JC. (2015). Robbins & Cotran Pathologic Basis of Disease. Philadelphia, PA: Elsevier Saunders; 2015.
  3. MedlinePlus. (2020). Hydronephrosis of one kidney. Retrieved April 30, 2021, from https://medlineplus.gov/ency/article/000506.htm 
  4. Preminger GM. (2020). Urinary Tract Obstruction. Merck Manual Consumer Version. Retrieved April 30, 2021, from https://www.merckmanuals.com/home/kidney-and-urinary-tract-disorders/obstruction-of-the-urinary-tract/urinary-tract-obstruction 
  5. Seifter JL. (2018). Urinary tract obstruction. Jameson J, & Fauci AS, & Kasper DL, & Hauser SL, & Longo DL, & Loscalzo J (Eds.), Harrison’s Principles of Internal Medicine, 20e. McGraw-Hill. https://accessmedicine-mhmedical-com.aucmed.idm.oclc.org/content.aspx?bookid=2129&sectionid=192281753
  6. Zeidel ML, O’Neill WC. Clinical manifestations and diagnosis of urinary tract obstruction and hydronephrosis. UpToDate. Retrieved April 30, 2021, from https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-urinary-tract-obstruction-and-hydronephrosis

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