- 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 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.
|Renal||Bladder inlet||Bladder outlet||Urethra|
|Acquired intrinsic defects|
|Acquired extrinsic defects||Trauma|
- 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)
|Hemodynamic effects||Tubule effects|
|Release of obstruction||Slow ↑ in GFR, which is variable|
Clinical presentation depends on the location, degree, and how quickly the obstruction develops.
Symptoms can include:
- 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:
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
- 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:
- 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
- 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
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.
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.
- Dmochowski R. R. Bladder outlet obstruction: etiology and evaluation. Reviews in Urology. 2005; 7 (Supplement 6): S3–S13.
- Kumar V, Abbas AK, Aster JC. (2015). Robbins & Cotran Pathologic Basis of Disease. Philadelphia, PA: Elsevier Saunders; 2015.
- MedlinePlus. (2020). Hydronephrosis of one kidney. Retrieved April 30, 2021, from https://medlineplus.gov/ency/article/000506.htm
- 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
- 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§ionid=192281753
- 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