Urinary Tract Obstruction & Postobstructive Diuresis

Where obstruction causes kidney injury

The bilateral rule. A single healthy kidney keeps serum creatinine near normal. Obstruction therefore produces AKI only when both kidneys are blocked, which can happen at the bladder outlet or urethra, in both ureters, or in the ureter of a solitary functioning kidney. Crystals or casts can also obstruct tubules from within (intratubular obstruction), and that form causes no hydronephrosis. Obstruction is the most reversible cause of AKI, so it should be excluded early in any unexplained case.

Drug-induced retention. Anticholinergics (antihistamines, tricyclics, antipsychotics) weaken detrusor contraction. Alpha-1 agonists such as pseudoephedrine tighten the bladder neck, and opioids blunt bladder sensation and emptying. An older man with BPH who gets one of these drugs is the classic setup. Neurogenic bladder from diabetes, multiple sclerosis, or spinal cord injury causes retention through failed detrusor contraction.

Retroperitoneal fibrosis. Fibrous tissue encases the aorta and ureters and pulls the ureters medially. It may be idiopathic, part of IgG4-related disease, or drug-induced by methysergide and other ergots. The idiopathic and IgG4-related forms respond to glucocorticoids, and stents or nephrostomies protect the kidneys in the meantime. Advanced cervical cancer is a classic cause of bilateral ureteral obstruction and uremia.

Recognition and diagnosis

Clinical picture. Complete obstruction causes anuria, which few other forms of AKI produce. Partial obstruction can swing between oliguria and polyuria. Look for suprapubic fullness or a palpable bladder, overflow dribbling, flank pain, or a known pelvic cancer. The urine sediment is usually bland.

Testing. A bedside bladder scan measures the post-void residual, and a large residual confirms outlet obstruction. Renal ultrasound is the best initial imaging for the upper tract because it is fast and needs no contrast; it shows hydronephrosis and suggests its level. Bilateral hydroureter points to a bladder or pelvic process. CT defines the cause (stone, mass, fibrosis) when needed.

Ultrasound can miss obstruction in the first hours, in a volume-depleted patient, and when fibrosis or tumor encases the collecting system so it cannot dilate. Repeat the ultrasound after hydration or obtain CT if suspicion persists. Conversely, dilation without obstruction occurs in pregnancy, vesicoureteral reflux, and an extrarenal pelvis.

Relieving the obstruction

Bladder outlet. Place a urethral (Foley) catheter, which is both diagnostic and therapeutic. Use a suprapubic catheter if a stricture or other barrier prevents urethral passage. Rapid, complete drainage is safe, and clamping to decompress gradually is unnecessary. Then address the cause: stop offending drugs, start an alpha-blocker such as tamsulosin before a voiding trial, and add a 5-alpha-reductase inhibitor or plan surgery for BPH.

Upper tract. Ureteral obstruction is relieved in one of two ways:

• a retrograde ureteral stent placed cystoscopically, which avoids an external drain and is preferred with coagulopathy
• an antegrade, image-guided percutaneous nephrostomy, which is favored when extrinsic tumor compression prevents a stent from passing

Fever or sepsis with an obstructed kidney (for example, an infected ureteral stone) is a urologic emergency. Antibiotics cannot sterilize an undrained system, so give IV antibiotics and decompress urgently with a stent or nephrostomy. Delay lithotripsy or ureteroscopy until the infection has cleared.

Recovery. How much function returns depends on how long and how completely the kidney was obstructed. Relief within days usually allows good recovery, whereas prolonged complete obstruction leaves permanent loss.

Chronic obstruction and postobstructive diuresis

Chronic partial obstruction. Long-standing back-pressure damages the distal nephron and collecting duct. The result is a concentrating defect with nephrogenic DI-like polyuria and nocturia, hyperkalemic distal (type 4) RTA from impaired potassium and hydrogen ion secretion, and hypertension. Voiding large volumes therefore does not exclude obstruction.

Postobstructive diuresis. After bilateral obstruction (or obstruction of a solitary kidney) is relieved, urine output can exceed 200 mL/h. The first phase is an appropriate excretion of retained urea, salt, and water. A pathologic phase may follow, driven by the tubular concentrating defect, and it can outlast the volume excess. Patients with chronic retention, a high creatinine, edema, or confusion (who cannot drink to thirst) are most at risk. Complications include volume depletion, hypokalemia, hypo- or hypernatremia, and hypomagnesemia.