Renal & Urinary
Postrenal AKI: obstruction workup and decompression
— Older man with rising creatinine, nocturia, weak stream, hesitancy, or palpable suprapubic fullness
— Woman with cervical/ovarian cancer, endometriosis, or prior pelvic radiation/surgery presenting with AKI
— Anuria or wildly fluctuating urine output (intermittent total obstruction)
— AKI with bland urine sediment and no clear prerenal or intrinsic etiology
— Flank pain + AKI in a patient with one kidney, transplant, or known stones
— New AKI after pelvic surgery (think ureteral injury)
— <1 week obstruction: full recovery expected
— 1–4 weeks: partial recovery
— >12 weeks: largely irreversible fibrosis

— BPH: gradual hesitancy, weak stream, nocturia, incomplete emptying, dribbling, overflow incontinence
— Urethral stricture: prior STI, instrumentation, catheter trauma, pelvic radiation
— Bladder neck obstruction, prostate cancer, anticholinergic/opioid medications causing acute retention
— Neurogenic bladder: diabetes, MS, spinal cord injury, prior pelvic surgery
— Nephrolithiasis: sudden severe colicky flank pain radiating to groin, nausea, hematuria
— Malignancy (cervical, prostate, bladder, colorectal, retroperitoneal lymphoma): subacute flank discomfort, weight loss, B-symptoms
— Retroperitoneal fibrosis: vague back/flank pain, often IgG4-related, may follow methysergide or ergot use
— Papillary necrosis: sickle cell, analgesic nephropathy, diabetes, pyelonephritis—sloughed papillae obstruct ureter
— Iatrogenic ureteral ligation after hysterectomy/colorectal surgery
— Anuria alternating with polyuria → intermittent complete obstruction
— Fever + flank pain + AKI → obstructed infected system (urosepsis)—surgical emergency
— Gross hematuria + clots → clot retention or bladder/upper-tract tumor
— Constitutional symptoms → malignancy or retroperitoneal disease

— Hypertension is common (volume retention, RAAS activation)
— Fever raises concern for obstructed pyelonephritis → urgent decompression
— Hypotension + obstruction + fever = urosepsis, ICU territory
— Suprapubic dullness, tenderness, or palpable bladder dome above pubis suggests >500 mL retention
— CVA tenderness with hydronephrosis or pyelonephritis
— Palpable flank mass in massive hydronephrosis or renal mass
— Digital rectal exam: enlarged, smooth prostate (BPH) vs. nodular/asymmetric (cancer); boggy/tender (prostatitis)
— Phimosis, meatal stenosis, palpable urethral stricture
— In women: pelvic exam for cervical mass, fixed adnexal mass, procidentia/uterine prolapse compressing ureters
— Saddle anesthesia, decreased rectal tone, lower-extremity weakness → cauda equina as cause of neurogenic retention—emergency MRI
— Diabetic autonomic neuropathy: orthostasis with chronic retention
— Often euvolemic or hypervolemic (edema, elevated JVP, crackles)
— Anuric patient with full bladder = retention until proven otherwise
— After decompression, monitor for orthostasis from postobstructive diuresis

— BMP: creatinine, BUN, K⁺ (watch for hyperkalemia), bicarbonate (non-anion-gap metabolic acidosis from type 4 RTA pattern or distal RTA in chronic obstruction)
— CBC: leukocytosis suggests infection
— Urinalysis with microscopy: typically bland sediment; hematuria suggests stone/tumor; pyuria + bacteriuria suggests infection
— Urine culture if any suspicion of UTI
— Coagulation studies if intervention anticipated
— Early obstruction: FeNa <1% (prerenal-like)
— Prolonged obstruction (>24–48h): FeNa >2% (tubular dysfunction)
— Key distinction: Urine indices cannot distinguish postrenal AKI reliably—imaging is required.
— >300 mL → place Foley catheter immediately
— Document pre- and post-catheterization urine volume (>400 mL on initial drainage confirms retention)
— Sensitivity ~90% for hydronephrosis; specificity high
— Look for hydronephrosis, hydroureter, bladder distension, post-void residual, stones, masses
— False negatives: Early obstruction (<24 h), volume-depleted patient, retroperitoneal fibrosis encasing ureters without dilation, staghorn calculi

— Gold standard for nephrolithiasis (sensitivity/specificity >95%)
— Identifies size, location, and degree of obstruction; perinephric stranding suggests inflammation
— Stones ≥10 mm or proximal ureteral stones unlikely to pass spontaneously → urology referral
— Evaluates urothelial malignancy, ureteral strictures, extrinsic compression
— Indicated for unexplained hematuria + obstruction, suspected upper-tract tumor
— Pregnancy, contrast allergy, severe CKD where iodinated contrast is risky
— Good for retroperitoneal fibrosis (T2 signal characteristics) and pediatric evaluation
— Differentiates obstructive vs. non-obstructive hydronephrosis (e.g., chronic dilation without functional obstruction)
— Quantifies split renal function—critical before nephrectomy decisions
— Performed by urology/IR at time of stent or nephrostomy placement
— Defines exact level and length of ureteral lesion
— Evaluates urethra, prostate, bladder for stricture, tumor, foreign body
— Allows stent placement
— Reflux, posterior urethral valves (pediatric), neurogenic bladder evaluation
— Outpatient evaluation of detrusor function vs. outlet obstruction in chronic retention

1. Is there infection above the obstruction? (fever, leukocytosis, pyuria, sepsis) → emergent decompression within hours
2. Is there severe hyperkalemia, acidosis, uremia, or volume overload? → dialysis indications regardless of decompression timing
3. Is the obstruction bilateral or in a solitary/transplant kidney? → decompression urgent (within 24 h)
4. Is the obstruction unilateral with normal contralateral kidney? → semi-elective (days), but treat pain and prevent infection
— Bladder outlet: Foley catheter; if unable to pass, suprapubic catheter
— Ureteral: Retrograde ureteral stent (cystoscopy) or percutaneous nephrostomy (IR)
— Renal pelvis/UPJ: Percutaneous nephrostomy preferred
— Stent: Less invasive, internal, ideal for stones and benign strictures, requires general anesthesia and ability to traverse obstruction retrograde
— Nephrostomy: Preferred in infected obstruction, malignant obstruction with distorted anatomy, pregnancy, coagulopathy, or when stent cannot be placed; allows pressure monitoring and antegrade access
— Calcium gluconate (membrane stabilization), insulin + dextrose, β2-agonist, then K⁺ removal (loop diuretic if making urine, patiromer/SZC, or dialysis)

— First-line: IV ketorolac 15–30 mg or IM (NSAIDs reduce ureteral smooth muscle tone and inflammation)—avoid in AKI with rising creatinine, single kidney, or hypovolemia
— Alternative/adjunct: IV morphine or hydromorphone for severe pain or when NSAIDs contraindicated
— Acetaminophen as adjunct
— Tamsulosin 0.4 mg daily × up to 4 weeks (α1-blocker relaxes distal ureter)
— Counsel on orthostasis, "floppy iris" if cataract surgery planned
— Not indicated for stones <5 mm (usually pass spontaneously) or >10 mm (need intervention)
— α1-blockers (tamsulosin, alfuzosin) start at Foley placement; continue 3–7 days before trial of void
— 5α-reductase inhibitors (finasteride, dutasteride): long-term reduction in prostate volume; takes 3–6 months for effect; reduces PSA by ~50%
— Empirical broad-spectrum for obstructed infection (piperacillin-tazobactam, carbapenem if ESBL risk)
— Tailor to urine and blood culture
— Pre-procedural prophylaxis per AUA guidelines before stent/nephrostomy
— Anticholinergics, opioids (precipitate retention)
— Nephrotoxins (aminoglycosides, IV contrast, NSAIDs if intrinsic damage developing)
— ACEi/ARB held during AKI; resume after recovery
— Replace 50–75% of urine output with 0.45% saline if patient becomes hypovolemic or hyponatremic
— Monitor electrolytes (K⁺, Mg²⁺, phosphate) q6–12 h
— Most diuresis is appropriate (excretion of retained urea/Na/water); do not over-replace

— First-line for suspected bladder outlet obstruction
— Use 16–18 Fr; if resistance at prostate, try Coudé-tip catheter
— If unable after 2 attempts → urology consult for suprapubic catheter or filiform/follower dilation
— Document pre-drainage residual volume
— Indications: failed urethral catheterization, urethral stricture, urethral trauma (e.g., pelvic fracture with blood at meatus—urethral catheterization contraindicated until retrograde urethrogram)
— Placed by urology under ultrasound guidance
— Placed via cystoscopy by urology
— Indications: ureteral stones, benign strictures, post-surgical leak, malignant compression amenable to stenting
— Complications: stent symptoms (frequency, urgency, hematuria), encrustation if left >3 months, migration, infection
— Placed by interventional radiology under ultrasound/fluoroscopy
— Preferred over stent in: infected obstruction (better drainage of purulent material), pregnancy, coagulopathy (smaller tract), malignant obstruction with distorted bladder anatomy, failed retrograde access
— Allows antegrade pyelography and conversion to internal stent later
— Ureteroscopy with laser lithotripsy (stones <2 cm)
— Shock wave lithotripsy (selected stones)
— Percutaneous nephrolithotomy (stones >2 cm, staghorn)
— TURP or laser prostatectomy for BPH refractory to medical therapy
— Ureteral reimplantation, ileal conduit, urinary diversion for complex strictures or malignancy

— BPH prevalence ~50% by age 60, ~90% by 85; the dominant cause of postrenal AKI
— Polypharmacy review: anticholinergics, opioids, decongestants, antihistamines, TCAs all precipitate retention
— Beers Criteria flags: oxybutynin, diphenhydramine, amitriptyline in older adults
— Atypical presentations: delirium may be the sole manifestation of retention or urosepsis
— Consider pelvic organ prolapse (cystocele, uterine procidentia kinking ureters), pelvic malignancy, fecal impaction
— Atrophic urethritis can mimic urinary symptoms but doesn't cause obstruction
— Small kidneys (<9 cm) and increased echogenicity suggest chronic disease; superimposed AKI may have less reserve
— Hydronephrosis may be subtle if parenchyma is thin
— Recovery after decompression is often incomplete
— Avoid iodinated contrast when possible; use MR urography or non-contrast CT
— Single functioning kidney → any obstruction causes AKI
— Ureteral stricture at uretero-vesical anastomosis is common (~3–5%) within first year
— Lymphocele compression also possible
— Ultrasound with Doppler is first-line; low threshold for percutaneous nephrostomy
— Hepatorenal physiology complicates AKI workup—always rule out postrenal cause before diagnosing HRS
— Avoid NSAIDs entirely; use cautious opioid dosing
— Tense ascites can rarely cause functional ureteral compression

— Physiologic hydronephrosis (R > L) develops by 20 weeks due to gravid uterus and progesterone-mediated ureteral relaxation; rarely causes AKI alone
— Pathologic obstruction: stones (1 in 1500 pregnancies), pyelonephritis, rarely retroperitoneal pathology
— Imaging: renal ultrasound first; if equivocal, MR urography without gadolinium; low-dose CT only if essential
— Avoid NSAIDs (third trimester—premature ductus closure); avoid fluoroquinolones
— Decompression of choice: double-J ureteral stent or percutaneous nephrostomy—both safe; stents require frequent exchange (every 4–6 weeks) due to encrustation in hypercalciuric pregnancy
— Antibiotics for pyelonephritis: ceftriaxone IV; admit threshold low
— Posterior urethral valves (PUV): Most common cause of bladder outlet obstruction in male infants; presents with antenatal hydronephrosis, weak urinary stream, palpable bladder, AKI in neonate; diagnosed by VCUG; treated with cystoscopic valve ablation
— Ureteropelvic junction (UPJ) obstruction: Most common upper-tract obstruction in children; often detected on antenatal ultrasound; managed with pyeloplasty if symptomatic or worsening function on MAG3 renogram
— Vesicoureteral reflux (VUR): Hydronephrosis without true obstruction; diagnosed by VCUG; managed with prophylactic antibiotics or surgical reimplantation
— Ureterocele, ectopic ureter, neurogenic bladder (spina bifida): Other pediatric considerations

— Occurs in ~50% after relief of bilateral or complete obstruction; typically urine output >200 mL/h × 2 h or >3 L/24 h
— Mechanisms: appropriate excretion of retained urea/Na/water (physiologic) vs. pathologic tubular concentrating defect
— Risks: hypovolemia, hyponatremia, hypokalemia, hypomagnesemia, hypocalcemia, hypophosphatemia
— Management: replace 50–75% of urine output with 0.45% NS; q6–12 h electrolytes; do not match output 1:1 (perpetuates diuresis)
— Decompression of chronically distended bladder can cause mucosal bleeding
— Usually self-limited; clamping the Foley intermittently is not recommended—drain completely
— Obstructed pyelonephritis carries mortality 25–60% without timely decompression
— Continued bacteremia until source controlled
— Pressure-induced tubular atrophy, interstitial fibrosis, irreversible loss of nephrons
— Permanent CKD risk increases with duration >2 weeks
— From sepsis, hypotension, or contrast during workup
— Prolongs recovery beyond simple decompression
— Rare; chronic massive distension can cause spontaneous rupture
— Infection, dislodgment, encrustation, bleeding, perforation
— Forgotten stents are a malpractice flashpoint—always document removal/exchange schedule
— Chronic obstruction impairs distal tubular function; may persist post-relief

— Inability to pass urethral catheter
— Suspected urethral injury (pelvic fracture, blood at meatus)
— Obstructed urosepsis
— Bilateral hydronephrosis on imaging
— Solitary kidney with obstruction
— Pediatric obstruction (PUV, severe UPJ)
— Need for percutaneous nephrostomy (sepsis, failed retrograde access, pregnancy with coagulopathy)
— AKI requiring dialysis (AEIOU criteria)
— Severe electrolyte derangements
— Diagnostic uncertainty between postrenal, intrinsic, and prerenal
— Post-decompression failure to recover
— Septic shock from urosepsis (lactate >4, vasopressors, MAP <65 despite fluids)
— Severe hyperkalemia with ECG changes
— Severe metabolic acidosis (pH <7.2) refractory to bicarbonate
— Hemodynamic instability during/after decompression
— Need for continuous renal replacement therapy
— AKI with creatinine >2× baseline
— Need for IV antibiotics, decompression, or pain control
— Postobstructive diuresis requiring monitoring
— Comorbidities limiting outpatient management
— Unilateral hydronephrosis from a small passing stone with normal contralateral kidney, normal creatinine, controlled pain → discharge with urology follow-up in 1–2 weeks
— BPH with mild retention, normal creatinine, successful trial of catheter → discharge with α-blocker and urology follow-up

— Urethra: stricture (instrumentation, STI, lichen sclerosus), posterior urethral valves (pediatric), trauma, foreign body, urethral cancer
— Bladder neck/prostate: BPH, prostate cancer, prostatitis, bladder neck contracture
— Bladder: stones, blood clots (clot retention), tumor (transitional cell carcinoma), neurogenic bladder (functional)
— Ureter (intrinsic): stones (calcium oxalate most common), urothelial cancer, blood clots, sloughed papilla, fungal ball, stricture (post-radiation, post-surgical, TB)
— Ureter (extrinsic): pelvic malignancy (cervical, prostate, bladder, colorectal), retroperitoneal fibrosis, retroperitoneal lymphadenopathy, AAA, pregnancy, endometriosis, iatrogenic ligation
— Renal pelvis/UPJ: stones, UPJ obstruction (congenital), tumor
— Acute, painful, unilateral: stone is overwhelmingly likely
— Subacute, painless, bilateral: malignancy or retroperitoneal fibrosis
— Chronic, intermittent, anuria-polyuria: intermittent obstruction (mobile stone, ball-valve tumor)
— Post-surgical (gyn or colorectal): ureteral injury (ligation, transection) → presents days later with flank pain, urinoma, or AKI
— Neurogenic bladder (diabetes, MS, spinal cord injury)
— Medication-induced retention
— Detrusor-sphincter dyssynergia

— Volume depletion, heart failure, cirrhosis, sepsis (pre-vasodilation phase), NSAIDs, ACEi/ARB
— BUN:Cr >20:1, FeNa <1%, FeUrea <35%, bland sediment
— Responds to volume resuscitation (or treatment of underlying low-flow state)
— Acute tubular necrosis (ATN): ischemic (prolonged prerenal), nephrotoxic (aminoglycosides, contrast, myoglobin, hemoglobin); muddy brown casts, FeNa >2%
— Acute interstitial nephritis (AIN): drug-induced (NSAIDs, PPIs, β-lactams, sulfonamides); fever, rash, eosinophilia, WBC casts, eosinophiluria (low sensitivity); biopsy confirmatory
— Glomerulonephritis: RBC casts, dysmorphic RBCs, proteinuria; serologies (ANCA, anti-GBM, complements, ANA, ASO, hepatitis)
— Vascular: thrombotic microangiopathy (TTP/HUS), atheroembolic disease (post-catheterization, livedo, eosinophilia, blue toes), renal artery stenosis with bilateral disease
— Imaging (renal ultrasound) is the single most useful test—hydronephrosis points to postrenal; bland sediment + no hydronephrosis suggests prerenal or early ATN; active sediment (casts, dysmorphic RBCs) suggests intrinsic
— Bladder scan identifies retention
— Urinalysis sediment is critical—postrenal sediment is usually bland unless infection or stone causes hematuria

— α1-blocker (tamsulosin 0.4 mg daily) indefinitely or until definitive therapy
— Consider 5α-reductase inhibitor if prostate >40 g (synergistic with α-blocker per MTOPS trial)
— Discuss surgical options (TURP, laser enucleation, prostatic urethral lift, water vapor therapy) if recurrent retention or failed medical therapy
— Avoid anticholinergics, decongestants, and unnecessary opioids
— 24-hour urine collection for metabolic workup (after recovery, ~6 weeks post-event): calcium, oxalate, citrate, uric acid, sodium, volume, pH
— Counsel fluid intake to achieve >2.5 L urine/day
— Dietary: low sodium (<2.3 g/day), normal calcium (1000–1200 mg/day from diet, not low-calcium), moderate animal protein, low oxalate if hyperoxaluria
— Thiazide for hypercalciuria, potassium citrate for hypocitraturia or uric acid stones, allopurinol for hyperuricosuria
— Long-term stent (exchange every 3 months) or nephrostomy
— Coordinate oncology, palliative care, urology
— Goals-of-care discussion: when to stop exchanging stents
— Glucocorticoids (prednisone 40–60 mg/day taper) ± tamoxifen or methotrexate
— Monitor with serial imaging and creatinine
— Clean intermittent catheterization (CIC) is preferred over chronic indwelling Foley to reduce infection risk
— Anticholinergics or β3-agonists (mirabegron) for detrusor overactivity once outlet is managed

— BMP at 48–72 h, 1 week, 2 weeks, and 4 weeks until creatinine plateaus
— Urinalysis at 1–2 weeks to assess for residual infection or proteinuria
— Document baseline creatinine for future reference
— Repeat renal ultrasound in 4–6 weeks to confirm resolution of hydronephrosis
— CT or MR urography if persistent symptoms, hematuria, or concern for missed malignancy
— Pre-procedure imaging before stent exchange
— Within 1–2 weeks for stone disease, BPH, stent management
— Stent exchange every 3 months for chronic indwelling stents
— Voiding trial 3–7 days after Foley placement for retention
— Recommended if creatinine does not return to baseline within 4 weeks
— CKD staging and longitudinal management
— Hydration (>2.5 L/day for stone formers)
— Dietary counseling per stone type
— Medication review at every visit—flag anticholinergics, decongestants, opioids in retention-prone patients
— Smoking cessation (bladder cancer risk)
— Pelvic floor therapy if appropriate
— Fever, flank pain, decreased urine output, gross hematuria, inability to void, suprapubic pain
— Worsening leg swelling, shortness of breath (volume overload)

— Foley insertion is usually implied consent in emergencies, but elective stent or nephrostomy requires explicit consent with discussion of risks (bleeding, infection, perforation, stent symptoms, need for repeat procedures), benefits, and alternatives
— Capacity assessment for elderly patients with delirium—if uremic encephalopathy impairs capacity, proceed under emergency consent or with surrogate decision-maker; document carefully
— Indwelling stents must be exchanged every 3 months; encrustation creates a non-removable stent, recurrent obstruction, and stone burden
— Best practice: stent registry, automated EHR reminders, mandatory exchange date documentation at insertion, patient-held stent card
— Recognized post-operative ureteral injury requires honest disclosure to the patient and family per ethical obligations of transparency
— Early recognition (<1 week) allows simple stent; delayed recognition leads to complex reimplantation or nephrectomy
— Risk management notification per institutional policy
— Malignant obstruction in a patient with advanced cancer raises the question: should we decompress?
— Discuss prognosis, expected benefit (days vs. months of survival), procedural burden (recurrent exchanges), and patient values
— Palliative care consultation appropriate
— Suspected non-accidental trauma (urethral injury in a child) → child protective services
— Sexual assault with urethral/genital injury → forensic protocols, law enforcement reporting per jurisdiction
— Discharge with stent or nephrostomy carries high risk of follow-up failure—ensure urology appointment is scheduled and confirmed before discharge
— Use teach-back to confirm patient understanding of stent symptoms vs. complications requiring ED return

— Calcium oxalate (most common, radiopaque)
— Uric acid (radiolucent, acidic urine; treat with alkalinization)
— Struvite (infection stones, Proteus/Klebsiella/Pseudomonas; staghorn calculi; alkaline urine)
— Cystine (rare, hexagonal crystals, hereditary cystinuria)


Postrenal AKI is rapidly reversible mechanical obstruction of urinary outflow that must be excluded first in every AKI workup with a bladder scan and renal ultrasound, then decompressed promptly—urgently in the setting of infection, bilateral disease, or a solitary kidney—using Foley, ureteral stent, or percutaneous nephrostomy as anatomy and infection dictate, followed by vigilant monitoring for postobstructive diuresis and structured follow-up to address the underlying cause and prevent recurrence.

