Eduovisual
Renal & Urinary
Nephrolithiasis: workup, management, and prevention
— Lifetime prevalence ~11% men, ~7% women; rising in both sexes and in adolescents.
— Peak age 30–50; recurrence ~50% within 5–10 years without prevention.
— Men > women historically, but the gap is narrowing due to obesity/metabolic syndrome.
— Calcium oxalate ~70–80% (most common overall)
— Calcium phosphate ~5–10% (associated with high urine pH, RTA type 1)
— Uric acid ~5–10% (low urine pH, gout, metabolic syndrome, tumor lysis)
— Struvite ~5–10% (urease-producing UTI: Proteus, Klebsiella, Ureaplasma)
— Cystine <1% (autosomal recessive cystinuria, presents in youth)
— Acute, severe, colicky flank pain radiating to groin or testicle/labia, often with nausea/vomiting and inability to find a comfortable position (writhing — contrast with peritonitis where patients lie still).
— Gross or microscopic hematuria (absent in ~10–15%, so its absence does not rule out).
— Prior stone history, family history, gout, IBD/short bowel, bariatric surgery, RTA, hyperparathyroidism, sarcoidosis, chronic UTIs, immobilization, ketogenic or high-protein/high-sodium diet, dehydration in hot climates.
— Fever, rigors, pyuria → obstructed infected stone is a urologic emergency requiring decompression within hours.
— Solitary kidney, transplant kidney, bilateral obstruction, AKI.
— Pregnancy with suspected stone.
Board pearl: A patient writhing in agony with CVA tenderness, hematuria, and a normal abdominal exam should make you order a non-contrast CT abdomen/pelvis, not an IVP. CT has replaced IVP as gold standard.
Step 3 management: Always check a urinalysis, BMP, and pregnancy test before imaging in reproductive-age women.
— Sudden-onset unilateral flank pain, waxing and waning every 20–60 minutes (peristaltic ureteral spasm against the obstruction).
— Pain migrates as the stone descends: flank → lateral abdomen → groin/testicle/labia → suprapubic + dysuria/urgency when stone reaches the ureterovesical junction (UVJ).
— Nausea/vomiting in 50%+ from shared celiac/splanchnic innervation.
— Ureteropelvic junction (UPJ)
— Crossing of iliac vessels (pelvic brim)
— Ureterovesical junction (UVJ) — most common; mimics cystitis
— Painless gross hematuria → consider stone but also rule out malignancy, especially >40.
— Recurrent UTIs with same organism → suspect struvite staghorn.
— Incidental stone on imaging → still warrants metabolic evaluation if recurrent or first stone with risk factors.
— Acute kidney injury → think bilateral stones or stone in solitary/transplant kidney.
— Prior stones, age at first stone, stone analysis if available.
— Family history (cystinuria, primary hyperoxaluria, Dent disease, RTA).
— Diet: sodium, animal protein, oxalate (spinach, nuts, chocolate, tea), vitamin C megadosing, low calcium intake (paradoxically increases oxalate absorption).
— Fluid intake and occupation (hot environments, low bathroom access).
— Medications: loop diuretics, topiramate, acetazolamide, indinavir, atazanavir, ceftriaxone, sulfadiazine, high-dose vitamin D.
— GI: Crohn disease, ileal resection, bariatric surgery → enteric hyperoxaluria.
— Endocrine: primary hyperparathyroidism, gout, type 2 diabetes (uric acid stones).
Key distinction: Stone pain is colicky and the patient moves constantly; peritonitis pain is constant and the patient lies still. This single observation steers the differential at the bedside.
Board pearl: A patient with Crohn disease post-ileal resection presenting with stones almost always has calcium oxalate from enteric hyperoxaluria — treat with calcium with meals and a low-oxalate diet.
— Restless, pacing, unable to lie still — hallmark of visceral colicky pain.
— Diaphoretic, pale, tachycardic from pain and vagal response.
— Tachycardia and mild hypertension from pain are expected.
— Fever ≥38°C, hypotension, or signs of sepsis change the disposition entirely — assume obstructed infected stone until proven otherwise.
— Tachypnea may reflect pain or metabolic acidosis (think sepsis or RTA contributing).
— Soft, non-peritoneal abdomen despite severe pain — a key contrast with surgical abdomen.
— Mild tenderness over the flank or lower quadrant; no rebound or guarding.
— Bowel sounds usually present, may be hypoactive from ileus.
— Costovertebral angle (CVA) tenderness on the affected side.
— Bilateral CVA tenderness or absent kidney sounds → consider bilateral obstruction.
— Examine testicles in men — referred pain mimics torsion; absent cremasteric reflex or transverse lie suggests torsion instead.
— In women, perform a pelvic exam if presentation is atypical to exclude ovarian torsion, ectopic pregnancy, PID, tubo-ovarian abscess.
— Dry mucous membranes, orthostasis from vomiting and poor intake.
— Adequate hydration is therapeutic and supports stone passage, but avoid aggressive fluid bolus in obstructed kidney — it worsens hydronephrosis and pain without expediting passage.
Step 3 management: Place the patient on continuous monitoring if febrile or hypotensive; obtain lactate, blood cultures, and urine culture before antibiotics, then start broad-spectrum coverage (e.g., piperacillin-tazobactam) and call urology for emergent decompression.
Board pearl: Hypotension + flank pain in a man >60 — do not anchor on stone. Get a bedside ultrasound to exclude ruptured AAA, which is the classic miss.
— Urinalysis with microscopy: hematuria (85–90%), crystals (envelope-shaped calcium oxalate, coffin-lid struvite, hexagonal cystine, rhomboid uric acid), pH (acidic <5.5 → uric acid; alkaline >7 → struvite or RTA), leukocyte esterase/nitrites.
— Urine culture: mandatory if pyuria, fever, or known recurrent UTI.
— BMP: creatinine (AKI from obstruction), calcium, bicarbonate (low in RTA), potassium.
— CBC: leukocytosis suggests infection; mild stress leukocytosis is common.
— Uric acid if uric acid stones suspected.
— β-hCG in reproductive-age women before imaging.
— PTH and ionized calcium if hypercalcemia or recurrent calcium stones.
— Non-contrast CT abdomen/pelvis (low-dose protocol when available): sensitivity ~97%, specificity ~95%. Identifies size, location, hydronephrosis, alternative diagnoses. First-line in nonpregnant adults.
— Renal/bladder ultrasound (POCUS or formal): first-line in pregnancy and children, and increasingly in young adults with classic presentation to reduce radiation. Detects hydronephrosis and large stones but misses ureteral stones.
— KUB X-ray: limited utility alone; useful to follow known radio-opaque stones (calcium-based are radio-opaque; uric acid and indinavir are radiolucent).
— MRI urography: alternative in pregnancy when ultrasound nondiagnostic.
Step 3 management: Choose ultrasound first in pregnancy and pediatrics; if nondiagnostic and clinical suspicion remains high, proceed to MRI without gadolinium before low-dose CT.
Board pearl: A radiolucent stone on KUB but visible on CT in a patient with gout or metabolic syndrome → uric acid stone; treat with urinary alkalinization (potassium citrate to pH 6.5–7) and the stone may dissolve without intervention.
Key distinction: Hydronephrosis on ultrasound confirms obstruction but does not localize the stone — CT is still needed for surgical planning if intervention is considered.
— Strain all urine and send any retrieved stone for crystallographic analysis (infrared spectroscopy or X-ray diffraction). Composition drives prevention strategy.
— Indications: recurrent stones, first stone in a high-risk patient (young age, family history, solitary kidney, nephrocalcinosis, non-calcium stone, bariatric/IBD, pediatric).
— Collect two 24-hour samples on usual diet, ≥6 weeks after acute episode/intervention.
— Measured: volume, calcium, oxalate, citrate, uric acid, sodium, potassium, magnesium, phosphate, pH, creatinine (validates completeness).
— Targets: volume >2.5 L/day, calcium <200 mg/day (women) / <250 mg/day (men), oxalate <40 mg/day, citrate >320 mg/day, sodium <100 mEq/day, uric acid <750/800 mg/day.
— Hypercalciuria + normal serum calcium → idiopathic hypercalciuria (most common); treat with thiazide.
— Hypercalciuria + hypercalcemia → primary hyperparathyroidism (check PTH); parathyroidectomy is definitive.
— Hypocitraturia + hypokalemia + non-anion-gap metabolic acidosis + alkaline urine → distal (type 1) RTA.
— Hyperoxaluria → enteric (IBD, bariatric), dietary, or primary (rare, severe, early-onset).
— Hyperuricosuria with acidic urine → uric acid stones.
— Low urine volume alone is the single most common abnormality.
Board pearl: Low urine citrate is a major modifiable risk factor — citrate complexes calcium and inhibits crystallization. Potassium citrate is the most versatile prevention drug across calcium oxalate, calcium phosphate (caution), and uric acid stones.
Step 3 management: Always obtain two 24-hour urines before starting prevention pharmacotherapy — empiric thiazides without data is a frequent wrong answer.
— Is there infection or sepsis? → emergent urologic decompression + IV antibiotics.
— Is there obstruction with AKI, solitary kidney, or bilateral stones? → urgent decompression.
— If neither, how likely is spontaneous passage? → driven by stone size and location.
— <5 mm: ~70–98% pass spontaneously, median 1–2 weeks.
— 5–7 mm: ~50% pass.
— 7–10 mm: ~25–50% pass.
— \>10 mm: rarely pass; plan intervention.
— Distal ureteral stones pass more readily than proximal.
— Renal pelvis stones often asymptomatic until they migrate.
— Outpatient management for stones ≤10 mm, controlled pain, no infection, no AKI, tolerating oral intake, reliable follow-up.
— Admission for intractable pain/vomiting, AKI, solitary kidney, infection, or stone >10 mm awaiting intervention.
— NSAIDs (ketorolac 15–30 mg IV or ibuprofen PO) — first-line; reduce ureteral spasm and inflammation. Avoid in AKI, CKD stage ≥3, pregnancy 3rd trimester, active bleeding.
— Opioids as adjunct or when NSAIDs contraindicated (morphine, hydromorphone). Use sparingly given opioid stewardship.
— Antiemetics (ondansetron, metoclopramide) as needed.
— IV fluids only to euvolemia — no evidence forced diuresis improves passage.
— Tamsulosin 0.4 mg daily × up to 4 weeks for distal ureteral stones 5–10 mm — modest benefit, well tolerated. Less useful for <5 mm or proximal stones.
Step 3 management: Discharge instructions: strain urine, hydrate, return precautions (fever, intractable pain, vomiting, anuria), urology follow-up in 1–2 weeks, repeat imaging if no passage by 4–6 weeks.
Board pearl: Tamsulosin's main role is distal ureteral stones 5–10 mm; counsel about orthostatic hypotension and retrograde ejaculation.
— Ketorolac 15 mg IV q6h or ibuprofen 600 mg PO q6h — first-line analgesia.
— Tamsulosin 0.4 mg PO daily for MET in eligible distal stones.
— Antiemetics PRN; IV fluids to euvolemia.
— Thiazide diuretic (hydrochlorothiazide 25 mg, chlorthalidone 25 mg, or indapamide 1.25–2.5 mg daily) for hypercalciuria — reduces urinary calcium by enhancing distal tubular reabsorption.
— Potassium citrate 10–20 mEq PO BID–TID for hypocitraturia — raises urinary citrate and pH.
— Dietary calcium 1000–1200 mg/day with meals — binds dietary oxalate in gut. Do not restrict calcium.
— Low sodium (<2300 mg/day) — reduces urinary calcium excretion.
— Moderate animal protein — high protein increases calcium and uric acid, lowers citrate.
— Pyridoxine (vitamin B6) in primary hyperoxaluria type 1.
— Same general measures; use caution with potassium citrate since alkalinization can promote calcium phosphate crystallization. Treat underlying distal RTA if present.
— Potassium citrate to alkalinize urine to pH 6.5–7.0 — can dissolve existing uric acid stones (rare for any stone type).
— Allopurinol 100–300 mg daily if hyperuricosuria persists or with gout.
— Reduce purine-rich foods, weight loss, treat metabolic syndrome.
— Complete surgical removal is essential (PCNL preferred for staghorn) — medical therapy alone fails.
— Culture-directed antibiotics; acetohydroxamic acid (urease inhibitor) is rarely used due to toxicity.
— High fluid intake (>3 L/day), urinary alkalinization to pH >7.5, low sodium, low animal protein.
— Tiopronin or D-penicillamine for refractory cases (chelate cystine).
Board pearl: Thiazides + potassium citrate is the most common prevention combination — thiazides cause hypokalemia and hypocitraturia, which citrate corrects synergistically.
Step 3 management: Always recheck a 24-hour urine 3–6 months after starting therapy to confirm targets are met and adjust.
— Stone >10 mm unlikely to pass.
— Failure of conservative management after 4–6 weeks.
— Infection with obstruction (emergent).
— AKI, solitary kidney, intractable pain or vomiting.
— Occupational requirement (pilots, certain professions).
— Percutaneous nephrostomy tube OR retrograde ureteral stent within hours.
— Definitive stone removal is deferred until infection is treated (typically 1–2 weeks of antibiotics).
— Both options are acceptable; choice depends on patient stability, anatomy, and local expertise. PCN preferred in sepsis/coagulopathy.
— Shock wave lithotripsy (SWL): non-invasive, focused acoustic waves fragment stones. Best for renal or proximal ureteral stones <2 cm, radio-opaque. Contraindications: pregnancy, bleeding diathesis, uncontrolled HTN, AAA, distal obstruction, morbid obesity. Lower stone-free rates for cystine and calcium oxalate monohydrate.
— Ureteroscopy (URS) with laser lithotripsy (holmium:YAG): flexible/semirigid scope; treats stones anywhere in ureter or kidney. First-line for most ureteral stones and increasingly for renal stones <2 cm. Often a stent is placed post-op.
— Percutaneous nephrolithotomy (PCNL): percutaneous tract into renal collecting system. First-line for stones >2 cm, staghorn calculi, lower pole renal stones >1 cm, complex anatomy. Highest stone-free rate, highest morbidity.
— Open or laparoscopic stone surgery: rare, reserved for complex anatomy or failed less-invasive approaches.
— Ureteral stents cause dysuria, urgency, flank pain with voiding ("stent symptoms") — counsel and prescribe alpha-blocker + anticholinergic if needed.
— Stents must be removed or exchanged within 3 months to avoid encrustation.
Step 3 management: A febrile patient with hydronephrosis and an obstructing stone needs decompression first — definitive lithotripsy is contraindicated during active infection because it risks urosepsis from bacterial release.
Board pearl: Staghorn (struvite) calculus → PCNL, not SWL. Complete clearance prevents recurrent UTIs and renal loss.
— Stone disease is common but atypical presentations dominate: minimal pain, isolated AKI, painless hematuria, urosepsis without classic colic.
— Always consider AAA, mesenteric ischemia, pyelonephritis, and malignancy in the differential — anchoring on stone is a frequent diagnostic error.
— NSAIDs are often contraindicated due to CKD, heart failure, anticoagulation, or GI bleeding risk → use acetaminophen + low-dose opioids for analgesia.
— Tamsulosin is generally safe; monitor for orthostatic hypotension and falls, and beware intraoperative floppy iris syndrome if cataract surgery is planned (hold tamsulosin if possible before ophthalmologic surgery).
— Avoid NSAIDs if eGFR <60 mL/min/1.73m² — risk of further AKI.
— Adjust dosing: allopurinol dose-reduced in CKD (start 50–100 mg daily, titrate by uric acid); HLA-B*5801 testing before initiation in high-risk populations (Han Chinese, Thai, Korean) to prevent SJS/TEN.
— Potassium citrate can cause hyperkalemia in advanced CKD — monitor potassium.
— Thiazides lose efficacy at eGFR <30; consider indapamide or chlorthalidone, which retain some activity longer.
— Imaging: avoid iodinated contrast if eGFR <30; gadolinium contraindicated <30 (NSF risk) — favor non-contrast CT or ultrasound.
— Less directly affected, but avoid acetaminophen >2 g/day in cirrhosis, and avoid NSAIDs due to variceal bleeding and hepatorenal risk.
— Opioids: reduce dose and frequency, avoid morphine (active metabolite accumulates) — favor hydromorphone or fentanyl.
— Many elderly are on anticoagulants — affects choice of SWL (contraindicated) vs URS (preferred).
— Diuretics, lithium, topiramate, vitamin D — review medication list for lithogenic drugs.
Step 3 management: In an elderly patient with CKD and a 6 mm distal stone, choose acetaminophen + tamsulosin + urology follow-up, not ketorolac.
Board pearl: AAA can mimic renal colic in men >60 — always image the aorta when imaging the kidneys in this demographic.
— Incidence ~1 in 1500 pregnancies, peaks in 2nd/3rd trimesters.
— Physiologic hydronephrosis of pregnancy (right > left from dextrorotated uterus, progesterone-mediated ureteral relaxation) complicates imaging.
— First-line imaging: renal/bladder ultrasound. If nondiagnostic, MRI without gadolinium. Low-dose CT only if absolutely necessary (3rd trimester preferred).
— Analgesia: acetaminophen first-line. NSAIDs contraindicated after 20 weeks (oligohydramnios, premature ductal closure). Opioids in moderation if needed.
— Tamsulosin is off-label in pregnancy — limited data, generally avoided; some experts permit short courses.
— Intervention when needed: ureteral stent or percutaneous nephrostomy is preferred; SWL and PCNL are contraindicated. Ureteroscopy with holmium laser is increasingly considered safe in experienced centers.
— Stents/PCNs encrust faster in pregnancy — exchange every 4–6 weeks.
— Antibiotics: avoid fluoroquinolones, trimethoprim (1st trimester), sulfonamides (3rd trimester); use beta-lactams.
— Rising incidence; higher likelihood of underlying metabolic or genetic etiology — every pediatric stone warrants full metabolic workup including 24-h urine and stone analysis.
— Consider cystinuria, primary hyperoxaluria, Dent disease, distal RTA, ketogenic diet (epilepsy), topiramate.
— Ultrasound is first-line imaging to minimize radiation; low-dose CT if needed.
— Hydration, dietary counseling, and treatment of underlying disorder are cornerstones.
— URS and SWL both used; PCNL for large/staghorn stones in specialized centers.
— Roux-en-Y gastric bypass increases enteric hyperoxaluria — counsel on calcium with meals, low oxalate, hydration, and consider lifelong monitoring.
Step 3 management: Pregnant patient with flank pain and ultrasound showing hydronephrosis but no visible stone → MRI urography without gadolinium is the next step.
Board pearl: A child with bilateral stones and a positive cyanide-nitroprusside test has cystinuria — treat with hydration, alkalinization, and tiopronin if refractory.
— Acute kidney injury — especially with bilateral obstruction, solitary kidney, or transplant; usually reversible if relieved <2 weeks.
— Chronic kidney disease — recurrent obstruction or staghorn calculi cause progressive parenchymal loss.
— Hydronephrosis with parenchymal atrophy — long-standing obstruction.
— Obstructed pyonephrosis/urosepsis — pus under pressure; mortality high without rapid decompression.
— Xanthogranulomatous pyelonephritis — chronic destructive infection, often with staghorn stone and Proteus; nephrectomy frequently required.
— Perinephric abscess.
— SWL: subcapsular/perinephric hematoma (~1%), steinstrasse ("stone street" — fragments obstructing ureter), transient hematuria, rarely worsening HTN or new-onset DM (debated).
— Ureteroscopy: ureteral perforation, avulsion (rare, catastrophic), stricture, UTI, stent symptoms.
— PCNL: bleeding requiring transfusion or angioembolization, pneumothorax/hemothorax (upper pole access), bowel injury, urinoma, sepsis.
— Stent complications: dysuria, hematuria, migration, encrustation, "forgotten stent" syndrome — track all stents in the EHR.
— ~50% recurrence within 10 years without prevention; ~80% lifetime if untreated. Recurrence is a quality measure and the central focus of long-term care.
— Nephrolithiasis is independently associated with CKD, hypertension, diabetes, metabolic syndrome, and cardiovascular events — treat the patient, not just the stone.
— Idiopathic hypercalciuria and primary hyperparathyroidism increase osteoporosis risk — consider DEXA in chronic stone formers, especially those on thiazides for years.
Step 3 management: Forgotten stents are a patient-safety event — at every stent placement, document removal/exchange date and use EHR-based tracking.
Board pearl: Steinstrasse post-SWL typically resolves spontaneously or with tamsulosin; persistent obstruction or infection requires ureteroscopy.
— Obstructed infected stone (fever, pyuria, hydronephrosis) — decompression within hours.
— AKI from bilateral obstruction or stone in solitary/transplant kidney.
— Anuria with bilateral stones.
— Stone in a renal transplant — always urgent given absence of contralateral function and immunosuppression.
— Septic shock from urosepsis — vasopressors, broad-spectrum antibiotics (piperacillin-tazobactam or carbapenem if ESBL risk), source control via decompression.
— Severe metabolic acidosis from sepsis.
— Significant hemorrhage post-PCNL requiring transfusion/angio.
— Intractable pain or vomiting despite ED management.
— AKI without sepsis.
— Stone >10 mm awaiting next-day intervention.
— Inability to tolerate oral intake or lack of reliable follow-up.
— Pregnancy with obstructing stone (OB + urology co-management).
— Stone ≤10 mm, controlled pain, no infection, normal renal function, tolerating PO, reliable follow-up.
— Discharge with NSAIDs/acetaminophen, tamsulosin if eligible, antiemetics, strainer, return precautions, urology follow-up 1–2 weeks.
— Nephrology for recurrent stones, metabolic workup, RTA, CKD, complex prevention.
— Endocrinology for primary hyperparathyroidism (after PTH/calcium confirm) — refer for parathyroidectomy planning.
— Genetics for cystinuria, primary hyperoxaluria, Dent disease.
— Dietitian for diet-driven recurrence.
CCS pearl: In CCS-style cases of urosepsis: order labs and cultures, start IV fluids and broad-spectrum antibiotics, consult urology for decompression, admit to ICU, and advance the clock. Do not schedule definitive lithotripsy during the acute infection — it is a frequent wrong move.
Step 3 management: Always confirm a follow-up appointment is booked before discharge, not just recommended — transition-of-care lapses drive readmissions.
— Fever, flank pain, CVA tenderness, pyuria, bacteriuria without obstruction. Constant pain rather than colicky. CT shows perinephric stranding without stone. Treat with antibiotics; admit if pregnant, septic, immunosuppressed, or unable to tolerate PO.
— Painless hematuria, especially in older smokers. CT urography or cystoscopy if hematuria without clear stone.
— Urothelial carcinoma can present with hydronephrosis mimicking stone obstruction.
— Sudden flank pain with hematuria; risk factors: atrial fibrillation, hypercoagulable state. LDH markedly elevated. CT with contrast shows wedge-shaped perfusion defect — easily missed on non-contrast CT for stones.
— Diabetes, sickle cell, NSAID abuse, pyelonephritis. Sloughed papillae cause obstruction mimicking stone.
— Nephrotic syndrome (especially membranous nephropathy), hypercoagulable. Flank pain, hematuria, proteinuria, elevated LDH.
— Prior instrumentation, radiation, TB, retroperitoneal fibrosis. Subacute flank pain with hydronephrosis but no stone.
— Retroperitoneal mass, lymphadenopathy, endometriosis, retroperitoneal fibrosis (IgG4-related).
— Hematuria from upstream lesion forms clot causing colic — "clot colic."
— Suprapubic pain, dysuria, frequency without flank involvement.
— Referred pain can mimic UVJ stone. Examine genitalia and obtain pelvic ultrasound when in doubt.
Key distinction: Stone colic causes hydronephrosis with a visible stone; pyelonephritis causes perinephric stranding without a stone; infarction causes a wedge defect on contrast CT — three different CT signatures for the same flank pain presentation.
Board pearl: In atrial fibrillation patient off anticoagulation with sudden flank pain and LDH >1000, think renal infarction, not stone. Get contrast CT.
— Ruptured or symptomatic AAA — man >60, pulsatile mass, hypotension, syncope, flank/back pain. Get bedside ultrasound immediately.
— Aortic dissection — tearing chest/back pain, BP differential between arms.
— Mesenteric ischemia — pain out of proportion to exam, atrial fibrillation, elevated lactate.
— Acute appendicitis — retrocecal appendix can cause right flank pain.
— Acute cholecystitis/biliary colic — right upper quadrant radiation; Murphy sign.
— Diverticulitis — left lower quadrant, fever, change in bowel habits.
— Bowel obstruction — distension, vomiting, obstipation.
— Pancreatitis — epigastric/back pain, elevated lipase.
— Perforated peptic ulcer — peritonitis, free air on imaging.
— Ectopic pregnancy — positive β-hCG, adnexal pain; emergency.
— Ovarian torsion — sudden unilateral pelvic pain, nausea; pelvic ultrasound with Doppler.
— Ruptured ovarian cyst, PID, tubo-ovarian abscess, endometriosis.
— Vertebral compression fracture, muscle strain, herpes zoster (look for dermatomal rash, which may follow pain by days).
— Lower lobe pneumonia or pulmonary embolism can refer pain to flank/abdomen — check oxygenation and chest imaging when atypical.
— Diabetic ketoacidosis — abdominal pain, vomiting; check glucose and anion gap.
— Adrenal hemorrhage — anticoagulated, septic, or post-trauma patients.
— Munchausen/factitious stone-passers — patients who feign or even introduce stones to obtain opioids; recognize patterns of multiple ED visits, refusal of imaging or stone collection.
Step 3 management: When the story does not fit (no hematuria, normal urinalysis, atypical demographics, hemodynamic instability), broaden the differential before anchoring on stone.
Board pearl: Herpes zoster can mimic flank colic for 2–3 days before the rash appears — ask about prior prodromal burning/tingling pain and re-examine the skin.
— Fluid intake to achieve urine output >2.5 L/day — single most effective intervention. Reduces recurrence by ~50%.
— Sodium restriction <2300 mg/day — lowers urinary calcium.
— Moderate animal protein (~0.8–1.0 g/kg/day) — high intake raises calcium and uric acid, lowers citrate.
— Normal dietary calcium 1000–1200 mg/day with meals — binds gut oxalate. Do not restrict calcium, even in calcium stone formers.
— Reduce dietary oxalate (spinach, rhubarb, nuts, chocolate, tea, beets) in hyperoxaluric patients.
— Limit added sugars and sugar-sweetened beverages; lemonade/citrus juice can modestly raise urinary citrate.
— Weight loss if obese; treat metabolic syndrome.
— Avoid high-dose vitamin C supplements (metabolized to oxalate).
— Calcium oxalate with hypercalciuria → thiazide.
— Hypocitraturia → potassium citrate.
— Uric acid → potassium citrate ± allopurinol.
— Cystine → alkalinization + tiopronin if refractory.
— Struvite → complete surgical clearance + culture-directed antibiotics.
— Primary hyperparathyroidism → parathyroidectomy.
— Distal RTA → potassium citrate, treat underlying cause (Sjögren, drugs).
— IBD/short bowel → calcium with meals, low oxalate, treat IBD, consider cholestyramine if bile acid malabsorption.
— Discontinue or substitute lithogenic medications when possible.
— Analgesia (short course), tamsulosin if MET indicated, antiemetics PRN.
— Hydration plan, urine strainer, return precautions.
— Booked urology follow-up and primary care follow-up.
— 24-hour urine kits scheduled at 6 weeks for recurrent or high-risk patients.
Step 3 management: The single highest-yield prevention recommendation on any exam is increased fluid intake to >2.5 L urine output/day — choose this first, then layer pharmacology.
Board pearl: Counsel that dietary calcium restriction worsens calcium oxalate stones by increasing free oxalate absorption — a counterintuitive but high-yield concept.
— Primary care or urology visit within 1–2 weeks to confirm passage, review pain control, reinforce hydration.
— Repeat imaging (KUB or ultrasound) at 4–6 weeks if passage uncertain or persistent symptoms.
— Send any passed stone for composition analysis — drives prevention.
— 6 weeks after acute episode/intervention, on usual diet, off short-term medications that distort results.
— Two 24-hour urine collections + serum chemistries (calcium, PTH, uric acid, bicarbonate, creatinine).
— Repeat 24-hour urine at 3–6 months after starting prevention therapy to confirm targets met, then annually for chronic stone formers.
— Renal ultrasound annually for recurrent stone formers, or every 1–2 years for low-risk patients with residual stones.
— Low-dose CT for symptomatic recurrence.
— Thiazides: check potassium, sodium, glucose, uric acid at 2–4 weeks then every 6–12 months; supplement potassium or pair with potassium citrate.
— Potassium citrate: monitor potassium (hyperkalemia, especially in CKD or with ACEi/ARB/spironolactone), serum bicarbonate, urinary citrate, urinary pH.
— Allopurinol: baseline CBC, LFTs, creatinine; HLA-B*5801 testing in high-risk ethnic groups; titrate to uric acid <6 mg/dL.
— Tiopronin/D-penicillamine: monitor for proteinuria, cytopenias, hepatotoxicity.
— Stones are a chronic, recurrent disease, not a one-time event — frame prevention as lifelong.
— Tie prevention to cardiovascular and bone health to motivate adherence.
— Address occupational dehydration (military, construction, athletes).
— Educate on lithogenic medications to discuss with all prescribers.
Step 3 management: A patient on chlorthalidone for calcium oxalate prevention who develops hypokalemia and cramps should be switched to or supplemented with potassium citrate, which corrects both potassium and citrate deficits.
Board pearl: Always document stone composition in the problem list — it changes management at every future encounter.
— Surgical interventions (URS, SWL, PCNL) require discussion of stone-free rates, need for repeat procedures, stent placement, bleeding, infection, ureteral injury. For PCNL, also disclose pneumothorax and transfusion risk.
— In emergent decompression for urosepsis, implied consent applies if the patient is obtunded; document the urgency and inability to obtain explicit consent, and involve surrogate when feasible.
— Renal colic is a recognized opioid prescribing pitfall — frequent ED visits, severe pain, easy escalation.
— Use NSAIDs first when not contraindicated; limit opioid scripts to short duration (3–5 days); check the state prescription drug monitoring program (PDMP) before each prescription.
— Recognize and address drug-seeking presentations without stigmatizing legitimate pain — imaging-confirmed stones guide judgment.
— A retained ureteral stent beyond 3 months risks encrustation, infection, and stone formation around the stent, sometimes requiring complex extraction.
— Mitigation: stent registries, EHR alerts, automatic scheduling of removal at the time of placement, and patient stent cards. This is a frequent patient safety quality measure.
— ED → urology handoff is a common failure point. Confirmed appointments beat "call to schedule" instructions.
— Hospital discharge after stone procedure: medication reconciliation, clear stent removal plan, PCP notification.
— Stone formers are often young and undergo repeat CTs. Use low-dose CT protocols, ultrasound, and KUB for follow-up where appropriate to limit cumulative radiation, especially in pregnancy and pediatrics.
— Recurrent UTIs with struvite stones may indicate catheter-associated infections in long-term care — reportable in some states as healthcare-acquired infections.
— Pilots and commercial drivers may have occupational restrictions until stone-free — counsel and document.
— Lower-income patients face barriers to follow-up and 24-h urine completion. Connect to social work and patient navigators to close prevention gaps.
Step 3 management: Always schedule stent removal at the time of placement and document it — this is the single most actionable safety intervention in stone care.
— Uric acid and cystine → acidic (<5.5)
— Struvite and calcium phosphate → alkaline (>7)
— Calcium oxalate → variable
— Calcium oxalate monohydrate → dumbbell
— Calcium oxalate dihydrate → envelope/bipyramid
— Uric acid → rhomboid/rosette, yellow-brown
— Cystine → hexagonal
— Struvite → coffin lid
— Radio-opaque: calcium oxalate, calcium phosphate, struvite (less dense), cystine (faintly)
— Radiolucent on KUB but visible on CT: uric acid, indinavir, xanthine
— Topiramate, acetazolamide → calcium phosphate (metabolic acidosis, alkaline urine).
— Indinavir, atazanavir → drug crystal stones, radiolucent.
— Ceftriaxone, sulfadiazine, triamterene → drug crystallization.
— Loop diuretics → hypercalciuria (contrast thiazides, which reduce it).
— Vitamin C megadosing → oxalate stones.
— Cystinuria — autosomal recessive (SLC3A1, SLC7A9); presents in adolescence.
— Primary hyperoxaluria — AR, AGXT mutation; oxalate everywhere (kidney, bone, heart); liver transplant curative.
— Dent disease — X-linked; low molecular weight proteinuria, hypercalciuria, nephrocalcinosis.
— MSK (medullary sponge kidney) — recurrent stones, ectatic collecting ducts on CT urography.
— Distal RTA (type 1) — hypokalemic NAGMA, alkaline urine, calcium phosphate stones, nephrocalcinosis.
— Crohn/short bowel → calcium oxalate (enteric hyperoxaluria).
— Gout/metabolic syndrome → uric acid.
— Recurrent UTI with Proteus → struvite/staghorn.
— Primary hyperparathyroidism → calcium phosphate or oxalate with hypercalcemia.
— Sarcoidosis → 1,25-vitamin D-mediated hypercalciuria.
— Bariatric (RYGB) → enteric hyperoxaluria.
Board pearl: A 30-year-old with adolescent-onset bilateral stones, family history, and hexagonal urine crystals → cystinuria. Confirm with cyanide-nitroprusside test or urinary cystine quantitation.
Key distinction: Loop diuretics increase urinary calcium (cause stones); thiazides decrease it (prevent stones).
— 35-year-old man with sudden severe right flank pain radiating to the groin, microscopic hematuria, afebrile, BUN/Cr normal. → Non-contrast CT abdomen/pelvis; if 5 mm distal ureteral stone → NSAIDs + tamsulosin + outpatient management with strainer.
— Febrile patient with flank pain, pyuria, hydronephrosis, leukocytosis. → IV fluids + broad-spectrum antibiotics + emergent urologic decompression (stent or PCN). Definitive lithotripsy is deferred.
— 28-year-old at 26 weeks with right flank pain, hydronephrosis on ultrasound, no visible stone. → MRI urography without gadolinium next; if intervention needed, ureteral stent.
— Recurrent calcium stones + elevated calcium → check PTH. High PTH → primary hyperparathyroidism → parathyroidectomy.
— Crohn disease s/p ileal resection with recurrent stones → enteric hyperoxaluria → calcium with meals + low oxalate diet, not calcium restriction.
— Obese diabetic with radiolucent stone on KUB visible on CT, acidic urine → uric acid stone; potassium citrate to alkalinize urine can dissolve the stone.
— Recurrent calcium phosphate stones + nephrocalcinosis + hypokalemic NAGMA + alkaline urine → distal RTA; treat with potassium citrate.
— Adolescent with bilateral stones, family history, hexagonal crystals → cystinuria; hydration + alkalinization + tiopronin.
— Recurrent Proteus UTIs with staghorn calculus → struvite; definitive treatment PCNL with complete clearance.
— 70-year-old man, smoker, hypertensive, with "renal colic" and hypotension → bedside ultrasound for AAA before anchoring on stone.
— 7 mm distal ureteral stone, normal renal function → NSAIDs + tamsulosin × 4 weeks, follow up with imaging.
— Patient returns 8 months after stent placement with flank pain and recurrent UTIs → encrusted stent; cystoscopy + complex extraction; teaches systems-level prevention.
Step 3 management: When a vignette gives you fever + hydronephrosis + stone, the answer is decompress now, not "schedule lithotripsy."
Board pearl: If the stem mentions hypocitraturia, the answer is almost always potassium citrate.
Nephrolithiasis is a chronic, recurrent disease in which acute care centers on imaging-guided pain control, identification and emergent decompression of obstructed infected stones, and size-appropriate disposition, while long-term care is built on stone composition analysis, two 24-hour urine collections, and a tailored regimen of hydration, dietary modification, and stone-type-specific pharmacotherapy to prevent recurrence.
— Non-contrast CT abdomen/pelvis (ultrasound in pregnancy/children), UA, urine culture if febrile, BMP, β-hCG; assess for fever, AKI, solitary kidney, bilateral obstruction — the four red flags that change disposition immediately.
— NSAIDs first (ketorolac/ibuprofen) unless contraindicated, tamsulosin for distal stones 5–10 mm, antiemetics, euvolemic hydration; emergent stent or PCN for obstructed infected stones with IV antibiotics; outpatient if ≤10 mm with no red flags.
— URS for most ureteral stones, SWL for renal/proximal stones <2 cm, PCNL for stones >2 cm and staghorn calculi; SWL contraindicated in pregnancy, bleeding diathesis, AAA.
— Urine output >2.5 L/day, normal dietary calcium with meals, low sodium, moderate protein; thiazide for hypercalciuria, potassium citrate for hypocitraturia/uric acid stones, allopurinol for hyperuricosuria, alkalinization + tiopronin for cystine, complete surgical clearance for struvite; treat primary hyperparathyroidism, RTA, IBD, obesity, and lithogenic medications.
Step 3 management: Every stone patient leaves with hydration counseling, a urine strainer, a scheduled urology follow-up, a stent-removal date if applicable, and a plan for 24-hour urine collection if recurrent or high-risk.
Board pearl: When in doubt on the exam, choose hydration for prevention and decompress before definitive treatment in obstructed infected stones — these two principles answer the majority of nephrolithiasis questions.