The Daily Differential — Sunday, May 17, 2026

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Nephrotic Syndrome

Nephrotic syndrome causes heavy protein loss, leading to edema, hypercoagulability, infection risk, and kidney injury. ED care focuses on recognizing...

At the Bedside

Core definition
Heavy proteinuria, hypoalbuminemia, edema, hyperlipidemia/lipiduria.
Usually proteinuria >3.5 g/day in adults.
Key history
New/worsening edema, frothy urine, weight gain, dyspnea, orthopnea.
Thrombotic symptoms: unilateral leg swelling, chest pain, dyspnea, neurologic deficits, flank pain.
Infection symptoms: fever, abdominal pain, cellulitis.
Secondary causes: diabetes, lupus, malignancy, HIV, hepatitis B/C, NSAIDs, lithium, heroin, malignancy.
Exam
Periorbital edema, dependent edema, ascites, pleural effusions.
Assess intravascular volume: tachycardia, orthostasis, dry mucosa vs pulmonary edema/JVD.
ED workup
UA with microscopy: proteinuria, oval fat bodies/fatty casts.
Urine protein/creatinine ratio if available.
CMP: creatinine, albumin, electrolytes.
CBC.
Lipid panel can be outpatient unless needed for admission workup.
Pregnancy test when relevant.
If dyspnea/chest pain: CXR, ECG, troponin, BNP as indicated; CT pulmonary angiography if PE concern.
If unilateral leg swelling: venous duplex.
If flank pain/AKI/hematuria: consider renal vein thrombosis.
ED management priorities
Treat life threats: PE, renal vein thrombosis, sepsis, pulmonary edema, AKI.
Salt restriction and loop diuretics for symptomatic edema.
Avoid overly aggressive diuresis if intravascularly depleted; nephrotic patients can look “wet” but be intravascularly dry.
Severe edema with hypoalbuminemia may require albumin-assisted diuresis, usually inpatient/nephrology-guided.
Anticoagulate confirmed VTE unless contraindicated.
Nephrology consult/admission for AKI, severe hypoalbuminemia, anasarca, refractory edema, suspected renal vein thrombosis, pulmonary edema, infection, or new severe nephrotic syndrome.
Disposition
Admit: AKI, hypoxia/pulmonary edema, anasarca impairing mobility/respiration, suspected/confirmed thromboembolism, serious infection, severe electrolyte disturbance, unreliable follow-up.
Outpatient nephrology: stable edema, preserved renal function, no thrombosis/infection, reliable follow-up.

A Classic Presentation

A 42-year-old man with diabetes presents with progressive leg swelling, frothy urine, and mild dyspnea. Exam shows periorbital edema, 3+ pitting edema, clear lungs, and normal oxygenation. UA shows 4+ protein and oval fat bodies; albumin is 1.8 g/dL, creatinine mildly elevated. He receives cautious IV diuresis, nephrology is consulted, and he is admitted due to AKI and severe hypoalbuminemic anasarca.

Study Directive

Memorize the nephrotic syndrome tetrad: proteinuria, hypoalbuminemia, edema, hyperlipidemia/lipiduria.
Make a complications checklist: VTE, renal vein thrombosis, infection, AKI, pulmonary edema.
Review UA microscopy images of oval fat bodies and fatty casts.
Practice disposition decisions using 3 scenarios: mild edema outpatient, anasarca with AKI admit, dyspnea with PE workup.
Read one concise review on adult nephrotic syndrome causes: diabetic nephropathy, membranous nephropathy, FSGS, minimal change, lupus.

Key Medications

Edema
- Furosemide 20–40 mg IV initial adult dose; higher doses often needed in chronic kidney disease or severe nephrotic edema. Titrate to urine output and renal function.
- Bumetanide 0.5–1 mg IV/PO may be used if poor furosemide response.
- Albumin 25% 25 g IV followed by loop diuretic may be used for severe hypoalbuminemic edema, but practice varies — discuss with nephrology/institutional protocol.
VTE treatment
- Unfractionated heparin: bolus 80 units/kg IV, then 18 units/kg/hr infusion, adjust per aPTT/anti-Xa protocol.
- Enoxaparin 1 mg/kg SC q12h if renal function adequate; adjust/avoid in severe renal impairment.
Infection
- Ceftriaxone 1–2 g IV daily depending on suspected source/severity.
- Broaden based on sepsis source and local antibiogram.
Hypertension/proteinuria
- ACE inhibitors/ARBs reduce proteinuria but are generally started outpatient or inpatient with renal/electrolyte monitoring, not reflexively in the ED.

High-Yield Pearls

Nephrotic syndrome is hypercoagulable because anticoagulant proteins are lost in urine while hepatic procoagulant synthesis increases.
Edematous does not always mean intravascularly overloaded; hypoalbuminemia lowers oncotic pressure and can cause third spacing.
Oval fat bodies under polarized light show “Maltese crosses” and are classic for nephrotic-range proteinuria.

Board Question

A patient with nephrotic syndrome develops acute pleuritic chest pain and dyspnea. Vitals show tachycardia and mild hypoxia. What complication is most concerning?

AHyperkalemic periodic paralysis
BPulmonary embolism
CAcute pancreatitis
DMyxedema coma

Reveal answer

Correct: B

Nephrotic syndrome causes urinary loss of anticoagulant proteins, especially antithrombin III, creating a hypercoagulable state. PE, DVT, and renal vein thrombosis are major complications.

Recent Literature

Review or guideline IPNA clinical practice recommendations for the diagnosis and management of children with steroid-resistant nephrotic syndrome
Pediatr Nephrol, 2020 · cited 369×

Full text · open access
Recent clinical Research Advances in Rituximab-Resistant Membranous Nephropathy
Kidney Med, 2026

Full text · open access

3 of 4

Non-Traumatic Hematuria

Hematuria ranges from benign cystitis to malignancy, glomerulonephritis, obstructing stones, anticoagulant-related bleeding, and clot retention. ED...

At the Bedside

Initial classification
Gross vs microscopic.
Painful vs painless.
Glomerular vs non-glomerular.
With or without clots/retention.
History
Dysuria, frequency, flank pain, fever, abdominal pain.
Clots, inability to void, decreased urine output.
Anticoagulants/antiplatelets.
Smoking, occupational exposures, age >35–40, prior malignancy.
Recent URI, rash, joint pain, edema, hypertension — suggests glomerulonephritis.
Exercise, menstruation contamination, recent instrumentation.
Exam
Vitals for sepsis/hemorrhage.
Abdominal/CVA tenderness.
Bladder distention.
GU exam when appropriate: meatal bleeding, testicular pathology, prostate tenderness.
Check for edema, rash, purpura, hypertension suggesting nephritic syndrome.
Testing
UA with microscopy: RBCs, WBCs, nitrites/leukocyte esterase, casts, protein.
Urine culture if infection possible.
CBC if gross hematuria, clots, anticoagulation, or systemic symptoms.
BMP/creatinine.
Coagulation studies if anticoagulated, liver disease, bleeding disorder.
Pregnancy test when relevant.
Type and screen if heavy bleeding or unstable.
Glomerular clues
RBC casts, dysmorphic RBCs, significant proteinuria, hypertension, edema, AKI.
Consult nephrology; admit if AKI, severe HTN, systemic disease, or rapidly progressive features.
Imaging
Suspected stone: noncontrast CT abdomen/pelvis is most sensitive; renal US useful for hydronephrosis, pregnancy, radiation avoidance.
Painless gross hematuria: malignancy until proven otherwise; ED imaging depends on stability/resources, but needs urology follow-up for cystoscopy and upper tract imaging.
Fever + obstruction/hydronephrosis = infected obstructed stone → antibiotics + urgent urologic decompression.
Clot retention management
Large-bore 3-way Foley, typically 22–24 Fr.
Manual irrigation to clear clots.
Continuous bladder irrigation if ongoing bleeding.
Urology consult for persistent clots, inability to irrigate, ongoing bleeding, significant anemia, suspected tumor.
Anticoagulant-associated hematuria
Do not assume anticoagulants are the only cause; malignancy and structural pathology still require evaluation.
Reverse anticoagulation only for life-threatening bleeding, hemodynamic instability, major anemia, urgent procedure, or uncontrolled bleeding.

A Classic Presentation

A 68-year-old smoker presents with painless gross hematuria and passage of clots. He is hemodynamically stable but cannot void. Bladder scan shows retention. A 24 Fr 3-way Foley is placed, clots are manually irrigated, and continuous bladder irrigation is started. Labs show stable hemoglobin and creatinine; urology is consulted because painless gross hematuria with clots is concerning for bladder malignancy.

Study Directive

Build a hematuria algorithm: unstable → resuscitate; retention → irrigate; infection/obstruction → antibiotics + urology; glomerular → nephrology.
Memorize glomerular clues: RBC casts, dysmorphic RBCs, proteinuria, HTN, edema, AKI.
Practice setting up continuous bladder irrigation and troubleshooting poor catheter drainage.
Review indications for CT stone protocol vs renal ultrasound vs outpatient cystoscopy.
Make a one-card anticoagulant reversal guide for warfarin, dabigatran, and factor Xa inhibitors.

Key Medications

Pain/renal colic
- Ketorolac 15 mg IV/IM once; avoid in renal failure, active bleeding risk, or severe CKD.
- Morphine 0.05–0.1 mg/kg IV q10–15 min PRN.
- Ondansetron 4 mg IV/ODT q6–8h PRN.
UTI/pyelonephritis
- Ceftriaxone 1 g IV once for pyelonephritis/complicated UTI initial ED therapy.
- Cephalexin 500 mg PO QID x5–7 days for uncomplicated cystitis when appropriate and local resistance acceptable.
- Nitrofurantoin 100 mg PO BID x5 days for uncomplicated cystitis only; not for pyelonephritis or poor renal function.
- TMP-SMX DS 1 tab PO BID x3 days for uncomplicated cystitis if local resistance acceptable; longer courses often needed for men/complicated UTI.
Sepsis/complicated infection
- Piperacillin-tazobactam 4.5 g IV q6h, or cefepime 2 g IV q8–12h depending on renal function/severity.
Anticoagulant reversal — major bleeding
- Warfarin: vitamin K 10 mg IV plus 4-factor PCC, typically 25–50 units/kg based on INR; check protocol.
- Dabigatran: idarucizumab 5 g IV total.
- Factor Xa inhibitors: andexanet alfa per drug/timing/dose protocol, or 4-factor PCC 50 units/kg if andexanet unavailable/institutional pathway supports it.
- These reversal doses vary by protocol; verify with pharmacy/reference.

High-Yield Pearls

Gross painless hematuria in an older adult is bladder cancer until proven otherwise.
Hematuria with clots is usually non-glomerular; glomerular bleeding typically does not clot and is associated with proteinuria/casts.
Infected obstructing stone is a urologic emergency requiring drainage, not just antibiotics.

Board Question

Which urinalysis finding most strongly suggests a glomerular source of hematuria?

ALarge blood with normal-appearing RBCs and clots
BPositive nitrites and leukocyte esterase
CRBC casts and significant proteinuria
DCalcium oxalate crystals

Reveal answer

Correct: C

RBC casts form within renal tubules and strongly suggest glomerulonephritis or renal parenchymal inflammation. Clots usually indicate a lower urinary tract or collecting system source rather than glomerular bleeding.

Recent Literature

Review or guideline [Non-infectious emergencies of the lower urinary tract and genitals]
Prog Urol, 2021 · cited 4×
Recent clinical Magnitude and outcome of urologic emergencies: prospective cohort study
BMC Emerg Med, 2026

Full text · open access

4 of 4

Normal Vaginal Delivery

Emergency physicians may need to manage imminent delivery without obstetric support. A calm, structured approach protects both mother and neonate and...

At the Bedside

Initial assessment
Gestational age, prenatal care, complications, parity, time/contraction frequency, rupture of membranes, bleeding, fetal movement.
Ask about multiple gestation, breech, prior C-section, placenta previa, preeclampsia, GBS status.
Vitals, IV access, fetal heart tones if time.
If crowning/imminent delivery, do not transfer; prepare for delivery.
Prepare
Call OB, pediatrics/neonatal team, nursing, respiratory therapy if available.
PPE, sterile towels, clamps/scissors, bulb suction, neonatal warmer, BVM, umbilical supplies.
Position mother in dorsal lithotomy or comfortable semi-recumbent position.
Delivery of head
Encourage pushing with contractions; controlled delivery of head to avoid rapid expulsion.
Support perineum; apply gentle pressure to fetal head.
Check for nuchal cord after head delivers:
Loose: slip over head.
Tight: clamp x2 and cut if cannot reduce.
Delivery of shoulders/body
Wait for restitution/external rotation.
Gentle downward traction to deliver anterior shoulder, then upward traction for posterior shoulder.
Do not pull forcefully.
If shoulder dystocia: call for help, McRoberts maneuver, suprapubic pressure; avoid fundal pressure.
After delivery
Dry and stimulate neonate immediately; keep warm.
Bulb suction only if secretions obstruct breathing; routine aggressive suctioning is not needed.
Delayed cord clamping 30–60 seconds if vigorous and no contraindication.
Clamp cord in two places and cut.
Assess Apgar at 1 and 5 minutes.
Skin-to-skin if stable.
Third stage
Placenta usually delivers within 30 minutes.
Do not forcibly pull placenta.
Inspect placenta for completeness.
Uterine massage and oxytocin after delivery to reduce postpartum hemorrhage.
Disposition
Mother and baby generally require transfer/admission to L&D/postpartum/newborn care.
Immediate escalation for hemorrhage, retained placenta, severe hypertension, seizure, maternal fever, nonvigorous neonate, prematurity, breech, cord prolapse, or shoulder dystocia.

A Classic Presentation

A 27-year-old G2P1 at 39 weeks arrives with contractions every 2 minutes and says she needs to push. The fetal head is crowning. You call OB/pediatrics, prepare warmer and delivery supplies, control delivery of the head, reduce a loose nuchal cord, deliver anterior then posterior shoulder with gentle traction, dry/stimulate the vigorous newborn, delay cord clamping, administer oxytocin after delivery, and monitor for placental delivery and hemorrhage.

Study Directive

Rehearse the normal delivery sequence out loud: head, nuchal cord, restitution, anterior shoulder, posterior shoulder, body, dry/stimulate, cord, placenta.
Memorize postpartum hemorrhage uterotonics and contraindications: methylergonovine = HTN; carboprost = asthma.
Practice shoulder dystocia algorithm: call help, McRoberts, suprapubic pressure, delivery of posterior arm, rotational maneuvers.
Review neonatal initial steps: warm, dry, stimulate, position airway, assess breathing/HR.
Watch one short procedural video of ED delivery and one of shoulder dystocia maneuvers.

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Mechanism Pearl of the Day: Across GU bleeding, nephrotic edema, testicular torsion, priapism, and delivery complications, the emergency is often a flow problem: blocked venous/lymphatic drainage, impaired arterial perfusion, obstructed urine outflow, or loss of oncotic pressure causing third spacing. Identify whether the organ needs decompression, reperfusion, volume control, or source control.

Key Medications

Postpartum hemorrhage prevention/treatment
- Oxytocin 10 units IM once after delivery, or 10–40 units in 1 L normal saline/LR IV infusion; rate varies by protocol.
- Tranexamic acid 1 g IV over 10 min for postpartum hemorrhage, ideally within 3 hours of birth; may repeat 1 g once if bleeding continues after 30 min or recurs within 24 hr.
- Methylergonovine 0.2 mg IM q2–4h PRN; avoid in hypertension/preeclampsia.
- Carboprost 250 mcg IM q15–90 min PRN, max total 2 mg; avoid in asthma.
- Misoprostol 800–1000 mcg PR or SL for hemorrhage when other uterotonics unavailable/adjunctive; dosing route varies by protocol.
GBS prophylaxis if laboring and indicated
- Penicillin G 5 million units IV loading dose, then 2.5–3 million units IV q4h until delivery.
- Ampicillin 2 g IV loading dose, then 1 g IV q4h.
- If severe penicillin allergy, regimen depends on susceptibility/risk — check protocol.
Analgesia
- Fentanyl 25–50 mcg IV q5–10 min PRN severe pain, cautious near delivery due to neonatal respiratory depression.
- Local lidocaine 1% for laceration repair; dose depends on volume/repair, max generally 4.5 mg/kg without epinephrine.

High-Yield Pearls

Never pull hard on the fetal head; controlled delivery and gentle traction prevent injury.
Fundal pressure is contraindicated in shoulder dystocia; use McRoberts and suprapubic pressure first.
Postpartum hemorrhage is most commonly due to uterine atony — massage and oxytocin are first-line.

Board Question

During an ED vaginal delivery, the fetal head delivers but the shoulders do not deliver with gentle traction. What is the best initial maneuver?

AFundal pressure
BMcRoberts maneuver with suprapubic pressure
CImmediate cesarean section in the ED
DForceful downward traction on the fetal head

Reveal answer

Correct: B

Shoulder dystocia is initially managed with McRoberts positioning and suprapubic pressure. Fundal pressure and forceful traction increase risk of uterine rupture, brachial plexus injury, and fetal harm.

Recent Literature

Review or guideline The Pathophysiology of Labor Dystocia: Theme with Variations
Reprod Sci, 2023 · cited 48×

Full text · open access
Recent clinical Evaluation of the natural birth prediction system for assessing cephalopelvic disproportion: a multicentre prospective study
Ann Med, 2026

Full text · open access

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At the Bedside

Study Directive

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