Eduovisual
Renal & Urinary
Post-streptococcal glomerulonephritis
— Triggered by specific virulence antigens: streptococcal pyrogenic exotoxin B (SpeB) and nephritis-associated plasmin receptor (NAPlr).
— Immune complexes deposit subepithelially → complement activation → glomerular injury.
— ~1–2 weeks after pharyngitis (throat strain)
— ~3–6 weeks after impetigo or pyoderma (skin strain)
— Contrast with IgA nephropathy, where hematuria is synpharyngitic (during, not after, infection).
— Most common in children 5–12 years; sporadic adult cases, especially in elderly, diabetics, alcohol-use disorder, and immigrants from endemic regions.
— Suspect in any patient presenting with abrupt cola-colored urine, edema, and hypertension after a recent upper respiratory or skin infection.
— Outbreaks occur in crowded settings, daycares, military barracks, and indigenous communities (e.g., remote Aboriginal, Pacific Islander, sub-Saharan populations).
— Outpatient pediatrician/internist must recognize early, distinguish from other glomerulonephritides, manage volume/BP, and arrange renal follow-up cadence.
— Decision points: who needs hospitalization, when to biopsy, antibiotic role, and counseling families about prognosis.
Board pearl: PSGN is the prototype of nephritic syndrome with LOW C3 and normal C4 — a finding that should immediately reorder your differential toward post-infectious GN, lupus nephritis, MPGN, or cryoglobulinemia. The latent period plus low C3 that normalizes by 6–8 weeks distinguishes PSGN from MPGN (persistently low) and lupus (low C3 and C4).
Step 3 management: First encounter is usually ambulatory — order UA, BMP, C3/C4, ASO/anti-DNase B, and arrange close BP/weight follow-up; admit only for severe HTN, AKI, or volume overload.
— Hematuria — gross "cola-," "tea-," or "smoky"-colored urine in ~30–50%; microscopic in nearly all.
— Edema — periorbital on awakening, dependent later in day; from sodium/water retention, not hypoalbuminemia.
— Hypertension — volume-dependent; can be severe, occasionally hypertensive encephalopathy.
— Oliguria and mild azotemia — usually transient.
— Recent sore throat (1–2 weeks prior) or skin infection/impetigo/scabies superinfection (3–6 weeks prior).
— Antibiotic treatment of the prior infection — does not reliably prevent PSGN (unlike rheumatic fever).
— Sick contacts, daycare/school exposure, crowded housing, recent travel to endemic regions.
— Prior episodes of hematuria (suggests IgA nephropathy or Alport, not PSGN, which is typically a one-time event).
— Family history of kidney disease, deafness (Alport), or autoimmune disease (lupus).
— Adults and elderly more often present with acute kidney injury, heart failure from volume overload, and require hospitalization.
— Diabetics may have prolonged courses and worse renal recovery.
— Nephrotic-range proteinuria (>3.5 g/day) is uncommon and should prompt biopsy consideration.
— Persistent hypocomplementemia beyond 8 weeks → reconsider MPGN, lupus, or C3 glomerulopathy.
— Hematuria can persist microscopically for 1–2 years; proteinuria resolves within 6 months in most children.
— Children: >95% complete recovery; adults: only ~60% fully recover, with rising risk of CKD/HTN.
Key distinction: PSGN latency 1–6 weeks vs. IgA nephropathy synpharyngitic hematuria (1–3 days after URI onset) — this single timing detail is one of the most tested points on the exam.
Board pearl: Ask about impetigo or scabies in summer/warm climates — skin-strain PSGN is easily missed because providers fixate on a "recent strep throat" history that may be absent.
— Child may look surprisingly well or, conversely, puffy and pale with malaise, headache, and anorexia.
— Assess growth parameters in children and document baseline weight — critical for tracking fluid status.
— Hypertension — measure on age- and height-appropriate cuff; ≥95th percentile in pediatrics defines stage 1, ≥95th + 12 mmHg = stage 2.
— Mild tachycardia from volume overload; bradycardia or AMS suggests hypertensive encephalopathy.
— Document orthostatics in adults to differentiate volume overload from depletion.
— Periorbital edema, most prominent in morning — pathognomonic-feeling finding in pediatric PSGN.
— Pharyngeal erythema/exudate usually resolved by the time GN appears (post-infectious latency).
— Funduscopy if BP markedly elevated — look for hypertensive retinopathy, papilledema.
— Listen for S3 gallop, displaced PMI, JVD, and pulmonary crackles — signs of volume overload and hypertensive heart strain.
— Adults more likely to manifest acute pulmonary edema; in elderly with limited cardiac reserve this can be the presenting complaint.
— Dependent pitting edema; scrotal/labial edema in severe cases.
— Hepatomegaly from volume overload, not intrinsic liver disease.
— Skin: look for healing impetigo, ecthyma, scabetic burrows, or residual desquamation of fingertips/perineum (post-scarlet fever).
— Headache, confusion, seizure, or focal deficits = hypertensive emergency / PRES — admit immediately.
Step 3 management: Daily weights, strict I/Os, and serial BPs are the bedside trifecta. Weight is the single most reliable bedside marker of resolving volume overload in PSGN — order it in your CCS case.
CCS pearl: Order "vital signs q4h," "daily weight," and "strict I/O" on admission orders — these are scored items that mirror real-world inpatient management of acute nephritis.
— Dysmorphic RBCs and RBC casts → glomerular hematuria.
— Proteinuria typically <3 g/day (sub-nephrotic); spot urine protein/creatinine ratio in clinic.
— Sterile pyuria possible; WBC casts uncommon — if present consider interstitial nephritis.
— Send urine specific gravity and Na to assess concentrating ability (often low FeNa from avid Na retention).
— Elevated BUN/Cr with mild AKI; track trend, not just snapshot.
— Hyperkalemia from AKI — get ECG if K >6 or rising rapidly.
— Mild dilutional hyponatremia common.
— Calculate eGFR using age-appropriate equation (Schwartz in children, CKD-EPI 2021 without race in adults).
— Mild normocytic anemia (dilutional + mild marrow suppression).
— Leukocytosis usually absent — if present rethink active infection or vasculitis.
— C3 LOW, C4 normal in ~90% of PSGN.
— Low C3 + low C4 → think lupus, cryoglobulinemia, endocarditis-associated GN.
— Persistently low C3 beyond 8 weeks → MPGN or C3 glomerulopathy.
— ASO titer — best after pharyngeal strep; rises 1–3 weeks, peaks 3–5 weeks.
— Anti-DNase B — best after skin infections (impetigo); ASO often negative due to lipid inhibition in skin.
— Streptozyme panel combines several antigens; sensitivity ~95%.
— Throat or skin cultures usually negative by GN onset.
— Renal ultrasound — kidneys normal or mildly enlarged and echogenic; rule out obstruction, congenital anomalies, or chronic disease (small kidneys = chronic).
— CXR if volume-overloaded — pulmonary edema, cardiomegaly.
Board pearl: A child with cola-colored urine, periorbital edema, hypertension, LOW C3, NORMAL C4, and elevated anti-DNase B = textbook PSGN — biopsy not required.
Key distinction: ASO may be falsely negative after impetigo; always send anti-DNase B if pyoderma is suspected.
— Classic child, recent strep, low C3 normalizes within 6–8 weeks, improving renal function.
— Empirically diagnosed, no biopsy needed — supportive care only.
— Anuria or rapidly progressive renal failure (RPGN picture) — exclude crescentic GN.
— Nephrotic-range proteinuria persisting beyond 4 weeks.
— Persistent hypocomplementemia >6–8 weeks — suggests MPGN, C3 glomerulopathy, lupus.
— Atypical age (adult, especially elderly) with diagnostic uncertainty.
— No documented streptococcal infection or negative serologies.
— Recurrent gross hematuria — favors IgA nephropathy.
— Light microscopy: diffuse proliferative endocapillary GN with neutrophil influx ("exudative GN").
— Immunofluorescence: granular "starry sky" pattern of IgG and C3 along capillary walls and mesangium.
— Three IF patterns described: starry sky (early), mesangial (resolving), and garland (heavy capillary wall deposits — worse prognosis).
— Electron microscopy: characteristic subepithelial "humps" of immune complex deposition — pathognomonic.
— ANA, anti-dsDNA, C1q — lupus.
— ANCA (MPO, PR3) — pauci-immune crescentic GN.
— Anti-GBM — Goodpasture.
— Cryoglobulins, RF, HCV, HBV, HIV — infection-related GN.
— Blood cultures — endocarditis-associated GN, especially in IV drug users and adults.
— SPEP/UPEP in adults — monoclonal gammopathy mimics.
Board pearl: Subepithelial humps on EM are the single most pathognomonic feature of PSGN — appears in stems describing a patient who underwent biopsy due to atypical course.
Step 3 management: In an outpatient adult with otherwise typical features, defer biopsy and recheck C3 at 6–8 weeks; persistent hypocomplementemia is the trigger to refer to nephrology for biopsy.
— Mild: microscopic hematuria, normal BP, normal Cr → outpatient with close follow-up (BP and weight in 2–3 days, then weekly).
— Moderate: gross hematuria, mild HTN controllable with diet/loop diuretic, mild Cr bump → outpatient or short observation; reassess in 24–48 h.
— Severe: hypertensive urgency/emergency, oliguria, AKI with hyperkalemia, pulmonary edema, encephalopathy → admit.
— Critical: RPGN, dialysis-requiring AKI, refractory hyperkalemia, seizures → ICU + nephrology.
— Sodium restriction (<2 g/day in adults; weight-based in kids).
— Fluid restriction to insensible losses + urine output in oliguric phase.
— Loop diuretic (furosemide IV or PO) is first-line for edema and HTN.
— Reduce by ≤25% in first hour for hypertensive emergency.
— Then to <95th percentile in 24–48 h in children; <140/90 in adults.
— Avoid abrupt drops → watershed cerebral ischemia.
— Treat only if active streptococcal infection is documented (positive culture or persistent symptoms).
— Antibiotics do NOT alter the course of established PSGN but reduce community spread.
— Treat household contacts in outbreak settings.
— Not indicated in uncomplicated PSGN.
— Reserve for biopsy-proven crescentic/RPGN variant — pulse methylprednisolone, then oral taper, sometimes with cyclophosphamide.
Step 3 management: Sodium restriction + loop diuretic + a single antihypertensive (CCB or loop) controls 90% of PSGN cases; resist the urge to layer agents before assessing volume response.
CCS pearl: Order "low-sodium diet," "fluid restrict 1000 mL/day," "furosemide IV," and "monitor weight, BP, K, Cr" — these are the four pillars on the CCS interface.
— Furosemide PO/IV — first-line.
— Pediatric: 1–2 mg/kg/dose, q6–12h.
— Adult: 20–80 mg IV/PO, titrate to UOP and weight.
— Monitor K, Mg, Na, Cr; replace as needed.
— Switch to oral once euvolemic; taper off as renal function recovers.
— Calcium channel blockers (amlodipine, nifedipine) — first-line add-on, especially in pediatrics.
— Avoid ACEi/ARB acutely — risk of hyperkalemia and worsening AKI in oliguric phase; can introduce later for residual proteinuria once Cr stable.
— Labetalol or nicardipine IV drip for hypertensive emergency.
— Hydralazine is an older but still acceptable option in pediatrics for acute severe HTN.
— ECG first; if peaked T waves, widened QRS → IV calcium gluconate to stabilize membrane.
— Insulin + dextrose, β2-agonist nebulizer to shift.
— Loop diuretic, sodium polystyrene/patiromer, or dialysis to remove.
— Penicillin V PO 250–500 mg QID × 10 days (or amoxicillin) — if active strep infection on culture.
— Benzathine penicillin G IM single dose — for adherence concerns or outbreak control.
— Cephalexin or clindamycin if penicillin allergic.
— Treat close contacts of index case in outbreak settings.
— Avoid NSAIDs — worsen AKI and Na retention.
— Hold nephrotoxins (aminoglycosides, IV contrast) during AKI phase.
— Renally dose all medications; recheck Cr-based dosing daily during admission.
Board pearl: Loop diuretic + CCB, NOT ACEi/ARB, is the right acute antihypertensive cocktail in PSGN — ACEi/ARB can precipitate hyperkalemia and AKI in the volume-overloaded, oliguric patient.
Step 3 management: Document medication reconciliation for any preexisting ACEi/ARB, NSAID, or K-sparing diuretic and hold them during the acute phase; restart selectively at follow-up.
— Acidosis (refractory metabolic acidosis, pH <7.1).
— Electrolytes (refractory hyperkalemia >6.5 with ECG changes).
— Ingestions (n/a here).
— Overload (pulmonary edema refractory to diuretics).
— Uremia (pericarditis, encephalopathy, BUN >100).
— Modality: intermittent hemodialysis if hemodynamically stable; CRRT if unstable or in ICU.
— Most PSGN patients needing dialysis recover renal function and can be weaned off within 1–2 weeks.
— Performed percutaneously under ultrasound guidance.
— Pre-procedure: correct BP <140/90, hold antiplatelets/anticoagulants, ensure platelets >50k, INR <1.5.
— Post-procedure: bedrest 6–24 h, monitor for gross hematuria, perinephric hematoma, AV fistula.
— Informed consent must include risk of bleeding (~1%), need for transfusion (~0.3%), nephrectomy (rare).
— Not routine; reserved for anti-GBM coexistence or severe crescentic GN as adjunct to immunosuppression.
— IV access, continuous BP monitoring (arterial line preferred).
— Nicardipine or labetalol infusion in adults.
— Sodium nitroprusside — avoid in renal failure due to thiocyanate accumulation.
— Reduce MAP by 20–25% in first hour, then gradual.
— Upright positioning, supplemental O2, BiPAP if needed.
— Aggressive IV furosemide ± nitroglycerin drip.
— Avoid morphine in renal failure.
CCS pearl: When ordering dialysis on CCS, include "place dialysis catheter," "consult nephrology," and "transfer to ICU" together — the simulator scores you on bundled, time-appropriate orders.
Board pearl: Crescentic transformation in PSGN is rare but devastating; persistent oliguria beyond 1 week or rising Cr despite supportive care mandates biopsy and consideration of pulse steroids.
— Often misdiagnosed because PSGN is "a pediatric disease" in many providers' minds — high index of suspicion needed.
— Higher rates of comorbid HTN, diabetes, CHF complicate fluid management.
— Acute kidney injury more severe, with up to 50% needing temporary dialysis and ~25% progressing to CKD.
— Mortality higher (5–10%) due to cardiovascular complications rather than renal failure per se.
— Edema and CHF often dominate over hematuria.
— Concomitant diabetes + PSGN can mimic diabetic nephropathy; biopsy more often required.
— Skin sources of strep (cellulitis, infected leg ulcers, diabetic foot infections) are common triggers.
— Higher risk of concurrent endocarditis-related GN — get blood cultures and echo if any murmur, fever, or IVDU history.
— Worse baseline renal reserve → lower threshold to admit, monitor closely.
— Adjust all medications to eGFR; avoid contrast, NSAIDs, and aminoglycosides.
— Higher risk of failure to recover baseline function — counsel about possible permanent eGFR decline.
— Cirrhosis-associated coagulopathy increases biopsy bleeding risk.
— Differential expands to include HCV cryoglobulinemic GN and HBV-associated MPGN — send hepatitis serologies in any adult with GN.
— Diuretic dosing trickier — risk of hepatorenal precipitation; use spironolactone-furosemide combinations cautiously.
— Hold NSAIDs, ACEi/ARB, K-sparing diuretics, metformin, SGLT2i during AKI.
— Reassess at each visit; restart based on eGFR trajectory.
Step 3 management: In any adult >50 with new GN, send blood cultures, hepatitis serologies, HIV, ANCA, ANA, and SPEP/UPEP — the post-infectious diagnosis must be earned, not assumed.
Board pearl: Adult PSGN carries a 20–30% risk of long-term CKD or HTN — counsel and arrange longitudinal nephrology follow-up at discharge.
— Peak age 5–12 years; rare under 3 (immature immune complex handling).
— >95% complete recovery of renal function.
— Boys > girls (~2:1).
— Outpatient management feasible in mild cases with reliable caregivers.
— Counsel families: hematuria can persist microscopically for 1–2 years, proteinuria up to 6 months — this is normal and does not signal failure.
— School avoidance only during active infection phase if streptococcal source is still contagious.
— PSGN in pregnancy is rare but must be distinguished from preeclampsia:
— Preeclampsia: HTN + proteinuria after 20 wks, normal C3, elevated LFTs, low platelets.
— PSGN: low C3, recent strep, RBC casts, normal LFTs/platelets.
— Manage with labetalol, nifedipine, methyldopa; avoid ACEi/ARB throughout pregnancy.
— Maternal-fetal medicine and nephrology co-management.
— Postpartum, follow renal function and BP for 6–12 months.
— Indigenous Australian, Pacific Islander, sub-Saharan African, indigenous American communities — outbreaks linked to skin infections, crowding, scabies co-infection.
— Public health response: treat index cases and close contacts with penicillin, treat scabies, improve housing/sanitation.
— Higher long-term risk of CKD and HTN — establish surveillance programs.
— Atypical presentations; consider concurrent opportunistic infections.
— HIV-associated nephropathy and HBV-MPGN should be excluded.
Board pearl: Normal C3 essentially excludes PSGN; in a pregnant patient with HTN and proteinuria, normal C3 should redirect you toward preeclampsia.
Step 3 management: Pediatric outpatient follow-up cadence — BP at 1 week, UA + BMP at 2 weeks, C3 at 6–8 weeks, then UA + BP every 3–6 months for 1–2 years.
— Hypertensive encephalopathy / PRES — seizures, AMS, cortical blindness; requires controlled BP reduction.
— Acute pulmonary edema — particularly in adults; can be presenting feature.
— Acute kidney injury — usually self-limited; dialysis-requiring in 1–5% of children, up to 25% of adults.
— Hyperkalemia with arrhythmia risk.
— Congestive heart failure from volume overload superimposed on baseline cardiac disease.
— Rapidly progressive (crescentic) glomerulonephritis — rare; biopsy-defined when >50% glomeruli show crescents. Worse renal prognosis; consider pulse steroids.
— Persistent proteinuria or nephrotic syndrome — should resolve in 3–6 months; persistence raises alternative diagnoses (MPGN, FSGS).
— Chronic kidney disease — up to 25% of adults with severe initial episode.
— Hypertension — may persist or recur years later; screen at every visit.
— Microalbuminuria — early marker of incomplete recovery; treat with ACEi/ARB once Cr stable.
— End-stage renal disease is rare from PSGN alone but contributes to CKD burden in endemic regions.
— PSGN is generally a one-time event — recurrent episodes should prompt reconsideration of diagnosis (IgA nephropathy, MPGN, hereditary nephritis).
— Re-exposure to nephritogenic strains can rarely cause recurrence in children.
— Pediatric: <1%, usually from hypertensive complications.
— Adult: 5–10%, driven by cardiovascular events and comorbid disease.
— PSGN can follow either pharyngitis or skin infection; rheumatic fever follows only pharyngitis.
— Penicillin prevents rheumatic fever but does not reliably prevent PSGN.
Key distinction: Persistent hematuria for years = expected microscopic course in PSGN, but recurrent gross hematuria episodes = IgA nephropathy until proven otherwise.
Board pearl: A child with PSGN does not need long-term penicillin prophylaxis (unlike rheumatic fever), because recurrence is rare.
— Stage 2 hypertension or symptomatic HTN.
— Cr >1.5× baseline or oliguria (<0.5 mL/kg/h).
— Pulmonary edema, significant edema, or weight gain >7% baseline.
— Hyperkalemia (K >5.5) or other significant electrolyte derangement.
— Inability to ensure outpatient follow-up; social complexity; pediatric caregiver concerns.
— Hypertensive emergency requiring IV antihypertensive infusion.
— Seizures, AMS, focal deficits, PRES on imaging.
— Refractory hyperkalemia, acidosis, or need for emergent dialysis.
— Pulmonary edema requiring positive pressure ventilation.
— Hemodynamic instability or coexisting sepsis.
— Nephrology — for any AKI, persistent low C3, atypical features, or need for biopsy.
— Pediatrics/pediatric nephrology — all pediatric cases beyond mildest.
— Cardiology — if pulmonary edema, hypertensive cardiomyopathy, or arrhythmia.
— Neurology — if encephalopathy, seizures, or focal deficits.
— Infectious disease — if endocarditis or alternative source suspected.
— Pediatric patients in adult facilities → transfer to children's hospital with pediatric nephrology and dialysis capability.
— Adults without local dialysis access → transfer.
— BP controlled on oral regimen ≥24 h.
— Trending downward Cr.
— Net diuresis with stable electrolytes.
— Tolerating oral intake.
— Reliable follow-up arranged within 3–7 days.
Step 3 management: Document the handoff between inpatient team and outpatient nephrologist/PCP explicitly — pending labs, BP medication titration plan, repeat C3 timing, and red-flag symptoms (decreased urine output, recurrent gross hematuria, severe headache).
CCS pearl: On CCS, "transfer to ICU" should be paired with continuous cardiac monitoring, arterial line, and nephrology consult — partial bundles lose points.
— Synpharyngitic hematuria (1–3 days post-URI), no latency.
— Normal C3/C4.
— Recurrent episodes of gross hematuria; chronic course.
— Biopsy: mesangial IgA deposits.
— Persistently low C3 beyond 8 weeks; type II (DDD) classically has C3 nephritic factor.
— Mixed nephrotic-nephritic picture.
— Tram-track basement membrane on biopsy.
— Low C3 AND low C4; positive ANA, anti-dsDNA.
— Systemic features: rash, arthritis, serositis, cytopenias.
— Biopsy for ISN/RPS class; treatment is immunosuppression.
— Pauci-immune crescentic GN.
— Normal complement, positive ANCA.
— Constitutional symptoms, sinus/lung involvement.
— RPGN + pulmonary hemorrhage.
— Normal complement; positive anti-GBM antibody.
— Linear IF on biopsy.
— Treat with plasmapheresis + immunosuppression urgently.
— Low C4, normal/low C3; positive cryoglobulins, RF.
— Often HCV-associated; palpable purpura, neuropathy.
— Low C3 ± low C4, positive blood cultures, vegetations on echo.
— Often in IVDU, prosthetic valves; immune complex–mediated.
— Persistently low C3, normal C4; C3 nephritic factor or complement regulator mutations.
— Chronic, often progressive.
Key distinction: Complement pattern is the single most useful initial discriminator — low C3/normal C4 = PSGN, MPGN type I, or C3 glomerulopathy; low C3/low C4 = lupus, cryoglobulinemia, endocarditis.
Board pearl: ASO + anti-DNase B negative in a low-C3 nephritis should make you broaden the differential and consult nephrology for biopsy.
— Drug-induced (NSAIDs, PPIs, antibiotics).
— Sterile pyuria, WBC casts, eosinophiluria; rash, fever, eosinophilia.
— No RBC casts; complement normal.
— Ischemic or nephrotoxic; muddy brown casts.
— No hematuria of glomerular type, no edema/HTN syndrome.
— Dysuria, frequency, suprapubic pain.
— Pyuria, bacteriuria; RBCs but no RBC casts or proteinuria.
— Triad: microangiopathic hemolytic anemia, thrombocytopenia, AKI.
— Bloody diarrhea preceding (Shiga toxin E. coli O157:H7).
— Schistocytes on smear; normal C3 in typical HUS, low in atypical.
— Palpable purpura (legs/buttocks), abdominal pain, arthralgias, GN.
— Normal complement; IgA deposition on biopsy.
— Children, often post-URI.
— Pheochromocytoma, renovascular HTN, drug-induced (cocaine, methamphetamine, sympathomimetics).
— Workup with metanephrines, renal artery imaging, toxicology screen.
— Flank pain, hematuria; CT or US confirms; no edema or HTN syndrome.
— Flank pain, hematuria, proteinuria; usually in nephrotic syndrome (membranous nephropathy).
— Hematuria, papillary necrosis; African ancestry, known sickle disease/trait.
Step 3 management: When a child presents with hematuria + purpura + abdominal pain, think HSP/IgA vasculitis, not PSGN — complement will be normal, and treatment differs (supportive ± steroids for severe abdominal/renal disease).
Board pearl: RBC casts on urinalysis are the great discriminator — they essentially confine you to glomerular disease and exclude AIN, ATN, UTI, and stones.
— Continue oral loop diuretic until euvolemic; taper based on weight/BP at follow-up.
— Continue antihypertensive (CCB most common) until BP stable off therapy.
— Hold ACEi/ARB initially; consider introducing later if persistent proteinuria after Cr normalizes.
— Reconcile pre-admission medications: restart maintenance therapies cautiously.
— Complete 10-day course if active strep infection documented.
— No long-term prophylactic penicillin — PSGN does not recur like rheumatic fever does.
— Treat household contacts only if outbreak setting or persistent transmission.
— Low-sodium diet (<2 g/day) while diuretics ongoing and during BP stabilization.
— Fluid restriction lifted once euvolemic.
— Avoid NSAIDs indefinitely while renal function is recovering; counsel on alternatives (acetaminophen).
— Encourage hand hygiene, skin hygiene, prompt treatment of skin infections.
— Update pneumococcal, influenza, COVID-19 vaccines per CDC schedule.
— No specific PSGN vaccine exists; group A strep vaccines are in trials.
— BP target <130/80 in adults with CKD.
— ACEi or ARB once stable for any persistent proteinuria.
— Glycemic control if diabetic.
— Annual UA, BMP, BP monitoring.
— Red-flag symptoms to return: decreased urine output, recurrent gross hematuria, severe headache, vision changes, leg swelling, shortness of breath.
— Explain expected microscopic hematuria duration (1–2 years) — to prevent unnecessary alarm.
Step 3 management: On discharge, schedule PCP follow-up in 3–7 days, nephrology in 4–6 weeks, and repeat C3 at 6–8 weeks — these dates should appear on the discharge summary, not in the "TBD" box.
Board pearl: Long-term BP and proteinuria surveillance are the highest-yield secondary prevention items — PSGN-related CKD often presents years later as HTN-attributed renal disease.
— Day 3–7 post-discharge: PCP visit — BP, weight, symptom check, medication tolerance.
— Week 2: UA, BMP — confirm Cr trending to baseline; assess proteinuria.
— Week 6–8: repeat C3 — should normalize; if not, refer to nephrology for biopsy.
— Months 3 and 6: UA, BMP, BP.
— Annually for 1–2 years: UA (for residual microscopic hematuria), BP.
— More intensive; nephrology involvement standard.
— Repeat eGFR, UA, urine protein/Cr ratio at 1, 3, 6, and 12 months.
— Consider continued nephrology follow-up at 1-year mark, especially if any residual proteinuria or HTN.
— Blood pressure — home BP monitoring encouraged.
— Weight — early indicator of recurrent fluid retention.
— Urine color and volume — caregivers/patients trained to watch for gross hematuria recurrence.
— Serum Cr/eGFR — trajectory matters more than single value.
— Spot urine protein/Cr ratio — should fall below 0.2 in children, 0.15 in adults.
— Return to school/work as tolerated once BP controlled and edema resolved.
— No specific exercise restrictions in uncomplicated recovery.
— Persistent microscopic hematuria is expected and does not indicate ongoing disease.
— PSGN does not run in families; siblings are not at increased intrinsic risk.
— Prompt treatment of future strep infections recommended for general health, not PSGN prevention.
— Long-term CKD risk is small in children, real in adults.
Step 3 management: Build a patient-portal message template for caregivers reporting microscopic hematuria months later — most need reassurance, not workup.
CCS pearl: "Schedule follow-up with PCP in 1 week" and "schedule follow-up with nephrology in 6 weeks" are scored items at end-of-case in nephritic syndrome simulations.
— Discuss bleeding (~1% major), hematoma (5–10% minor), transfusion (~0.3%), AV fistula, very rare nephrectomy/death.
— In pediatrics, assent from child + consent from parent/guardian; document both.
— Discuss alternatives (observation, empirical management) when clinical picture is typical PSGN.
— Some jurisdictions require reporting of streptococcal outbreaks (especially in schools, daycares, military, indigenous communities).
— Notify public health when PSGN clusters appear — facilitates contact tracing and source identification (e.g., scabies + strep co-epidemic).
— Invasive group A strep disease is reportable in most US states.
— Pediatric-to-adult transition of chronic mild kidney disease is a known gap — children with residual proteinuria can be lost to follow-up; build warm handoffs.
— Hospital-to-outpatient handoff: ensure repeat C3 and BP plan are documented in legible discharge summary and patient-portal note.
— Medication reconciliation errors common — explicit instructions on which pre-admission medications to resume and when.
— PSGN disproportionately affects under-resourced communities (overcrowding, skin infections, limited access to primary care).
— Address social determinants: housing density, skin/scabies treatment, hygiene resources, school nursing access.
— Avoid NSAIDs and IV contrast during AKI phase — common iatrogenic harms.
— Avoid ACEi/ARB in acute oliguric phase — hyperkalemia and AKI worsening.
— Drug dosing errors in pediatric weight-based dosing — double-check furosemide and antihypertensive doses.
— Use closed-loop communication for handoff between ED, floor, and ICU teams.
— Adolescent patients may have privacy concerns about contagious skin infections; discuss confidentially when developmentally appropriate.
Board pearl: A child returns to school with persistent microscopic hematuria — no work, school, or activity restriction is warranted. Counsel teachers and school nurses to prevent unnecessary stigmatization.
Step 3 management: Always confirm scheduled follow-up appointment exists before discharge — "follow-up arranged" without a date is a documented safety gap.
— Pharyngitis → PSGN: 1–2 weeks.
— Impetigo/pyoderma → PSGN: 3–6 weeks.
— IgA nephropathy: 1–3 days (synpharyngitic).
— Low C3, normal C4 = PSGN classic.
— Low C3 + low C4 = lupus, cryoglobulin, endocarditis.
— C3 normalizes by 6–8 weeks.
— ASO best for pharyngeal source.
— Anti-DNase B best for skin source.
— Streptozyme = combined panel; ~95% sensitive.
— LM: diffuse endocapillary proliferative GN with neutrophils.
— IF: granular "starry sky" IgG + C3.
— EM: subepithelial humps (pathognomonic).
— Children: >95% complete recovery.
— Adults: 60% complete recovery, 25% CKD, 5–10% mortality (cardiovascular).
— Recurrence is rare.
— Sodium restriction, fluid restriction, loop diuretic, CCB.
— Avoid ACEi/ARB acutely.
— Antibiotics only for active infection; do not prevent PSGN.
— No prophylactic penicillin (unlike rheumatic fever).
— Persistent low C3 → MPGN / C3 glomerulopathy.
— Pulmonary hemorrhage → anti-GBM.
— Palpable purpura → IgA vasculitis (HSP).
— Crescents on biopsy → RPGN; consider pulse steroids.
— NAPlr (nephritis-associated plasmin receptor).
— SpeB (streptococcal pyrogenic exotoxin B).
— Subepithelial immune complex deposits.
— Children 5–12, M>F.
— Outbreaks in crowded settings.
— Indigenous/under-resourced populations disproportionately affected.
Board pearl: Memorize the trio — low C3, anti-DNase B (or ASO), subepithelial humps — these three findings together = PSGN with near certainty.
Key distinction: PSGN does NOT prevent recurrent streptococcal infection — there is no immunity from one episode; long-term prophylaxis is unwarranted.
— 8-year-old with sore throat 2 weeks ago presents with periorbital edema, tea-colored urine, BP 140/90.
— UA: RBC casts, 2+ protein. C3 low, C4 normal. ASO elevated.
— Answer: PSGN; supportive care, loop diuretic, sodium restriction. Do not biopsy.
— 6-year-old with healing crusted lesions on legs for 4 weeks now has gross hematuria.
— ASO normal, anti-DNase B elevated.
— Tests how well you know skin-source serology.
— 55-year-old diabetic with cellulitis 4 weeks ago, now Cr 3.0, low C3.
— Question: Next step? → Biopsy (atypical age, severe AKI).
— Same nephritic presentation but with low C3 AND low C4 → lupus.
— Persistent low C3 at 8 weeks → MPGN.
— Normal C3 + RBC casts shortly after URI → IgA nephropathy.
— PSGN patient with BP 180/120 and headache → hypertensive emergency → IV labetalol or nicardipine, lower MAP 20–25% in first hour. Avoid sodium nitroprusside.
— PSGN patient started on lisinopril develops K 6.5 and rising Cr → answer: stop ACEi; not appropriate in acute oliguric phase.
— Family asks how long microscopic hematuria will persist → up to 1–2 years; reassure.
— Pediatrician asks whether prompt penicillin for next strep infection prevents recurrence → No; PSGN is not prevented by antibiotics (unlike rheumatic fever).
— EM shows subepithelial humps → PSGN.
— Linear IgG → anti-GBM.
— Tram-track basement membrane → MPGN.
— IgA mesangial deposits → IgA nephropathy.
— School outbreak of impetigo with multiple PSGN cases → notify public health, treat scabies/strep in cohort, improve hygiene access.
Step 3 management: When the stem asks "next best step" in classic PSGN, the answer is almost always supportive care + outpatient follow-up, NOT biopsy or immunosuppression — resist over-testing.
Board pearl: If the stem mentions "starry sky" or "humps," the diagnosis is locked — focus your answer on management or prognosis.
Post-streptococcal glomerulonephritis is an immune complex–mediated nephritic syndrome occurring 1–2 weeks after streptococcal pharyngitis or 3–6 weeks after impetigo, characterized by low C3/normal C4, elevated ASO or anti-DNase B, subepithelial "humps" on EM, and managed with supportive care — sodium restriction, loop diuretics, and a calcium channel blocker — while avoiding ACEi/ARB acutely, with excellent pediatric prognosis and meaningful adult CKD risk requiring long-term follow-up.
Board pearl: The single highest-yield distinguishing fact: PSGN = low C3, normal C4, with C3 normalizing within 8 weeks — persistent hypocomplementemia is your trigger to biopsy and chase MPGN, lupus, or C3 glomerulopathy.
Step 3 management: Build the discharge plan around scheduled labs, scheduled visits, and explicit medication reconciliation — PSGN is a disease where the follow-up plan IS the treatment plan.