Nephrology & Internal Medicine & Family Medicine
Glomérulonéphrite | Clinique Omicron Québec
Glomerulonephritis refers to a heterogeneous group of inflammatory conditions affecting the renal glomeruli - microscopic filtration units of the kidney consisting of a capillary surrounded by specialized cells (podocytes, mesangial cells, endothelial cells). Clinical symptoms include glomerular hematuria (deformed red blood cells - acanthocytes), proteinuria, hypertension and altered renal function to varying degrees depending on etiology and severity. Classically, a distinction is made between nephritic syndrome (macroscopic hematuria + hypertension + edema + oliguria + moderate proteinuria) and nephrotic syndrome (massive proteinuria >3.5 g/d + hypoalbuminemia + edema + hyperlipidemia + lipiduria), but many glomerulonephritic patients present a mixed picture. Rapidly progressive glomerulonephritis (RPGN), characterized by renal deterioration over days to weeks with epithelial crescents on biopsy, is an absolute nephrological emergency. Precise diagnosis relies on renal biopsy, which enables histological classification, etiological orientation and therapeutic decision - early immunosuppressive treatment is decisive in preserving renal function.
Classification, pathophysiology, and clinical syndromes
- General Pathophysiology of Glomerulonephritis: immunological mechanisms: deposition of circulating immune complexes (CIC) in glomeruli → activation of complement (classical pathway) → recruitment of inflammatory cells → glomerular damage - examples: post-streptococcal glomerulonephritis + lupus + cryoglobulinemia + anti-glomerular basement membrane antibodies (anti-GBM): cross-reactivity with GBM type IV collagen → Goodpasture's syndrome (anti-GBM + pulmonary hemorrhage + necrotizing glomerulonephritis) + ANCA (anti-neutrophil cytoplasmic antibodies): antibodies directed against proteins in PNN granules (proteinase 3 - PR3 - for c-ANCA + myeloperoxidase - MPO - for p-ANCA) → ANCA+ vasculitides (granulomatosis with polyangiitis - GPA - Wegener + microscopic polyangiitis - PAM + eosinophilic granulomatosis with polyangiitis - GEPA - Churg-Strauss) → pauci-immune GNRP (no immunological deposits visible on IF); cellular mechanisms : proliferation of mesangial cells (mesangioproliferative GN) + proliferation of Bowman's capsule cells (epithelial crescents) + infiltration by macrophages and T lymphocytes → glomerular necrosis; consequences of glomerular damage: hematuria (rupture of the GBM → passage of red blood cells into Bowman's space → microscopic or macroscopic hematuria + acanthocytes - dysmorphic red blood cells pathognomonic of a glomerular origin) + proteinuria (alteration of the selectivity of GBM → passage of albumin and other proteins → glomerular-type proteinuria) + reduced GFR (reduced filtration surface + inflammation) + sodium and water retention → hypertension + edema + oligoanuria if severe
- Clinical Classification of Glomerulonephritis: Acute nephritic syndrome: gross hematuria («Coca-Cola» or brick-red urine) + sudden onset hypertension + edema (especially facial edema upon waking) + oliguria + moderate proteinuria (1-3 g/day) + red blood cell casts in urine sediment (pathognomonic—red blood cells clumped in Tamm-Horsfall matrix within tubules) + moderate renal function impairment—prototype: post-infectious glomerulonephritis (post-streptococcal); pure nephrotic syndrome: massive proteinuria (>3.5 g/day in adults + >40 mg/m²/h in children) + hypoalbuminemia<30 gl) + œdèmes importants (déclives ascite épanchements pleuraux) hyperlipidémie (ldl ++ cholestérol total élevé) lipidurie (corps gras ovales au sédiment) état pro-thrombotique (pertes urinaires d'antithrombine iii protéine c s → risque de tvp ep thrombose la veine rénale) — pas ou peu d'hématurie dfg souvent préservé initialement prototype : syndrome néphrotique à lésions glomérulaires minimes (snlgm) ; impur (mixte) protéinurie massive hématurie hta altération fonction rénale glomérulonéphrite membranoproliférative lupique iga sévère rapidement progressive (gnrp) détérioration rapide (jours semaines) ± histologie croissants épithéliaux (>50 % of glomeruli) → emergency → urgent histological diagnosis + immediate intensive immunosuppression; chronic glomerulonephritis: persistent proteinuria ± microscopic hematuria ± hypertension ± slow and progressive decline in GFR → evolution towards end-stage renal disease (ESRD) in the absence of treatment
- Etiologies and Main Histological Forms primitive glomerulonephritis (idiopathic - no causative systemic disease): IgA nephropathy (Berger's disease): most common primary glomerulonephritis worldwide (30-40 % of renal biopsies for GN) - mesangial deposits of polymeric IgA → lectin-mediated complement activation → episodic macroscopic hematuria (often postENT infection - synchronous in 24-72h - different from post-streptococcal GN which occurs 10-14 days later) + persistent microscopic hematuria + variable proteinuria + hypertension - Oxford score (MEST-C) : mesangial (M) + endocapillary (E) + segmental (S) + tubulointerstitial (T) + crescentic (C) lesions → guides prognosis and treatment + minimal glomerular lesion nephrotic syndrome (MGNLS): child +++ (80 % of nephrotic syndromes in children) + adult (25 %) - normal MO + negative IF + ME: effacement of podocyte pedicels - prototype of pure nephrotic syndrome + excellent prognosis if corticosensitive + segmental and focal glomerulosclerosis (SFG): sclerosing lesions in some glomeruli (segmental) + some glomeruli (focal) - primary (idiopathic) or secondary (obesity + HIV + heroin + sickle cell anemia + compensatory hypertrophy - single kidney) - impure nephrotic syndrome + frequent resistance to corticoids + extramembranous glomerulonephritis (EMG) : subepithelial IgG deposits (granular in IF) → «comb-tooth» image in ME - adult ++ - anti-PLA2R antibodies (phospholipase A2 receptor - present in 70-80 % of primary GEM) - pure nephrotic syndrome - high risk of renal vein thrombosis + membranoproliferative glomerulonephritis (MPGN) : mesangial + subendothelial deposits → double-contour GBM thickening («streetcar rail» - ME) - types I (CIC) + II (dense deposit disease - C3) + III - impure nephrotic syndrome + low complement (C3 ± C4); secondary glomerulonephritis (systemic diseases): systemic lupus erythematosus (SLE - lupus nephritis - ISN/RPS classification classes I-VI) + ANCA+ vasculitides (GPA + PAM + GEPA) + Goodpasture's syndrome (anti-GBM) + diabetes (diabetic nephropathy - the most common secondary glomerulopathy) + amyloidosis + cryoglobulinemia (associated HCV) + Henoch-Schönlein purpura (IgA - child) + post-infectious glomerulonephritis (post-streptococcal - GASBH - Streptococcus pyogenes)
Diagnosis, treatment and special situations
| Clinical situation | Diagnosis | Treatment and follow-up |
|---|---|---|
| Diagnostic workup for glomerulonephritis Urine sediment — biopsy — immunology |
Diagnostic workup of glomerulonephritis follows a two-stage approach: confirmation of glomerular nature of renal involvement + identification of etiology; confirmation of glomerular involvement: urinalysis with sediment: microscopic hematuria (>3 RBCs/field) → phase-contrast microscopy: acanthocytes (dysmorphic bicycle bell-shaped red blood cells - pathognomonic if >5 %) + hematic cylinders (pathognomonic of active GN) + granular cylinders + lipiduria (oval fatty bodies + esterified cholesterol) if nephrotic syndrome + 24h proteinuria or proteinuria/creatinuria ratio (ACR - albumin-to-creatinine ratio) : glomerular proteinuria → albumin predominates (vs. tubular proteinuria → small proteins predominate) + renal function tests: creatinine + estimated GFR (CKD-EPI 2021) + urea + ionogram; immunological work-up guided by clinical presentation: serum complement (C3 + C4 + CH50): low in immune-complex GN (lupus + post-streptococcal GN + GNMP) → normal in pauci-immune GN (ANCA+) and Goodpasture's syndrome + ANCA (c-ANCA/anti-PR3 + p-ANCA/anti-MPO): vasculitides → pauci-immune GN → GNRP + anti-GBM antibodies : Goodpasture's syndrome → GNRP + AAN + anti-dsDNA (lupus) + anti-Sm + antiphospholipid antibodies + cryoglobulins + protein electrophoresis + immunofixation (gammopathy + amyloidosis) + HBV + HCV + HIV serology + ASLO (antistreptolysin O) + anti-DNAse B (streptococcus) + anti-PLA2R (primary GEM - IgG4) + blood cultures if endocarditis suspected ; percutaneous renal biopsy: reference examination for histological diagnosis of GN - indications: adult nephrotic syndrome (>1 year) + persistent microscopic hematuria + significant (>1 g/d) unexplained proteinuria + GNRP + follow-up of lupus nephritis + contraindications: single functional kidney + uncontrolled hypertension + coagulation disorders + active infection + insufficient cooperation + treatment: ultrasound guidance + local anesthesia + bed rest 6-8h post-biopsy + blood pressure monitoring + post-biopsy macroscopic hematuria (5-10 % - most often spontaneously resolving) - the 3 essential tissue analyses: light microscopy (MO - PAS + Jones + Masson + HE staining) + direct immunofluorescence (IF - IgG + IgA + IgM + C3 + C1q + fibrin - «comb-tooth» or mesangial or subendothelial appearance) + electron microscopy (EM - localization of deposits + effacement of podocyte pedicels) | General therapeutic approach to glomerulonephritis: nephroprotective measures common to all GN (background treatment regardless of etiology): blood pressure control: target BP <130/80 mmHg (KDIGO 2021) → IEC (ramipril + perindopril) or ARA2 (losartan + telmisartan): 1st line (reduction in proteinuria + nephroprotection independent of antihypertensive effect - reduction in glomerular intracapillary hydrostatic pressure) → double renin-angiotensin blockade (ACEI + ARB2): not recommended (risk of hyperkalemia + acute renal failure) + SGLT2 inhibitors (dapagliflozin - Forxiga + empagliflozin - Jardiance): nephroprotection demonstrated in proteinuric chronic kidney disease (DAPA-CKD 2020 trial + CREDENCE - 39 % reduction in risk of renal progression) → now recommended as 1st line in proteinuric chronic GN (KDIGO 2024) + sparsentan (dual endothelin-1 and angiotensin II - AT1 antagonist): FDA 2023 approved for IgA nephropathy + GSF - availability in Canada under evaluation + proteinuria reduction: optimize RAAS blockade + sodium restriction (2 g Na/d) + statins if hyperlipidemia (nephrotic syndrome) + prophylactic anticoagulation: DVT + renal vein thrombosis - high risk if albuminemia <25 g/L + GEM → LMWH or VKA depending on bleeding risk |
| Rapidly progressive glomerulonephritis (RPGN) Emergency — croissants — intensive immunosuppression |
GNRP is a nephro-immunological emergency - every hour lost worsens renal prognosis; definition: rapid deterioration of renal function (doubling of creatinine in 50 % of glomeruli (proliferation of Bowman's capsule cells + macrophages → compression of glomerulus → sclerosis); immunological classification of GNRP (3 types): type I (anti-GBM - 10-15 %): IgG anti-collagen IV α3 antibody → fixation on GBM → complement activation → glomerular necrosis + alveolar hemorrhage if antibody cross-reactive with alveolar basement membrane (Goodpasture's syndrome) - normal complement - biopsy: linear IgG deposits (IF) - diagnosis: anti-GBM ELISA (sensitivity 95 %) + type II (immune complexes - 15-20 %): granular Ig deposits (IF) → lupus + post-infectious GN + cryoglobulinemia + severe IgA → low complement - diagnosis according to etiology + type III (pauci-immune - ANCA+ - 60-65 %): most frequent GNRP - ANCA positive (anti-PR3 or anti-MPO) → no deposits in IF (hence «pauci-immune») - forms: GPA (formerly Wegener's - anti-PR3 + ENT + lung + kidney involvement) + PAM (anti-MPO + kidney ++ + lung) + GEPA (anti-MPO + asthma + eosinophilia + polyangiitis); emergency work-up for suspected GNRP: ANCA (c-ANCA + p-ANCA + anti-PR3 + anti-MPO) + anti-GBM + AAN + complement + CBC + coagulation panel + renal function + proteinuria + urine sediment + renal imaging (echo) + FOGD and chest x-ray (alveolar hemorrhage - Goodpasture's syndrome + GPA) + renal biopsy URGENTLY (ideally within 24-48h) | Treatment of GNRP - therapeutic emergency: pauci-immune ANCA+ GNRP (GPA + PAM): induction of remission: rituximab (Rituxan - anti-CD20 - 375 mg/m² IV × 4 weeks or 1 g × 2 at 2-week intervals) : equivalent to cyclophosphamide for induction (RAVE 2010 trial + RITUXVAS) + preferred in severe forms from the outset and if subsequent pregnancy desired - cyclophosphamide IV (0.6-0.75 g/m²/4 weeks - EUVAS regimen) or PO (2 mg/kg/d) : alternative if rituximab not available + methylprednisolone IV (250-1,000 mg/d × 3 days - bolus IV) → relay prednisone 1 mg/kg/d PO → gradual decrease over 3-6 months + plasma exchange : indicated if creatinine >500 µmol/L or dialysis-dependent OR active alveolar hemorrhage (PEXIVAS 2020 trial - mixed results on renal prognosis but possible benefit in severe alveolar hemorrhage) → 7 exchanges × 14 days (plasma volume × 1.5 per exchange + albumin 4 %); remission maintenance: rituximab 500 mg IV every 6 months × 2 years (superior to azathioprine in the MAINRITSAN 2014 study) or azathioprine 2 mg/kg/d PO (less effective than rituximab but accessible); GNRP type I (anti-GBM): bolus methylprednisolone IV + cyclophosphamide + intensive plasma exchanges (14 exchanges in 21 days - eliminates circulating anti-GBM antibodies) → poor renal prognosis if creatinine >600 µmol/L at presentation (oligoanuria + 100 % of crescents → chronic dialysis unavoidable in most cases) - but treatment nonetheless indicated to prevent pulmonary relapses + cure of less advanced forms; GNRP type II (immune complexes): treatment of causative disease + corticosteroids depending on cause |
| IgA nephropathy (Berger's disease) The most frequent primary GN |
IgA nephropathy (N-IgA) is characterized by mesangial deposits of galactose-deficient polymeric IgA → lectin and alternate pathway complement activation → mesangial inflammation; clinical presentation: recurrent macroscopic hematuria (episodes synchronous with upper airway infections - latency 24-72h - «synpharyngitic hematuria» - to be distinguished from post-streptococcal LN - latency 10-21 days) + persistent microscopic hematuria between episodes + variable proteinuria (mild to nephrotic) + hypertension + progressive GFR impairment in 30-40 % of cases at 20 years + Oxford score (MEST-C): M (mesangial hypercellularity) + E (endocapillary lesions) + S (segmental sclerosis) + T (tubular atrophy/interstitial fibrosis) + C (crescents) → T1-T2 and C2 = poor prognostic markers; poor prognostic factors: persistent proteinuria >1 g/d + uncontrolled hypertension + low GFR at presentation + high MEST-C score + associated GSF-type lesions; PRISMMED Calculator and International IgAN Prediction Tool prognostic tool: predicts risk of progression to CKD at 5 and 10 years → guides intensity of immunosuppressive therapy; renal biopsy: mesangial IgA deposits (IF) ± IgG + C3 + C1q negative (vs Henoch-Schönlein purpura where IgA also present but systemic context: purpura + arthritis + abdominal pain) | Treatment of IgA nephropathy: optimal nephroprotective measures first (before any immunosuppressive treatment): ACE inhibitor or ARB2 at maximum tolerated dose (target BP 1 g/d) + SGLT2 inhibitor (dapagliflozin 10 mg/d) → 30-40 % reduction in proteinuria in studies + sodium restriction + weight control + smoking cessation + re-evaluation after 3-6 months of optimization : if persistent proteinuria >0.5-1 g/d despite optimal nephroprotective treatment → consider specific treatment; new N-IgA target therapies: sparsentan (Filspari - dual ET-A + AT1 antagonist): approved FDA 2023 (PROTECT trial) - significant reduction in proteinuria + possible slowing of renal progression - Health Canada approval pending + iptacopan (factor B inhibitor of the alternative complement pathway - PO): FDA 2024 approved (APPLAUSE-IgAN trial) - 38 % reduction in proteinuria → Health Canada approval pending + ileal targeted-release budesonide (Nefecon - Tarpeyo): targeting ileal Peyer's patches (site of IgA galactose-deficient production) → 27-50 % reduction in proteinuria (NefIgArd phase 3 trial) - FDA 2023 approved + Health Canada approval pending + systemic corticosteroids: prednisone 0.5-1 mg/kg/d × 6-8 months → reduction in proteinuria but significant adverse effects (diabetes + hypertension + infections) → risk-benefit debated - STOP-IgAN study: no renal benefit vs. long-term nephroprotective treatment alone + TESTING (high-dose corticosteroids): stopped prematurely (severe infections) + lower-dose regimen under evaluation |
| Ne Corticosensitivity — rituximab — anti-PLA2R |
Nephrotic syndrome with minimal glomerular lesions (SNLGM): the most common NG in children (80 % of nephrotic syndromes 60 years with GEM (oncological workup: CT TAP + PSA + mammography + colonoscopy) + lupus nephritis (ISN/RPS classes I-VI): class III (focal) + IV (diffuse) → most severe → aggressive treatment; thrombotic risk in nephrotic syndrome: albumin <25-30 g/L → risk of DVT + PE + renal vein thrombosis (particularly in GEM - risk of renal vein thrombosis of 25-35 %) → prophylactic anticoagulation discussed if albumin <25 g/L (VKA or LMWH) | Treatment of SNLGM: corticosteroids (1st line - corticosensitivity in 80-90 % in adults): prednisone 1 mg/kg/d (maximum 80 mg/d) × 4-16 weeks → slow decrease over 6 months - complete remission (proteinuria 2 years) + mycophenolate mofetil (MMF) 1,000-1,500 mg × 2/d: less nephrotoxic than ICNs - option in recurrent SNLGM + cyclophosphamide (2 mg/kg/d × 8-12 weeks): historical option - reduced long-term recurrences but risk of gonadal toxicity; treatment of GEM: spontaneous remission in 30 % of primary GEM (especially if anti-PLA2R titre low and spontaneously decreasing) → wait 6 months if moderate nephrotic syndrome + albuminemia >25-30 g/L → immunosuppressive treatment if severe nephrotic syndrome + thrombotic complications + decline in GFR or absence of remission at 6 months: rituximab (375 mg/m² × 4 infusions 1 week apart - MENTOR 2019 trial: superior to cyclophosphamide + corticosteroids at 24 months for complete remission) + cyclosporine or tacrolimus: alternative if rituximab unavailable + modified Ponticelli treatment (corticosteroids alternated with chlorambucil or cyclophosphamide × 6 months): historical regimen still in use + anti-PLA2R monitoring: titer decreasing → good therapeutic response → cure possible |
| Lupus nephritis Classes ISN/RPS — hydroxychloroquine — belimumab |
Lupus nephritis (LN) is one of the most severe visceral impairments of systemic lupus erythematosus (SLE) - it occurs in 40-60 % of lupus patients in the first 10 years of the disease and represents a major factor in morbidity and mortality; ISN/RPS 2003 classification (revised 2018): class I: minimal mesangial deposits (normal MO) - class II: proliferative mesangial LN - class III: focal GN (50 % of affected glomeruli - most severe - crescents possible) - class V: membranous GN (nephrotic syndrome) - class VI: advanced sclerosing GN (>90 % of sclerotic glomeruli) - classes III + IV = most severe → intensive immunosuppressive treatment essential + frequent combined classes III-IV + V; NL diagnostic workup: lupus ACTIVITY: NAA + anti-dsDNA (correlated with renal activity) + complement (C3 + C4 + low CH50) + CBC + 24h proteinuria + urinary sediment (hematic cylinders) + renal function - renal biopsy: essential to classify NL + assess activity (index of activity and chronicity - NIH) + decide intensity of immunosuppressive treatment - repeat biopsy («protocol» biopsy): evaluated in clinical trials - recommended in cases of renal relapse or therapeutic resistance; poor prognostic factors: class IV + high chronicity index (fibrosis + tubular atrophy) + presence of fibro-cellular crescents + high creatinine at presentation + massive proteinuria + uncontrolled hypertension + history of renal relapse + African or Hispanic ethnicity (genetic factors - FCGR2A + FCGR3B polymorphism). | Treatment of lupus nephritis: hydroxychloroquine (Plaquenil): indicated in all lupus patients (including pregnant patients) - reduces lupus relapses including renal relapses by 30-50 % + reduces cardiovascular risk + protects against thrombosis → dose: 5 mg/kg/d PO (maximum 400 mg/d) → annual ophthalmological monitoring after 5 years (risk of late retinopathy); induction of remission classes III-IV (± V): mycophenolate mofetil (MMF - CellCept): 2-3 g/d PO × 6 months → equivalent to cyclophosphamide IV for induction (ASPREVA 2009 trial - Contreras 2004) → preferred in women of childbearing age (no gonadotoxicity unlike cyclophosphamide) + bolus methylprednisolone IV (500 mg-1 g × 3 days) + prednisone 0.5 mg/kg/d → gradual tapering - or cyclophosphamide IV (EUROLUPUS regimen: 500 mg × 6 every 2 weeks - equivalent to NIH high-dose regimen with less toxicity) + methylprednisolone bolus → corticosteroid taper + voclosporin (Lupkynis - new-generation calcineurin inhibitor): FDA approved 2021 + Health Canada 2022 → combination MMF + voclosporin + corticoids → superior results to MMF alone in the AURORA-1 trial (complete remission rate at 52 weeks: 40.8 % vs. 22.5 %) + belimumab (Benlysta - anti-BAFF/BLyS): FDA + Health Canada approved for active NL (addition to standard therapy) - BLISS-LN 2020 trial: reduced risk of renal complications by 32 % + reduced corticosteroids; remission maintenance: MMF 1-2 g/d × at least 3 years + hydroxychloroquine + gradual reduction in corticosteroids → goal: corticosteroid withdrawal or dose ≤5 mg/d prednisone equivalent within 12-18 months; monitoring and therapeutic goals: complete remission: proteinuria <0.5 g/d + stable creatinine (≤15 % above baseline) + inactive urine sediment + normalized complement + anti-dsDNA in decline |
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Acanthocytes and Red Blood Cell Casts – Irreplaceable Markers of Urine Sediment devant toute hématurie inexpliquée, l'analyse du sédiment urinaire par microscopie en contraste de phase est indispensable pour distinguer une hématurie d'origine glomérulaire d'une hématurie urologique. La présence d'acanthocytes (>5 % des hématies) et surtout de cylindres hématiques est pathognomonique d'une glomérulonéphrite active — elle oriente d'emblée vers la néphrologie et peut éviter des explorations urologiques inutiles. Cet examen simple et peu coûteux est malheureusement sous-utilisé en pratique courante au Québec.
Situations requiring urgent medical assessment
Rapid deterioration of kidney function (doubling of creatinine in days to weeks) + hematuria + proteinuria → Probable GNRP -> ANCA+, anti-GBM+, AAN urgent -> Renal biopsy within 24-48h + urgent nephrology consult + do not wait for biopsy to initiate methylprednisolone bolus if GNRP is very probable.
Goodpasture's syndrome: hemoptysis + rapidly progressive renal failure + positive anti-GBM → Emergency → immediate plasmapheresis + cyclophosphamide + IV methylprednisolone + resuscitation if massive alveolar hemorrhage.
Nephrotic syndrome + albumin <20 g/L + sudden unilateral flank pain + gross hematuria → Renal vein thrombosis (complication of nephrotic syndrome — especially MGS) → renal echo-Doppler + angio-CT + urgent anticoagulation.
Palpable purpura + arthralgias + hematuria + proteinuria + abdominal pain in a child or young adult → Henoch-Schönlein purpura (IgA vasculitis) → hospitalization if severe renal + digestive involvement + pediatric/nephrology consultation.
Consult at Clinique Omicron
Clinique Omicron physicians perform initial screening for glomerular damage (urinalysis with sediment, proteinuria, renal function) and urgent referral to nephrology in cases of suspected active glomerulonephritis or RPGN. Follow-up for patients with chronic glomerulonephritis—blood pressure control, RAAS blockade adjustment, SGLT2 inhibitor prescription, and renal function monitoring—is provided at several service points in Quebec and via telemedicine. To make an appointment, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not replace the advice of a physician or nephrologist. Any suspected kidney damage should be promptly evaluated by a healthcare professional, especially rapidly progressive forms, which are medical emergencies.
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