{"id":24986,"date":"2026-02-28T22:54:45","date_gmt":"2026-03-01T02:54:45","guid":{"rendered":"https:\/\/cliniqueomicron.ca\/syndrome-nephrotique\/"},"modified":"2026-09-14T19:52:15","modified_gmt":"2026-09-14T23:52:15","slug":"nephrotic-syndrome","status":"publish","type":"page","link":"https:\/\/cliniqueomicron.ca\/en\/syndrome-nephrotique\/","title":{"rendered":"Nephrotic syndrome: proteinuria, causes and treatment | Clinique Omicron"},"content":{"rendered":"<div data-elementor-type=\"wp-page\" data-elementor-id=\"24986\" class=\"elementor elementor-24986\" data-elementor-post-type=\"page\">\n\t\t\t\t<div class=\"elementor-element elementor-element-a47a170 e-flex e-con-boxed e-con e-parent\" data-id=\"a47a170\" data-element_type=\"container\" data-e-type=\"container\" data-settings=\"{&quot;ekit_has_onepagescroll_dot&quot;:&quot;yes&quot;}\">\n\t\t\t\t\t<div class=\"e-con-inner\">\n\t\t\t\t<div class=\"elementor-element elementor-element-85a4c10 elementor-widget elementor-widget-html\" data-id=\"85a4c10\" data-element_type=\"widget\" data-e-type=\"widget\" data-settings=\"{&quot;ekit_we_effect_on&quot;:&quot;none&quot;}\" data-widget_type=\"html.default\">\n\t\t\t\t<div class=\"elementor-widget-container\">\n\t\t\t\t\t<!DOCTYPE html>\n<html lang=\"fr\">\n<head>\n<meta charset=\"UTF-8\">\n<meta name=\"viewport\" content=\"width=device-width, initial-scale=1.0\">\n<title>Nephrotic syndrome: proteinuria, causes and treatment | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"Nephrotic syndrome is defined by massive proteinuria, hypoalbuminemia, edema and hyperlipidemia. GEM, lipoid nephrosis, GSFS, renal biopsy, corticosteroids and rituximab in Quebec.\">\n<meta name=\"keywords\" content=\"syndrome n\u00e9phrotique, prot\u00e9inurie syndrome n\u00e9phrotique, hypoalbumin\u00e9mie, syndrome n\u00e9phrotique causes, GEM glom\u00e9rulon\u00e9phrite membraneuse, n\u00e9phrose lipo\u00efdique, GSFS syndrome n\u00e9phrotique, biopsie r\u00e9nale syndrome n\u00e9phrotique, rituximab GEM, syndrome n\u00e9phrotique Qu\u00e9bec\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n@import url('https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap');\n\n.co-wrap * {\n  font-family: 'Poppins', sans-serif;\n  box-sizing: border-box;\n}\n.co-wrap {\n  max-width: 1100px;\n  margin: 0 auto;\n  padding: 30px 0 60px;\n  margin-top: 10px;\n}\n.co-label {\n  font-family: 'Cinzel', serif;\n  font-size: 14px;\n  font-weight: bold;\n  letter-spacing: 1px;\n  text-transform: uppercase;\n  color: #4D6577;\n  margin-bottom: 14px;\n  display: block;\n}\n.co-wrap h1 {\n  font-size: 32px;\n  font-weight: 500;\n  color: #323C52;\n  margin: 0 0 22px;\n  line-height: 1.2;\n  letter-spacing: 0.5px;\n}\n.co-intro {\n  font-size: 16px;\n  font-weight: 400;\n  line-height: 1.75;\n  color: #4D6577;\n  margin-bottom: 36px;\n  padding-bottom: 32px;\n  border-bottom: 1px solid rgba(77,101,119,.2);\n}\n.co-wrap h2 {\n  font-size: 20px;\n  font-weight: 600;\n  color: #323C52;\n  margin: 32px 0 12px;\n  letter-spacing: 0.3px;\n}\n.co-wrap p {\n  font-size: 15px;\n  font-weight: 400;\n  color: #4D6577;\n  line-height: 1.7;\n  margin-bottom: 14px;\n}\n.co-list {\n  list-style: none;\n  padding: 0;\n  margin: 12px 0 24px;\n}\n.co-list li {\n  font-size: 15px;\n  font-weight: 400;\n  color: #4D6577;\n  padding: 10px 14px 10px 38px;\n  margin-bottom: 8px;\n  border-radius: 6px;\n  position: relative;\n  background: rgba(77,101,119,.06);\n  border-left: 3px solid #4D6577;\n}\n.co-list li::before {\n  content: \"\u2713\";\n  position: absolute;\n  left: 12px;\n  font-weight: 700;\n  color: #4D6577;\n}\n.co-table {\n  width: 100%;\n  border-collapse: collapse;\n  margin: 14px 0 22px;\n  font-size: 14px;\n  border-radius: 8px;\n  overflow: hidden;\n}\n.co-table thead tr {\n  background: #323C52;\n  color: #fff;\n}\n.co-table thead th {\n  padding: 11px 16px;\n  text-align: left;\n  font-weight: 600;\n  font-size: 13px;\n}\n.co-table tbody tr:nth-child(even) {\n  background: rgba(77,101,119,.06);\n}\n.co-table tbody tr:nth-child(odd) {\n  background: #fff;\n}\n.co-table td {\n  padding: 10px 16px;\n  color: #4D6577;\n  border-bottom: 1px solid rgba(77,101,119,.12);\n  font-size: 14px;\n  vertical-align: top;\n}\n.co-table td:first-child {\n  font-weight: 600;\n  color: #323C52;\n}\n.co-infobox {\n  display: flex;\n  gap: 12px;\n  background: rgba(77,101,119,.06);\n  border-radius: 8px;\n  border-left: 4px solid #4D6577;\n  padding: 14px 18px;\n  margin: 18px 0 28px;\n  font-size: 14px;\n  font-weight: 400;\n  color: #4D6577;\n  line-height: 1.65;\n}\n.co-infobox .ico {\n  font-size: 18px;\n  flex-shrink: 0;\n}\n.co-urgence {\n  background: #fff8f8;\n  border-left: 5px solid #c0392b;\n  border-radius: 6px;\n  padding: 20px 26px;\n  margin: 24px 0 32px;\n}\n.co-urgence .co-urgence-titre {\n  font-size: 13px;\n  font-weight: 700;\n  color: #c0392b;\n  letter-spacing: 1.5px;\n  text-transform: uppercase;\n  margin-bottom: 10px;\n}\n.co-urgence p {\n  color: #5a2020;\n  font-size: 14px;\n  margin: 0 0 10px;\n  line-height: 1.7;\n}\n.co-urgence p:last-child {\n  margin-bottom: 0;\n}\n.co-disclaimer {\n  font-size: 13px;\n  color: #8a9aaa;\n  font-style: italic;\n  border-top: 1px solid rgba(77,101,119,.15);\n  padding-top: 24px;\n  margin-top: 40px;\n  line-height: 1.6;\n}\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n\n  <span class=\"co-label\">Nephrology &amp; Internal Medicine &amp; Family Medicine<\/span>\n  <h1>Nephrotic syndrome<\/h1>\n<style>.oc-fiche-cta{margin:8px 0 34px;padding:22px 24px;border:1.5px solid rgba(50,60,82,.15);border-left:4px solid #FF611C;border-radius:12px;background:#F4F6F8;font-family:Poppins,sans-serif}.oc-fiche-cta-t{font-size:18px;font-weight:600;color:#323C52;margin:0 0 4px;line-height:1.35}.oc-fiche-cta-x{font-size:15px;color:#4D6577;margin:0 0 14px;line-height:1.55}.oc-fiche-cta-b{display:flex;flex-wrap:wrap;gap:10px}.oc-fiche-cta-b a{display:inline-flex;align-items:center;justify-content:center;min-height:44px;padding:10px 18px;border-radius:8px;font-size:14px;font-weight:600;text-decoration:none;box-sizing:border-box}.oc-fiche-cta-b .oc-p{background:#FF611C;color:#fff}.oc-fiche-cta-b .oc-p:hover{background:#E04E0C}.oc-fiche-cta-b .oc-s{background:#fff;color:#323C52;border:1.5px solid rgba(50,60,82,.25)}@media (max-width:600px){.co-wrap h1{font-size:24px;line-height:1.25;text-transform:none}.oc-fiche-cta{padding:18px 16px}.oc-fiche-cta-b a{flex:1 1 100%}body .co-wrap > .co-table,body .co-wrap > .co-table tbody,body .co-wrap > .co-table tr,body .co-wrap > .co-table td{display:block;width:100%;box-sizing:border-box}body .co-wrap > .co-table{min-width:0;table-layout:auto}body .co-wrap > .co-table thead{display:none}body .co-wrap > .co-table tr{margin:0 0 10px;border:1px solid rgba(77,101,119,.18);border-radius:8px;overflow:hidden}body .co-wrap > .co-table td{padding:9px 12px;border:0}body .co-wrap > .co-table td:first-child{font-weight:600;color:#323C52;background:rgba(77,101,119,.07)}#ocw{transform:scale(.8);transform-origin:bottom right}}<\/style><div class=\"oc-fiche-cta\" data-oc-cta=\"fiche-haut-consult\"><p class=\"oc-fiche-cta-t\">Obtenir un avis adapt\u00e9 \u00e0 votre situation<\/p><p class=\"oc-fiche-cta-x\">Consultation en clinique ou en t\u00e9l\u00e9consultation, partout au Qu\u00e9bec.<\/p><div class=\"oc-fiche-cta-b\"><a class=\"oc-p\" href=\"https:\/\/cliniqueomicron.ca\/rendez-vous\/\">Make an appointment<\/a><a class=\"oc-s\" href=\"https:\/\/cliniqueomicron.ca\/consultation-en-ligne\/\">Consult online<\/a><a class=\"oc-s\" href=\"tel:+15146063350\">514 606-3350<\/a><\/div><\/div>\n\n\n  <div class=\"co-intro\">\n    Nephrotic syndrome (NS) is a clinico-biological syndrome defined by the association of massive proteinuria (\u2265 3.5 g\/24 h in adults + or urinary protein\/creatinine ratio \u2265 300 mg\/mmol) + hypoalbuminemia (serum albumin &lt; 30 g\/L) + peripheral declining edema + and hyperlipidemia (hypercholesterolemia + hypertriglyceridemia), resulting from damage to the glomerular filtration membrane - mainly at the level of podocytes (specialized visceral epithelial cells lining the outer surface of the glomerular basement membrane) - leading to massive protein loss in the urine, exceeding the capacity of compensatory hepatic synthesis. The cascade pathophysiology is as follows: podocyte injury (depending on the underlying cause) \u2192 increased glomerular protein permeability \u2192 massive proteinuria \u2192 hypoalbuminemia \u2192 reduced plasma oncotic pressure \u2192 hydrosodic leakage to the interstitial sector \u2192 edema + relative hypovolemia \u2192 activation of the renin-angiotensin-aldosterone system (RAAS) \u2192 hydrosodic retention \u2192 worsening of edema. Hepatic synthesis of lipoproteins is increased in response to hypo-oncotia (replacement lipoproteins) \u2192 hyperlipidemia. Urinary leakage of natural anticoagulant proteins (antithrombin III + protein C + protein S) + hyperlipidemia + hypovolemia \u2192 major prothrombotic state (renal venous thrombosis ++ + DVT + PE - risk of thrombosis particularly high in membranous glomerulonephritis). Positive diagnosis of SN is biological - simple and rapid - but the underlying cause requires in the vast majority of cases a renal biopsy to guide specific treatment.\n  <\/div>\n\n  <h2>Clinico-biological tetrad<\/h2>\n  <ul class=\"co-list\">\n    <li><strong>Massive proteinuria :<\/strong> \u2265 3.5 g\/24 h or urine protein\/creatinine ratio \u2265 300 mg\/mmol on a urine sample + SN proteinuria is mainly selective (albumin ++ + in minimally lesioned forms) or non-selective (albumin + globulins in other glomerulonephritis)<\/li>\n    <li><strong>Hypoalbuminemia:<\/strong> serum albumin &lt; 30 g\/L + severe if &lt; 20 g\/L \u2192 hydrops + thrombotic + infectious + nutritional complications + hypoalbuminemia reduces the bound fraction of many drugs \u2192 increased drug toxicity (warfarin + phenytoin + furosemide)<\/li>\n    <li><strong>Edema :<\/strong> bilateral soft declivities + scooping + periorbital on awakening (characteristic of children) + ascites + pleural effusion + anasarca in severe forms<\/li>\n    <li><strong>Hyperlipidemia :<\/strong> hypercholesterolemia (high LDL + low HDL) + hypertriglyceridemia + total lipidemia may exceed 20-30 mmol\/L + lipiduria (lipid cylinders + oval fatty bodies in urine sediment) + increased long-term cardiovascular risk<\/li>\n    <li><strong>Associated complications :<\/strong> prothrombotic state (renal venous thrombosis - particularly in GEM - DVT + pulmonary embolism) + bacterial infections (urinary loss of IgG + opsonins + hypoalbuminemia \u2192 relative immune deficiency \u2192 pneumococcus + encapsulated germ infections) + acute renal failure (hypovolemia + thrombi + nephrotoxics)<\/li>\n  <\/ul>\n\n  <h2>Main causes according to age and clinical picture<\/h2>\n\n  <table class=\"co-table\">\n    <thead>\n      <tr>\n        <th>Etiology<\/th>\n        <th>Epidemiology<\/th>\n        <th>Features<\/th>\n        <th>Specific treatment<\/th>\n      <\/tr>\n    <\/thead>\n    <tbody>\n      <tr>\n        <td>Minimal glomerular lesions (LGM - Lipoid nephrosis)<\/td>\n        <td>Leading cause in children (90 % of childhood SN) + young adults + peak 2-6 years old<\/td>\n        <td>Pure SN + selective (albumin only) + normal light microscopy + electron microscopy: erasure of podocytic feet + rapid response to corticoids (94 %) + frequent recurrences (40-60 %) + no progression to CKD in general<\/td>\n        <td>Prednisone 60 mg\/m\u00b2 \u00d7 4-6 weeks + decrease + cortico-resistant forms: cyclosporine + tacrolimus + rituximab<\/td>\n      <\/tr>\n      <tr>\n        <td>Extra-membranous glomerulonephritis (EMG)<\/td>\n        <td>Leading cause of adult SN (20-40 + and &gt; 60) + 80 % idiopathic (anti-PLA2R ++) + 20 % secondary (cancer + HBV + lupus + NSAIDs)<\/td>\n        <td>Non-selective SN + anti-PLA2R (phospholipase A2 receptor) antibodies positive in 70-80 % of idiopathic forms (pathognomonic) + biopsy: subepithelial deposits + basement membrane thickening + \"spikes\" on silver impregnation + high risk of renal venous thrombosis (up to 40 %)<\/td>\n        <td>Rule of thirds (1\/3 spontaneous remission + 1\/3 remission on treatment + 1\/3 progressive CKD) \u2192 treatment if persistent proteinuria &gt; 6 months or CKD: rituximab (375 mg\/m\u00b2 \u00d7 4 or 1 g \u00d7 2) + or cyclophosphamide + corticoids (Ponticelli protocol) + anti-PLA2R monitoring as biomarker of activity<\/td>\n      <\/tr>\n      <tr>\n        <td>Segmental and focal hyalinosis (GSFS)<\/td>\n        <td>Adult + African-American populations ++ + often secondary (obesity + nephron reduction + HIV + heroin)<\/td>\n        <td>Non-selective SN + focal and segmental glomerular sclerosis lesions on biopsy + often associated with hypertension + microscopic hematuria + frequent progression to CKD + cortico-resistant in 50-60 % of primary cases<\/td>\n        <td>Prednisone 1 mg\/kg\/d \u00d7 16 weeks (primary forms) + if resistant: cyclosporine + tacrolimus + mycophenolate + treatment of secondary factors (weight loss + HIV)<\/td>\n      <\/tr>\n      <tr>\n        <td>Diabetic nephropathy<\/td>\n        <td>World's leading cause of adult nephrotic syndrome in Western countries + type 1 and 2 diabetes + progressive albuminuria over 10-20 years<\/td>\n        <td>Progression from microalbuminuria (30-300 mg\/d) to macroalbuminuria then SN + concomitant diabetic retinopathy in 90 % \u2192 if absent \u2192 biopsy recommended (other cause) + biopsy: basement membrane thickening + mesangial expansion + Kimmelstiel-Wilson nodules<\/td>\n        <td>ACE inhibitor or ARB II (renal protection ++ + proteinuria reduction) + SGLT2 (dapagliflozin + empagliflozin - proven nephroprotection) + GLP-1 + glycemic + lipid control + strict BP<\/td>\n      <\/tr>\n      <tr>\n        <td>Renal amyloidosis (AL and AA)<\/td>\n        <td>Elderly adults + multiple myeloma (AL) + chronic inflammatory diseases (AA)<\/td>\n        <td>SN severe + progressive + hepatomegaly + macroglossia (AL) + serum free light chain assay + immunofixation + fat or rectal biopsy (screening) + renal biopsy (confirmation) \u2192 amyloid deposits Congo red + bright green in polarized light<\/td>\n        <td>AL: chemotherapy + autograft if eligible (daratumumab + bortezomib) + AA: treatment of underlying inflammatory disease<\/td>\n      <\/tr>\n      <tr>\n        <td>Lupus nephropathy (classes III-IV-V)<\/td>\n        <td>Young woman + lupus + class V = pure membranous \u2192 SN + class III\/IV = proliferative + hematuria + cylinders<\/td>\n        <td>Complementary C3 + C4 low + AAN positive + anti-native DNA high (lupus activity) + renal biopsy: ISN\/RPS classification<\/td>\n        <td>Mycophenolate mofetil + corticoids (induction) + belimumab + voclosporin (class V + III\/IV) \u2192 rituximab if refractory<\/td>\n      <\/tr>\n    <\/tbody>\n  <\/table>\n\n  <h2>Renal biopsy - indications in SN<\/h2>\n  <ul class=\"co-list\">\n    <li><strong>Adult :<\/strong> systematic renal biopsy for any first presentation of NS in adults (unless type 2 diabetes with obvious diabetic retinopathy + progressive NS over years \u2192 sufficient probability of diabetic nephropathy not to biopsy straight away)<\/li>\n    <li><strong>Children aged 1 to 12 with no atypical signs:<\/strong> empirical treatment with prednisone (90 % of LGM + cortico-sensitive) + biopsy reserved for cortico-resistant + or frequent recurrent + or atypical forms (macroscopic hematuria + hypertension + CKD + age 12 years)<\/li>\n    <li><strong>Contraindications to biopsy :<\/strong> single kidney + uncorrected coagulation disorder + uncontrolled hypertension + active infection \u2192 correct before biopsy<\/li>\n  <\/ul>\n\n  <div class=\"co-infobox\">\n    <span class=\"ico\">\u2119\ufe0f<\/span>\n    <span>Idiopathic extra-membranous glomerulonephritis (GEM) is the leading cause of SN in adults over 40, and is associated in 70-80 % of cases with anti-phospholipase A2 receptor antibodies (anti-PLA2R) - a discovery by Beck et al. (NEJM 2009) that has transformed management. Anti-PLA2R is pathognomonic of primary GEM + allows diagnosis without biopsy in some cases + and is a biomarker for monitoring activity and response to treatment (rituximab). A decrease in anti-PLA2R levels precedes clinical remission by several months.<\/span>\n  <\/div>\n\n  <h2>Symptomatic treatment - common to all forms<\/h2>\n  <ul class=\"co-list\">\n    <li><strong>Sodium restriction:<\/strong> &lt; 2 g sodium per day (strict low-salt diet) + avoid salt-rich processed foods + essential for controlling oedema<\/li>\n    <li><strong>Diuretics :<\/strong> furosemide (Lasix\u00ae) 40-120 mg\/day po + or IV if refractory edema + monitor kalemia + creatinine + natremia + hypoalbuminemia reduces furosemide efficacy (less well transported to tubules) \u2192 IV albumin infusion before furosemide if albumin &lt; 20 g\/L + refractory edema<\/li>\n    <li><strong>ACEI or ARB II :<\/strong> reduction of proteinuria (30-50 %) + long-term renal protection + indicated in all causes of SN (even if no diabetes + even if normotensive) \u2192 combination ACEI + ARB II not recommended (hyperKalemia + ARF)<\/li>\n    <li><strong>Statins :<\/strong> atorvastatin or rosuvastatin for hyperlipidemia + reduced long-term cardiovascular risk (chronic SN)<\/li>\n    <li><strong>Prophylactic anticoagulation :<\/strong> if albumin &lt; 20-25 g\/L + or GEM (very high risk of renal vein thrombosis + PE) \u2192 low-molecular-weight heparin or warfarin depending on context + bleeding risk vs thrombotic risk to be assessed<\/li>\n    <li><strong>Vaccinations :<\/strong> pneumococcal vaccine (risk of pneumococcal infections ++) + varicella vaccine if na\u00efve (immunosuppression) + HBV vaccine if IEC\/rituximab<\/li>\n  <\/ul>\n\n  <div class=\"co-urgence\">\n    <div class=\"co-urgence-titre\">Medical consultation recommended<\/div>\n    <p>Seek prompt medical attention if progressive bilateral edema of the lower limbs + swollen eyelids on awakening + frothy urine (proteinuria) + or shortness of breath appear - a simple urine test (dipstick + urine protein\/creatinine ratio) will confirm proteinuria and initiate investigation. Refer to the emergency department if signs of thrombosis (pain + swelling of a limb + dyspnea) + or acute renal failure (oliguria + very high creatinine) + or severe infection develop in the context of a known NS. For a complete nephrotic syndrome workup (24-hour proteinuria + albumin + lipids + creatinine + immunological workup) and referral to nephrology, Clinique Omicron offers consultations at its points of service in Quebec and via telemedicine. To book an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\" style=\"color:#c0392b;font-weight:600;text-decoration:none;\">cliniqueomicron.ca<\/a>.<\/p>\n  <\/div>\n\n  <h2>Consult at Clinique Omicron<\/h2>\n  <p>Clinique Omicron's specialized physicians and nurse practitioners (SPNs) diagnose nephrotic syndrome through an initial blood and urine test (proteinuria + albumin + creatinine + lipids + urine sediment), initiate symptomatic treatment (sodium restriction + furosemide + ACEI\/ARB II + statins + prophylactic anticoagulation if indicated), refer to nephrology for renal biopsy and cause-specific treatment, and ensure longitudinal follow-up of proteinuria + renal function + complications. Consultations are available at several points of service in Quebec, and via telemedicine. To book an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\" style=\"color:#4D6577;font-weight:600;text-decoration:none;\">cliniqueomicron.ca<\/a>.<\/p>\n\n  <p class=\"co-disclaimer\">The contents of this page are provided for information purposes only and do not replace the advice of a physician or nephrologist. Nephrotic syndrome requires renal biopsy in adults to identify the cause and guide specific treatment. Prophylactic anticoagulation should be discussed with the nephrologist according to the individual risk profile - it is particularly important in extra-membranous glomerulonephritis.<\/p>\n\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p>Syndrome n\u00e9phrotique : prot\u00e9inurie, causes et traitement | Clinique Omicron N\u00e9phrologie &amp; M\u00e9decine interne &amp; M\u00e9decine de famille Syndrome n\u00e9phrotique Le syndrome n\u00e9phrotique (SN) est un syndrome clinico-biologique d\u00e9fini par l&#8217;association d&#8217;une prot\u00e9inurie massive (\u2265 3,5 g\/24 h chez l&#8217;adulte + ou ratio prot\u00e9ine\/cr\u00e9atinine urinaire \u2265 300 mg\/mmol) + d&#8217;une hypoalbumin\u00e9mie (albumine s\u00e9rique &lt; 30&hellip;&nbsp;<a href=\"https:\/\/cliniqueomicron.ca\/en\/syndrome-nephrotique\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Nephrotic syndrome: proteinuria, causes and treatment | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Syndrome n\u00e9phrotique | Brossard | Clinique Omicron","_metasync_otto_description":"Syndrome n\u00e9phrotique Syndrome n\u00e9phrotique est une condition m\u00e9dicale qui peut n\u00e9cessiter une \u00e9valuation et un suivi m\u00e9dical appropri\u00e9s. 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