Nephrotic Syndrome (Supportive)
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Nephrotic Syndrome (Supportive)
Nephrotic Syndrome is a kidney disorder characterized by a cluster of symptoms resulting from damage to the glomeruli, the tiny filtering units within the kidneys. The hallmark features include massive proteinuria (excretion of more than 3.5 grams of protein per day in adults), hypoalbuminemia (low blood albumin levels), edema (swelling), and hyperlipidemia (elevated blood lipids). This occurs when the glomerular filtration barrier becomes excessively permeable, allowing large proteins—primarily albumin—to leak into the urine. The condition is not a single disease but rather a clinical syndrome that can arise from various underlying pathologies affecting the kidneys.
Recognizing Nephrotic Syndrome (Supportive)
Common symptoms and warning signs to look for
Waking up with puffy eyes and facial swelling, especially in the morning
Noticeable swelling in legs, ankles, and feet that leaves indentations when pressed
Foamy or bubbly urine that persists even after flushing
Unexplained weight gain from fluid retention despite normal eating habits
Persistent fatigue and feeling of heaviness throughout the body
What a Healthy System Looks Like
In a healthy state, the glomerular filtration barrier functions as a sophisticated molecular sieve, allowing water and small solutes to pass into the urine while retaining essential proteins in the bloodstream. This barrier consists of three layers: the fenestrated endothelium, the glomerular basement membrane (GBM), and the podocytes with their interdigitating foot processes. The podocytes, specialized epithelial cells, form slit diaphragms between their foot processes that regulate protein passage. Under normal conditions, less than 150 mg of protein is lost in urine daily, with albumin being effectively retained due to its size and negative charge. The kidneys maintain plasma oncotic pressure by preserving albumin, which is crucial for keeping fluid within blood vessels. The renin-angiotensin-aldosterone system (RAAS) and other hormonal mechanisms finely regulate glomerular filtration rate and protein handling, ensuring homeostasis.
How the Condition Develops
Understanding the biological mechanisms
Nephrotic Syndrome develops through several interconnected pathophysiological mechanisms: (1) Podocyte injury - The primary event in most cases involves damage to podocytes, whether from immune-mediated mechanisms, genetic mutations, toxic exposures, or systemic diseases. This disrupts the slit diaphragm and alters the negative charge barrier. (2) Glomerular basement membrane disruption - Structural damage to the GBM increases permeability to proteins, particularly albumin. (3) Massive proteinuria - As the filtration barrier fails, large quantities of albumin (3.5-20+ g/day) leak into the urine, leading to hypoalbuminemia. (4) Hypoalbuminemia and oncotic pressure collapse - Low serum albumin reduces plasma oncotic pressure, causing fluid to shift from intravascular to interstitial spaces, resulting in edema. (5) Compensatory hepatic protein synthesis - The liver attempts to compensate for protein loss by increasing synthesis of albumin and lipoproteins, but this also increases production of cholesterol, triglycerides, and lipoproteins, causing hyperlipidemia. (6) Sodium and water retention - RAAS activation and increased antidiuretic hormone (ADH) occur secondary to intravascular volume depletion sensed by baroreceptors, further exacerbating edema. (7) Hypercoagulability - Loss of antithrombin III and other anticoagulant proteins in urine, combined with increased hepatic synthesis of procoagulant factors, creates a prothrombotic state. (8) Immune dysfunction - Loss of immunoglobulins (IgG) and complement factors increases infection risk.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| 24-Hour Urine Protein | <150 mg/day | <150 mg/day | Diagnostic hallmark; nephrotic range proteinuria defined as >3,500 mg/day (3.5 g/day); quantifies severity and monitors treatment response |
| Urine Albumin-to-Creatinine Ratio (UACR) | <30 mg/g | <30 mg/g | Spot urine test; >3,500 mg/g suggests nephrotic-range proteinuria; useful for screening and monitoring |
| Serum Albumin | 3.5-5.0 g/dL | >3.5 g/dL | Typically <3.0 g/dL in nephrotic syndrome; <2.5 g/dL indicates severe disease; inversely correlates with edema severity |
| Total Cholesterol | <200 mg/dL | <200 mg/dL | Often elevated >300 mg/dL in nephrotic syndrome due to compensatory hepatic lipoprotein synthesis |
| LDL Cholesterol | <100 mg/dL | <100 mg/dL | Frequently elevated; contributes to accelerated atherosclerosis; often >160 mg/dL in active disease |
| Triglycerides | <150 mg/dL | <150 mg/dL | Elevated due to decreased lipoprotein lipase activity and increased hepatic synthesis |
| Serum Creatinine | 0.7-1.3 mg/dL (male), 0.6-1.1 mg/dL (female) | 0.8-1.1 mg/dL (male), 0.6-0.9 mg/dL (female) | May be normal in pure nephrotic syndrome; elevated in nephritic features or chronic kidney disease overlap |
| eGFR | >90 mL/min/1.73m² | >90 mL/min/1.73m² | Often preserved in minimal change disease; may be reduced in focal segmental glomerulosclerosis or advanced disease |
| Serum Sodium | 135-145 mEq/L | 138-142 mEq/L | May be dilutional hyponatremia due to water retention; monitor during diuretic therapy |
| Serum Potassium | 3.5-5.0 mEq/L | 3.8-4.5 mEq/L | Monitor closely with diuretic use; hypokalemia common with aggressive diuresis |
| Serum Calcium (Total and Ionized) | 8.5-10.5 mg/dL (total) | 9.0-10.0 mg/dL | May be low due to hypoalbuminemia (corrected calcium calculation needed); ionized calcium more accurate |
| Serum IgG | 700-1,600 mg/dL | >700 mg/dL | Often reduced due to urinary losses; contributes to infection risk |
| Antithrombin III | 80-120% | >80% | Reduced in nephrotic syndrome; contributes to hypercoagulable state and thrombosis risk |
| C3 and C4 Complement | C3: 90-180 mg/dL, C4: 10-40 mg/dL | Normal ranges | Low C3 suggests post-infectious or membranoproliferative glomerulonephritis; helps differentiate etiology |
| Hepatitis B and C Serologies | Negative | Negative | Hepatitis B associated with membranous nephropathy; Hepatitis C with cryoglobulinemia and MPGN |
| ANA, Anti-dsDNA | Negative | Negative | Positive in lupus nephritis, which can present with nephrotic features |
| Kidney Biopsy | Normal glomerular architecture | Normal | Definitive diagnosis; distinguishes minimal change disease, FSGS, membranous nephropathy, membranoproliferative GN, amyloidosis |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Primary Glomerular Diseases","contribution":"60-70% of nephrotic syndrome cases","assessment":"Kidney biopsy essential; minimal change disease (children), FSGS (adults, especially African Americans), membranous nephropathy (Caucasian adults), membranoproliferative GN"}
{"cause":"Systemic Diseases","contribution":"30-40% of adult cases","assessment":"Diabetes mellitus (diabetic nephropathy), lupus nephritis, amyloidosis (serum free light chains, fat pad biopsy), vasculitis (ANCA testing)"}
{"cause":"Infections","contribution":"Significant cause in endemic areas and specific populations","assessment":"Hepatitis B and C serologies, HIV testing, malaria in endemic regions, streptococcal infection history (post-infectious GN)"}
{"cause":"Malignancy-Associated","contribution":"10% of membranous nephropathy in patients >60 years","assessment":"Age-appropriate cancer screening, serum protein electrophoresis, imaging for solid tumors; paraneoplastic workup"}
{"cause":"Drug-Induced","contribution":"Increasing recognition as cause","assessment":"Medication history: NSAIDs, pamidronate, interferon, lithium, gold, penicillamine; timing of drug exposure relative to onset"}
{"cause":"Genetic/Familial","contribution":"15-30% of steroid-resistant cases in children; rare in adults","assessment":"Family history, early onset (<1 year), genetic testing for NPHS1, NPHS2, WT1 mutations; consanguinity"}
{"cause":"Allergic/Immune Triggers","contribution":"Particularly in minimal change disease","assessment":"History of atopy, allergic rhinitis, eczema, food allergies; response to steroids; eosinophilia"}
{"cause":"Environmental Toxins","contribution":"Less common but recognized","assessment":"Exposure history: mercury, lead, hydrocarbons; occupational exposures; heroin use (FSGS)"}
Risks of Inaction
What happens if left untreated
{"complication":"Thromboembolic Disease","timeline":"Risk present throughout active disease; highest in first 6 months","impact":"20-40% risk of venous thrombosis (renal vein thrombosis, DVT, PE); arterial thrombosis (stroke, MI) also increased; leading cause of morbidity; can be life-threatening"}
{"complication":"Severe Infections","timeline":"Ongoing risk while proteinuria persists","impact":"Loss of IgG and complement factors increases susceptibility to encapsulated bacteria (Streptococcus pneumoniae, Haemophilus influenzae); spontaneous bacterial peritonitis; cellulitis; pneumonia; can be fatal"}
{"complication":"Progression to Chronic Kidney Disease/ESRD","timeline":"Variable: months to decades depending on etiology","impact":"FSGS and membranous nephropathy can progress to ESRD requiring dialysis or transplantation; minimal change disease rarely progresses if treated"}
{"complication":"Accelerated Atherosclerosis","timeline":"Progressive over years","impact":"Severe hyperlipidemia promotes premature cardiovascular disease; increased risk of myocardial infarction and stroke even in young patients"}
{"complication":"Acute Kidney Injury","timeline":"Can occur at any time","impact":"Hypovolemia from aggressive diuresis, sepsis, or contrast exposure can precipitate AKI; nephrotic syndrome with nephritic features more prone to rapid progression"}
{"complication":"Protein Malnutrition","timeline":"Progressive with persistent proteinuria","impact":"Severe hypoalbuminemia (<2.0 g/dL) causes poor wound healing, impaired immune function, muscle wasting, growth retardation in children"}
{"complication":"Hypovolemic Shock","timeline":"Acute risk with severe edema and aggressive diuresis","impact":"Intravascular volume depletion can lead to hypotension, pre-renal azotemia, acute tubular necrosis; requires careful fluid management"}
{"complication":"Vitamin D Deficiency and Bone Disease","timeline":"Progressive over months to years","impact":"Loss of vitamin D-binding protein causes deficiency; hypocalcemia; secondary hyperparathyroidism; bone demineralization; increased fracture risk"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"24-Hour Urine Collection for Protein","purpose":"Quantify protein loss and confirm nephrotic range","whatItShows":"Total protein excretion; nephrotic range defined as >3.5 g/day in adults, >50 mg/kg/day in children; also assesses creatinine clearance"}
{"test":"Spot Urine Protein-to-Creatinine Ratio (UPCR)","purpose":"Estimate protein excretion from single sample","whatItShows":"Correlates with 24-hour collection; >3.5 mg/mg suggests nephrotic-range proteinuria; convenient for monitoring"}
{"test":"Complete Blood Count","purpose":"Assess for anemia and infection","whatItShows":"Hemoglobin may be normal or reduced; white count may indicate infection; platelets may be elevated (reactive)"}
{"test":"Comprehensive Metabolic Panel","purpose":"Assess kidney function, electrolytes, albumin","whatItShows":"Serum creatinine, BUN, eGFR, albumin (low), total protein (low), electrolytes, calcium (may need correction for albumin)"}
{"test":"Lipid Panel","purpose":"Characterize hyperlipidemia","whatItShows":"Elevated total cholesterol, LDL, triglycerides; may see lipoprotein abnormalities; cardiovascular risk assessment"}
{"test":"Serum Protein Electrophoresis (SPEP)","purpose":"Assess for monoclonal gammopathy","whatItShows":"M-spike suggests multiple myeloma or monoclonal gammopathy of renal significance (MGRS) causing amyloidosis or light chain deposition"}
{"test":"Immunoglobulin Levels (IgG, IgA, IgM)","purpose":"Assess immune status","whatItShows":"IgG typically reduced due to urinary losses; increased infection risk correlates with IgG <600 mg/dL"}
{"test":"Complement Levels (C3, C4)","purpose":"Help identify etiology","whatItShows":"Low C3 suggests post-infectious GN, MPGN, or lupus; normal complements in minimal change, FSGS, membranous"}
{"test":"Autoimmune Panel","purpose":"Screen for systemic causes","whatItShows":"ANA, anti-dsDNA (lupus), ANCA (vasculitis), anti-PLA2R antibodies (membranous nephropathy), anti-GBM antibodies"}
{"test":"Infectious Disease Screening","purpose":"Identify infectious triggers","whatItShows":"Hepatitis B surface antigen, Hepatitis C antibody, HIV test, syphilis serology, ASO titer (post-streptococcal)"}
{"test":"Kidney Ultrasound","purpose":"Assess kidney size and structure","whatItShows":"Usually normal or enlarged kidneys in acute nephrotic syndrome; small kidneys suggest chronic disease; rules out obstruction"}
{"test":"Kidney Biopsy","purpose":"Definitive diagnosis","whatItShows":"Light microscopy, immunofluorescence, and electron microscopy identify specific pathology (MCD, FSGS, membranous, MPGN, amyloidosis, diabetic changes)"}
{"test":"Coagulation Studies","purpose":"Assess thrombosis risk","whatItShows":"Antithrombin III level (often reduced), D-dimer, fibrinogen; prothrombotic state assessment"}
{"test":"Age-Appropriate Cancer Screening","purpose":"Rule out malignancy-associated nephrotic syndrome","whatItShows":"In patients >60 with membranous nephropathy: chest CT, colonoscopy, PSA, mammography as indicated"}
Our Treatment Approach
How we help you overcome Nephrotic Syndrome (Supportive)
Phase 1: Diagnosis and Initial Stabilization (Weeks 1-4)
{"phase":"Phase 1: Diagnosis and Initial Stabilization (Weeks 1-4)","focus":"Confirm diagnosis, identify etiology, control edema, prevent complications","interventions":"Complete diagnostic workup including quantification of proteinuria, assessment of serum albumin, lipid panel, and infectious/autoimmune screening. Kidney biopsy if etiology unclear (adults) or steroid-resistant (children). Initiate sodium restriction (<2g/day). Begin diuretic therapy (loop diuretics, often combined with thiazides for synergistic effect) for edema management. Monitor electrolytes closely. Assess thrombosis risk; consider prophylactic anticoagulation if high risk (albumin <2.0-2.5 g/dL, immobilization, prior thrombosis). Vaccinate against pneumococcus and influenza. ACE inhibitors or ARBs to reduce proteinuria. Statin therapy for hyperlipidemia.\n"}
Phase 2: Disease-Specific Treatment (Weeks 4-24)
{"phase":"Phase 2: Disease-Specific Treatment (Weeks 4-24)","focus":"Treat underlying cause, induce remission","interventions":"Minimal Change Disease: High-dose corticosteroids (prednisone 1 mg/kg/day, max 80mg) for 4-16 weeks, then slow taper; 80-90% achieve remission. FSGS: Steroids (longer course 3-6 months); calcineurin inhibitors (tacrolimus, cyclosporine) for steroid-resistant or dependent cases; consider rituximab. Membranous Nephropathy: Conservative management for 6 months if low risk; high-risk patients receive rituximab or cyclophosphamide + steroids (Ponticelli regimen). Lupus Nephritis: Immunosuppression per ISN/RPS class (my cophenolate mofetil, cyclophosphamide, steroids). Diabetic Nephropathy: Optimize glycemic control, ACEi/ARB, SGLT2 inhibitors, finerenone. Amyloidosis: Treat underlying plasma cell dyscrasia or inflammatory disease.\n"}
Phase 3: Maintenance and Relapse Prevention (Months 6-12)
{"phase":"Phase 3: Maintenance and Relapse Prevention (Months 6-12)","focus":"Maintain remission, manage relapses, minimize steroid exposure","interventions":"Gradual taper of immunosuppression while monitoring for relapse. For steroid-dependent or frequently relapsing minimal change disease: consider calcineurin inhibitors, mycophenolate, or rituximab to minimize steroid side effects. Continue ACEi/ARB at maximally tolerated dose to maintain proteinuria reduction. Ongoing dietary sodium restriction. Monitor lipids; continue statin therapy if indicated. Regular monitoring of kidney function, proteinuria, albumin, and electrolytes every 4-8 weeks. Patient education on infection avoidance and warning signs of relapse. Address cardiovascular risk factors aggressively. Bone protection if prolonged steroid use (calcium, vitamin D, bisphosphonates).\n"}
Phase 4: Long-Term Management and Complication Surveillance (Year 1+)
{"phase":"Phase 4: Long-Term Management and Complication Surveillance (Year 1+)","focus":"Sustained remission or chronic management, prevent progression","interventions":"For sustained remission: Continue ACEi/ARB, maintain lifestyle modifications, monitor periodically (every 3-6 months). For persistent proteinuria or chronic disease: Ongoing immunosuppression as needed, management of CKD complications (anemia, bone disease, acidosis). Regular cardiovascular risk assessment and management. Continued vigilance for thrombotic complications. For progressive disease despite therapy: Consider clinical trials, advanced immunosuppression, or preparation for renal replacement therapy. Transplant evaluation if approaching ESRD. Genetic counseling if hereditary nephrotic syndrome. Support groups and mental health support for chronic disease burden.\n"}
Diet & Lifestyle
Recommendations for optimal recovery
Lifestyle Modifications
Regular moderate exercise: 150 minutes/week as tolerated; avoid during severe edema or acute illness, Leg elevation: Elevate legs above heart level 30 minutes 3-4 times daily to reduce edema, Compression stockings: 20-30 mmHg to reduce peripheral edema and venous stasis, Weight monitoring: Daily weights; report gain >3 lbs in 24 hours or >5 lbs in a week, Smoking cessation: Critical for cardiovascular protection, Avoid prolonged immobility: Increases thrombosis risk; ambulate regularly, Sleep with head elevated: Reduces periorbital edema, Stress management: Meditation, yoga, counseling to support immune function, Infection avoidance: Good hygiene, avoid sick contacts, promptly treat infections, Avoid live vaccines while on immunosuppression
Recovery Timeline
What to expect on your healing journey
Phase 1 (Weeks 1-4): Diagnosis and initial stabilization. Confirm nephrotic-range proteinuria, assess serum albumin and lipids, complete infectious and autoimmune workup. Kidney biopsy if indicated. Initiate sodium restriction and diuretic therapy for edema. Begin ACEi/ARB therapy. Assess thrombosis risk. Initiate specific treatment based on underlying cause (steroids for minimal change disease, etc.).
Phase 2 (Weeks 4-24): Active treatment and remission induction. Continue disease-specific immunosuppression. Monitor for response (decreasing proteinuria, rising albumin, resolving edema). Adjust diuretics as edema improves. Manage hyperlipidemia with statins. Monitor for treatment side effects (infection, hyperglycemia, bone loss). For steroid-responsive minimal change disease, remission often occurs within 2-4 weeks.
Phase 3 (Months 6-12): Maintenance therapy and relapse prevention. Gradual taper of immunosuppression while monitoring for relapse. For steroid-dependent disease, transition to steroid-sparing agents. Continue ACEi/ARB. Regular monitoring every 4-8 weeks. Patient education on recognizing relapse signs. Maintain lifestyle modifications.
Phase 4 (Year 1+): Long-term management. For sustained remission: Continue monitoring every 3-6 months, maintain ACEi/ARB, lifestyle modifications. For chronic or relapsing disease: Ongoing management with immunosuppression as needed, management of complications, cardiovascular risk reduction. For progressive disease: Consider advanced therapies, clinical trials, or preparation for renal replacement therapy.
Note: Timelines are highly variable. Minimal change disease often responds within weeks. FSGS and membranous nephropathy may require months to assess treatment response. Some patients achieve sustained remission; others have relapsing courses requiring long-term management.
How We Measure Success
Outcomes that matter
Complete remission: Urine protein <300 mg/day (or UPCR <0.3) and normal serum albumin
Partial remission: 50% reduction in proteinuria and protein <3.5 g/day
Serum albumin >3.0 g/dL (ideally >3.5 g/dL)
Resolution of edema
Stable or improved kidney function (eGFR)
Normalization of lipid profile
No thrombotic complications
No serious infections
Maintenance of normal blood pressure (<130/80 mmHg)
Minimal or no steroid side effects
Good quality of life and functional status
Sustained remission off immunosuppression (for responsive cases)
No progression to chronic kidney disease stage 4 or 5
Frequently Asked Questions
Common questions from patients
What is the difference between nephrotic syndrome and nephritic syndrome?
Nephrotic syndrome is characterized by massive proteinuria (>3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia, with relatively preserved kidney function and minimal urine sediment changes. Nephritic syndrome features hematuria (blood in urine with red blood cell casts), hypertension, reduced kidney function, and milder proteinuria. Some conditions can have mixed features. The distinction is important because it points to different underlying causes and treatment approaches.
Can nephrotic syndrome be cured?
The prognosis depends entirely on the underlying cause. Minimal change disease in children has an excellent prognosis with 80-90% achieving complete remission with steroids, though relapses are common. In adults, minimal change disease also responds well to treatment. Membranous nephropathy may spontaneously remit in 30% of cases, persist in 30%, and progress in 30%. FSGS is more challenging, with variable response to treatment and higher risk of progression to kidney failure. Secondary causes (like diabetic nephropathy or lupus) require treatment of the underlying disease.
Why does nephrotic syndrome cause swelling?
The swelling (edema) occurs due to a combination of factors: (1) Low albumin from protein loss reduces the oncotic pressure that normally keeps fluid in blood vessels, causing fluid to leak into tissues; (2) The kidneys sense reduced effective blood volume and activate the renin-angiotensin-aldosterone system, causing sodium and water retention; (3) Antidiuretic hormone increases, promoting water retention. This combination of fluid shifting out of vessels and the kidneys holding onto salt and water results in edema, often most noticeable around the eyes (periorbital edema) due to loose tissue there.
Is nephrotic syndrome hereditary?
Most cases are not hereditary. However, certain genetic mutations can cause congenital or familial forms of nephrotic syndrome. Congenital nephrotic syndrome (presenting within the first 3 months of life) is often genetic, with mutations in genes like NPHS1 (Finnish type) or NPHS2 (podocin). Familial FSGS can result from genetic mutations in podocyte proteins. Genetic testing is recommended for children with steroid-resistant nephrotic syndrome, congenital onset, or family history. Adult-onset nephrotic syndrome is rarely genetic.
How long do I need to take steroids for nephrotic syndrome?
Treatment duration varies by diagnosis and response. For minimal change disease, initial treatment is typically 4-16 weeks of high-dose prednisone (1 mg/kg/day), followed by a slow taper over several months. Total initial treatment may be 3-6 months. For FSGS, longer courses (3-6 months or more) may be needed. Membranous nephropathy treatment varies based on risk stratification. Steroid-sparing agents (calcineurin inhibitors, mycophenolate, rituximab) are often used for steroid-dependent or resistant cases, or to minimize steroid side effects. Never stop steroids abruptly—always taper under medical supervision.
What are the warning signs of a relapse?
Watch for: (1) Return of foamy or bubbly urine; (2) New or worsening swelling in legs, ankles, or around eyes; (3) Unexplained weight gain from fluid retention; (4) Increased fatigue; (5) Decreased urine output; (6) Shortness of breath from fluid accumulation. Contact your doctor immediately if you notice these signs. Regular monitoring of urine protein with dipsticks at home can help catch relapses early. Prompt treatment of relapses improves outcomes.
Medical References
- 1.KDIGO Glomerular Diseases Work Group. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int. 2021;100(4S):S1-S276. doi:10.1016/j.kint.2021.05.021 - Comprehensive international guidelines for diagnosis and management of nephrotic syndrome.
- 2.Rovin BH, Adler SG, Barratt J, et al. Executive summary of the KDIGO 2021 Guideline for the Management of Glomerular Diseases. Kidney Int. 2021;100(4):753-779. doi:10.1016/j.kint.2021.08.006 - Summary of key recommendations.
- 3.Waldman M, Crew RJ, Valeri A, et al. Adult minimal-change disease: clinical characteristics, treatment, and outcomes. Clin J Am Soc Nephrol. 2007;2(3):445-453. doi:10.2215/CJN.03531006 - Clinical outcomes in adult minimal change disease.
- 4.Beck LH Jr, Bonegio RGB, Lambeau G, et al. M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. N Engl J Med. 2009;361(1):11-21. doi:10.1056/NEJMoa0810457 - Landmark study identifying PLA2R as target antigen in membranous nephropathy.
- 5.D'Agati VD, Kaskel FJ, Falk RJ. Focal segmental glomerulosclerosis. N Engl J Med. 2011;365(25):2398-2411. doi:10.1056/NEJMra1106556 - Comprehensive review of FSGS pathogenesis and treatment.
- 6.Kerlin BA, Ayoob R, Smoyer WE. Epidemiology and pathophysiology of nephrotic syndrome-associated thromboembolic disease. Clin J Am Soc Nephrol. 2012;7(3):513-520. doi:10.2215/CJN.10181011 - Review of thrombosis risk in nephrotic syndrome.
- 7.Gipson DS, Massengill SF, Yao L, et al. Management of childhood onset nephrotic syndrome. Pediatrics. 2009;124(2):747-757. doi:10.1542/peds.2008-1559 - Pediatric nephrotic syndrome management guidelines.
Ready to Start Your Healing Journey?
Our integrative medicine experts are ready to help you overcome Nephrotic Syndrome (Supportive).