Glomerulonephritis
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Glomerulonephritis
Glomerulonephritis is an inflammatory kidney disease where the tiny filtering units of the kidneys (glomeruli) become inflamed and damaged, impairing their ability to filter waste and excess fluids from the blood. This can occur suddenly (acute) or develop gradually over years (chronic), leading to proteinuria, hematuria, high blood pressure, and progressive kidney failure if left untreated. It can be triggered by infections, autoimmune diseases, or occur as a primary kidney disorder, affecting both children and adults with varying severity.
Recognizing Glomerulonephritis
Common symptoms and warning signs to look for
Cola-colored or tea-colored urine indicating blood in the urine
Foamy or frothy urine suggesting protein leakage
Swelling in face, hands, feet, or legs from fluid retention
Persistent high blood pressure that is difficult to control
Decreased urine output or changes in urination frequency
What a Healthy System Looks Like
Healthy glomeruli function as the kidney's microscopic filtration factories, with approximately 1 million glomeruli in each kidney. Each glomerulus consists of a tight cluster of capillaries (tuft) surrounded by Bowman's capsule. Blood enters through the afferent arteriole under controlled pressure, where the glomerular filtration barrier - composed of fenestrated endothelial cells, the glomerular basement membrane (GBM), and podocyte foot processes - selectively filters blood. This barrier allows water, electrolytes, and small molecules to pass into the urinary space while retaining blood cells and large proteins like albumin. The filtrate then enters the renal tubules for further processing. In a healthy state, the glomeruli filter about 180 liters of blood daily while maintaining impermeability to proteins larger than 70 kDa, preserving essential nutrients while removing metabolic waste.
How the Condition Develops
Understanding the biological mechanisms
Glomerulonephritis develops through several distinct immunological and inflammatory mechanisms: (1) Immune complex deposition - Circulating immune complexes (antigen-antibody complexes) deposit in the glomerular mesangium or subendothelial/subepithelial spaces, activating complement via the classical pathway (C1q, C4, C2, C3) and generating membrane attack complex (C5b-9) that damages podocytes and endothelial cells. (2) Anti-GBM antibody formation - Autoantibodies directly attack type IV collagen in the glomerular basement membrane, causing linear immunofluorescence patterns and rapid, severe glomerular destruction as seen in Goodpasture's syndrome. (3) Alternative complement pathway dysregulation - Uncontrolled activation of C3 convertase leads to C3 deposition without immune complexes, seen in C3 glomerulopathy and dense deposit disease. (4) Podocyte injury - Direct damage to podocyte foot processes causes proteinuria and effacement, disrupting the selective filtration barrier. (5) Mesangial proliferation - Inflammatory mediators stimulate mesangial cell proliferation and matrix expansion, reducing filtration surface area. (6) Crescent formation - Severe glomerular injury triggers parietal epithelial cell proliferation and macrophage infiltration, forming cellular crescents that compress the glomerular tuft and cause rapid progression to kidney failure. (7) Tubulointerstitial fibrosis - Chronic inflammation leads to scarring of surrounding tissue, further compromising kidney function.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| eGFR (Estimated Glomerular Filtration Rate) | 90-120 mL/min/1.73m² | >90 mL/min/1.73m² | Declines with glomerular damage; rapid decline suggests active disease requiring urgent intervention |
| 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) | Elevated when glomerular filtration is impaired; rising creatinine indicates disease progression |
| Urine Protein-to-Creatinine Ratio (UPCR) | <0.2 g/g | <0.15 g/g | Quantifies proteinuria; >3.5 g/g indicates nephrotic-range proteinuria; key marker of glomerular damage |
| Urine Albumin-to-Creatinine Ratio (UACR) | <30 mg/g | <10 mg/g | Early marker of glomerular damage; elevated in diabetic and non-diabetic glomerular disease |
| Complement C3 | 90-180 mg/dL | 100-150 mg/dL | Low in post-infectious GN, lupus nephritis, MPGN; consumed in immune complex-mediated disease |
| Complement C4 | 10-40 mg/dL | 15-30 mg/dL | Low in lupus nephritis, cryoglobulinemia, hepatitis C-associated GN |
| ANA (Antinuclear Antibodies) | Negative or <1:40 | Negative | Positive in lupus nephritis and other autoimmune causes of glomerulonephritis |
| Anti-dsDNA Antibodies | <100 IU/mL | Negative | Specific for lupus nephritis; levels correlate with disease activity |
| ANCA (Anti-Neutrophil Cytoplasmic Antibodies) | Negative | Negative | Positive in pauci-immune glomerulonephritis (Wegener's/granulomatosis with polyangiitis, microscopic polyangiitis) |
| Anti-GBM Antibodies | Negative | Negative | Positive in Goodpasture's syndrome; requires urgent treatment to prevent irreversible kidney failure |
| Serum Albumin | 3.5-5.0 g/dL | >4.0 g/dL | Low in nephrotic syndrome due to urinary protein loss; <3.5 g/dL indicates significant proteinuria |
| Kidney Biopsy | Normal glomerular architecture | No inflammation, no immune deposits | Gold standard for diagnosis; shows pattern of injury, immune deposits, and guides treatment |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Post-Infectious Immune Complex Deposition","contribution":"Most common cause of acute glomerulonephritis in children","assessment":"Recent streptococcal infection history, low complement C3, elevated ASO or anti-DNase B titers, typical latency period"}
{"cause":"Autoimmune Dysregulation (Lupus, Vasculitis)","contribution":"Major cause of glomerulonephritis in adults","assessment":"ANA, anti-dsDNA, ANCA panels; systemic symptoms (rash, arthritis, sinusitis); biopsy shows immune deposits or pauci-immune pattern"}
{"cause":"IgA Nephropathy","contribution":"Most common primary glomerulonephritis globally","assessment":"Persistent microscopic hematuria, often with concurrent upper respiratory infection (synpharyngitic); mesangial IgA deposits on biopsy"}
{"cause":"Genetic Predisposition","contribution":"Family history increases risk for IgA nephropathy, Alport syndrome, thin basement membrane disease","assessment":"Family history of kidney disease, genetic testing for COL4A mutations, early onset disease"}
{"cause":"Environmental Toxins and Medications","contribution":"NSAIDs, gold, penicillamine, captopril can cause membranous nephropathy; heroin, silica exposure","assessment":"Medication history, occupational exposures, drug cessation trial"}
{"cause":"Chronic Infections","contribution":"Hepatitis B, Hepatitis C, HIV, endocarditis, infected shunts","assessment":"Viral serologies, blood cultures, echocardiogram; treat infection to resolve glomerular disease"}
{"cause":"Malignancy-Associated","contribution":"Solid tumors (lung, colon, breast) and lymphomas can cause membranous nephropathy","assessment":"Age-appropriate cancer screening, tumor markers, imaging; paraneoplastic autoantibodies (THSD7A, PLA2R)"}
{"cause":"Complement Dysregulation","contribution":"C3 glomerulopathy, dense deposit disease, atypical HUS","assessment":"Low C3 with normal C4, genetic testing for complement regulatory proteins, C3 nephritic factor"}
{"cause":"Membranous Nephropathy (Primary or Secondary)","contribution":"Leading cause of nephrotic syndrome in adults","assessment":"Anti-PLA2R antibodies, rule out secondary causes (hepatitis, lupus, drugs, malignancy); subepithelial deposits on biopsy"}
Risks of Inaction
What happens if left untreated
{"complication":"Rapidly Progressive Glomerulonephritis (RPGN)","timeline":"Weeks to months","impact":"Crescent formation causes irreversible glomerular destruction; without treatment, progresses to end-stage kidney disease within months; requires urgent immunosuppression"}
{"complication":"Chronic Kidney Disease (CKD) Progression","timeline":"Years","impact":"Persistent inflammation causes progressive scarring; gradual decline in kidney function from stage 1 to stage 5; may require dialysis or transplantation"}
{"complication":"End-Stage Renal Disease (ESRD)","timeline":"Variable (months to decades)","impact":"Complete kidney failure requiring dialysis or transplantation; significantly reduced life expectancy; cardiovascular mortality 10-20x higher than general population"}
{"complication":"Nephrotic Syndrome Complications","timeline":"Progressive with heavy proteinuria","impact":"Severe edema, infections from immunoglobulin loss, thromboembolism from hypercoagulable state, accelerated cardiovascular disease, malnutrition"}
{"complication":"Cardiovascular Disease","timeline":"Present from early disease","impact":"Hypertension accelerates atherosclerosis; glomerular disease patients have 2-3x increased cardiovascular mortality; leading cause of death in CKD"}
{"complication":"Electrolyte Emergencies","timeline":"Acute or chronic","impact":"Hyperkalemia causes life-threatening cardiac arrhythmias; severe hyponatremia or hypernatremia cause neurological symptoms; metabolic acidosis accelerates bone loss"}
{"complication":"Pulmonary Hemorrhage (Goodpasture's)","timeline":"Acute, life-threatening","impact":"Anti-GBM disease can cause massive pulmonary bleeding; respiratory failure; requires emergency plasmapheresis and immunosuppression"}
{"complication":"Permanent Kidney Damage","timeline":"Months to years","impact":"Glomerular scarring (glomerulosclerosis) is irreversible; lost nephrons cannot regenerate; early treatment preserves remaining kidney function"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"Urinalysis with Microscopy","purpose":"Initial screening for glomerular disease","whatItShows":"Hematuria (RBCs), proteinuria, RBC casts (pathognomonic for GN), dysmorphic RBCs (indicate glomerular origin), WBCs, granular casts"}
{"test":"Urine Protein Quantification","purpose":"Quantify protein loss","whatItShows":"24-hour urine protein or UPCR; nephrotic range >3.5 g/day; guides treatment intensity and prognosis"}
{"test":"Serum Creatinine and eGFR","purpose":"Assess kidney function","whatItShows":"Baseline and trend of kidney function; rising creatinine indicates active disease or progression"}
{"test":"Complement Levels (C3, C4)","purpose":"Identify immune complex-mediated disease","whatItShows":"Low C3 suggests post-infectious GN, C3 glomerulopathy, or lupus; low C4 suggests lupus or cryoglobulinemia; normal complements suggest IgA nephropathy or ANCA-associated disease"}
{"test":"Autoantibody Panel","purpose":"Identify autoimmune cause","whatItShows":"ANA and anti-dsDNA for lupus; ANCA for vasculitis; anti-GBM for Goodpasture's; anti-PLA2R for membranous nephropathy"}
{"test":"Infectious Disease Workup","purpose":"Identify infectious trigger","whatItShows":"ASO and anti-DNase B (streptococcal); hepatitis B and C serologies; HIV testing; blood cultures if endocarditis suspected"}
{"test":"Kidney Biopsy","purpose":"Definitive diagnosis and classification","whatItShows":"Light microscopy (cellularity, crescents, sclerosis), immunofluorescence (immune deposit pattern and type), electron microscopy (ultrastructural details); guides specific treatment"}
{"test":"Serum Albumin and Lipid Panel","purpose":"Assess nephrotic syndrome","whatItShows":"Hypoalbuminemia <3.5 g/dL, elevated cholesterol and triglycerides in nephrotic syndrome"}
{"test":"CBC and Coagulation Studies","purpose":"Assess complications","whatItShows":"Anemia from CKD; hypercoagulable state in nephrotic syndrome (elevated fibrinogen, decreased antithrombin III)"}
{"test":"Renal Ultrasound","purpose":"Assess kidney size and structure","whatItShows":"Kidney size (small kidneys suggest chronicity), echogenicity, rule out obstruction; normal or enlarged kidneys in acute GN"}
Our Treatment Approach
How we help you overcome Glomerulonephritis
Phase 1: Diagnosis and Acute Stabilization (Weeks 1-4)
{"phase":"Phase 1: Diagnosis and Acute Stabilization (Weeks 1-4)","focus":"Establish diagnosis, control blood pressure, reduce proteinuria, address urgent complications","interventions":"Complete diagnostic workup including kidney biopsy if indicated. Aggressive blood pressure control with ACE inhibitors or ARBs (reduce proteinuria and slow progression). Diuretics for edema management. Sodium restriction (<2g/day). Treat any identified infection (antibiotics for streptococcal infection). Monitor electrolytes closely. Address nephrotic syndrome complications (anticoagulation if indicated, statins for hyperlipidemia). For rapidly progressive GN with crescents: urgent high-dose corticosteroids, cyclophosphamide or mycophenolate, possible plasmapheresis for anti-GBM disease or severe vasculitis.\n"}
Phase 2: Disease-Specific Immunosuppression (Weeks 4-24)
{"phase":"Phase 2: Disease-Specific Immunosuppression (Weeks 4-24)","focus":"Target underlying immune mechanism to induce remission","interventions":"Tailored immunosuppressive therapy based on biopsy and serologies: Lupus nephritis (my cophenolate mofetil or cyclophosphamide + steroids per ISN/RPS class); IgA nephropathy (fish oil, possible steroids if proteinuria >1g/day or declining GFR); Membranous nephropathy (rituximab or calcineurin inhibitors if high risk); ANCA vasculitis (rituximab or cyclophosphamide + steroids); Minimal change disease (high-dose steroids). Continue ACEi/ARB. Monitor for infection due to immunosuppression. Regular lab monitoring (weekly initially, then monthly).\n"}
Phase 3: Maintenance and Relapse Prevention (Months 6-18)
{"phase":"Phase 3: Maintenance and Relapse Prevention (Months 6-18)","focus":"Maintain remission, taper immunosuppression, prevent relapses","interventions":"Gradual taper of corticosteroids. Continue maintenance immunosuppression as indicated (mycophenolate, azathioprine, low-dose steroids). Continue ACEi/ARB indefinitely if tolerated. Monitor proteinuria, kidney function, and inflammatory markers. Screen for relapse (rising proteinuria, hematuria, creatinine). Address cardiovascular risk aggressively (statins, antiplatelet therapy). Lifestyle modifications (smoking cessation, weight management, exercise). Vaccinations (influenza, pneumococcal) before or between immunosuppressive courses.\n"}
Phase 4: Long-Term Management and Kidney Protection (Month 18+)
{"phase":"Phase 4: Long-Term Management and Kidney Protection (Month 18+)","focus":"Preserve remaining kidney function, manage chronic complications, prepare for ESRD if needed","interventions":"Long-term blood pressure control (target <130/80 mmHg). Continue renoprotective medications. Monitor for CKD complications (anemia, bone disease, acidosis). Dietary counseling (protein moderation, sodium restriction). Regular nephrology follow-up (every 3-6 months). Screen for cardiovascular disease. If progressive CKD: prepare for renal replacement therapy (dialysis education, transplant evaluation). Support groups and mental health support. Consider clinical trials for refractory cases.\n"}
Diet & Lifestyle
Recommendations for optimal recovery
Lifestyle Modifications
Blood pressure monitoring: Home BP monitoring daily; target <130/80 mmHg, Smoking cessation: Critical - smoking accelerates kidney damage and cardiovascular disease, Regular moderate exercise: 150 minutes/week of walking, swimming, cycling - improves cardiovascular health and blood pressure, Weight management: Achieve healthy BMI; obesity worsens proteinuria and CKD progression, Stress management: Chronic stress elevates blood pressure and cortisol; meditation, yoga, breathing exercises, Sleep hygiene: 7-8 hours nightly; sleep apnea screening (common in CKD and worsens hypertension), Avoid dehydration: Maintain adequate hydration unless fluid-restricted, Limit alcohol: Moderate consumption only; avoid if blood pressure poorly controlled, Infection prevention: Hand hygiene, avoid sick contacts, vaccinations (before immunosuppression), Medication compliance: Take ACEi/ARB and immunosuppressants exactly as prescribed
Recovery Timeline
What to expect on your healing journey
Phase 1 (Weeks 1-4): Acute diagnosis and stabilization; kidney biopsy if indicated; initiate blood pressure control with ACEi/ARB; treat any infection; manage edema with diuretics; begin immunosuppressive therapy if rapidly progressive or severe nephrotic syndrome; weekly monitoring of labs.
Phase 2 (Weeks 4-24): Active immunosuppressive treatment based on specific diagnosis; monitor for treatment response (declining proteinuria, stable/improving kidney function); manage side effects of medications; infection prophylaxis if on high-dose steroids or potent immunosuppressants; monthly lab monitoring.
Phase 3 (Months 6-18): Taper immunosuppression if in remission; continue maintenance therapy as indicated; monitor for relapse; address cardiovascular risk factors; lifestyle modifications firmly established; labs every 2-3 months.
Phase 4 (Month 18+): Long-term maintenance; regular nephrology follow-up every 3-6 months; monitor for CKD complications if kidney function reduced; screen for cardiovascular disease; prepare for ESRD if progressive decline; many patients achieve stable remission with preserved kidney function.
Note: Timelines vary significantly by glomerulonephritis type. Post-infectious GN often resolves in weeks. Minimal change disease responds within weeks to steroids. IgA nephropathy and membranous nephropathy follow courses over years. Lupus nephritis requires long-term management with flares and remissions.
How We Measure Success
Outcomes that matter
Proteinuria reduction: <0.5 g/day or >50% reduction from baseline
Resolution of hematuria: No RBCs or minimal on urinalysis
Blood pressure control: <130/80 mmHg consistently
Stable or improving eGFR: Decline <5 mL/min/year
Resolution of edema: No peripheral or facial swelling
Normalization of complement levels (if previously low)
Reduction or normalization of autoantibody titers
Absence of RBC casts on urinalysis
Stable serum albumin >3.5 g/dL (if nephrotic)
No disease flares for 12+ months
Successful taper of corticosteroids without relapse
Maintenance of remission on minimal immunosuppression
Good quality of life and functional status
No hospitalizations for disease complications
Frequently Asked Questions
Common questions from patients
What is the difference between glomerulonephritis and chronic kidney disease?
Glomerulonephritis is a specific type of kidney disease affecting the glomeruli (filtering units), while chronic kidney disease (CKD) is a broader term for any progressive loss of kidney function. Glomerulonephritis is one of many causes of CKD. Think of it this way: all glomerulonephritis can lead to CKD if untreated, but not all CKD is caused by glomerulonephritis. Other causes of CKD include diabetes, hypertension, polycystic kidney disease, and interstitial nephritis. Glomerulonephritis specifically involves inflammation and immune-mediated damage to the glomeruli.
Can glomerulonephritis be cured?
The prognosis depends on the specific type and severity. Post-infectious glomerulonephritis often resolves completely within weeks to months, especially in children. Minimal change disease usually responds completely to steroids. However, many forms like IgA nephropathy, lupus nephritis, and membranous nephropathy are chronic conditions that require long-term management. Early diagnosis and appropriate treatment can induce remission, prevent progression to kidney failure, and preserve kidney function. Even when not 'cured,' many patients maintain stable kidney function for decades with proper treatment. Rapidly progressive forms require urgent intervention to prevent irreversible damage.
Why is my urine dark or foamy?
Dark, cola-colored, or tea-colored urine indicates hematuria (blood in urine) - red blood cells leaking through inflamed glomeruli. This is a hallmark of glomerulonephritis. Foamy or frothy urine indicates proteinuria (protein in urine) - albumin and other proteins passing through damaged glomerular filters. Both occur because inflammation damages the glomerular filtration barrier that normally keeps blood cells and large proteins in the bloodstream. These findings require prompt medical evaluation to determine the cause and initiate treatment.
Will I need a kidney biopsy?
A kidney biopsy is often necessary for definitive diagnosis and treatment planning, especially in adults with unexplained glomerulonephritis. The biopsy reveals the pattern of injury, type of immune deposits, and presence of crescents or scarring - information critical for choosing the right treatment. However, biopsies may be deferred in classic presentations (such as post-streptococcal GN in children) or when contraindicated (bleeding disorders, single kidney). The procedure is generally safe with ultrasound guidance and local anesthesia, with serious complications occurring in less than 1% of cases.
What medications will I need to take?
Treatment is individualized based on the specific type of glomerulonephritis. Common medications include: ACE inhibitors or ARBs (reduce proteinuria and protect kidneys), corticosteroids (reduce inflammation), immunosuppressants (mycophenolate, cyclophosphamide, azathioprine, rituximab - suppress the immune system), diuretics (reduce edema), and medications to control blood pressure and cholesterol. For nephrotic syndrome, blood thinners may be needed to prevent clots. Treatment duration varies from months to years, and some patients require lifelong medication to maintain remission.
Can I exercise with glomerulonephritis?
Yes, moderate exercise is generally beneficial and encouraged. Regular physical activity helps control blood pressure, reduces cardiovascular risk, improves mood, and maintains overall health. However, avoid high-intensity exercise during acute flares or when proteinuria is severe, as extreme exertion can temporarily increase protein in urine. Start with low-impact activities like walking, swimming, or cycling. Stay well-hydrated. Consult your nephrologist about exercise guidelines specific to your condition and current kidney function. Dialysis patients can and should exercise, including during dialysis sessions.
Medical References
- 1.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.2021.05.015 - Comprehensive international guidelines for diagnosis and management of all glomerular diseases.
- 2.Floege J, Amann K. Primary Glomerulonephritides. Lancet. 2016;387(10032):2036-2048. doi:10.1016/S0140-6736(16)00272-5 - Clinical review of primary glomerular diseases.
- 3.Beck LH Jr, Salant DJ. Glomerular and Tubulointerstitial Diseases. Prim Care. 2017;44(4):669-692. doi:10.1016/j.pop.2017.07.006 - Primary care perspective on glomerular diseases.
- 4.Jennette JC, Falk RJ. Pathogenesis of Antineutrophil Cytoplasmic Autoantibody-Mediated Disease. Nat Rev Rheumatol. 2014;10(7):463-473. doi:10.1038/nrrheum.2014.56 - Mechanisms of ANCA-associated vasculitis.
- 5.Wyatt RJ, Julian BA. IgA Nephropathy. N Engl J Med. 2013;368(25):2402-2414. doi:10.1056/NEJMra1206793 - Comprehensive review of the most common glomerulonephritis.
- 6.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 discovery of anti-PLA2R antibodies in membranous nephropathy.
Ready to Start Your Healing Journey?
Our integrative medicine experts are ready to help you overcome Glomerulonephritis.