Membranous Nephropathy in Oman: Symptoms, Causes & Treatment | aihealz
Nephrologymoderate
Membranous Nephropathy.Care & specialists in Oman
In Oman, membranous Nephropathy is managed by nephrologists. Membranous nephropathy (MN) is the most common cause of nephrotic syndrome in non-diabetic adults of European ancestry, accounting for roughly 20-30% of biopsy-proven adult nephrotic syndrome. It is driven by deposition of subepithelial immune complexes on the outer surface of the glomerular basement membrane, with thickening visible on light microscopy and characteristic spikes on silver staining.
Membranous nephropathy (ICD-10: N04.2 nephrotic syndrome with diffuse membranous glomerulonephritis) is a histologic pattern of glomerular disease defined by subepithelial immune complex deposits on the glomerular basement membrane (GBM), with diffuse thickening of the GBM and characteristic spikes seen on Jones silver stain. The cellular mechanism involves IgG4-predominant autoantibodies binding to a podocyte antigen — most commonly the M-type phospholipase A2 receptor (PLA2R), responsible for 70-80% of primary cases — at the podocyte slit diaphragm. Bound antibody activates the complement membrane attack complex (C5b-9) in situ, damaging podocytes and producing massive proteinuria. Newer antigens include thrombospondin type-1 domain-containing 7A (THSD7A, 1-5%), neural epidermal growth factor-like 1 protein (NELL1, particularly in malignancy-associated MN), semaphorin 3B, protocadherin 7, and exostosin 1/2 (in lupus-associated cases).
key facts
Prevalence
Annual incidence approximately 1-2 per 100,000 adults in Western populations; accounts for 20-30% of adult nephrotic syndrome (KDIGO 2021)
Demographics
Male:female ratio approximately 2:1; predominantly affects White and East Asian adults; rare in children
Avg. age
Peak age 50-60 years; bimodal distribution with smaller peak in 20-40-year-olds; older onset (over 65) raises suspicion of malignancy-associated MN
Global cases
No reliable global figure; estimated several hundred thousand prevalent cases worldwide given incidence and 5-year prevalence on therapy
Specialist
Nephrology
§ 02
How you might notice it
The key symptoms of Membranous Nephropathy are: Foamy, frothy urine that persists from morning to evening — the visible expression of heavy proteinuria., Generalized peripheral edema, often starting in the ankles and progressing to the thighs, scrotum or vulva, and abdomen; periorbital edema is common in the morning., Sudden weight gain (5-15 kg) from fluid retention over weeks to months., Fatigue and reduced exercise tolerance from hypoalbuminemia and overall systemic effects of nephrotic syndrome., Sometimes hypertension (40-50% of patients at presentation) with associated headache or blurred vision., Microscopic hematuria in roughly 30-50% of patients; macroscopic hematuria is uncommon and suggests a different diagnosis., Symptoms of venous thromboembolism — unilateral leg swelling with calf tenderness, pleuritic chest pain, breathlessness, or flank pain — from renal-vein thrombosis or deep-vein thrombosis, particularly in severe nephrotic syndrome..
01Foamy, frothy urine that persists from morning to evening — the visible expression of heavy proteinuria.
02Generalized peripheral edema, often starting in the ankles and progressing to the thighs, scrotum or vulva, and abdomen; periorbital edema is common in the morning.
03Sudden weight gain (5-15 kg) from fluid retention over weeks to months.
04Fatigue and reduced exercise tolerance from hypoalbuminemia and overall systemic effects of nephrotic syndrome.
05
§ 03
How it’s diagnosed
diagnosis
Diagnosis starts with confirmation of nephrotic syndrome — proteinuria over 3.5 g/24 hours (or urinary protein-to-creatinine ratio over 3.5 g/g) with hypoalbuminemia under 30 g/L, edema, and hyperlipidemia. Serum and urine immunofixation rules out paraprotein-associated disease. Hepatitis B and C serology, HIV testing, autoimmune panel (ANA, anti-dsDNA, complement C3 and C4, anti-Ro, anti-La, anti-thyroid), serum anti-PLA2R antibody, age-appropriate cancer screening, and review of medications all proceed in parallel. Anti-PLA2R antibody by indirect immunofluorescence or ELISA is positive in 70-80% of primary MN and is approximately 99% specific. A positive anti-PLA2R titer combined with nephrotic syndrome and absence of secondary causes can sometimes confirm primary MN without biopsy (KDIGO 2021), but renal biopsy remains the gold standard. Biopsy shows diffuse subepithelial immune deposits on electron microscopy with characteristic GBM spikes, granular IgG (predominantly IgG4 in primary disease, IgG1/IgG3 in secondary or lupus-associated) and C3 on immunofluorescence, and positive PLA2R or THSD7A staining when applicable. Disease stages (Ehrenreich-Churg I to IV) reflect deposit location and basement membrane thickening. Risk stratification at diagnosis uses proteinuria magnitude, serum albumin, eGFR, anti-PLA2R titer, and rate of change — KDIGO 2021 separates low, moderate, high, and very-high risk to guide treatment. Imaging (renal ultrasound) excludes obstruction and assesses kidney size; chest CT, colonoscopy, mammography, and PSA are obtained based on age and risk profile.
Key tests
01
24-hour urine protein or urinary protein-to-creatinine ratio (uPCR)Quantifies proteinuria; over 3.5 g/24h or uPCR over 3.5 g/g defines nephrotic-range and orients treatment risk
02
Serum albumin, lipid profile, creatinine, eGFRConfirms nephrotic syndrome and assesses baseline kidney function; albumin under 25 g/L raises thrombosis risk
§ 04
Treatment & cost
medical treatments
✓Rituximab (1 g IV days 1 and 15, or 375 mg/m2 weekly × 4)
✓Cyclophosphamide-based Ponticelli regimen (alternating months of methylprednisolone pulses + oral steroid and oral cyclophosphamide 2-2.5 mg/kg/day) for 6 months
✓Calcineurin inhibitors (cyclosporine 3.5-5 mg/kg/day or tacrolimus 0.05-0.1 mg/kg/day) plus low-dose prednisolone
✓ACE inhibitor or ARB at maximally tolerated dose
§ 05
Causes & risk factors
known causes
Anti-PLA2R autoantibodies (primary MN)
Circulating IgG4 antibodies against the M-type phospholipase A2 receptor on podocytes bind in situ and form subepithelial immune complexes that activate complement and damage podocytes. Found in 70-80% of primary MN. Antibody titer correlates with disease activity and treatment response.
Anti-THSD7A and other novel antigens (primary MN)
Thrombospondin type-1 domain-containing 7A (1-5%), NELL1 (often malignancy-associated), semaphorin 3B (pediatric), protocadherin 7, and exostosin 1/2 (lupus-associated) account for most non-PLA2R primary cases. Discovery of new antigens has reduced the proportion of idiopathic disease.
Hepatitis B virus infection
Subepithelial deposition of HBV antigen-antibody complexes causes secondary MN, particularly in regions of high HBV prevalence (sub-Saharan Africa, Asia). Treatment of HBV with antivirals can induce remission of MN. HCV is a rarer cause.
Class V lupus nephritis is the prototype; Sjögren-associated MN, sarcoidosis-related MN, and IgG4-related disease are recognized. Exostosin 1/2-positive MN often signals lupus.
Solid organ malignancy
Up to 25% of MN in patients over 65 is paraneoplastic, most commonly with lung, colon, prostate, breast, or stomach cancer. NELL1-positive MN has the strongest cancer association. Age-appropriate screening (chest CT, colonoscopy, mammography, PSA) is mandatory at diagnosis.
Drugs and toxin exposure
NSAIDs, gold salts, penicillamine, captopril, mercury (including skin-lightening creams), and trastuzumab can induce MN. Withdrawal of the agent often leads to remission within months.
risk factors
§ 06
Living with it
01Vaccinate against hepatitis B universally to prevent the most common cause of secondary MN globally.
02Avoid chronic NSAID use without medical supervision; review medications regularly.
03Maintain age-appropriate cancer screening, particularly after age 50.
04Manage autoimmune diseases (lupus, Sjögren) according to specialist guidance to reduce renal complications.
05Monitor blood pressure, lipids, and urinalysis in patients with risk factors or family history of glomerular disease.
06Avoid mercury exposure (some skin-lightening creams, traditional remedies, occupational hazards) — a recognized cause of MN in some populations.
recommended foods
•Sodium 2-3 g/day (less than 5 g salt) for edema control
•Protein 0.8-1.0 g/kg/day in non-severe disease; higher with active losses, lower in CKD progression per dietitian advice
•
§ 07
When to seek help
why see a nephrology
Nephrology referral is essential for any adult with nephrotic-range proteinuria. Specialists confirm diagnosis with biopsy, identify secondary causes, perform risk stratification, and select immunosuppression. Tertiary glomerular disease centers offer access to rituximab and clinical trials of newer agents.
01Venous thromboembolism (renal vein thrombosis, deep-vein thrombosis, pulmonary embolism) in up to 25% of patients with severe nephrotic syndrome (albumin under 25 g/L).
02Progression to chronic kidney disease and end-stage renal disease in 30-50% of untreated nephrotic-range patients over 10 years.
03Accelerated cardiovascular disease from dyslipidemia, hypertension, and endothelial dysfunction.
04Infections, especially encapsulated organisms (pneumococcus, Hib) from urinary loss of IgG and complement factors, plus opportunistic infections during immunosuppression.
05Adverse effects of long-term immunosuppression: bone marrow suppression, infertility, malignancy (cyclophosphamide), nephrotoxicity (calcineurin inhibitors), infusion reactions (rituximab).
Primary (autoimmune) membranous nephropathy70-80% of cases; circulating IgG4 autoantibodies against podocyte antigens (anti-PLA2R in 70-80%, anti-THSD7A in 1-5%, newer antigens in the remainder). Treated with KDIGO-recommended immunosuppression in high-risk patients.
Secondary membranous nephropathy20-30% of cases. Causes include hepatitis B (subepithelial HBV antigens), hepatitis C, syphilis, schistosomiasis, lupus (class V lupus nephritis), Sjögren, sarcoidosis, malignancy (especially solid tumors in patients over 65), and drugs (NSAIDs, gold, captopril, penicillamine, mercury). Treatment targets the underlying cause.
Malignancy-associated membranous nephropathyUp to 25% of MN in patients over 65 is associated with occult solid malignancy (lung, gastrointestinal, prostate, breast). NELL1-positive MN has particular association with cancer. Age-appropriate cancer screening is recommended at diagnosis.
Lupus membranous nephropathy (class V)WHO/ISN class V lupus nephritis with membranous pattern, often combined with proliferative lesions (mixed III+V or IV+V). Treatment follows lupus nephritis protocols rather than primary MN regimens.
Recurrent membranous nephropathy in renal allograftApproximately 40% of patients with primary MN have biopsy-proven recurrence in a kidney transplant; anti-PLA2R-positive recipients are at higher risk. Rituximab is effective.
Living with Membranous Nephropathy
Timeline
Proteinuria typically begins to fall within 6-12 weeks of starting ACE inhibitor or ARB, and within 3-6 months of starting immunosuppression. Complete remission (proteinuria under 0.3 g/day) usually takes 12-24 months on rituximab and 6-12 months on cyclophosphamide-based regimens. Anti-PLA2R titers fall before proteinuria, often within 3-6 months of effective therapy. Edema resolves within weeks of diuretic and protein response. Sustained remission after rituximab can last several years; re-treatment is timed by titer rebound and proteinuria recurrence.
Lifestyle
01Restrict dietary sodium to 2-3 g/day to control edema and blood pressure.
02Take ACE inhibitor or ARB consistently at the prescribed dose; never stop suddenly without medical advice.
03Adhere to immunosuppression schedule and infection prophylaxis (PJP, varicella, vaccinations).
04Maintain regular outpatient blood and urine monitoring during active treatment.
05Stop smoking; tobacco worsens cardiovascular and renal outcomes.
06Engage in moderate exercise once edema and thrombosis risk are stable, with anticoagulation if indicated.
Daily management
01Weigh yourself at the same time daily and report sudden gain of more than 1.5 kg over 48 hours.
Complementary approaches
Obinutuzumab and other anti-CD20 agents (clinical trial setting)Second-generation anti-CD20 monoclonal antibodies under investigation for primary MN; early data suggest deeper B-cell depletion and possible advantage in rituximab-resistant disease.
Adrenocorticotropic hormone (ACTH) gelUsed in some North American centers for refractory MN; small studies show modest remission rates. Cost and availability limit use.
Choosing a doctor
Choose a nephrologist with experience in glomerular diseases — KDIGO-aligned protocols, access to anti-PLA2R testing, and a working relationship with renal pathology, oncology, and hepatology. Tertiary centers with dedicated glomerular disease clinics or trial enrolment are preferred for high-risk or refractory disease.
Membranous nephropathy is a kidney disease in which antibody complexes deposit on the outer surface of the glomerular basement membrane, thickening it and causing massive protein loss in the urine. It is the most common cause of adult nephrotic syndrome in non-diabetic patients of European ancestry and is treated with ACE inhibitors and, in higher-risk patients, immunosuppression.
What are the symptoms of membranous nephropathy?▾▴
The main symptoms are foamy urine, generalized swelling (ankles, face, abdomen), unexplained weight gain, fatigue, and sometimes high blood pressure. Severe disease can cause renal vein thrombosis or pulmonary embolism, with leg swelling, chest pain, or sudden dyspnea — all requiring urgent evaluation.
How is membranous nephropathy diagnosed?▾▴
Diagnosis combines a 24-hour urine showing over 3.5 g protein, hypoalbuminemia, and a renal biopsy showing subepithelial immune deposits with characteristic GBM spikes. Anti-PLA2R antibody testing identifies 70-80% of primary cases and is approximately 99% specific. Secondary causes (hepatitis B, lupus, malignancy, drugs) are excluded with targeted tests.
What causes membranous nephropathy?▾▴
About 70-80% of cases are primary autoimmune disease driven by antibodies against the podocyte protein PLA2R (or THSD7A and other antigens). The remaining 20-30% are secondary to hepatitis B, lupus, malignancy (especially in older adults), and drugs such as NSAIDs, gold, captopril, penicillamine, and mercury.
Does membranous nephropathy go away on its own?▾▴
Roughly one-third of untreated patients spontaneously achieve complete or partial remission within 12-24 months, especially those with proteinuria under 3.5 g/day. Another third stabilize with persistent proteinuria, and a final third progress to kidney failure. Risk-stratified treatment with rituximab or cyclophosphamide significantly improves outcomes for high-risk patients.
Is rituximab effective for membranous nephropathy?▾▴
Yes. Rituximab is now KDIGO-recommended first-line therapy for moderate-to-high-risk primary membranous nephropathy. The MENTOR trial (NEJM 2019) showed sustained remission at 24 months in 60% on rituximab versus 20% on cyclosporine, with comparable safety. It is given as two 1 g IV infusions 2 weeks apart, sometimes repeated based on anti-PLA2R titer.
How long does treatment take for membranous nephropathy?▾▴
Supportive therapy with ACE inhibitor or ARB is continued indefinitely. Immunosuppression with rituximab or cyclophosphamide is given over weeks but takes 6-24 months to produce maximum remission. Sustained remission can last years; rituximab may be repeated based on rising anti-PLA2R titer or relapsing proteinuria.
What is the role of anti-PLA2R antibody?▾▴
Anti-PLA2R antibody confirms primary MN with about 99% specificity and is positive in 70-80% of patients. Titers correlate with disease activity and predict response to treatment. Serial monitoring guides duration of therapy: falling titers precede proteinuria reduction by months and antibody-negative remissions are more stable.
Can membranous nephropathy lead to kidney failure?▾▴
Yes, in 30-50% of untreated patients with sustained nephrotic-range proteinuria over 10 years. Risk-stratified treatment substantially reduces this rate. Predictors of progression include male sex, older age, proteinuria over 8 g/day, declining eGFR, high anti-PLA2R titer, and significant chronic injury on biopsy.
Why is screening for cancer important in older adults with MN?▾▴
Up to 25% of MN cases in patients over 65 are paraneoplastic, most commonly with lung, colon, breast, or prostate cancers. NELL1-positive MN has particularly strong cancer association. Age-appropriate screening (chest CT, colonoscopy, mammography, PSA) is recommended at diagnosis, and cancer treatment often resolves the kidney disease.
Can hepatitis B cause membranous nephropathy?▾▴
Yes. Chronic hepatitis B is the most common cause of secondary MN globally, particularly in endemic regions. HBV antigens form subepithelial immune complexes that damage the basement membrane. Treatment with entecavir or tenofovir alafenamide induces MN remission in many patients without additional immunosuppression.
What is the risk of blood clots in MN?▾▴
Nephrotic syndrome creates a prothrombotic state by urinary loss of antithrombin and increased hepatic synthesis of fibrinogen. Renal vein thrombosis, deep-vein thrombosis, and pulmonary embolism affect up to 25% of patients with serum albumin under 25 g/L. Prophylactic anticoagulation is considered in high-risk patients using validated risk models.
Is membranous nephropathy hereditary?▾▴
Most cases are not directly inherited, but strong HLA-DQA1 and PLA2R1 risk alleles increase susceptibility — the highest odds ratios in any common autoimmune disease. Family clustering is uncommon. Children with MN should be evaluated for inherited podocyte disorders and viral causes.
Can MN come back after a kidney transplant?▾▴
Yes. Recurrence in the allograft occurs in approximately 40% of patients with primary MN, often within the first 2 years post-transplant. Pre-transplant anti-PLA2R-positive recipients are at highest risk. Rituximab effectively induces remission in most recurrent cases.
Do I need to avoid certain medications with MN?▾▴
Yes. NSAIDs and naproxen worsen kidney function and edema. Drug-induced MN can be caused by gold, penicillamine, captopril, mercury-containing creams, and certain biologic agents. Always review new prescriptions and supplements with your nephrologist, especially during immunosuppression.
What diet helps with membranous nephropathy?▾▴
Restrict salt to 2-3 g/day to control edema and blood pressure. Moderate protein intake (0.8-1.0 g/kg/day) is usually appropriate. Mediterranean-style eating with vegetables, fish, olive oil, and limited red meat supports cardiovascular health. Avoid grapefruit juice if on cyclosporine or tacrolimus. A renal dietitian helps individualize the plan.
Can membranous nephropathy occur in pregnancy?▾▴
Yes, though uncommon. Pregnancy can also cause MN-like findings in pre-eclampsia, which usually resolve after delivery. Confirmed MN in pregnancy is managed by nephrology and high-risk obstetrics with calcineurin inhibitors and careful blood pressure control; ACE inhibitors and rituximab are generally avoided.
How often is monitoring needed during remission?▾▴
After remission, urine protein, serum creatinine, and serum albumin are checked every 3 months in the first year and every 6 months thereafter. Anti-PLA2R titer is repeated every 3-6 months for the first 2 years; rising titers prompt earlier re-evaluation. Long-term cardiovascular risk monitoring is essential.
Are calcineurin inhibitors still used for MN?▾▴
Yes, as second-line therapy or in patients who cannot receive rituximab or cyclophosphamide. Cyclosporine and tacrolimus induce remission in 60-70% but have a high relapse rate after withdrawal and risk of nephrotoxicity. They are also used in pregnancy and post-transplant recurrence.
What is the Ponticelli regimen?▾▴
The Ponticelli regimen alternates monthly courses of methylprednisolone pulses with oral steroid (months 1, 3, 5) and oral cyclophosphamide 2-2.5 mg/kg/day (months 2, 4, 6). It is highly effective (80-85% remission at 24 months in the original trial) and remains first-line in high-risk MN, especially with declining eGFR or unavailability of rituximab.
Can I exercise with membranous nephropathy?▾▴
Yes, with adjustments. Moderate aerobic activity is encouraged once edema is controlled. Patients on anticoagulation should avoid contact sports. Resistance training helps maintain lean mass during steroid therapy. Restart progressively after rituximab infusions and report new symptoms or infections promptly.
Sometimes hypertension (40-50% of patients at presentation) with associated headache or blurred vision.
06Microscopic hematuria in roughly 30-50% of patients; macroscopic hematuria is uncommon and suggests a different diagnosis.
07Symptoms of venous thromboembolism — unilateral leg swelling with calf tenderness, pleuritic chest pain, breathlessness, or flank pain — from renal-vein thrombosis or deep-vein thrombosis, particularly in severe nephrotic syndrome.
08Dyspnea and reduced exercise capacity from pleural effusions or pulmonary embolism.
09Abdominal discomfort from ascites or hepatic congestion in advanced fluid overload.
10Symptoms of any underlying disease in secondary MN — joint pain and dry eyes in autoimmune disease, hepatitis symptoms in hepatitis B-associated MN, or cancer-specific symptoms in malignancy-associated MN.
early warning signs
•Foamy urine that does not clear with a single flush
•New persistent ankle or periorbital edema in an adult without obvious cause
•Unexplained weight gain of more than 3 kg over 2 weeks
•Mild dyspnea on exertion with leg swelling
•Routine urinalysis showing 3+ or 4+ protein on dipstick
● emergency signs
•Pleuritic chest pain or sudden dyspnea — suspect pulmonary embolism in a patient with nephrotic syndrome and proceed to CT pulmonary angiography
•Acute unilateral flank pain with macroscopic hematuria — exclude renal vein thrombosis with Doppler ultrasound or CT venogram
•Severe acute oliguria with rising creatinine — exclude superimposed acute kidney injury (intravascular volume depletion, drug nephrotoxicity, crescentic transformation)
•Sepsis with peritoneal signs in patients with ascites — exclude spontaneous bacterial peritonitis
•Severe hypertension (over 180/110 mmHg) with end-organ symptoms — emergency BP control
03
Anti-PLA2R antibody (ELISA and/or indirect immunofluorescence)Diagnoses primary MN with 70-80% sensitivity and 99% specificity; serial titers track treatment response
04
Renal biopsy with light, immunofluorescence, electron microscopy, and PLA2R/THSD7A immunohistochemistryGold standard diagnostic test; distinguishes primary from secondary disease, stages disease, and assesses chronic injury
Age-appropriate cancer screeningExcludes paraneoplastic MN, particularly in patients over 65; CT chest/abdomen/pelvis, colonoscopy, mammography, PSA, and other organ-specific tests as appropriate
07
Renal vein and lower-limb Doppler ultrasoundIdentifies renal vein thrombosis or DVT in symptomatic or high-risk patients (albumin under 25 g/L)
Outlook
Outlook in MN follows the rule of thirds without treatment but is substantially better with risk-stratified KDIGO-aligned care. Low-risk patients have spontaneous complete or partial remission rates of 30-35% within 12-24 months. With immunosuppression, complete or partial remission is achieved in 60-80% of moderate-to-high-risk patients. Long-term renal survival at 10 years exceeds 80% in patients achieving sustained remission, versus 35-50% in those with persistent nephrotic-range proteinuria. The MENTOR trial showed sustained remission at 24 months in 60% on rituximab versus 20% on cyclosporine, with similar safety. Predictors of poor outcome include male sex, older age, severe baseline proteinuria over 8 g/day, declining eGFR, high anti-PLA2R titer, and chronic damage on biopsy (interstitial fibrosis over 25%). Recurrence after transplantation occurs in approximately 40% of primary MN recipients and is treated effectively with rituximab. Cardiovascular and thromboembolic complications remain significant contributors to morbidity and mortality and require integrated management.
Male sexnon-modifiable
Male:female ratio approximately 2:1; men also tend to have higher anti-PLA2R titers and worse outcomes if untreated.
Age over 50non-modifiable
Peak incidence at 50-60 years; age over 65 increases the probability of paraneoplastic disease and worsens prognosis.
HLA-DQA1 and PLA2R1 risk allelesgenetic
Strong genetic associations with primary anti-PLA2R MN (Stanescu NEJM 2011), with odds ratios up to 79 in homozygotes for risk alleles. Genetic testing is research-only at present.
Chronic hepatitis B infectionmodifiable
HBV is the most important cause of secondary MN globally, particularly in children and young adults in endemic regions. Universal HBV vaccination reduces incidence.
Active autoimmune disease (lupus, Sjögren)modifiable
Class V lupus nephritis and Sjögren-associated MN; control of the underlying disease often improves renal outcomes.
Solid organ malignancymodifiable
Particularly lung, gastrointestinal, breast, and prostate cancers in older adults. Treatment of the cancer often induces MN remission.
NSAID and other drug usemodifiable
Chronic NSAID use, gold, penicillamine, captopril, mercury, and certain biologic agents have been implicated. Drug review is essential at diagnosis.
Mediterranean-style pattern with vegetables, fish, olive oil, and limited red meat
•Adequate calcium (1000-1200 mg/day) and vitamin D 800-2000 IU/day during steroid therapy
foods to avoid
•Excess sodium (over 5 g salt/day), processed and restaurant foods high in salt
•Excessive animal protein that accelerates hyperfiltration
•Grapefruit juice in patients on cyclosporine or tacrolimus
•NSAIDs and naproxen without medical supervision; they worsen edema and renal function
Hypovolemic acute kidney injury from over-diuresis or sepsis superimposed on chronic disease.
choosing the right hospital
01Day-case renal biopsy service with experienced ultrasound-guided operators
02Renal pathology with electron microscopy and PLA2R/THSD7A immunohistochemistry
03Anti-PLA2R antibody testing locally or via reliable referral
04Rituximab infusion capacity and KDIGO-aligned glomerular disease pathway
05Multidisciplinary input from hepatology, oncology, and rheumatology for secondary causes
Essential facilities
Tertiary glomerular disease clinicsRenal transplant centers managing recurrent MNHepatology services for HBV-associated MNOncology centers for paraneoplastic MNLupus nephritis specialty clinics
Compare →
02Take ACE inhibitor or ARB and diuretic as prescribed; do not skip doses.
03Inspect legs daily for new swelling, redness, or calf tenderness (DVT signs).
04Maintain immunosuppression schedule; avoid contact with known infectious cases during B-cell depletion.
05Monitor blood pressure at home twice weekly during initial therapy.
06Attend scheduled urine, blood, and anti-PLA2R titer measurements as agreed with the nephrology team.
Exercise
Moderate aerobic activity is safe and beneficial once severe edema is controlled. Patients on anticoagulation should avoid contact sports. Resistance training supports lean mass during steroid therapy. Restart progressively after rituximab infusions and check for any new infection or flare before increasing intensity.