In March 2026, We performed 80 endometriosis surgeries. learn more > We performed 80 endometriosis surgeries. In March 2026, We performed 80 endometriosis surgeries. learn more >

Home >Nephrology > Glomerulonephritis

Glomerulonephritis

Glomerulonephritis is not a single disease - it is an entire category of kidney conditions united by one mechanism: inflammation of the glomeruli, the microscopic filtering units within the kidney. Some forms are mild and self-resolving. Others progress to kidney failure within months if not treated aggressively. The mistake most often made with glomerulonephritis is underestimating it - attributing the haematuria and proteinuria to something simpler, and deferring the kidney biopsy that would have changed the management entirely. At Shree Hospitals, our glomerulonephritis treatment in Mumbai is biopsy-guided and pathology-driven. We do not treat a label - we treat the histological diagnosis.

(24×7 Emergency Care)

1800-268-4000

(24×7 Emergency Care)

1800-268-4000

Our Approach in Managing Glomerulonephritis

GN management starts at the microscope. Our kidney inflammation specialist team in Mumbai, India takes a biopsy-first, protocol-second approach - because treating IgA nephropathy identically to membranous nephropathy, or lupus nephritis identically to minimal change disease, produces entirely different outcomes. The diagnosis must be specific before the treatment can be appropriate.

Clinical Presentation & Pattern Recognition

GN presents as one of two syndromes - or a combination.

Nephrotic syndrome: heavy proteinuria (>3.5g/day), hypoalbuminaemia, oedema, hyperlipidaemia, lipiduria - glomerular barrier dysfunction
Nephritic syndrome: haematuria and proteinuria, hypertension, oliguria, oedema, azotaemia - glomerular inflammatory injury
Rapidly Progressive GN (RPGN) - crescentic GN causing acute severe kidney failure over days to weeks - a nephrology emergency requiring immediate biopsy and treatment

Laboratory Evaluation

24-hour urine protein or UACR - quantifying proteinuria is essential for diagnosis and monitoring
Urine microscopy - dysmorphic red cells and red cell casts confirm glomerular origin of haematuria
Serum C3, C4, ANA, anti-dsDNA - lupus nephritis evaluation
ANCA (PR3, MPO) - pauci-immune GN (Granulomatosis with Polyangiitis, Microscopic Polyangiitis)
Anti-GBM antibodies - Goodpasture's syndrome; rapidly fatal without immediate treatment
ASO titre, C3, C4 - post-streptococcal GN evaluation
Hepatitis B, C serology - membranous and MPGN can be infection-related
Serum protein electrophoresis - paraproteinaemic GN

Kidney Biopsy - The Definitive Step

A kidney biopsy is mandatory in most non-resolving GN presentations. Treating without histological diagnosis risks either over-immunosuppression or under-treatment.

Light microscopy, immunofluorescence, and electron microscopy together define the diagnosis
Key histological diagnoses: IgA nephropathy, Focal Segmental Glomerulosclerosis (FSGS), Minimal Change Disease (MCD), Membranous Nephropathy, Lupus Nephritis (class I–VI), ANCA vasculitis, anti-GBM disease, Post-infectious GN

Disease-Specific Treatment

Immune-mediated kidney disease treatment is determined by the biopsy result.
Minimal Change Disease: high-dose oral prednisolone; typically steroid-responsive; relapsing cases managed with Cyclophosphamide or Rituximab
FSGS: steroids first-line; steroid-resistant FSGS - Cyclosporine, Tacrolimus, or Rituximab; genetic FSGS does not respond to immunosuppression
Membranous Nephropathy: PLA2R antibody-positive cases managed with Rituximab (now first-line over Cyclophosphamide); RAAS blockade for proteinuria in low-risk cases
IgA Nephropathy: RAAS blockade for proteinuria control; Budesonide (Nefecon/Tarpeyo) for high-risk patients; Sparsentan - dual endothelin-angiotensin receptor antagonist - emerging therapy
Lupus Nephritis: class III/IV - Mycophenolate mofetil + steroids (induction), then maintenance MMF; Belimumab and Voclosporin as adjunctive therapies
ANCA vasculitis: Rituximab or Cyclophosphamide for induction; Azathioprine or Rituximab for maintenance; plasma exchange for severe presentations
Anti-GBM disease: plasma exchange + Cyclophosphamide + steroids - initiated within hours of diagnosis

Supportive Management

RAAS blockade - reduces haematuria and proteinuria progression rate in all proteinuric GN
BP control to <130/80 mmHg
Salt and fluid restriction in nephrotic syndrome with oedema
Anticoagulation - in severe nephrotic syndrome (albumin <2g/dL) due to hypercoagulable state from urinary antithrombin loss
Infection prophylaxis during immunosuppression - Pneumocystis prophylaxis with Cotrimoxazole, vaccination review

Long-Term Monitoring

Proteinuria and eGFR at every visit - the two most important GN progression markers
Immunosuppression toxicity monitoring - CBC, liver function, glucose, blood pressure
Relapse detection and early reinduction - most GN requires years of follow-up
CKD transition management when eGFR persistently below 60 despite treatment.

Happy Patients & Their Case Stories

A young woman who noticed her urine was tea-coloured two days after a throat infection. She was initially managed for a UTI elsewhere. When the haematuria persisted and a dipstick showed 3+ protein, she came to Shree Hospitals. Urine microscopy confirmed red cell casts. Kidney biopsy showed IgA nephropathy with Oxford M1E0S0T0C0 classification.

Mr. Sarvesh L

Presented with generalised oedema, anasarca, and serum albumin of 1.6g/dL. 24-hour urine protein was 9.4g. Kidney biopsy confirmed PLA2R-positive membranous nephropathy. He was started on Rituximab (two doses) alongside RAAS blockade and anticoagulation.

Mr. karan . L

How to Identify Glomerulonephritis?

The two hallmarks of GN are haematuria and proteinuria - together they point to the glomerulus before any other diagnosis is made.

Signs that should prompt nephrology evaluation rather than routine management:

Blood in urine without a urological cause - no stone, no infection, no prostate issue
Frothy urine persisting beyond a few days - not a UTI, not dehydration
Swelling of the face and legs appearing over days - without cardiac or liver cause
Haematuria following a throat or skin infection by 1–3 weeks - post-infectious GN
Haematuria appearing alongside haemoptysis - anti-GBM disease or ANCA vasculitis, both requiring emergency treatment
Any combination of rash, joint pain, and haematuria and proteinuria - systemic autoimmune disease affecting kidneys
Rapidly rising creatinine without an obvious pre-renal or obstructive cause

Immune-mediated kidney disease does not wait - and neither should its evaluation. If a urine dipstick shows blood and protein together and the basic workup does not find a urological cause, a nephrology opinion and consideration of kidney biopsy should happen within days, not months. Seek glomerulonephritis treatment in Mumbai at a centre where the full diagnostic pathway - biopsy, immunofluorescence, and pathology interpretation - is available and acted on promptly.

Important FAQs - Glomerulonephritis

Is glomerulonephritis always serious?

Not always - post-infectious GN in children typically resolves spontaneously. But some forms, like anti-GBM disease or RPGN, can destroy kidney function within weeks without treatment. Histological diagnosis determines urgency.

Is a kidney biopsy painful or risky?

It is performed under local anaesthesia with ultrasound guidance. Most patients experience mild discomfort and require a few hours of observation post-procedure. Serious complications - significant bleeding requiring intervention - occur in less than 1% of cases at experienced centres.

Can glomerulonephritis be cured?

Some forms - minimal change disease, post-infectious GN - achieve complete and sustained remission. Others - IgA nephropathy, membranous - require long-term management to maintain remission and prevent progression.

What is the difference between nephrotic and nephritic syndrome?

Nephrotic syndrome features heavy proteinuria, low albumin, and oedema - a barrier function problem. Nephritic syndrome features haematuria, hypertension, and impaired kidney function - an inflammatory injury pattern. Some GN types produce features of both.

Can lupus nephritis come back after treatment?

Yes - lupus nephritis relapses in approximately 30–50% of patients over 10 years. Long-term maintenance immunosuppression and regular monitoring are standard of care.

Treatments for Glomerulonephritis at Shree Hospitals

Comprehensive glomerulonephritis diagnosis and immunotherapy in Mumbai - biopsy-guided, histology-specific, and protocol-driven.

Kidney Biopsy

The definitive diagnostic procedure. Percutaneous ultrasound-guided biopsy with immediate specimen processing for light microscopy, immunofluorescence, and electron microscopy - enabling precise histological diagnosis before any immunosuppression is initiated.

Rituximab Therapy

Monoclonal anti-CD20 antibody therapy - now first-line for PLA2R-positive membranous nephropathy, and a key agent in steroid-resistant MCD, FSGS, and ANCA vasculitis immune-mediated kidney disease management.

Mycophenolate Mofetil (MMF) Protocol

Standard induction and maintenance therapy for lupus nephritis class III/IV. Administered with careful monitoring of white cell count, liver function, and BP during the immunosuppression period.

Nefecon/Budesonide for IgA Nephropathy

Targeted oral steroid with predominantly gut-level action - reducing mucosal IgA production at its source. Used in high-risk IgA nephropathy patients with persistent nephrotic syndrome-range or significant proteinuria.