Mesangial Proliferative Glomerulonephritis: Understanding Causes, Symptoms, and Treatment Options
Mesangial proliferative glomerulonephritis (MPGN) is a group of kidney disorders characterized by diffuse proliferation of mesangial cells and increased mesangial matrix within the glomeruli—the tiny filtering units of the kidneys. This pathological change disrupts normal kidney function, leading to a range of clinical symptoms including hematuria (blood in urine), proteinuria (excess protein in urine), hypertension, and progressive decline in renal function. The condition is broadly categorized into two main types: IgA-dominant and non-IgA forms, each with distinct immunological profiles and disease progression patterns.
Recognizing the Clinical Signs
One of the most common features of mesangial proliferative glomerulonephritis is microscopic hematuria, which is detectable only through urinalysis. However, a significant subset of patients—particularly those diagnosed with IgA nephropathy, a major subtype of MPGN—may experience recurrent episodes of visible, or gross, hematuria. These flare-ups often coincide with upper respiratory infections or other immune triggers, suggesting a close link between immune system activation and kidney inflammation.
In addition to abnormal urinalysis results, many individuals develop proteinuria that can range from mild to nephrotic-range levels. When protein loss becomes substantial, it may lead to swelling (edema), particularly in the legs and around the eyes. Over time, uncontrolled proteinuria and persistent high blood pressure can accelerate kidney damage, increasing the risk of chronic kidney disease (CKD) or even end-stage renal disease (ESRD).
Diagnosis Through Kidney Biopsy
Definitive diagnosis of mesangial proliferative glomerulonephritis requires a kidney biopsy, which allows pathologists to examine tissue samples under a microscope. The hallmark finding is an increase in mesangial cell numbers and expansion of the mesangial matrix. Immunofluorescence staining further helps differentiate between IgA nephropathy—where IgA immune complexes deposit in the mesangium—and non-IgA forms, which may involve other immunoglobulins like IgG or complement components.
Treatment Strategies Based on Disease Severity
Management of MPGN depends heavily on the severity of histological changes and clinical presentation. In milder cases, especially when proteinuria is minimal and kidney function remains stable, a conservative approach is typically recommended. This includes strict control of blood pressure using medications such as ACE inhibitors (e.g., lisinopril) or angiotensin receptor blockers (ARBs, e.g., losartan), both of which also reduce protein leakage and protect long-term kidney health.
Lifestyle modifications play a supportive role—patients are advised to avoid nephrotoxic substances, including certain over-the-counter painkillers like NSAIDs, and to prevent infections that could trigger disease flares, such as colds or strep throat.
Advanced Cases: Immunosuppressive Therapy
For patients with more aggressive disease—characterized by heavy proteinuria (>1g/day), rapidly declining kidney function, or severe histopathological findings—immunosuppressive therapy becomes essential. Corticosteroids such as prednisone are commonly prescribed, sometimes in combination with other agents like mycophenolate mofetil, cyclophosphamide, or azathioprine. These drugs work by suppressing the overactive immune response believed to drive kidney inflammation.
Recent advances have also introduced targeted therapies for specific subtypes, especially in primary MPGN linked to complement system dysregulation. Drugs like eculizumab, a monoclonal antibody that inhibits complement activation, are being explored in selected cases, offering hope for improved outcomes in difficult-to-treat scenarios.
Prognosis and Long-Term Outlook
The long-term prognosis varies widely among individuals. Patients with mild histological changes and responsive symptoms often maintain good kidney function for years. However, those with frequent relapses, uncontrolled hypertension, or significant scarring (glomerulosclerosis) on biopsy face a higher risk of progressive kidney failure. Regular monitoring through blood tests, urine analysis, and blood pressure checks is crucial to adjust treatment and slow disease progression.
With early detection and personalized management plans, many people living with mesangial proliferative glomerulonephritis can achieve remission or stabilize their condition, preserving quality of life and minimizing complications.