What Is Endocapillary Proliferative Glomerulonephritis?

Endocapillary proliferative glomerulonephritis (EPGN) is a histopathological diagnosis defined by specific microscopic findings in kidney tissue. Under light microscopy, physicians observe proliferation of both endothelial cells within the glomerular capillaries and mesangial cells. This distinctive cellular overgrowth disrupts normal filtration structures and is often accompanied by clinical signs of acute kidney injury.

Key Diagnostic Features of EPGN

One of the hallmark characteristics of this condition is immune complex deposition, which can be detected through immunofluorescence testing. Typically, deposits of immunoglobulin G (IgG) and complement component C3 are found along the glomerular basement membrane. These immune markers suggest an underlying immune-mediated process triggering inflammation.

Electron microscopy further confirms the diagnosis by revealing subepithelial electron-dense deposits that appear as "hump-like" structures. These humps represent aggregated immune complexes lodged between the podocytes and the basement membrane, contributing to glomerular damage and proteinuria.

Primary Clinical Association: Acute Glomerulonephritis

In most cases, endocapillary proliferative glomerulonephritis corresponds to acute glomerulonephritis, particularly post-infectious forms such as those following streptococcal infections. When a patient presents with symptoms like hematuria, hypertension, edema, and reduced kidney function, and biopsy reveals EPGN, the clinical diagnosis typically points to acute glomerulonephritis.

It's important to note: while acute glomerulonephritis usually shows EPGN on biopsy, not all cases of EPGN are due to typical post-infectious causes. The pathological pattern is a clue, not a final diagnosis—further investigation is essential.

Differential Diagnoses and Other Possible Causes

Beyond acute glomerulonephritis, several other systemic conditions can manifest with identical or similar histological features. One notable example is cryoglobulinemia, an immune complex-mediated vasculitis often associated with hepatitis C, autoimmune diseases, or lymphoproliferative disorders. In such cases, circulating cryoglobulins deposit in the glomeruli, leading to endocapillary proliferation and renal impairment.

Less Common but Important Considerations

Rare diseases such as lupus nephritis (particularly Class III or IV), IgA nephropathy during acute flares, or even certain bacterial endocarditis-related immune complex glomerulonephritis may also present with EPGN patterns. Therefore, when EPGN is identified, clinicians must perform a comprehensive workup—including serological tests, viral panels, and autoimmune markers—to rule out secondary causes.

Accurate diagnosis hinges on integrating clinical presentation, laboratory data, and histopathological findings. Treating the underlying cause—whether infection, autoimmunity, or paraproteinemia—is crucial for improving long-term renal outcomes.