IgA nephropathy, also known as Berger disease, is the most common primary glomerulonephritis and the most prevalent chronic glomerular disease in the world. It was first described morphologically by Dr. Jean Berger (nephrologist) and Nicole Hinglais (microscopist) in 1968 by electron microscopy. Later, immunofluorescence microscopy was used to show more specific findings associated with the disease, such as deposits of IgA in the mesangial matrix and its subsequent proliferation, types of immunoglobulins, and complement. The hallmark of the disease is the deposition of IgA in the glomerular mesangium, causing progressive kidney disease in a majority of patients. Because gross hematuria often follows an episode of upper tract respiratory infection, IgA nephropathy is also called synpharyngitic glomerulonephritis. Other names used are IgA nephritis, IgA-IgG nephropathy, nephropathy with mesangial IgA, and IgG deposits. Major clinical risk factors for progression are hypertension, proteinuria, and reduced GFR; whereas, microscopic hematuria is not a significant risk factor for the progressive loss of renal function. The Oxford classification involves scoring based histologic findings, including mesangial hypercellularity, endocapillary proliferation, segmental glomerulosclerosis, tubular atrophy, or interstitial fibrosis.[1][2][3]