The etiology of most chronic nephritis is not clear. Acute streptococcal infections with nephritis that persist for more than 1 year can turn into chronic glomerulonephritis. However, most chronic nephritis does not result from acute nephritis. Other bacterial and viral infections, especially hepatitis B virus infection, can also cause chronic nephritis. Because chronic nephritis is not a separate disease, its pathogenesis varies. Most of them are immune complex diseases, which can be caused by the deposition of circulating soluble immune complexes in the glomerulus, which can be formed by antigens (intrinsic glomerular antigens or exogenous implanted antigens) and antibodies in the glomerulus in situ, activating complement and causing tissue damage. Alternatively, immune complexes may be used to activate complement through a “bypass system” of bacterial toxins and metabolites deposited locally in the glomerulus, resulting in a series of inflammatory reactions leading to glomerulonephritis. Non-immune mediated kidney damage may also play an important role in the development and progression of chronic nephritis. According to the present findings, this non-immune mechanism may include the following factors: (1) glomerulopathy causing intrarenal arteriosclerosis; (2) glomerular damage caused by compensatory changes in renal hemodynamics; (3) hypertensive effects on glomerular structure and function; (4) super-negative charge state of the glomerular thylakoid membrane.