Taken together, these results show that immunoglobulins, including IgA, found in renal tissues may be secondary phenomena derived from systemic immune reactions rather than primary etiologic agents [34]. control the etiologic substances acting against renal cells; if this system fails, the disease progresses to end stage renal disease. Each renal disease has its characteristic pathologic lesions where immune cells and immune proteins, such as immunoglobulins and complements, are infiltrated. These immune cells and immune proteins may control the etiologic substances involved in renal pathologic lesions. Also, genetic renal diseases and cancers may originate from a protein deficiency or malfunctioning protein under the PHS. A unified pathogenesis for renal diseases, including acute glomerulonephritis, idiopathic nephrotic syndrome, immunoglobulin A nephropathy, genetic renal diseases such as Alport syndrome, and malignancies such as Wilms tumor and renal cell carcinoma, is usually proposed using the PHS hypothesis. Keywords:Acute glomerulonephritis, Alport syndrome, Idiopathic nephrotic syndrome, IgA nephropathy, Renal cell carcinoma, Wilms tumor == Introduction == Kidneys are constructed of a variety of different renal cell types. Each renal cell has its own cell-fate and characteristic cell-receptors and produces characteristic proteins that cannot be produced by other renal cells. Injury of a kind of renal cells impairs total renal function and induces an imbalance in total body health. Although the etiology or precise pathogenesis of most of renal RAF709 diseases remains unknown, it is obvious that there are etiologic substances associated with all acute or chronic kidney diseases. Each renal disease has its characteristic pathologic lesions. In renal biopsy findings, various immune cells and immune proteins, including immunoglobulins and match (C) proteins, are commonly seen. These immune cells and immune proteins originate in the host and are observed not only in renal disease lesions, but also in all pathologic lesions of nearly all human diseases. Therefore, it is believed RAF709 that immune cells and immune proteins may perform the same function in all pathologic lesions associated with the diseases. It has been proposed that this immune system of the host controls the etiologic substances harmful to host organ cells [1]. The author has proposed a unified model of immunopathogenesis for infectious diseases and infection-related immune diseases, includingMycoplasma pneumoniaepneumonia, influenza pneumonia, acute respiratory distress syndrome, and Kawasaki disease, based on the protein-homeostasis-system (PHS) hypothesis [15]. In this paper, a common mode of pathogenesis for kidney diseases from acute glomerulonephritis (AGN) to renal cell carcinoma based on the PHS hypothesis is usually proposed. == The protein-homeostasis-system hypothesis == Multicellular organisms are constructed of numerous kinds of cells whose main constituents are proteins. Furthermore, all biological activities, including embryonic development, biochemical reactions, physiological phenomena and pathologic processes, are performed by proteins that are encoded in genomic deoxyribonucleic acids (DNAs). Therefore, intracellular and systemic protein homeostasis should be managed for the health of the IL1R2 antibody host. Because every cell of an organism is usually separated and guarded by a cell membrane, communication across cells is required. The intercellular communications are performed by mainly proteins such as cytokines for maintenance of the healthy state of an organism. Thus, the healthy state of the organisms may be controlled by an interacting protein network, designated the PHS [1]. There are etiologic substances involved in all human diseases. The substances may have an affinity to certain target organ cells and they bind and signal the cells, since the eventual symptoms and indicators of all diseases result from cell injury at a molecular level. The etiologic substances may be of variable size and possess different biochemical RAF709 characteristics. They can be classified largely as substances originating from exogenous sources, such as pathogens and natural toxins from animals, plants, and environment factors, or RAF709 as substances originating from the host cells, such as damage (or danger)-associated molecular patterns (DAMPs) from hurt host cells and proteolytic enzymes and proinflammatory cytokines from activated immune cells. The etiologic substances are also classified into two parts: the protein substances and the non-protein substances. The protein substances, including previously named pathogenic proteins (PPs), may have a variety of sizes, similar RAF709 to monoamines, small peptides (310 amino acid residues) such as neuropeptides and peptide hormones, larger peptides (1230 amino acid residues) that can attach to T cell receptors (TCR), small proteins, and larger protein complexes. The non-protein substances that can be harmful to host cells are also variably sized, including elements such as real oxygen and carbon monoxide, drugs (chemicals), natural biochemicals such as vitamins and fatty acids, lipopolysaccharides, DNAs and ribonucleic acids (RNAs), and other large complexes (Fig. 1). It is proposed that this immune/repair system is usually a part of the PHS of the host, and that it controls these substances based on the size and biochemical house of the substances. Briefly, the adaptive immune system controls protein substances according to their size and biochemical.