**1. Introduction**

A wide variety of bacterial infection-related renal diseases are known, among which the most common is acute kidney injury (AKI) [1], which occurs as part of multiple organ failure. Changes in hemodynamics and cytokine expression are thought to be involved in the pathogenesis of AKI.

Bacterial infections also cause renal injury, partly through immune mechanisms. For example, glomerulonephritis (GN) can develop following streptococcal upper respiratory tract or skin infections with a latent period of approximately 10 days. As streptococcal infections are usually cured when GN is diagnosed and there is a distinct infection-free latent period, the GN has been referred to as poststreptococcal acute glomerulonephritis (PSAGN) [2–4].

In previous years, most cases of AGN were PSAGN in children; however, probably owing to the improvement of living environments and the adequate usage of antibiotics, the incidence of PSAGN has been decreasing, particularly in developed countries [4]. Whereas PSAGN is still the most common cause of pediatric AGN, adult AGN cases have been increasing, and those associated with non-streptococcal infections, particularly infections by *Staphylococcus aureus*, are now as common as PSAGN [5]. Thus, a major shift in the epidemiology of AGN has occurred. In Japan, cases of PSAGN, which accounted for more than two-thirds of AGN cases in the 1970s, decreased to about 30% after the 1980s, whereas AGN cases associated with *S. aureus* infections reached 30% in the 1990s [6].

Furthermore, in adult AGN patients, the infection is usually still present at the time when GN is diagnosed. Based on these backgrounds, instead of "postinfectious AGN", the disease concept of infection-related glomerulonephritis (IRGN) has recently been proposed [5]. Notably, whereas in most patients, PSAGN resolves without any specific therapy, the prognosis of patients with IRGN is poor, and older patients, particularly those with an immunocompromised background, such as diabetes mellitus, malignancies, or alcoholism, are reported to be at high risk [7]. Controlling the underlying infection and managing complications are essential for the treatment of IRGN, and immunosuppressive therapy is generally not recommended. However, the prompt diagnosis of IRGN is often difficult because specific diagnostic biomarkers have not yet been identified.

We herein present an overview of our recent understanding of the pathogenesis of bacterial IRGN. Accumulated data suggest that the disease concept of bacterial IRGN can be further expanded, and glomerular deposition of nephritis-associated plasmin receptor (NAPlr), originally considered to be a candidate nephritogenic protein for PSAGN [8] and related plasmin activity [9], can be used as general diagnostic biomarkers of bacterial IRGN. Although infections of various viruses, mycobacteria, fungi, or protozoa are also known to cause IRGN [1], they are not within the scope of this article.
