Infection-associated glomerulonephritis is divided into three main categories according to the source of infection, bacterial infections, viral infections, fungal and protozoal infections resulting in glomerulopathies. I. Bacterial infection-associated glomerulonephritis 1. post-streptococcal infection nephritis Post-streptococcal infection nephritis mainly occurs in children and adolescents, secondary to infection with strains of streptococci in the pharynx or skin (pustulosis), with clinical manifestations mostly of acute nephritis syndrome and good prognosis. The etiological spectrum of post-infectious glomerulonephritis has changed in the last decade. In developed countries, the incidence of nephritis after acute streptococcal infection has gradually decreased. Recent series have shown that acute nephritis due to streptococcal infection is only 28-47%, while Staphylococcus aureus or Staphylococcus epidermidis was isolated in 12-24% of cases and Gram-negative bacteria in 22% of cases. Atypical post-infectious glomerulonephritis mostly involves immune-compromised adults, such as patients with alcoholism, diabetes mellitus and drug addiction. While typical acute post-streptococcal nephritis in children tends to resolve spontaneously within a few weeks, the prognosis for post-infectious glomerulonephritis in immunocompromised adults is poor, with less than 50% of patients found to be in complete remission at long-term follow-up. Diagnostic renal biopsy pathology is required when the diagnosis is doubtful, or in order to assess prognosis and determine treatment options. Typical renal pathology presents as acute intracapillary proliferative glomerulonephritis with granular immune complex deposition in the thylakoid region and capillary loops. The symptoms of acute nephritis syndrome usually last less than 2 weeks. Less than 4% of post-streptococcal infections in children present with nephritis as massive proteinuria and occasionally acute renal insufficiency with crescent formation. The prognosis for the acute phase is excellent in pediatric patients, whereas mortality in older patients can be as high as 20%. Although the long-term prognosis of nephritis after streptococcal infection remains controversial, with a 15-year follow-up finding an incidence of end-stage renal disease (ESRD) of only 1%, the prognosis for older patients with persistent proteinuria is poor. The current treatment for streptococcal infections is still penicillin (or erythromycin in case of penicillin allergy) is preferred to clear the causative organism, reduce the formation of immune complexes, and prevent transmission of streptococci between relatives and contacts. When the immune complexes formed after streptococcal infection have led to glomerular damage, the application of antibiotics is of little help in nephritis itself. Patients with clinical manifestations of severe hypertension and congestive heart failure (mainly seen in adults) require hospitalization, and hypertension and edema mostly improve with symptomatic treatment with diuresis. Adult patients with persistent abnormal urinalysis for >6 months, especially with urinary protein >1g/d, similar to other glomerular diseases presenting as proteinuria, require ACEI or ARB therapy. Shock therapy with intravenous methylprednisolone may be considered for the treatment of patients presenting with acute and crescentic nephritis, although there is no evidence from randomized controlled trials (RCTs). 2. Infective endocarditis-associated glomerulonephritis With the widespread use of antibiotics and changes in prevalence, the natural progression of infective endocarditis-associated glomerulonephritis has also changed. In the United States, infective endocarditis is diagnosed at 40 cases per million population per year and is increasingly common in the elderly population and in those without underlying cardiac disease. Intravenous drug use, prosthetic heart valve replacement, and structural changes in the heart are also high risk factors for the disease. Staphylococcus aureus has replaced Streptococcus aureus as the main causative agent of infective endocarditis. The incidence of S. aureus endocarditis-associated glomerulonephritis ranges from 22% to 78%, with the highest risk in the intravenous drug-taking population. Typical pathology on renal biopsy shows focal segmental proliferative glomerulonephritis, often with focal crescent formation. Some patients present with diffuse intracapillary proliferative lesions with or without crescent formation. The short-term prognosis of this type of nephritis is good and is associated with the use of highly targeted antibiotics for 4 to 6 weeks and rapid clearance of the infection site. 3, shunt nephritis Shunt nephritis is an immune complex-mediated glomerulonephritis caused by chronic infection at the shunt site after ventriculo-atrial (or jugular vein) shunt in patients with hydrocephalus. After ventriculo-ventricular vascular shunts for hydrocephalus, their renal disease manifests as microscopic hematuria and proteinuria, mostly at the nephrotic level, occasionally with elevated blood creatinine and hypertension, which may be accompanied by prolonged fever or signs of chronic infection. The typical pathology on renal biopsy is type 1 membranoproliferative glomerulonephritis with immunofluorescence of IgG, IgM and C3 granular deposits and electron-dense deposits in the thylakoid region and subendothelium on electron microscopy. If the infection is diagnosed and treated early, the kidney prognosis in shunt nephritis is good. The infection rate at the ventricular vascular shunt is 30%. 0.7-2% of these infections present as glomerulonephritis, most often 2 months to several years after shunt surgery. The pathogens of infection are usually Staphylococcus epidermidis and Staphylococcus aureus. Untimely antibiotic treatment due to delayed diagnosis and delayed removal of the drainage tube will result in poor renal prognosis. 2. Viral infection-associated glomerulonephritis 1. Hepatitis C virus (HCV) infection-associated glomerulonephritis HCV infection is a public health problem, with approximately 130 million to 170 million people infected worldwide. We are also a country with a high prevalence of hepatitis C at about 3%. Hepatitis C often causes extrahepatic symptoms including mixed cryoglobulinemia, abnormal lymphocyte proliferation syndrome and renal lesions. HCV infection involving the kidneys is most commonly accompanied by type 2 cryoglobulinemia. Clinical manifestations include proteinuria, microscopic hematuria, hypertension, and mild or moderate renal damage. The most common type of pathology on renal biopsy is type 1 MPGN. small- and medium-vessel renal artery vasculitis may be present simultaneously. Immunofluorescence usually shows IgM, IgG, and C3 deposits in the thylakoid region and capillary wall. Electron microscopy shows immune complexes visible under the endothelium and may have histology-like material as cryoglobulin deposits. In addition to MPGN, other types of glomerulopathies include IgAN, MN, post-infectious nephritis, thrombotic microangiopathy, FSGS, and fibrillary tentacle-like immune nephritis. Even patients with liver disease without clinical and/or biological evidence of proteinuria and type 2 cryoglobulinemia (mixed polyclonal IgG, monoclonal IgM, RF-positive cryoglobulin) should be tested for HCV and HCV-mRNA, excluding hepatitis C virus infection. Similarly, patients with HCV infection should be tested annually for proteinuria, hematuria and renal function to clarify the presence of HCV-associated nephritis. Treatment of HCV-associated nephropathy is aimed at reducing or eliminating HCV replication and reducing the formation of immune complexes and deposition in the glomerulus (including cryoglobulins) due to HCV. There is a lack of evidence-based medical evidence and safe and effective drugs to treat HCV infection in patients with concomitant CKD. However, we can learn from the anti-HCV treatment for non-CKD population. At CKD stage 1 and 2, the antiviral treatment regimen is the same as in the general population, with a combination of pegylated interferon and ribavirin antiviral therapy, and the dose of ribavirin is gradually increased according to the patient’s tolerance. For patients with CKD stages 3, 4 and 5 who are not on dialysis, pegylated interferon is used as monotherapy and the dose is adjusted according to the level of renal function. Ribavirin is mainly excreted by the kidneys and tends to accumulate in red blood cells, leading to hemolytic anemia, and is not recommended at GFR <50 ml/min. Concomitant HCV infection and mixed cryoglobulinemia (IgG/IgM), proteinuria or progressive nephropathy with nephrotic ranges, or acute recurrent cryoglobulinemia may be considered with antiviral therapy along with methylprednisolone and/or immunosuppressive agents, plasma exchange, etc. The best long-term prognostic indication for HCV-associated nephritis is sustained negative virologic testing (defined as HCV-mRNA conversion) 6 months after cessation of antiviral therapy. 2. Hepatitis B virus (HBV) infection-associated nephritis Approximately one-third of the world's population has previous or current serologic evidence of hepatitis B virus infection, and 350 million people have chronic infection, making HBV one of the most common human pathogens. Whether patients with concomitant hepatitis B virus infection may develop nephropathy is currently unpredictable. Types of hepatitis B virus-associated nephritis include: membranous nephropathy, membranoproliferative nephritis, focal segmental glomerulosclerosis, and IgA nephropathy. Membranous nephropathy is the most common type of hepatitis B virus-mediated nephritis, especially in children, with a high rate of spontaneous remission and a good prognosis. Hepatitis B virus-mediated nephritis in adults, is usually progressive. Patients with nephrotic syndrome and abnormal liver function have a worse prognosis. Current research evidence demonstrates the effectiveness of applying interferons or nucleoside analogues for the treatment of hepatitis B virus (HBV) infection. For example, lamivudine, adefovir, entecavir, tipifovir and tenofovir have been evaluated and their antiviral efficacy has been confirmed in clinical data or randomized controlled studies with long-term follow-up (2 to 5 years). However, there is no data demonstrating the efficacy of these anti-HBV-infective agents in HBV-associated nephritis, and there are no RCT studies for the treatment of hepatitis B virus-mediated nephritis, so evidence-based treatment recommendations or guidelines have not been established. As with clinical practice guidelines for the general population, patients with HBV-associated nephritis should follow standard clinical practice guidelines for the treatment of HBV infection, with antiviral medications dosed according to renal function status. However, there is no rigorous evidence-based medical evidence on whether to add glucocorticoids and immunosuppressive therapy for patients with massive proteinuria. Only a few, single-center, observational clinical studies have concluded that in the absence of HBV replication, glucocorticoids and/or immunosuppressive therapy can be added for short periods of time and in small doses, and that HBV replication indicators should be closely monitored during treatment. 3. human immunodeficiency virus infection-associated nephritis (HIVAN) Approximately 5 million people worldwide are infected with HIV each year. nephropathy is a relatively common complication in patients with AIDS. HIV-associated nephropathy is the most common cause of HIV in patients with CKD, and is particularly common in Africa. If left untreated, HIV-associated nephropathy quickly progresses to end-stage renal disease. Renal pathology often presents as collapsed focal segmental glomerulosclerosis with microcystic tubular changes. In HIV patients with proteinuria or decreased renal function, the prognosis is poor or death is increased. data from RCTs suggest that Highly Active Antiretroviral Therapy (HAART) is beneficial in protecting and improving renal function in HIV patients. Therefore KDIGO clinical guidelines recommend that all HIV-infected patients should be initiated on antiretroviral therapy (1B) regardless of CD4 count. With HAART treatment, HIV viral load decreases and renal function improves; HIV viral load increases and renal function deteriorates. HIV-1 replication has been shown to be an independent risk factor for chronic impairment of renal function in the progression of HIV disease. Third, protozoan infection-associated glomerulonephritis Schistosoma, filarial parasites, Plasmodium and other protozoan and helminthic infections can also cause different types of glomerulonephritis. Schistosomiasis is a chronic infectious parasitic disease that can be transmitted by both humans and animals. It is common in Asia, Africa and South America. The life history of schistosomes is complex. Adult worms are parasitic in the blood of the mesenteric and portal veins of humans, cattle, pigs or other mammals. There are five types of glomerular pathology in schistosomiasis. type 1 is the earliest and most common type of injury and is characterized clinically by asymptomatic proteinuria and pathology characterized by deposition of IgM, C3 and schistosome antigens in the thylakoid region, with light microscopy of thylakoid hyperplasia, mild lesions, focal or diffuse hyperplasia. type 2 lesions are more common and mostly present as a nephrotic syndrome with deposition of C3 and schistosome antigens in the capillaries and glomerular Type 3 clinical manifestations include proteinuria, hypertension, renal insufficiency, and pathology showing glomerular thylakoid capillary lesions with deposits of IgG, C3, and in advanced stages IgA. type 4 is a focal segmental lesion with deposits of IgG, IgA, and IgM, manifested by massive proteinuria, hypertension, and progressive decline in renal function. type 5 progresses to amyloidosis with proteinuria, abnormal renal function, and much less elevated blood pressure. Patients with new-onset, worsening nephrotic syndrome tend to have Salmonella co-infection. The pathology of filarial nephritis manifests as diffuse glomerular lesions, including MPGN, MCD and chronic sclerosing nephritis, collapsed FSGS; microfilariae can be found in the lumen of small arteries, glomeruli, peritubular capillaries, tubules and interstitium. Plasmodium infections usually cause acute kidney injury or proliferative glomerulonephritis, including MN and MPGN. Treatment of glomerulonephritis due to various protozoan and helminthic infections is first and foremost with an adequate dose and sufficient course of antiparasitic drugs to eradicate the pathogenic microorganisms and help prevent or reduce renal pathology. Glucocorticoids or immunosuppressants are not recommended for the treatment of protozoal infectious glomerulonephritis. In the treatment of infection-associated glomerulonephritis, the first and most important thing is to choose a highly targeted anti-infective therapy according to the pathogenic organism and to adjust the dose and course of anti-infective drugs according to the status of renal function; in the presence of massive proteinuria, or nephrotic syndrome, if there is no active infectious lesion or viral replication in the clinical judgment In case of massive proteinuria or nephrotic syndrome, if there is no active infection or viral replication, glucocorticoids and/or immunosuppressive drugs can be applied in a timely and appropriate manner according to the degree of renal lesions.