Chronic pyelonephritis
If the susceptible factors such as urinary tract obstruction, malformation and low immune function persist, and the antibacterial treatment fails to completely control the submucosal inflammation or small abscess of the renal pelvis formed in the stage of acute pyelonephritis, small scars can be left, causing intrarenal obstruction, resulting in repeated attacks and slow prolongation of the disease.
Some people believe that autoimmunity may be involved in the pathogenesis of chronic pyelonephritis. Some patients found pathogenic bacteria in urine culture during acute pyelonephritis, but in the later chronic process, there was no pathogenic bacteria in urine culture, and the disease still gradually entered chronic pyelonephritis. It is speculated that after renal infection, the body produces antibodies against Escherichia coli, and the renal tissue has common antigenicity with these bacteria. After the pathogen disappears, the antibody continues to react with renal tissue antigen, resulting in renal damage. It has been found that there is a renal tubular antigen (Tamm Horsfall protein, called THP), which has the same antigenicity with Escherichia coli. The antibody against Escherichia coli can simultaneously resist the THP of renal tubular epithelial cells, which may be related to the occurrence of chronic inflammation of renal interstitium.
Recent studies have found that in any chronic kidney disease, once there is inflammatory cell infiltration in renal stroma, it may cause renal tissue injury through cytokine release, and the occurrence and development of chronic pyelonephritis may also be related to this.
The existence of L-type bacteria makes the treatment of pyelonephritis more difficult. These bacteria were first discovered by Lister, so they are named L-type bacteria. Its formation is due to the rupture of the cell membrane of the pathogenic bacteria under the treatment of antibiotics or the action of antibodies, complement and lysozyme, only the protoplasm remains, and it continues to survive hidden in the hypertonic area of renal medulla. General antibiotics can not completely kill it. When the living environment improves, L-type bacteria return to their original shape and continue to grow and reproduce, so as to rekindle pyelonephritis, resulting in the delay and refractory of the disease. According to the survey, L-type bacteria can be found in about 20% of chronic pyelonephritis with negative urine culture.