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Apostematous pyelonephritis.
Last reviewed: 04.07.2025
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Causes apostematous pyelonephritis.
There are four pathogenetic stages leading to the development of apostematous nephritis.
- Recurrent short-term bacteremia. Microorganisms can enter the blood via pyelolymphatic and pyelovenous reflux from extrarenal foci of infection located in the urinary system. A small amount of infection does not lead to the development of sepsis. Bacteria die, and their decay products are excreted in the urine. In this case, the membrane of the glomerular hemocapillaries is damaged, which becomes permeable to microorganisms.
- With repeated entry of bacteria into the blood, some of them can pass through the membrane and enter the lumen of the capsule, and then into the lumen of the first-order convoluted tubule. If the outflow through the intrarenal tubules is not impaired, the process can be limited to the appearance of bacteriuria.
- In case of intrarenal urine stasis or slowing of the outflow through the tubules (obstruction of the urinary tract, relative dehydration of the body), microorganisms that have entered the lumen of the glomerular capsule and the first-order convoluted tubule begin to multiply rapidly. Despite contact with foci of infection, the epithelium and basement membrane are not damaged in these sections.
- As they move along the convoluted tubule, the multiplied microorganisms enter the urine, which is an unfavorable environment for them. Massive bacterial aggression against the relatively weakly protected cells of the tubular epithelium begins. At the same time, a violent but delayed leukocyte reaction occurs, accompanied by the penetration of a large number of leukocytes into the lumen of the tubules. The epithelial cells disintegrate and die. The basement membrane ruptures in many places. The heavily infected contents of the second-order convoluted tubule penetrate into the interstitial tissue of the kidney. If the microflora is virulent enough and the body's defenses are weakened, the primary peritubular infiltrates become suppurative. The pus is localized in the superficial layers of the renal cortex, since this is where most of the second-order convoluted tubules are located. The abscesses are small (peritubular infiltrates cannot reach large sizes), there are many of them (massive invasion of infection occurs through a significant number of glomeruli). They are poorly delimited by a leukocyte and connective tissue shaft. Due to insufficient isolation, significant resorption of purulent inflammation products is observed. This can lead to both local (acute degeneration, up to necrosis of the tubular epithelium) and general disorders caused by acutely developed infectious-septic toxemia. Among the general disorders, changes in the function of the cardiovascular, nervous, respiratory systems, and liver come to the fore. Secondary (toxic-septic) degenerative changes in the contralateral kidney are possible, up to total necrosis of the tubular epithelium and cortical necrosis, leading to the development of acute renal failure. With a protracted course of apostematous nephritis, other manifestations of the pathological process can be observed. With a satisfactory protective reaction and normal virulence of the flora, individual apoaemes merge, are delimited by a denser cellular, and then connective tissue shaft, turning into abscesses. At the same time, the fibroplastic reaction intensifies. The connective tissue of the kidney grows, coarsens. Focal infiltrates consisting of lymphocytes and plasma cells appear in it. The intima of many intrarenal arteries thickens. Some veins thrombose. As a result, zones of relative ischemia of the renal parenchyma may occur. In other cases, the inflammatory process spreads to the entire connective tissue stroma of the organ, which is subject to diffuse massive infiltration by polymorphonuclear leukocytes. This is why severe changes occur in the intrarenal vessels (arterial thrombosis) with the formation of local ischemia zones. Superinfection can often lead to the development of a renal carbuncle against the background of apostematous nephritis.
The kidney affected by apostematous nephritis is enlarged, blue-cherry or blue-purple in color. Its fibrous capsule is thickened, the perirenal fat capsule is edematous. After removing the capsule, the surface bleeds. Multiple foci of inflammation are visible on it, looking like pustules 1-2.5 mm in diameter, located singly or in groups. With a large number of pustules, the kidney becomes flaccid (due to edema and dystrophy of the parenchyma). Small pustules are visible not only in the cortex, but also in the medulla (in rare cases, they are contained only in the medulla.)
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Symptoms apostematous pyelonephritis.
Symptoms of apostematous nephritis largely depend on the degree of disturbance of urine passage. In hematogenous (primary) apostematous nephritis, the disease manifests itself suddenly (often after hypothermia or overwork from an intercurrent infection). The disease begins with a sharp increase in body temperature (up to 39-40°C or more), which then quickly decreases; severe chills, profuse sweating. Symptoms of severe intoxication appear: weakness, tachycardia, headache, nausea, vomiting, adynamia, decreased blood pressure. On the 5th-7th day, pain in the lumbar region intensifies, which at the beginning of the disease is dull. This is explained by the involvement of the fibrous capsule of the kidney in the process or the rupture of pustules.
Usually, from the very beginning of the disease, painfulness is determined upon palpation of the corresponding area, an enlarged kidney. In primary apostematous nephritis, the process can be bilateral, but the disease does not always begin simultaneously on both sides. There may be no changes in the urine at first. Later, leukocyturia, proteinuria, true bacteriuria, microhematuria are detected. The blood picture is characteristic of sepsis: hyperleukocytosis, a shift in the blood formula to the left, toxic granularity of leukocytes, hypochromic anemia, increased ESR, hypoproteinemia.
With a protracted course, the pain in the kidney area increases, rigidity of the muscles of the anterior abdominal wall on the affected side and symptoms of peritoneal irritation appear. Infection through the lymphatic tract can penetrate into the pleura and cause the development of exudative pleurisy, empyema. Septicemia, septicopyemia occur. Extrarenal foci of purulent inflammation can be observed - in the lungs (metastatic pneumonia), in the brain (brain abscess, basal meningitis), in the liver (liver abscess) and other organs. Acute renal failure and liver failure develop, jaundice occurs.
Apostematous nephritis, if not treated in a timely manner or incorrectly, can lead to urosepsis.
Secondary apostematous nephritis, unlike primary, usually begins 2-3 days (sometimes later) after an attack of renal colic. Sometimes it develops against the background of chronic obstruction of the urinary tract, as well as soon after surgery on the kidney or ureter for urolithiasis, after resection of the bladder, adenomectomy. Most often, the process appears when the postoperative period is complicated by obstruction of the urinary tract, urinary fistula of the kidney or ureter. The disease begins with chills and increased pain in the lumbar region. Subsequently, primary and secondary apostematous nephritis proceed almost identically.
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Where does it hurt?
Forms
A distinction is made between primary and secondary acute purulent pyelonephritis. Primary acute purulent pyelonephritis occurs against the background of a previously unchanged kidney, secondary - against the background of an existing disease (for example, urolithiasis). In case of obstruction of the urinary tract, the process is unilateral, in case of hematogenous origin - bilateral.
Diagnostics apostematous pyelonephritis.
Diagnosis of apostematous nephritis is based on the analysis of anamnestic data, clinical signs, results of laboratory, X-ray and radiological examination methods. The level of leukocytes in the blood taken from the finger and both lumbar regions is compared (leukocytosis will be higher on the affected side). On the general radiograph of the lumbar region, the shadow of the affected kidney is enlarged, the contour of the lumbar muscle on this side is absent or smoothed, and a curvature of the spinal column towards the affected organ is noted. Due to inflammatory edema of the perirenal tissue, a rim of rarefaction is visible around the kidney. With the development of the pathological process in the pelvis or ureter, a shadow of a urinary stone is observed. Excretory urography is informative. There is no mobility of the kidney during breathing on urograms. Urinary function is reduced or absent, the intensity of the shadow of the contrast agent secreted by the affected kidney is low, the organ is enlarged, the second-order calyces are not contoured or are deformed. Kidney enlargement can be detected using a tomogram and ultrasound. The following symptoms of apostematous pyelonephritis are revealed during an echographic examination:
- hypoechoic foci in the parenchyma with initial dimensions of up to 2-4 mm:
- thickening of the cortex and medulla of the kidney:
- increased echogenicity of the perirenal tissue:
- capsule thickening up to 1-2 mm:
- deformation of the cups and pelvis;
- thickening of the walls of the renal pelvis.
Dopplerography reveals local depletion of the vascular pattern, especially in the cortical layer.
Dynamic scintigraphy reveals a violation of vascularization, secretion and excretion. The obstructive type of renogram indicates a pathological process in the kidney.
When performing spiral CT, it is possible to obtain the following signs of the disease:
- non-uniform decrease in kidney density;
- thickening of the renal parenchyma.
Primary apostematous nephritis is differentiated from infectious diseases, subphrenic abscess, acute cholecystopancreatitis, acute cholangitis, acute appendicitis, acute pleurisy.
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Treatment apostematous pyelonephritis.
Treatment of apostematous nephritis involves emergency surgery. The kidney is exposed by subcostal lumbotomy, then decapsulated. Abscesses are opened. The retroperitoneal space is drained, and if the passage of urine is impaired, its free outflow is ensured by applying a nephrostomy. Renal drainage is maintained until the patency of the urinary tract is restored, the acute inflammatory process is eliminated, and kidney function is normalized.
Recently, internal drainage of the kidney by installing a stent has been increasingly used. Most urologists perform drainage of the renal pelvis, both in primary and secondary apostematous nephritis. However, a number of urologists do not drain the kidney in primary apostematous nephritis. As experience shows, nephrostomy drainage installed during surgery does not function with normal urine outflow after surgery. Urine is discharged naturally. In case of a bilateral severe process, drainage of the kidney is mandatory. In the postoperative period, antibacterial and detoxifying therapy are carried out, and general disorders are corrected. After the acute inflammation subsides, treatment of apostematous nephritis is carried out according to the scheme used for chronic pyelonephritis.
In case of total pustular kidney damage in elderly patients with severe intoxication and good function of the opposite kidney, it is recommended to perform nephrectomy immediately. However, due to the fact that in primary apostematous pyelonephritis the possibility of damage to the second kidney is not excluded, indications for nephrectomy should be sharply limited. Organ-preserving surgery, if performed in a timely and correct manner, with adequate postoperative treatment, provides a satisfactory result.
Unfortunately, sometimes the operation is too late. It should be remembered that intensification of antibacterial therapy without combined action on the local focus does not give the expected result. In such a case, early surgical treatment of apostematous nephritis should be recommended.
Forecast
Bilateral apostematous pyelonephritis has an unfavorable prognosis, with mortality reaching 15%. The possibility of developing late severe complications after organ-preserving surgeries (frequent exacerbations of chronic pyelonephritis, nephrogenic arterial hypertension, shrinkage of the operated kidney, stone formation, etc.) dictates the need for lifelong active medical examination of patients.