Pyelonephritis pathological anatomy. Pyelonephritis

Pyelonephritis- an infectious disease in which the renal pelvis, its calyces and the substance of the kidneys are involved in the process with a predominant lesion of the interstitial tissue. In this regard, pyelonephritis is interstitial (interstitial) nephritis. It can be one- or two-sided.

Intermediate nephritis- a broader concept than pyelonephritis. It denotes, firstly, a type of kidney inflammation of any etiology with a predominant interest in the interstitium, and secondly, a special disease in which this inflammation is its only and main expression (for example, phenacetin interstitial nephritis). Based on clinical and morphological data, acute and chronic pyelonephritis are distinguished.

Pyelonephritis usually has a recurrent course in the form of attacks of acute pyelonephritis. The pathological anatomy of acute and chronic pyelonephritis is different. In acute pyelonephritis, at the height of the disease, plethora and leukocyte infiltration of the pelvis and calyces, foci of necrosis of the mucous membrane, and a picture of fibrinous pyelitis are detected. The interstitial tissue of all layers of the kidney is edematous, infiltrated with leukocytes, multiple miliary abscesses and hemorrhages are common.

Diffuse leukocyte infiltration of the interstitial tissue of the kidney.

The tubules are in a state of dystrophy, their lumens are clogged with cylinders of desquamated epithelium and leukocytes. The process is focal or diffuse in nature. The kidney(s) are enlarged, its tissue is swollen, full of blood, the capsule is easily removed. The cavities of the pelvis and calyces are dilated, filled with cloudy urine or pus, their mucous membrane is dull, with areas of hemorrhage.

On the section, the kidney tissue is variegated, yellow-gray areas are surrounded by an area of plethora and hemorrhage, abscesses are found. Chronic pyelonephritis is characterized by a diversity of changes, since sclerotic processes, as a rule, are combined with exudative-necrotic ones.

On histological examination, changes in the pelvis and calyces are reduced to their sclerosis, lymphoplasmacytic and leukocyte infiltration, polyposis of the mucous membrane and metaplasia of the transitional epithelium into stratified squamous epithelium. In the kidney tissue, chronic interstitial inflammation is expressed with the proliferation of connective tissue, encapsulation of abscesses and macrophage resorption of purulent-necrotic masses. The tubules undergo deep degeneration and atrophy.

The surviving tubules become sharply stretched, their epithelium is flattened, the lumens are filled with thick colloid-like contents, and the kidney resembles the structure of the thyroid gland (“thyroid kidney”). The damage to the glomeruli is less pronounced compared to the tubules. Glomerulosclerosis is predominantly extracapillary in nature.

Arteries and veins undergo sclerosis. It should be emphasized that changes in renal tissue in chronic pyelonephritis are focal. Areas of interstitial inflammation, atrophy and sclerosis are surrounded by relatively preserved renal tissue, in which signs of regenerative hypertrophy can be found.

This feature of the process determines the characteristic appearance of the kidneys in chronic pyelonephritis: the sizes of the left and right kidneys are not the same, their surface is coarsely lumpy, the section shows fields of scar tissue, alternating with relatively preserved renal parenchyma, the pelvis is dilated, their walls are thickened and whitish.

At the end of chronic pyelonephritis, a pyelonephritic wrinkled kidney develops, which is characterized by uneven cicatricial wrinkling, tight adhesion of the kidney tissue to the capsule, sclerosis of the pelvis and pelvic tissue, and asymmetry of the process in both kidneys. These signs, although relative, make it possible to distinguish pyelonephrotic nephrocirrhosis from nephrosclerosis and nephrocirrhosis of other etiologies.

“Pathological anatomy”, A.I. Strukov

Based on clinical and morphological data, acute and chronic pyelonephritis is distinguished, which usually has a recurrent course in the form of attacks of acute pyelonephritis.

Etiology and pathogenesis. Pyelonephritis is an infectious disease. Its causative agents can be various infections (Escherichia coli, Enterococcus, Streptococcus, Staphylococcus, Proteus, etc.), but in most cases it is Escherichia coli. More often, microbes are introduced into the kidneys by an ascending route from the ureters, bladder, and urethra (urogenic ascending pyelonephritis). The urogenic rise of infection is facilitated by dyskinesia of the ureters and pelvis, increased intrapelvic pressure (vesicorenal and pyelorenal reflux), as well as reabsorption of the contents of the pelvis into the veins of the medulla of the kidneys (pyelovenous reflux). Ascending pyelonephritis often complicates those diseases of the genitourinary system in which the outflow of urine is obstructed (stones and strictures of the ureters, strictures of the urethra, tumors of the genitourinary system), so it often develops during pregnancy. Infectious agents can penetrate the kidney, including the pelvis, through the bloodstream (hematogenous descending pyelonephritis). This path of occurrence of pyelonephritis is observed in many infectious diseases (typhoid fever, influenza, tonsillitis, sepsis). Lymphogenous introduction of infection into the kidneys (lymphogenous pyelonephritis) is also possible; the source of infection in these cases is the large intestine and genitals.

For the development of pyelonephritis, the penetration of infection into the kidneys is not enough. Its occurrence is determined by the reactivity of the body and a number of local reasons that cause disruption of the outflow of urine and urinary stasis. The same reasons explain the possibility of a recurrent chronic course of the disease.

Pathological anatomy. Changes in acute and chronic pyelonephritis are different.

For acute pyelonephritis at the height of the disease, plethora and leukocyte infiltration of the pelvis and calyces, foci of necrosis of the mucous membrane, and a picture of fibrinous pyelitis are detected. The interstitial tissue of all layers of the kidney is swollen and infiltrated with leukocytes; Multiple miliary abscesses and hemorrhages are common. The tubules are in a state of dystrophy, their lumens are clogged with cylinders of deflated epithelium and leukocytes. The process is focal or diffuse in nature.

Bud(kidneys) are enlarged, the tissue is swollen, full of blood, the capsule is easily removed. The cavities of the pelvis and calyces are dilated, filled with cloudy urine or pus, their mucous membrane is dull, with areas of hemorrhage. On the section, the renal tissue is variegated, yellow-gray areas are surrounded by an area of plethora and hemorrhage, abscesses are found.

Chronic pyelonephritis is characterized by diversity of changes, since sclerotic processes, as a rule, are combined with exudative-necrotic ones. Changes in the pelvis and calyces are reduced to their sclerosis, lymphoplasmacytic infiltration, polyposis of the mucous membrane and metaplasia of the transitional epithelium into stratified squamous epithelium. In the kidney tissue, chronic interstitial inflammation is expressed with the proliferation of connective tissue, encapsulation of abscesses and macrophage resorption of purulent-necrotic masses. The tubules undergo dystrophy and atrophy. The preserved tubules are sharply stretched and the kidney resembles the thyroid gland in structure. Predominantly periglomerular and extracapillary glomerulosclerosis is expressed. Arteries and veins are sclerotic.

Changes in renal tissue in chronic pyelonephritis are focal in nature: areas of interstitial inflammation, atrophy and sclerosis are surrounded by relatively preserved renal tissue, in which signs of regenerative hypertrophy can be found. This ability of the process determines the characteristic appearance of the kidneys in chronic pyelonephritis: the sizes of the kidneys are not the same, their surface is coarsely lumpy, the section shows fields of scar tissue, alternating with relatively preserved renal parenchyma; the pelvis is dilated, their walls are thickened and whitish.

At the end of chronic pyelonephritis, a pyelonephritic wrinkled kidney or pyelonephritic wrinkled kidney develops. This is characterized by uneven cicatricial wrinkling, the formation of dense adhesions between the kidney tissue and the capsule, sclerosis of the pelvis and pelvic tissue, and asymmetry of the process in both kidneys. These signs, although relative, make it possible to distinguish pyelonephritic nephrosclerosis from nephrosclerosis and nephrocirrhosis of other etiologies.

Complications. In acute pyelonephritis, the progression of the purulent process leads to the fusion of large abscesses and the formation of a kidney carbuncle, the connection of purulent cavities with the pelvis (pyonephrosis), the transition of the process to the fibrous capsule (perinephritis) and perinephritis (paranephritis). Acute pyelonephritis can be complicated by necrosis of the pyramidal papillae (papilonecrosis), which develops as a result of the toxic effect of bacteria in conditions of urinary stasis. This complication of pyelonephritis occurs more often in patients with diabetes. Rarely, pyelonephritis becomes a source of sepsis. When the purulent process is limited during the scarring period, chronic kidney abscesses can form. In chronic pyelonephritis, especially unilateral, the development of nephrogenic arterial hypertension and arteriolosclerosis in the second (intact) kidney is possible. Bilateral pyelonephritic shrinkage of the kidneys leads to chronic renal failure.

Exodus. In acute pyelonephritis, the outcome is usually recovery. Its severe complications (pyonephrosis, sepsis, papillonecrosis) can cause death. Chronic pyelonephritis with kidney shrinkage often ends in azotemic uremia. With the development of nephrogenic arterial hypertension, death in chronic pyelonephritis is sometimes associated with the complications that occur with hypertension (cerebral hemorrhage, myocardial infarction, etc.).

PYELONEPHRITIS (pyelonephritis; grech, pyelos trough, vat + nephritis) - a nonspecific inflammatory process with predominant damage to the interstitial tissue of the kidney and its pyelocaliceal system.

Clinicians abandoned the term “pyelitis”, because there is no isolated lesion of the pelvis (renal pelvis, T.). Since in the initial stages of P. a picture of interstitial nephritis is morphologically observed (see), some urologists propose to designate such a disease by the term “interstitial nephritis”. However, despite the morphol, the identity of this form of nephritis and P., it is still more appropriate to use the term “pyelonephritis”, since it most correctly reflects the pathogenetic, morphological and clinical essence of the disease. In some cases, when the primary inflammatory focus occurs in the bladder, the term “cystopyelonephritis” is used.

There are acute and chronic P.

Statistics

P. is the most common kidney disease (see). Analysis of large pathological material presented by N. Dutz et al. (1968), showed that in 6-18% of all autopsies signs of hron were established. P. In women, P. is observed 2 times more often than in men. In 75% of cases, the disease occurs in women under the age of 40, in most cases during pregnancy. Elderly men become ill with P. more often than women; This is mainly due to impaired urodynamics due to prostate adenoma (see) and other diseases of the genitourinary system. Children most often become ill with P. under the age of 3 years, and girls are 3 times more likely than boys.

According to Ditscherlein (G. Ditscherlein, 1969), P. develops in 25.7% of people with diabetes. Almost 40% of patients suffering from kidney tuberculosis also experience pyelonephritis. And vice versa, it is possible that a tuberculosis focus may appear in a kidney previously affected by P. According to A.Ya. Yaroshevsky (1971), Shenet (D. Sclione) et al. (1974), in 9-10% of cases of glomerulonephritis (see), P. joins. In recent years, there has been an increase in cases of P.'s disease and its frequent atypical course. This is due not so much to improved diagnostics as to the sharply increased virulence of microorganisms as a result of their acquired resistance to antibiotics, as well as changes in the course of inf. process in the kidney due to suppression of immune reactions during antibiotic therapy, the presence of sensitization and superinfection in patients.

Classification

There are primary and secondary P. Primary P. is otherwise called uncomplicated, secondary - complicated, and some clinicians - obstructive. Primary P. is observed in 20%, secondary - in 80% of cases among all patients with P.

Primary P. is not preceded by any disorders of the kidneys or urinary tract; Secondary P. is based on organic or functional processes in the kidneys and urinary tract, which reduce the resistance of the kidney tissue to infection and disrupt the passage of urine. Depending on whether one or two kidneys are affected, P. is distinguished as unilateral and bilateral. According to the nature of the process, P. is divided into acute (serous and purulent), chronic and recurrent. Depending on the route of infection, P. is distinguished between hematogenous and urinogenic (ascending). In addition, P.'s course may have features associated with the patient's age, changes in his general physiological condition, the presence of another pathol, process; in this regard, they distinguish: P. in childhood (including in newborns), P. in elderly people, in patients with diabetes mellitus, glomerulonephritis, in patients with spinal cord damage, P. in persons with a kidney transplant (so called pyelonephritis of a transplanted kidney).

Etiology and pathogenesis

Many factors play a role in the occurrence and development of P., among which the type and nature of the infectious agent, the presence of changes in the kidney and urinary tract that contribute to the fixation of infectious agents in them and the development of the process, the routes of penetration of infectious agents into the kidney, and the general condition of the body are of particular importance. , its immunobiol. reactivity.

The causative agents of P. are predominantly Escherichia coli, staphylococcus, Proteus, representatives of the genus Klebsiella, Pseudomonas, less commonly Enterococcus, Streptococcus; there is often a mixed flora.

In patients with acute P., a pure culture of Escherichia coli is determined in the urine in 49%, mixed flora (Escherichia coli, staphylococcus, Proteus and Enterococcus) in 35%, staphylococcus in 10%, staphylococcus and streptococcus in 5% of cases. Patients have chronic P. pure culture of Escherichia coli is found in 25%, mixed (Escherichia coli, staphylococcus, streptococcus, Proteus, etc.) - in 68%, only coccal flora - in 6% of cases. It has been proven that the species composition of the microflora in P. changes as a result of antibacterial therapy (microorganisms that were almost never encountered before are often sown); The biol, the properties of the pathogens have also changed, acquiring etiol, the value of the L-form of bacteria, especially when hron occurs. P. and its exacerbations.

The primary foci of infectious agents, from where they can be introduced into the kidney, are any purulent-inflammatory processes (dental caries, pneumonia, furunculosis, mastitis, cholecystitis, osteomyelitis, inflammatory foci in the genitourinary system, etc.).

There are the following ways of penetration of infectious agents into the kidney: hematogenous, along the wall of the ureter, along its lumen in the presence of vesicoureteral reflux (see).

In elucidating the mechanism of penetration of infectious agents into the kidney tissue and the development of the inflammatory process in it, the doctrine of renal pelvic reflux played a large role.

For pathogens to penetrate from the pelvis into the renal parenchyma, two conditions are necessary: a violation of the integrity of the urothelium in the fornicale zone of the calyx and an increase in intrapelvic pressure, which is a consequence of a violation of the outflow of urine - vesicoureteral reflux. Penetration of infection into the renal parenchyma can occur without damage to the fornix urothelium - through the canalicular route with subsequent transfer of inf. agent from the tubules into the interstitial tissue.

Infection of the kidney through the hematogenous route occurs as follows: microorganisms from the pelvis penetrate the general blood flow through the venous or lymph vessels of the kidney, and then, returning through the arterial system to the same kidney, cause an inflammatory process in it. Sclerosis of the adipose tissue of the renal sinus (renal sinus, T.), caused by intermittent pyelosinus refluxes, is of significant importance in P.'s development. The resulting pedunculitis (see) leads to lymph and venous stasis in the kidney parenchyma. Venous congestion adversely affects lymphatic drainage from the kidney and contributes to impaired permeability of the vascular wall with subsequent penetration of microorganisms into the tissue. The hematogenous route occurs not only in the presence of inf. focus in distant organs and tissues, but also when it is localized in the genitourinary system. Microorganisms from the organs of this system can penetrate through the lymphatic vessels into the general circulation and enter the kidney. Penetration into the kidney inf. started in the lymph, vessels from the intestines has not been proven.

Primary bacterial P. may be preceded by abacterial interstitial nephritis (see). Combinations of allergic, chemical, physical and bacterial factors create a unique wedge, manifestations of the disease. The pathogenetic factors of interstitial nephritis include the adverse effects of certain medications and their metabolites (sulfonamides, anti-tuberculosis drugs, vitamin D in high doses, phenacetin, analgesics). P., which is preceded by abacterial interstitial nephritis, occurs mainly in adults. Kidney dysplasia contributes to P.'s development in children.

Functional and morphological changes in the urinary tract of a congenital and acquired nature, leading to disruption of urodynamics, starting from the nephron and ending with the urethra, have a significant role in P.’s development. In patients with impaired urinary passage, P. is observed 12 times more often, and predominantly purulent forms of acute P. develop.

Hron, P.'s course is largely due to immunopathology. process. Bacterial antigens, remaining in the kidney parenchyma for a long time after the disappearance of viable microbes, contribute to the progression of P.

Along with local factors, the weakening of the body’s defenses, hypovitaminosis, trophic disorders, neurohumoral disorders, diseases of the liver, vascular system, diabetes mellitus, gout, nephrocalcinosis, potassium deficiency, abuse of analgesics (phenacetin, etc.), and extrarenal lesions are important in the occurrence of P. inflammation (enteritis, tonsillitis, etc.), inflammatory processes of the genitourinary system.

Pathological anatomy

P. is characterized by focal and more often unilateral kidney damage. Even with bilateral damage, the degree of changes in different parts of the organ is not the same. Significant difficulties are presented by Gistol, the distinction between urinogenic and hematogenous P.

There are P. focal and diffuse. Macroscopically, the kidneys in focal acute P. do not have any specific changes; with diffuse damage, they can be swollen with a slightly expanded and flabby cortex and hyperemic mucous membrane of the pelvis.

In acute serous P., there is swelling of the stroma of the medulla and cortex, congestion of the microvasculature (color Fig. 1), dystrophic-necrobiotic changes in the epithelium of the proximal and distal tubules, and dilatation of their lumen. In areas of maximum tubuloegstelial lesions, the stromal exudate contains an admixture of polymorphonuclear leukocytes. The glomeruli remain intact.

With focal purulent P., peritubular or intratubular accumulations of polymorphonuclear leukocytes, cellular detritus and homogeneous protein masses are observed within several nephrons (tsvetn. Fig. 2 and 3). With diffuse purulent P., there may be destruction of the walls of the tubules (tubulorrhexis), and sometimes the capsule of the glomeruli (invasive glomerulitis) with the formation of urinary leaks.

In the lumen of the dilated tubules, protein-leukocyte casts and colonies of microbes are visible (color. Fig. 4). The progression of purulent inflammation can result in apostematous nephritis, an isolated abscess or carbuncle of the kidney, representing large areas of merging abscesses and foci of necrosis. Kidney carbuncle is often complicated by purulent paranephritis (print. Fig. 5). In patients with decompensated diabetes mellitus, P. may be complicated by necrosis of the pyramidal papillae (see Renal papilla necrosis).

P. is often preceded and accompanied by bacteriuria (see), its degree can reach 105 or more bacteria in 1 ml of urine. Bacteriuria is absent only when there is obstruction of the ureter or the formation of a closed (non-emptying) abscess in the kidney parenchyma. However, bacteriuria is not equivalent to P.

In the blood, the activity of lactate dehydrogenase, transaminase, leucine aminopeptidase, alkaline phosphatase increases, general proteolytic activity and the level of trypsin inhibitor increase. Trypsin-like activity increases in urine. An increase in the level of residual nitrogen, urea, and creatinine in the blood indicates bilateral kidney damage.

In severe cases of P., especially in the absence or slight leukocyturia, as well as indications of previous cystitis, it is necessary to examine the curvature of the spine and the upper urinary tract. For this purpose, survey radiography, excretory urography (see), ultrasound scanning, radioisotope renography (see Radioisotope renography), chromocystoscopy (see). Plain radiography allows you to determine the position and size of the kidneys, identify the shadows of radiopaque stones in the projection of the urinary tract, blurred contour of the psoas major muscle and the shadow of the kidney. Excretory urography reveals an increase in the size and intensity of the kidney shadow, limitation of its displacement during breathing, delay or absence of filling of the upper urinary tract with a contrast agent. With moderate urodynamic disorders, expansion of the upper urinary tract above the site of obstruction to the outflow of urine is characteristic. Urokinemography and fluoroscopy can reveal calyx dyskinesia. Infiltrative changes in the renal parenchyma lead to displacement of the calyces, compression and elongation of their necks, and protrusion of the outer contour of the kidney.

Purulent foci in the upper pole of the kidney lead to limited mobility of the diaphragm, the appearance of effusion in the pleural cavity, and a sharp limitation of the mobility of the affected kidney (Fig. 1).

Chromocystoscopy determines the patency of the urinary tract, and by reducing the color intensity of the urine secreted by the affected kidney, the degree of impairment of its function can be assessed. The absence of urine output from the mouth of the ureter is an indication for diagnostic and treatment. catheterization of the upper urinary tract (see Catheterization of the urinary tract). The discharge of purulent urine through a catheter under pressure indicates severe urostasis. The subsequent pyelourotherography helps clarify the nature and extent of kidney damage and determine the level and cause of urinary tract occlusion. In this case, it is necessary to drain the urinary tract (see Drainage).

Radiol, studies in acute serous P. reveal minor changes in reno- and scanograms. Deeper lesions of the parenchyma are accompanied by a slowdown and decrease in accumulation, and an increase in the half-life of the radionuclide.

With urostasis, the renogram curve has an ascending direction. Scanograms with dynamic scintigraphy show defects in radionuclide accumulation corresponding to foci of inflammation, especially extensive with renal carbuncle. Radioisotope cystourenography, voiding cystourethrography (examination during urination) can detect vesicoureteral reflux.

Differential diagnosis. Acute P. must be differentiated with necrosis of the renal papillae (see Renal papillae necrosis), in which there is a discharge of sequestered papillae or their fragments in the urine, more intense and constant hematuria. Destruction of the papilla is detected on pyelograms in the form of a defect in the filling of the calyx, corresponding in shape to the sequestrum, penetration of the radiopaque solution into the medulla of the kidney in the form of a ring-shaped shadow, uneven contour of the papilla, reminiscent, but according to Yu. A. Pytel, the flame of a fire.

Symptoms similar to acute P. are found in patients with pyonephrosis (see) with occlusion of the ureter and with infection of hydronephrosis (see).

The calculous form occurs due to the fact that purulent-inflammatory damage to the kidneys and upper urinary tract is complicated by secondary nephrolithiasis (see Kidney stone disease). The disease is accompanied by pain in the lumbar region, attacks of renal colic, persistent microscopic hematuria, and the passage of urinary stones (see). The primary nature of P. is confirmed by the fact that symptoms of inflammatory damage to the kidney are detected before the formation of a calculus in it.

The tubular form is sometimes leading to the wedge, manifestations of hron. P. Due to damage to the tubules, uncompensated losses of sodium and potassium occur in the urine, and acidosis develops (see). A persistent decrease in the total amount of sodium leads to hyponatremia, hypovolemia, hypotension, and a decrease in glomerular filtration. The latent tubular form, during exacerbation of P. or another disease, can suddenly manifest itself as symptoms of acute renal failure (see).

The anemic form is associated with the loss of the kidney's ability to produce erythroioetins. Persistent hypochromic anemia is sometimes the most pronounced sign of latent P.

Rare forms: chronic. P. proceeds with a predominance of symptoms of the disease. tract (enterorenal form) or with dysfunction of the adrenal glands, manifested by a picture of Addisonism (see Addison's disease).

Diagnosis

For a reliable diagnosis, it is necessary to establish in the patient at least five characteristic signs of P. (pyuria, bacteriuria, corresponding functions, kidney disorders, corresponding X-ray and radiological changes, kidney biopsy data). About half of the patients indicate a history of acute P. or the presence in the past of signs characteristic of this disease. When analyzing urine using the Kakovsky-Addis, Amburger or Nechiporenko method, leukocyturia is determined, which is facilitated by the use of peroxidase staining. Of particular importance is the qualitative analysis of leukocyturia, the identification of Sternheimer-Malbin cells and active leukocytes in urine sediment.

In case of unreliable indicators of leukocyturia, clarification is necessary using provocative tests. Among them, the most common is the prednisolone test. An increase in the intensity of leukocyturia by more than 100%, the appearance of active leukocytes, an increase in the degree of bacteriuria in urine samples 1-3 hours after intravenous administration of 30-40 mg of prednisolone phosphate is characteristic of latent P. In such patients, after the administration of prednisolone, the number of leukocytes in the blood, taken from the skin of the lumbar region, can be more than 20% higher than the number of leukocytes in blood obtained from a finger. Leukocyturia) in patients with latent 11. can be provoked by the administration of pyrogenal, radiocontrast substances, some antianemic drugs, and forcing diuresis.

Some urologists consider hron to be the most important for making a diagnosis. P. identification of true bacteriuria - a high microbial count (105 and above) in urine obtained from the middle portion during urination or using suprapubic puncture of the bladder. In this case, for indicative quantitative studies of bacteriuria, triphenyltetrazolium chloride or nitrite tests, the immersion plate method or a glucose-specific paper test are usually used; for more accurate ones, inoculate on solid media. However, not in all cases hron. P. true bacteriuria is detected, and its presence does not mean that the process is localized specifically in the upper urinary tract.

With chronic P. there is leukocytosis with a shift of the leukocyte formula to the left, acceleration of ROE, anemia, and the phenomena of aniso- and poikilocytosis. Dysproteinemia is characteristic. For exacerbation of chronic P. may indicate the appearance of C-reactive protein, an increase in the content of lactate dehydrogenase, succinate dehydrogenase, and an increase in the overall proteolytic activity of plasma.

Severe disturbances of homeostasis occur with bilateral hron. P., aggravated by renal failure (see). A study of kidney function first of all reveals a decrease in their ability to adequately respond to loads of ammonium chloride, sodium bicarbonate, and a drop in maximum tubular secretion. Subsequently, the coefficients of renal purification for creatinine and urea decrease, the phenomena of acidosis increase, azotemia appears, the osmolarity of urine decreases accordingly, the maximum density is set below 1.028 with a concentration test according to Volhard (see Kidneys, research methods). Zimnitsky test (see Zimnitsky test) reveals nocturia (see), hypo- or isosthenuria (see).

Immunol, research (reaction of blast transformation and migration of leukocytes, content of immunoglobulins, etc.) in many patients hron. P. show a decrease in the body's defenses. An increase in the titer of specific antibodies to one of the types of microorganisms isolated from the urine of patient P. allows us to consider it the causative agent of the disease and assess the degree of activity of the inflammatory process.

Diagnosis chronic. P. can be confirmed using a puncture biopsy of the kidney. Morphol, signs of hron. P., according to A. M. Wichert et al. (1980), are the following changes: focal interstitial sclerosis with infiltration of lymphoid-histiocytic elements, neutrophils; atrophy of the epithelium of the tubules in the area of interstitial sclerosis with expansion of their lumen and filling with thickened colloid-like masses - the so-called. thyroidization of tubules; periglomerular extracapsular sclerosis, internal dropsy of the glomerulus (glomerulohidrosis); grouping up to 10-15 glomeruli in one low-magnification field of view of a microscope; productive endarteritis and perivascular sclerosis with deformation of the wall and lumen of the vessel. In patients with high arterial hypertension, hypertrophy and hyperplasia of the juxtaglomerular apparatus with hypergranulation of epithelioid cells are often detected. Due to the focal nature of kidney damage, individual morphol, signs may be absent, which still does not allow excluding the diagnosis hron. P. and dictates the need for further observation and re-examination of patients.

Differential diagnosis.

Chron. P. most often has to be differentiated from kidney tuberculosis (see Extrapulmonary tuberculosis), glomerulonephritis (see), hypertension (see), as well as similar changes in the kidneys with collagenosis, diabetes mellitus, gout (a distinctive feature of these diseases is that that they are accompanied by symmetrical damage to the kidneys, whereas chronic P. is either a one-sided process or asymmetrically affects the right and left kidneys). With kidney tuberculosis, unlike hron. P. destructive changes predominate over sclerotic ones, which is determined radiographically. Cystoscopy reveals a characteristic picture of tuberculous cystitis, and mycobacterium tuberculosis can be isolated from urine culture.

Atony and dilatation of the pelvis with chronic. P. is similar, according to pyelography, with the initial stage of hydronephrosis (see). It is possible to distinguish them by identifying chronic diseases in the urine of patients. P. latent bacteriuria and pyuria.

Using radioisotope renography against the background of forced diuresis in patients with hydronephrosis, a worsening of urine outflow is established in comparison with previous data; with chronic P. the half-life of the radionuclide is often prolonged.

Treatment

Treatment should be based on eliminating the causes of the disease: sanitation of probable sources of infection in the body, prompt correction of urodynamic disorders, increasing the body's defenses. A rationally constructed antibacterial therapy is required based on bacterial data, urine examination and antibiogram. First, a drug more effective against the pathogen is prescribed, preferably an antiseptic (nitrofurans, 5-NOC, nevigramon, nitroxoline, sulfonamides). Among antibiotics, it is advisable to use drugs that have minimal nephrotoxic effects (semi-synthetic Penicillins, chloramphenicol, erythromycin, gentamicin, ceporin). Antibacterial therapy should be continued continuously for at least 2 months. with changing medications every 7-10 days. With the persistent disappearance of leukocyturia and bacteriuria, active leukocytes in the urine, and normalization of blood tests, you can proceed to the use of intermittent courses of antibacterial agents, first at intervals of 1 - 2 weeks, and then longer. In the remission phase, it is justified to carry out preventive courses of antibacterial therapy and physiotherapeutic procedures for 2-4 weeks. in autumn and spring. The effectiveness of antibacterial treatment increases by following a diet that excludes spicy foods, increasing water load, and using herbal diuretics (kidney tea, diuretic tea). To activate the immune system, prodigiosan, an autovaccine made from a microbial culture obtained by urine culture, is used.

In severe patients with terminal stage hron, renal failure, according to special indications, hemodialysis (see), hemofiltration (see), peritoneal dialysis (see), kidney transplantation (see).

Prognosis and Prevention

The prognosis is more favorable with early diagnosis and timely treatment of the disease. With advanced anatomical and functional changes in the parenchyma of the kidney and urinary tract, it worsens. Timely intensive long-term therapy reduces the frequency of disease relapses and prolongs the life of patients for many years. Stable remission can be achieved in 50% of cases.

Prevention: adequate treatment of acute P.; elimination of foci of infection in the body, especially diseases of the genitourinary system (cystitis, prostatitis, epididymitis, etc.); Timely correction of urodynamic disorders in urolithiasis and prostate adenoma is important.

Complicated forms of chronic pyelonephritis

Xanthogranulomatous pyelonephritis occurs in both adults and children (mainly females). Many researchers believe that xanthogranulomatous P. occurs as a result of long-term treatment of purulent P. with antibiotics, which leads to changes in the properties of microorganisms, impaired lipid metabolism, and phlebitis of the intrarenal veins. With xanthogranulomatous P., destruction of the kidney tissue occurs with the release of a lipoid substance. The causative agent of the disease is most often Proteus, less often Escherichia coli, Staphylococcus aureus, mixed flora. The disease occurs mainly due to obstruction of the ureter and affects one kidney diffusely or its individual segments. In the parenchyma of the kidney, granulation tissue grows, containing a large amount of fat, giving it a yellow-brown, golden color. The kidney is enlarged, tuberous, shrouded in sclerotic tissue, often containing accumulations of pus. In the parenchyma, lamellar accumulations of granulomatous foam cells are found - histiocytes containing lipids and lymphocytic infiltrates.

Patients are bothered by pain in the lower back and hypochondrium, and the temperature rises. The kidney is usually enlarged and can be easily palpated as a tumor-like formation. Arterial hypertension, leukocytosis, leukocyturia, proteinuria are often observed. Plain radiography often reveals stones in the kidney, and excretory urografin shows a picture of a “silent kidney.” Preoperative diagnosis of xanthogranulomatous P. is possible using arteriography, but the final diagnosis is established during surgery based on biopsy data. Nephrectomy is indicated for diffuse kidney damage. In the early stage of the disease, excision of xanthogranulomatous nodes or resection of the kidney can be performed. The prognosis for most patients after surgery is favorable.

Hypertensive form. Arterial hypertension is observed on average in 32% of patients chronically. P. Its malignant course is observed in 10% of cases. This form of P. is more common at a young age in females. Among children, girls are also predominantly affected by the hypertensive form of P.

The main cause of hypertension in P. is the inflammatory process in the interstitial tissue of the kidney with vascular sclerosis and significant impairment of the organ’s blood circulation. Wrinkling of the kidney most quickly occurs when the venous and lymphatic outflow is disturbed, which occurs with pedunculitis, which often complicates P. The renin-angiotensin-aldosterone system, according to H. Sarre et al. (1971), Linder (F. Linder, 1972), etc., may not take part in the genesis of hypertension in P. It is possible that high blood pressure during chronic P. depends on the kidney losing its ability to produce the so-called. antihypertensive substance.

Arterial hypertension can also occur at the beginning of P.; in such cases, according to Yu. A. Pytelya (1978), it has a central neurohumoral genesis, the inclusion of renal and other pressor mechanisms occurs subsequently.

Wedge, manifestations - prolonged headaches, anemia, thirst, polyuria, sometimes low-grade fever, decreased performance.

Radirisotope renography, rheography, and renal angiography are the most valuable diagnostic methods that make it possible to establish the presence of P. and the localization of the lesion (Fig. 3, 4).

Conservative treatment is ineffective. Kidney resection or nephrectomy, especially in the early stages of unilateral P., lead to recovery in most patients; hypertension, according to V. S. Gagarinov and I. S. Kamyshan (1973), A. Ya. Pytel (1977), disappears after nephrectomy in an average of 70% of those operated on. With arterial hypertension caused by bilateral hron. P., sometimes they resort to kidney enterorevascularization or kidney transplantation.

Pyelonephritis in pregnant women

P.'s frequency in pregnant women ranges from 2-10%, and it can occur in women in labor and postpartum, i.e. throughout the so-called. gestational period. Some clinicians use the term “gestational pyelonephritis”, highlighting its individual forms: P. of pregnant women, P. of women in labor and P. of postpartum women.

Gestational P. has its own patterns of development and course characteristics. Pathogens of P. in pregnant women are Escherichia coli, Klebsiella, Proteus; in postpartum women - enterococcus, E. coli. In the pathogenesis of gestational P., a large role belongs to physiol, hormonal changes that occur in the body of pregnant and postpartum women. Qualitative and quantitative changes in the composition of various hormones (estrogens, progesterone, hydrocortisone, etc.), changes in anatomical relationships during pregnancy predispose to disturbances in the uro- and hemodynamics of the upper urinary tract, contribute to infection of the kidney tissue and the occurrence of an inflammatory process, especially if the presence of which in a woman’s body - or inf. hearth.

Most often, right-sided P. is observed, which depends not only on compression of the ureter by the pregnant uterus, but also on the characteristics of the right ovarian vein (dilation, varicose changes). Women often get sick during their first pregnancy. This is explained by insufficient adaptation of the body to the changes that occur during pregnancy (hormonal, immunological). In most women, P. occurs at the end of the second - beginning of the third trimester of pregnancy (20-26 weeks and 32-34 weeks), when hormonal ratios change most significantly. P. in postpartum women most often appears on the 4-6th and 12-14th days after birth, i.e. during those periods when postpartum complications occur - metrothrombophlebitis (see), metroendometritis (see), etc.

Wedge, P.'s picture at different stages of pregnancy has features depending on the degree of disturbance in the passage of urine through the upper urinary tract: in the first trimester, severe pain is observed in the lumbar region; in the second and third trimesters of pregnancy with P., postpartum women have mild pain. Acute P. usually does not have a significant effect on the course of pregnancy (see); in chronic cases, miscarriage (see), premature birth (see), toxicosis of pregnant women (see) is often observed. In acute P., childbirth occurs spontaneously and does not require special manipulations; with chronic In 10% of cases, it is necessary to resort to artificial early induction of labor. Caesarean section (see) for P. in pregnant women is permissible according to strict obstetric indications, and preference should be given to the extraperitoneal method.

In the diagnosis of gestational P., great importance belongs to the data of laboratory methods (leukocytosis, neutrophil shift to the left, moderate hypochromic anemia, leukocyturia, bacteriuria). Determining the degree of disturbance in the passage of urine from the upper urinary tract is achieved using chromocystoscopy. Untimely release of indigo carmine in the second and third trimesters of pregnancy with a wedge, P.'s picture is an indication for catheterization of the ureters in order not only to restore the passage of urine, but also to prevent bacterial shock. Roentgenol, examination of women throughout pregnancy is undesirable due to possible harmful effects on the fetus. The kidneys in pregnant women are examined using ultrasound scanning (see Ultrasound diagnostics).

Treatment of gestational P. should be comprehensive, individual, taking into account the characteristics of the course of P. in pregnant women and postpartum women. To avoid harmful effects on the fetus in the first trimester of pregnancy, only natural and semi-synthetic Penicillins (ampicillin, carbenicillin, etc.) are used. In the II and III trimesters of pregnancy, in addition to the listed penicillins, antibiotics of the aminoglycoside group (gentamicin, kanamycin), cephalosporins, macrolides (erythromycin), and lincomycin are prescribed. Throughout pregnancy, the use of antibiotics of the tetracycline, levomycetin series and streptomycin is contraindicated due to adverse effects on the fetus. In the second and third trimesters of pregnancy, along with antibiotics, other anti-inflammatory drugs (furagin, 5-NOK, nevigramon, urosulfan) are used. P.'s treatment in postpartum women is carried out taking into account the possible influence of drugs through mother's milk on the newborn. In addition to this therapy, pregnant and postpartum women are prescribed low-toxic diuretics (uregit, furosemide). Replenishment of protein balance is achieved by transfusion of albumin, plasma, and blood; For detoxification purposes, low-molecular solutions (hemodez, reopolyglucin) are administered. The success of treatment largely depends on the timely restoration of the impaired passage of urine, which is achieved by bilateral catheterization of the ureters, which is performed on febrile patients who have had no effect from antibiotic therapy during the day or who have not received any treatment. If there is no effect from catheterization of the ureters and antibacterial therapy for 2-3 days (hectic fever, chills), an operation is indicated - decapsulation of the kidney (see), opening of purulent foci, imposition of a nephrostomy (see Nephrostomy). The inflammatory process in the kidney often continues after the end of the postpartum period; therefore, further monitoring of these patients by a urologist is required.

The prognosis with timely diagnosis and early rational therapy is favorable. If the process is severe and treatment is ineffective, adverse consequences are possible - transition to chronic. P., the emergence of a hypertensive form of P., etc.

Prevention of gestational P. involves identifying urinary tract diseases in antenatal clinics in non-pregnant women and their timely treatment. The presence of leukocyturia and bacteriuria in pregnant women requires appropriate treatment; if there is no effect, hospitalization in a specialized hospital is necessary.

Pyelonephritis in children

In pediatrics, P. is usually considered as a microbial inflammatory lesion of the tubules, interstitial tissue, and renal collecting system, clinically manifested as inf. disease, especially in young children and newborns, leukocyturia (see), bacteriuria (see) and impaired renal function.

The main factors contributing to the occurrence of P. in children are congenital and acquired uropathy, causing urodynamic disturbances. Of great importance are urinary reflux and dysplasia of the kidney parenchyma, metabolic and drug-induced nephropathies, as well as immunodeficiency states, changes in the hormonal regulation of kidney functions, primary and secondary tubulopathies, nephrolithiasis, kidney mobility with impaired urodynamics and blood microcirculation, vulvovaginitis, cystitis.

The causative agents of P. in children are most often Escherichia coli, Proteus, and Pseudomonas aeruginosa.

The main wedge, manifestations of P. in children are dysuria, flu-like syndrome, abdominal pain, lower back pain, intoxication, dyspeptic disorders, asthenic conditions of the child. In the wedge, picture in newborns and children of the first 3 months. life is dominated by symptoms of general intoxication with dysfunction of the gastrointestinal tract. tract; in preschool children - intoxication, pain and dysuria; at school age, intoxication manifests itself in the form of asthenia. The wedge, P.'s picture, is most pronounced in children with urodynamic disorders.

According to P.'s activity in children, three degrees are distinguished. Activity I degree is not clinically manifested; the disease is detected accidentally during laboratory tests during clinical examination, when registering a child for kindergarten, nursery, etc. With activity of the second degree wedge, manifestations of the disease may be absent, P. is detected according to laboratory tests (leukocytosis, neutrophilia with band shift, acceleration of ROE, positive reaction to C-reactive protein, etc.). The highest activity (III degree) is characterized by symptoms of intoxication, leukocytosis, neutrophilia with band shift, leukocyturia, bacteriuria, biochemical. changes in blood and urine.

In children, there are acute, chronic with exacerbations (wavy) and latent course of P. Depending on the activity and duration of the disease, there are three degrees of impairment and damage to kidney function. I degree of impairment of the function and condition of the kidneys is characterized by dysrhythmia of the tubular system (the rhythm of excretion of electrolytes and various metabolites in the urine during the day is disrupted). According to the Zimnitsky test, nocturia (see), low specific gravity of urine in the evening and night hours are detected. In case of impaired renal function of the second degree, homeostasis may not be changed, but when it is disturbed, metabolic acidosis (see), hyponatremia (see), hyperphosphaturia, hyperchloruria (see), hypernatriuria are observed. The final stage (III degree) of renal dysfunction is hron, renal failure (see).

The long course of P. is characterized by the addition of an allergic component, and at the age of over 10 years, autoimmune reactions are possible.

The basic principles of P.'s treatment in children should include the following measures: elimination of the microbial factor with short courses of antibacterial drugs (ampicillin, chloramphenicol, furagin, biseptol, etc.); influence on the main pathogenetic links of the process with antihistamines and antiserotonin drugs, anticoagulants, diuretics; restoration of renal hemodynamic disorders (aminophylline, Temisal, adonis infusion, etc.); reducing the load on the kidneys with diet therapy (limiting animal proteins); carrying out symptomatic therapy (hypotensive, correcting metabolic changes in the content of potassium, sodium, phosphorus, calcium, acids, bases and other substances in the blood and urine); increasing the resistance of kidney tissue to inf. beginning (pentoxyl, dibazol, anabolic hormones for 30-40 days); elimination of the causes that contributed to the occurrence of II. in children (elimination of hidden foci of infection, treatment of abnormalities in the development of the kidneys and urinary tract). When involved in patol, the process of the liver and bile ducts shows choleretic agents. In cases of repeated exacerbation of P., antibacterial therapy is also carried out in a short course. Children with interstitial nephritis, deformation of the pyelocaliceal system due to autoimmune changes in the body after sanitation of urine are recommended to be treated with resokhin drugs (eg, delagil) for 6-12 months. and more. In severe cases of P. occurring with chronic, renal failure, especially in children with congenital or acquired uropathy, peritoneal dialysis (see), hemodialysis (see) and other methods of extrarenal blood purification, and sometimes kidney transplantation are indicated (see. ).

P.'s prognosis in children is usually favorable. Antibacterial therapy started early and the elimination of causes predisposing to the development of P. lead to recovery. The prognosis for children with P., accompanied by chronic renal failure, is more serious.

P.'s prevention in children should include recording and examination of families at high risk for kidney and urinary tract diseases; medical examination of children born to mothers with toxicosis of pregnancy; early X-ray urological examination of children born to mothers who suffered from various diseases in the first half of pregnancy, and also took medications, especially progesterone. Those at risk for P.'s development are children who, during the prevention of rickets with vitamin D, have a positive Sulkovich test (high calcium content). There is a high risk of developing P. in children from families whose members suffer from metabolic disorders characterized by calciuria, oxalaturia, uraturia, and excretion of other nephrotoxic substances in the urine. A preventive measure in these cases is the correction of identified metabolic disorders before the disease manifests itself. The basis of P.’s prevention in children should be to treat. measures that include not only the use of antibacterial drugs, but also the elimination of factors predisposing to the occurrence of a microbial inflammatory process in the kidneys and urinary tract.

Bibliography: Abramova 3. Causative agents of pyelonephritis in pregnant and postpartum women, Akush, and gynek., No. 10, p. 40, 1976; Velikanov K. A. et al. The state of immunity in patients with chronic pyelonephritis, Urol, and nephrol., N "6, p. 16, 1977; Wichert A. M., Kozdoba O. A. and Arabidze G. G. Puncture kidney biopsy in the diagnosis of chronic pyelonephritis, Ter. arkh., t. 52, no. 4, p. 13, 1980; Voino-Yasenetsky A. M. Pyelonephritis in patients with glomerulonephritis, Klin, med., t. 47, No. 8, p. 50, 1969; aka, Xanthogranulomatous pyelonephritis, Urol, and nephrol., No. 1, p. 52, 1971; Ganzen T.N. Morphological diagnosis of pyelonephritis according to incisional and puncture biopsy of the kidney, Arch. pathol., t. 36, no. 1, p. 30, 1974; Gudzenko P. N. and Nabukhotny T. K. Primary pyelonephritis in children, Kyiv, 1976, bibliogr.; Ezersky R. F. Pyelonephritis in children, L., 1977, bibliogr.; Ignatova M. S. and Veltishchev Yu. E. Kidney diseases in children, p. 181, M., 1973; Ignatova M. S. et al. Immunological aspects of pyelonephritis, Sov. med., no. 10, p. 24, 1978; Lopatkin N. A., Pugachev A. G. and Rodoman V. E. Pyelonephritis in children, M., 1979, bibliogr.; Multi-volume guide to pathological anatomy, ed. A. I. Strukova, vol. 7, p. 121, M., 1964; Moskalev M. N. To the doctrine of the etiology of pyelonephritis, Kyiv, 1913; Pytel A. Ya. Pelvic-renal refluxes and their clinical significance, M., 1959, bibliogr.; aka, Unilateral chronic pyelonephritis and hypertension, Urology, No. 1, p. 3.1960; Pytel A. Ya. and Pugachev A. G. Essays on pediatric urology, p. 92, M., 1977; Pytel A. Ya. and Pytel Yu. A. X-ray diagnosis of urological diseases, M., 1966; Pytel A. Ya. et al. Pyelonephritis, M., 1977, bibliogr.; Pytel Yu. A. Emphysematous pyelonephritis, Urol, and nephrol., No. 4, p. 52, 1967; Pytel Yu. A., Grashchenkova Z. P. and Gurtova B. L. Pyelonephritis in pregnant women, Obstetrics and Gynecology, No. 1, p. 53, 1979; Pytel Yu. A., Zolotarev I. I. and Grigoryan V. A. On the pathogenesis of pyelonephritis in pregnant women and in the postpartum period, Urol, and nephrol., No. 4, p. 47, 1981; Pytel Yu. A. et al. The value of surgical biopsy in the diagnosis of pyelonephritis, Sov. med., no. 11, p. 88, 1973; Rodoman V. E. et al. Consequences of acute pyelonephritis suffered during pregnancy, Akush, and gynec., No. 8, p. 52, 1974; Svistelin D.P. About the combination of glomerulo- and pyelonephritis, Arkh. pathol., t. 36, no. 10, p. 43, 1974; Serov V.V. Morphological basis of kidney immunopathology, M., 1968; Sum-Shik E. R. Pyelonephritis of pregnant women, M., 1967, bibliogr.; Shekhtman M. M. Kidney diseases and pregnancy, M., 1980, bibliogr. ; Shulutko B.I. On the issue of the combination of glomerulonephritis and pyelonephritis, Ter. arkh., t. 52, no. 4, p. 21, 1980; Breunung M. u. In r e and n and n g M. Die Harnweginfektion, S. 35, Lpz., 1974; Brown A. D. The effects of pregnancy on the lower urinary tract, Clin. Obstet. Gynec., v. 5, p. 151, 1978; Carris S. K. a. Schmidt J. D. Emphysematous pyelonephritis, J. Urol. (Baltimore), v. 118, p. 457, 1977; Hep-t i n s t a 1 1 R. H. Pathology of end-stage of kidney disease, Amer. J. Med., v. 44, p. 656, 1968; Marchant D. J. Urinary tract infections in pregnancy, Clin. Obstet. Gynec., v. 21, p. 921, 1978; Die Pyelonephritis, hrsg. v. H. Losse u. M. Kienitz, Stuttgart, 1967, Bibliogr.; Quinn E. L. a. K a s s E. H. Biology of pyelonephritis, Boston, 1960, bibliogr.; R e n y i - V a m o s F. a. B a-logh F. Pyelonephritis, Budapest, 1979; Stamey Th. Urinary infections, Baltimore, 1972, bibliogr.; Y 1 a h o s L. a. o. Unilateral emphysematous pyelonephritis, Europ. Urol., v. 5, p. 220, 1979.

A. Ya. Pytel, K. A. Velikanov; 3. P. Grashchenkova (ac.), V. P. Lebedev (ped.), N. K. Permyakov (pat. an.).

All diseases, depending on what is primarily affected - glomeruli or tubules, diseases are divided into: 1. Glomerulopathies a) glomerulonephritis b) idiopathic nephrotic syndrome (lipoid nephrosis) c) renal amyloidosis d) diabetic glomerulosclerosis e) Hepatic glomerulosclerosis
2. Tubulopathies a) acute (Acute renal failure - acute renal failure) b) chronic (myeloma kidney, gouty kidney)
GLOMERULONEPHRITIS – non-purulent inflammation of the glomeruli of the kidney. Classification of glomerulonephritis. According to etiology, they are: a) infectious-allergic b) of unknown nature. According to topography: a) extracapillary b) intracapillary. According to the nature of inflammation - a) serous b) fibrinous d) hemorrhagic e) mixed
According to the course: a) acute, b) subacute, c) chronic, d) terminal.
Chronic is divided into a) membranous b) mesangial c) fibroplastic
V.V. Serov identified 5 main forms of glomerulonephritis based on clinical and anatomical features: a) post-streptococcal, b) extracapillary proliferative c) membranous d) mesangial e) fibroplastic
The disease manifests itself with renal and extrarenal symptoms:
Renal symptoms include a) oliguria d) proteinuria e) hematuria e) cylindruria. Extrarenal symptoms include: 1) arterial hypertension 2) left ventricular hypertrophy, 3) dysproteinemia, 4) edema 5) hyperazotemia and uremia
In acute glomerulonephritis, the kidneys are slightly enlarged; based on their macroscopic appearance they are called variegated kidneys; the disease lasts for 10-12 months; the changes that occur are often reversible and patients recover. Less commonly, acute renal failure (ARF) occurs. In the glomeruli, changes occur in Stage 3: a) exudative, b) exudative-proliferative, c) proliferative. With necrosis of capillary loops, necrotizing glomerulonephritis occurs.
Chronic glomerulonephritis is divided into a) membranous b) mesangial c) fibroplastic. It leads to sclerotic changes, the kidneys decrease in size, their surface is fine-grained, the tissue is dense (secondary wrinkled kidney) - this ends in uremia (CRF).
AMYLOIDOSIS often occurs against the background of chronic infections, rheumatoid arthritis, and purulent diseases. Amyloidosis occurs in 4 stages a) latent - the kidney does not change externally b) proteinuric - the kidney is enlarged, dense, the cortex is wide pale, the medulla is full-blooded, called the “big sebaceous kidney” c) nephrotic - amyloid is deposited and in medulla, the kidney is called “large white” d) azotemic - the kidneys decrease in size, are dense, large-lumpy, called “amyloid-wrinkled kidneys” and patients often die from chronic renal failure
TUBULOPATHY. The leading one is acute tubulopathy or acute renal failure (ARF). The cause of the pathology is a) intoxication b) infection. The kidneys are enlarged in size, the boundary between the layers is clear, the cortex is pale, the medulla is full-blooded, there is edema in the stroma, dystrophy in the epithelium (hyaline droplet, vacuolar, fatty) patients can survive only with the use of hemodialysis. Macroscopically, such a kidney is called “sublimate” or “sulfanilamide” because occurs when poisoned by these substances. The morphological substrate of acute renal failure includes a) necrosis of the convoluted tubule epithelium, b) impaired blood and lymph circulation in the kidneys,
The disease occurs in 3 stages: a) initial (shock), b) oligo-anuric, c) restoration of diuresis. If the patient survives, the kidney structure is completely restored.
PYELONEPHRITIS is a purulent disease of the pelvis, calyces and stroma of the kidneys. More often caused by Escherichia coli, the infection penetrates the kidney in different ways: a) hematogenous (descending) b) urogenic (ascending) c) lymphogenic. Promote the development of inflammation: a) disruption of urine outflow b) urinary stasis. Pyelonephritis can be acute or chronic. Acute illness often ends in recovery. Chronic pyelonephritis ends with a pyelonephrotic wrinkled kidney. Microscopically, the kidney resembles thyroid tissue and is therefore called the “thyroid kidney.”
Complications of pyelonephritis include: a) carbuncle - accumulation of pus b) pyonephrosis - when the carbuncle communicates with the pelvis c) perinephritis - inflammation of the kidney capsule d) paranephritis - inflammation of the perirenal tissue e) papillonecrosis - necrosis of the papillae of the pyramids
URINOLOGICAL DISEASE - causes 1. General (metabolic disorders) 2. Local (inflammation and urinary stasis). As a rule, it is combined with pyelonephritis, so the complications are the same, but when the ureter is blocked, hydronephrosis is possible.
POLYCYSTIC KIDNEY is a congenital pathology when the kidneys sharply increase in size, consist of a large number of cysts, patients die from chronic renal failure.
NEPHROSCLEROSIS - kidney sclerosis is a morphological substrate of chronic renal failure (CRF). It is divided into a) primary wrinkled kidney, when the vessels are primarily affected (atherosclerosis, hypertension, less commonly periarteritis nodosa, etc.) and b) secondary wrinkled kidney, when the stroma or glomeruli are primarily affected (glomerulonephritis, pyelonephritis, amyloidosis, tuberculosis, kidney stone disease, etc.) The appearance of these kidneys is different. They are reduced in size, dense, wrinkled, but the surface in some cases is fine-grained (hypertension, glomerulonephritis) in other cases coarsely lumpy (atherosclerosis, pyelonephritis). With nephrosclerosis, blood pressure increases, causing left ventricular hypertrophy.
UREMIA is a chronic renal failure that occurs in most kidney diseases. The kidneys cannot excrete nitrogenous wastes (urea, creatinine), they accumulate in the blood and are then released through all organs of excretion - the gastrointestinal tract, skin, serous membranes, respiratory organs, and fibrinous or fibrinous-hemorrhagic inflammation occurs there (gastritis, enteritis, bronchitis, pneumonia, pleurisy, pericarditis, powdery skin, etc.)
KIDNEY TUMORS. Organ-specific cancers include a) hypernephroid cancer and b) nephroblastoma. Organ-nonspecific cancers arise from the pelvis. Histological forms of pelvic cancer include: a) transitional cell b) glandular (against the background of metaplasia) c) squamous cell, the most common of them is transitional cell

- an infectious disease in which the renal pelvis, its calyces and the substance of the kidneys are involved in the process with a predominant lesion of the interstitial tissue. In this regard, pyelonephritis is interstitial (interstitial) nephritis. It can be one- or two-sided.

Based on clinical and morphological data, acute and chronic pyelonephritis is distinguished, which usually has a recurrent course in the form of attacks of acute pyelonephritis.

Etiology and pathogenesis

. Pyelonephritis is an infectious disease. Its causative agents can be various infections (Escherichia coli, Enterococcus, Streptococcus, Staphylococcus, Proteus, etc.), but in most cases it is Escherichia coli. More often, microbes are introduced into the kidneys by an ascending route from the ureters, bladder, and urethra (urogenic ascending pyelonephritis). The urogenic rise of infection is facilitated by dyskinesia of the ureters and pelvis, increased intrapelvic pressure (vesicorenal and pyelorenal reflux), as well as reabsorption of the contents of the pelvis into the veins of the medulla of the kidneys (pyelovenous reflux). Ascending pyelonephritis often complicates those diseases of the genitourinary system in which the outflow of urine is obstructed (stones and strictures of the ureters, strictures of the urethra, tumors of the genitourinary system), so it often develops during pregnancy. Infectious agents can penetrate the kidney, including the pelvis, through the bloodstream (hematogenous descending pyelonephritis). This path of occurrence of pyelonephritis is observed in many infectious diseases (typhoid fever, influenza, tonsillitis, sepsis). Lymphogenous introduction of infection into the kidneys (lymphogenous pyelonephritis) is also possible; the source of infection in these cases is the large intestine and genitals.

Pathological anatomy.

Changes in acute and chronic pyelonephritis are different.

For acute pyelonephritis

at the height of the disease, plethora and leukocyte infiltration of the pelvis and calyces, foci of necrosis of the mucous membrane, and a picture of fibrinous pyelitis are detected. The interstitial tissue of all layers of the kidney is swollen and infiltrated with leukocytes; Multiple miliary abscesses and hemorrhages are common. The tubules are in a state of dystrophy, their lumens are clogged with cylinders of deflated epithelium and leukocytes. The process is focal or diffuse in nature.

Bud

(kidneys) are enlarged, the tissue is swollen, full of blood, the capsule is easily removed. The cavities of the pelvis and calyces are dilated, filled with cloudy urine or pus, their mucous membrane is dull, with areas of hemorrhage. On the section, the renal tissue is variegated, yellow-gray areas are surrounded by an area of plethora and hemorrhage, abscesses are found.

Chronic pyelonephritis is characterized by

diversity of changes, since sclerotic processes, as a rule, are combined with exudative-necrotic ones. Changes in the pelvis and calyces are reduced to their sclerosis, lymphoplasmacytic infiltration, polyposis of the mucous membrane and metaplasia of the transitional epithelium into stratified squamous epithelium. In the kidney tissue, chronic interstitial inflammation is expressed with the proliferation of connective tissue, encapsulation of abscesses and macrophage resorption of purulent-necrotic masses. The tubules undergo dystrophy and atrophy. The preserved tubules are sharply stretched and the kidney resembles the thyroid gland in structure. Predominantly periglomerular and extracapillary glomerulosclerosis is expressed. Arteries and veins are sclerotic.

Complications.

In acute pyelonephritis, the progression of the purulent process leads to the fusion of large abscesses and the formation of a kidney carbuncle, the connection of purulent cavities with the pelvis (pyonephrosis), the transition of the process to the fibrous capsule (perinephritis) and perinephritis (paranephritis). Acute pyelonephritis can be complicated by necrosis of the pyramidal papillae (papilonecrosis), which develops as a result of the toxic effect of bacteria in conditions of urinary stasis. This complication of pyelonephritis occurs more often in patients with diabetes. Rarely, pyelonephritis becomes a source of sepsis. When the purulent process is limited during the scarring period, chronic kidney abscesses can form. In chronic pyelonephritis, especially unilateral, the development of nephrogenic arterial hypertension and arteriolosclerosis in the second (intact) kidney is possible. Bilateral pyelonephritic shrinkage of the kidneys leads to chronic renal failure.

Exodus.

In acute pyelonephritis, the outcome is usually recovery. Its severe complications (pyonephrosis, sepsis, papillonecrosis) can cause death. Chronic pyelonephritis with kidney shrinkage often ends in azotemic uremia. With the development of nephrogenic arterial hypertension, death in chronic pyelonephritis is sometimes associated with the complications that occur with hypertension (cerebral hemorrhage, myocardial infarction, etc.).

Pyelonephritis pathological anatomy. Pyelonephritis

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Etiology and pathogenesis