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Children are cute creatures that quite often make us parents pretty worried. Moms and dads pay special attention to the general health of their beloved children. This is not surprising, since only a healthy baby can be truly happy. Unfortunately, things don't always turn out well. These or other ailments quite often burst into the life of a child, and quite suddenly. Those children who day after day adhere to all the rules of a healthy lifestyle are no exception. site) will talk about diseases such as papillary and cortical necrosis kidneys in children. After reading the information provided, you can find out everything you need about the causes of development, symptoms, diagnosis, as well as methods of treating these ailments.

What is papillary necrosis of the kidneys in children?

In fact, this condition in most cases is a consequence of such ailments as diabetes mellitus, pyelonephritis, nephrolithiasis, hypertension and some others. Very rarely, this ailment makes itself felt as a primary kidney disease. By this disease is meant a condition in which there is a clear circulatory disorder directly in the pyramids of the kidneys. Modern doctors and specialists distinguish two forms of this disease - these are unilateral and bilateral necrosis.

What is renal cortical necrosis?

This condition is characterized by damage to the interlobular arcuate arteries, which can cause the development of ischemic necrosis of the entire renal tissue. We draw your attention to the fact that this pathology is observed, as a rule, in infants only.

What are the causes of papillary and cortical necrosis?

As for the first condition, it occurs as a result of exposure to the body of the child Escherichia coli. Infection can occur both by contact and hematogenous route. If we talk about the reasons for the development of the second condition, then in this case, bacterial infections such as staphylococcus, meningococcal infection, streptococcus and some others are to blame.

What is the clinical manifestation of papillary necrosis of the kidneys?

The very first symptoms of this pathology are considered to be a significant deterioration in the general well-being of the child against the background of the main ailment. The baby has a fever, chills and oligoanuria. In addition, the face also has hematuria, leukocyturia and bacteriuria. In the urine of such children, you can see separate parts of the renal papillae. In the presence of this disease, the child is also disturbed by quite strong pain sensations, which can be observed both in the abdomen, and in the lower back, or in the region of the kidney itself. When passing urine tests, there is also a clear leukocytosis.

What are the symptoms of renal cortical necrosis in children?

The most common signs of this disease include: hyperazotemia, oligoanuria, electrolyte disorders, as well as some other symptoms that are observed in renal failure. Note that the strength of the manifestation of all these signs directly depends on the degree of the necrotic process.

How are these conditions diagnosed?

To identify these pathologies, such a diagnostic method as excretory urography is used. Excretory urography is an X-ray method for examining the urinary tract, which is based on the ability of the kidney to excrete certain radiopaque substances.

What are the treatments for these ailments?

As for the therapy of papillary necrosis, it involves the treatment of an existing bacterial infection. In this case, the sick child is prescribed drugs with a wide antimicrobial spectrum of action. But in the case of cortical necrosis, in the very first place, all efforts are directed to the elimination of signs of acute renal failure. In this case, antibacterial and symptomatic therapy comes to the rescue, based on the use of antihypertensive, as well as diuretic drugs.

This is the destruction of the papillae of the kidneys, due to ischemia of the Malpighian pyramids. Manifested by episodes of renal colic, nagging pain in the lower back, hematuria, discharge of necrotic papillae. It is diagnosed with the help of general and bacteriological analysis of urine, excretory urography, ureteropyeloscopy. Antibacterial therapy, peripheral vasodilators, anticoagulants, antiaggregants, membrane stabilizers, antioxidants, hemostatics, venotonics are prescribed for treatment. If necessary, catheterization and stenting of the ureter, pelvis, decapsulation of the kidney, nephrostomy, partial and total nephrectomy are performed.

ICD-10

N17.2 Acute renal failure with medullary necrosis

General information

The disease was first described in 1877 by the German physician and pathologist Nikolaus Friedreich. Papillary renal necrosis (necrotizing papillitis, necrosis of the renal papillae), according to various sources, is diagnosed in 0.3-1% of patients in urological and nephrological hospitals. In those suffering from pyelonephritis, the prevalence of pathology reaches 3%.

Women get sick twice as often as men. In half of the cases, papillary necrosis occurs at the age of 30-40. In 75% of patients, necrotizing papillitis develops chronically with a gradual progressive increase in renal dysfunction. In 58% of cases, the inflammatory-destructive process is bilateral. According to the results of observations, ischemic destruction of the upper part of the Malpighian pyramids is associated with diabetes mellitus and sickle cell anemia, however, in recent years, it has increasingly occurred in other pathological conditions.

The reasons

Necrotizing papillitis is a polyetiological disease that develops against the background of other pathological conditions or the intake of nephrotoxic substances. A prerequisite for the occurrence of necrosis are the features of the anatomical structure of the medullary substance - hypoxia of the renal papillae is facilitated by a combination of relatively poor vascularization of the anatomical structure and high osmotic pressure in this area. Specialists in the field of modern urology and nephrology have established several groups of causes that cause papillary destruction:

• Impaired blood supply to the brain. Insufficient blood flow to the papillary apparatus is observed with changes in the vascular wall in patients with atherosclerosis, diabetes mellitus, and vasculitis. Ischemia of papillary structures is provoked by diseases in which thrombosis of renal microvessels is possible, most often sickle cell anemia is complicated by necrotic papillitis, less often - coagulopathy, DIC and other hypercoagulable conditions.
• Increased intrapelvic pressure. With obstruction of the urinary tract, the outflow of urine is disturbed with its accumulation in the pelvis system. The resulting pyelorenal reflux contributes to the seeding of the renal papillae with bacteria contained in urine, and the onset of an inflammatory reaction. In most cases, pelvic hypertension is formed when the ureter is obstructed by a stone, neoplasm, accidental ligation during surgery, and the presence of a ureterovaginal fistula.
• Purulent diseases of the kidneys. Secondary inflammation of the tops of the renal pyramids complicates the course of severe purulent-destructive processes. Massive reproduction of infectious pathogens that secrete proteolytic exotoxins contributes to the formation of purulent infiltrates and melting of the kidney parenchyma, involvement in the destruction of papillae. Papillary necrosis can develop against the background of pyelonephritis, apostematous nephritis, pyonephrosis, renal carbuncle, abscess.
• drug nephropathy. Long-term uncontrolled use of certain over-the-counter analgesics and antipyretics leads to disruption of medullary blood flow, deterioration of cortical and medulla perfusion, and the development of analgesic nephropathy. In the most severe cases, against the background of pronounced changes in the direct vessels that feed the renal papillae, their gross ischemic destruction occurs. NSAIDs also have a direct toxic effect on the renal medulla, which exacerbates papillary necrotic processes.

Pathogenesis

There are three main pathogenetic mechanisms for the development of renal papillary necrosis - angiopathic, vasocompressive, infectious, which often combine with each other, leading to an ischemic infarction of the medulla with its subsequent purulent fusion and rejection of necrotic masses. Reducing the lumen of the papillary arterioles due to thickening of the intima, thickening of the wall, compression by purulent foci or interstitium infiltrated with urine, complete obturation of their lumen with blood clots contribute to the occurrence of ischemia and tissue destruction.

The situation is aggravated by the narrowing of the diameter of the vessels supplying the papillae towards the top, which increases the viscosity of the incoming blood. An additional factor that enhances ischemic processes during obstruction of the urinary organs is inflammation and venous hyperemia of fatty tissue, into which urine penetrates. The ischemic papilla can undergo complete or partial destruction with damage to individual areas in the center or periphery. In severe cases, the entire Malpighian pyramid is necrotized, with multiple localization - the medullary layer of the affected kidney throughout. When an infection is attached, the necrotic process is complicated by an inflammatory reaction.

Classification

The systematization of the forms of papillary necrosis takes into account the mechanism and dynamics of the development of the disease, the severity of clinical symptoms. Nephrologists distinguish between primary necrotic papillitis, which occurs as a result of impaired blood supply without previous infectious and inflammatory pathology, and secondary, caused by ischemia of the medulla against the background of inflammatory and sclerotic changes in the parenchyma and renal sinus.

With an initial lesion of the papilla, they speak of a papillary form of destruction, with the primary formation of focal infarctions in the inner brain zone, followed by involvement of the tops of the Malpighian pyramids, they speak of a medullary form. Taking into account the characteristics of the flow, they distinguish:

• Acute papillary necrosis. The disease is characterized by a stormy clinical picture, severe intoxication, and an ambiguous prognosis. An acute course is more typical for papillits that complicate pyelonephritis, other purulent nephrological diseases, and nephrolithiasis.
• Chronic papillary necrosis. Symptoms are usually mild and nonspecific. A relapsing course is possible. Often, chronic papillitis is detected in angiopathy, sickle cell anemia and is diagnosed only after a thorough examination of the patient.

Symptoms of renal papillary necrosis

The clinical picture of the disease is characterized by a variety of symptoms, most of which are nonspecific. Often with papillary necrosis, renal colic occurs due to the separation of a necrotic papilla, which may be accompanied by nausea, vomiting, and stool retention. Typical are constant pulling pains in the lumbar region, excretion of blood in the urine.

Patients have an intoxication syndrome of varying severity: subfebrile or febrile fever, chills, headache, excessive sweating, weakness. A pathognomonic sign of necrotic papillitis, which is found only at a late stage of the disease, is the excretion of dead areas of the renal parenchyma in the form of grayish masses with inclusions of lime salts in the urine. In the chronic course, laboratory symptoms may predominate with little or no clinical symptoms.

Complications

In the case of a bacterial infection, apostematous pyelonephritis occurs, manifested by the formation of small abscesses in the cortical layer of the kidney. With an extensive lesion, a clinical picture of acute renal failure is revealed - oliguria or anuria, an increase in the level of urea and plasma creatinine, impaired consciousness due to azotemia.

The chronic course of necrotizing papillitis often leads to chronic renal failure, which is complicated by the development of decompensated metabolic acidosis and multiple organ failure. In 40% of cases, patients are diagnosed with nephrolithiasis with a high risk of formation of staghorn stones. Massive papillary necrosis is often accompanied by profuse bleeding, which is life-threatening and requires emergency care.

Diagnostics

Due to the polymorphism of the clinical picture and the absence of pathognomonic signs in the early stages of the disease, diagnosis is often difficult. Difficulties in diagnosis are also due to the latent development of renal papillary necrosis against the background of another pathology of the urinary system (pyelonephritis, nephrolithiasis). The plan for examining a patient with suspected necrotizing papillitis includes the following laboratory and instrumental methods:

• Clinical analysis of urine. Papillary necrosis is characterized by micro- and macrohematuria, leukocyturia, bacteriuria, the appearance of Sternheimer-Malbin cells. In the later stages, necrotic masses are found in the form of pieces of gray tissue of an oblong or triangular shape. The method is supplemented with a bacteriological examination of urine with the determination of the sensitivity of the flora.
• Intravenous urography. On the pictures obtained during excretory urography, blurred outlines of the fornix zone, small shadows of calcifications, an annular shadow in the lumen of the renal pelvis, fornico-medullary fistulas are visible. With complete rejection of the papilla, a filling defect is detected on the radiograph. A characteristic sign of total necrosis is the flow of contrast into the kidney parenchyma (a symptom of the “bonfire flame”).
• Ureteropyeloscopy. For nephroscopy, a flexible endoscope is used, which is inserted retrograde (through the urethra) or antegrade (through the abdominal wall), which makes it possible to assess the condition of the ureters and the pyelocaliceal system of the kidneys. With papillitis, multiple destructions of the renal papillae are observed, which is often accompanied by bleeding from the fornic zone.

In a clinical blood test with papillary renal necrosis, signs of bacterial inflammation are determined: neutrophilic leukocytosis with an increase in the number of stab cells, an increase in ESR. For a comprehensive assessment of the state of the urinary system, ultrasound and CT of the kidneys and other organs of the retroperitoneal space are performed. These methods are less informative in the diagnosis of necrosis of the renal papillae, but allow the identification of concomitant pathological conditions - urolithiasis, pyelonephritis.

Differential diagnosis of necrotizing papillitis is carried out with acute and chronic pyelonephritis, kidney tuberculosis, nephrolithiasis, developmental anomalies (medullary hypoplasia, renal dysplasia, tubulomedullary dilatation), hydronephrosis, pelvic-renal reflux, malignant neoplasms. In addition to the observation of a urologist or nephrologist, the patient may need to consult an oncologist, infectious disease specialist, endocrinologist, hematologist.

Treatment of renal papillary necrosis

The choice of medical tactics is determined by the causes and characteristics of the course of necrotic papillitis. If possible, treatment should be etiopathogenetic, aimed at correcting the primary disorder, which was complicated by papillary necrosis, restoring normal hemoperfusion of the renal parenchyma, and combating uroinfection. In an acute course, an important role is played by the relief of the symptoms that have arisen - renal colic, occlusion of the pelvis and ureter with necrotic masses, bleeding from damaged papillae.

Combination therapy for acute papillary renal necrosis provides for a standard treatment regimen for the underlying disease, against which papillitis developed, in combination with such medications and invasive methods as:

• Antibacterial drugs. Antibiotic therapy, if possible, is prescribed taking into account the sensitivity of the pathogen that caused the inflammatory process. The most effective is the use of uroantiseptics without nephrotoxic action - fluoroquinolones, nitrofurans, cephalosporins, fosfomycins, macrolides, derivatives of nalidixic and pipemidic acids.
• Means for improving renal hemodynamics. When choosing a medication, the causes of ischemia are taken into account. Peripheral vasodilators are recommended as basic ones, which, if necessary, are supplemented with direct anticoagulants, antiplatelet agents. Auxiliary drugs are antioxidants and membrane stabilizers that increase the ischemic resistance of papillary structures.
• Hemostatic therapy. Means for stopping bleeding are indicated with the predominance of signs of severe and massive hematuria in the clinical picture. Usually fresh frozen or antihemophilic plasma, aminocaproic acid preparations, fibrinolysis inhibitors, etamsylate analogues are used. The use of hemostatics is limited in papillary necrosis caused by thrombosis.
• Removal of necrotic masses. If the sloughing tissue of the papilla causes occlusion of the renal pelvis and ureters, they are catheterized. Subsequent stenting of the ureter can reduce pelvic hypertension and ensure a normal passage of urine. Necrotic masses can also be removed during ureteroscopy, retrograde or percutaneous nephroscopy (pyeloscopy).

With an increase in symptoms against the background of ongoing conservative therapy, the occurrence of therapeutically resistant acute pyelonephritis lasting more than 2-3 days, intractable profuse hematuria, surgical treatment is recommended. With a bilateral necrotic process, organ-preserving interventions are preferable - nephrostomy, decapsulation of the kidney, resection (partial nephrectomy) to remove the area with bleeding papillary structures. Radical nephrectomy is performed only for unilateral papillitis with total irreversible necrosis of the medullary layer and sufficient functionality of the contralateral kidney.

Treatment of chronic papillary necrosis involves long-term combined antibiotic therapy with broad-spectrum uroseptic antibiotics, nitrofurans, sulfonamides. Antimicrobial agents are used for 4-6 months in 8-14 day courses with interruptions, while it is recommended to prescribe drugs from at least two different groups, taking into account data on the sensitivity of the microflora. Treatment is supplemented with the use of peripheral vasodilators, anticoagulants, venotonic agents from the rutoside group.

Forecast and prevention

With early diagnosis and pathogenetic therapy, it is possible to regenerate the epithelium with the restoration of all kidney functions. The prognosis for necrosis of the renal papillae is relatively favorable. Thanks to the use of modern antibacterial drugs, mortality in acute necrotizing papillitis has been reduced from 50% to 10%.

Prevention of papillary necrosis consists in the timely treatment of infectious processes of the urinary system, nephrolithiasis, systemic vasculitis, toxic kidney damage, and the reasonable prescription of NSAIDs. An important link in the prevention of the disease is dispensary observation of patients at risk with careful medical control of diabetes mellitus, sickle cell anemia.

RENAL NECROSIS (PAPILLARY AND CORTICAL)(synonyms: papillonekrosis, necrotizing pyelonephritis).

Papillonekrosis. Etiology and pathogenesis. Most often it occurs as a complication of various diseases (diabetes mellitus, nephrolithiasis, etc.), less often - as a primary kidney lesion. In adults, a common cause of papillonecrosis is analgesic nephropathy resulting from long-term use of analgesics. The leading role in the development of the disease belongs to Escherichia coli, which penetrates into the papillae of the kidneys more often by contact (from the mucous membrane of the pelvis), in some patients - by the hematogenous route. The development of the disease is facilitated by an increase in pressure in the pelvis, followed by a circulatory disorder in the pyramids of the kidneys, which can also be observed in hypertension, thrombosis, etc. Papillary necrosis can be one- or two-sided, accompanied by damage to one or more papillae, which differ in sharp pallor and are clearly demarcated from adjacent tissue. Abscesses and an ulcerative necrotic process with rejection of the affected areas are often found in them. Morphologically, significant neutrophilic infiltration is noted in the affected papillae, with a protracted course of the disease - sclerosis.

Papillonekrosis) is the clinical picture. The main clinical signs are an acute onset with a deterioration in the general condition against the background of the underlying disease (diabetes mellitus, etc.), severe pain in the lumbar region, high fever, chills, oliguria, and other symptoms of acute renal failure. Severe leukocyturia and bacteriuria, hematuria, and sometimes pieces of renal papillae in the urine are observed. Possible recovery, death, as well as the transition to a relapsing course, characterized by bouts of pain in the abdomen, lower back, in the area of ​​the affected kidney, and. Relapses usually occur during an exacerbation of the underlying disease and under the influence of other factors (overwork, infections, etc.). During this period, increased ESR, marked leukocytosis, limited tubular functions and glomerular filtration in some patients. With excretory urography, deformation of the cups is revealed, in the later stages - a picture of chopped off papillae.

Papillonekrosis) - d diagnosis. It is based on the sudden appearance of a septic condition and signs of acute renal failure in the presence of a pronounced urinary syndrome.

Papillonekrosis must be differentiated from acute pyelonephritis, urolithiasis complicated by a bacterial infection.

Treatment. It should be aimed at eliminating the bacterial infection using drugs with a broad antimicrobial spectrum of action, which have minimal or moderate nephrotoxicity and do not cause an allergic reaction in a particular patient. Gentamicin (0.4 mg / kg 2 times a day), erythromycin (at the age of 2 years - 5-8 mg / kg 4 times a day, after 2 years - 0.5-1.0 g / day) and other drugs are prescribed in courses of 7-10 days. In case of recurrent papillonecrosis, in addition to repeated courses of antibiotic therapy, it is necessary to take measures to increase the body's reactivity. The development of acute renal failure requires appropriate tactics.

Cortical necrosis of the kidneys. It is observed mainly in infancy against the background of a bacterial infection (streptococcus, staphylococcus, intestinal and meningococcal infection, etc.) and is caused by damage to the interlobular and arcuate arteries, leading to ischemic necrosis of the renal tissue. In the cortical layer of the kidneys, necrosis of glomerular loops is found, total or in the form of foci.

Clinical picture. Clinical manifestations and outcome of cortical necrosis depend on the extent of the necrotic process. Symptoms of acute renal failure (oligoanuria, hyperazotemia, electrolyte disorders), hematuria are leading in focal and total necrosis, which, as a rule, ends in death. With focal cortical necrosis, reverse development of renal failure and recovery are possible. In such patients, excretory urography after a few months often reveals calcifications at the site of necrosis foci.

Kidney necrosis is a pathological process that manifests itself in swelling, denaturation and coagulation of cytoplasmic proteins, cell destruction. The most common causes of necrotizing kidney injury are interruption of the blood supply and exposure to pathogenic products of bacteria or viruses.

The kidney is a paired bean-shaped organ, its main function is to form urine and regulate the body's chemical homeostasis (blood filtration). The right kidney is slightly shorter, usually located 2-3 cm below the left kidney, it is more susceptible to any diseases. On the upper parts of the kidneys there are adrenal glands that produce the hormones adrenaline and aldosterone, which in turn regulate fat, carbohydrate and water-salt metabolism, the functioning of the circulatory system, the muscles of the skeleton and internal organs.

It is known that among the numerous diseases of the kidneys that affect more women than men, which is associated with physiological characteristics, there are extremely severe forms of damage to this organ as a result of various complications.

Types of kidney necrosis

Complex pathological changes in the kidneys occur with cortical necrosis.

This is a rare disorder in which there is complete or partial loss of tissue on the outside of the kidneys, while the inside of the kidneys may remain intact. This type of necrosis is manifested by the same symptoms as any manifestation of renal failure.

There is a sudden and sharp decrease in urine production and blood is found in it, an increase in body temperature is noted. Blood pressure rises or falls, cardiac and cardiogenic pulmonary edema appears. Cortical necrosis, as a rule, occurs due to blockage of small arteries that feed the cortical substance.

Cortical necrosis affects the kidneys at any age.

In children, and not infrequently in infants, the cause of necrosis can be bacterial infection of the blood, dehydration (dehydration) and acute (hemolytic-uremic syndrome). In adults - bacterial sepsis. In half of the cases, necrosis affects the cortex of the kidneys of women with a sudden separation of the placenta, with its incorrect location, uterine bleeding, blockage of the artery by amniotic fluid, etc.

Other possible causes include rejection of a transplanted kidney, inflammation of the pancreas, traumatic injury, snakebite, and arsenic poisoning. Organic and functional disorders can be expressed by destructive processes in the medulla of the kidney - this leads to necrosis of the renal tubules (papillae) or necrotic papillitis.

The development of the disease is accompanied by prolonged vasospasm, thrombosis, atherosclerosis, kidney injury, abuse of analgesics, the process of dissolving and removing stones from the kidneys and gallbladder, and urinary infection. There is a high risk of acute tubular necrosis in patients who have suffered severe injuries and injuries, in those who undergo surgery for a dissecting aortic aneurysm.

If the lack of oxygen (ischemia) of the papilla is not associated with inflammation of the kidneys, then necrosis of the renal papillae is called primary, secondary - if its development is associated with inflammation of the kidney tissue (pyelonephritis). Rejection of the affected papilla causes bleeding and ureteral occlusion. Clinical manifestations of primary necrosis are usually characterized by a chronic relapsing course, and secondary are combined with manifestations of pyelonephritis.

The detachment of the calcified papilla causes renal colic, and after this, the appearance of blood in the urine is also characteristic. As a result of a decrease in filtration or an increase in reabsorption in the kidneys, the amount of urine decreases. It is possible to confirm the presence of pathology only by identifying characteristic changes in the shape of small cups. The remission period should be aimed at improving microcirculation, eliminating bacteriuria and arterial hypertension.

With early diagnosis, kidney function is partially restored, but most patients are indicated for kidney transplantation or permanent dialysis, a procedure that performs the functions of the kidneys. Currently, any kidney disease is successfully diagnosed and treated. Continuous examination allows you to detect and prevent the development of necrosis in advance.

Recovery depends on the stage of the disease, a fatal outcome is possible during the transition to a relapsing course. During treatment, all actions should be aimed at eliminating the bacterial infection with the help of drugs with a wide antimicrobial spectrum of action, and at increasing the body's reactivity.

Expert editor: Mochalov Pavel Alexandrovich| MD therapist

Education: Moscow Medical Institute. I. M. Sechenov, specialty - "Medicine" in 1991, in 1993 "Occupational diseases", in 1996 "Therapy".

Every person suffering from at least some chronic pathology should be aware of the first signs of death of kidney tissue, which is called renal necrosis.

kidney necrosis

Necrosis of the kidneys is the process of necrosis of the cells of the kidney tissue. As a result of the research, it was found that kidney necrosis is characterized by swelling of cells and protein structures in them, followed by destruction (lysis).

Necrotic changes in the kidneys can occur as a result of severe intoxication with any poisonous substances, as a result of the development of autoimmune processes in the human body. Quite often, the cause of the destruction of kidney cells is a decrease in blood flow in the organ itself. With a decrease in the degree of blood supply, ischemia and hypoxia of the cellular system of the kidney develops, and then the destruction of cells.

Violation of blood flow to the kidney may occur due to thrombosis of the renal vessels or obstruction of the urinary tract by a stone or neoplasm.

Often, kidney necrosis develops in pregnant women and parturient women, this is due to heavy bleeding from the uterine cavity or premature detachment of a normal or pathologically placed placenta.

In children, this pathology occurs against the background of a viral or bacterial disease as a complication of dehydration (with profuse vomiting or diarrhea).

Kinds

Necrosis of epithelial cells of convoluted tubules

Toxic substances affect the most sensitive areas of the kidneys - the epithelium of the tubular apparatus.

The role of toxic substances can be:

• Pesticides that are part of various toxic substances or detergents;
• Heavy metal compounds, often mercury, lead and arsenic;
• Ethylene glycol is a representative of organic solvents.

In the photo, necrotic changes in the epithelial cells of the convoluted tubules of the kidneys or acute tubular necrosis - micropreparation

A. - Non-nuclear cells; B. - Preserved nuclei in the cells of the loop of Henle; B. The vessels are filled with blood and dilated.
Also, a possible cause of acute tubular necrosis can be an injury, which consists in severe squeezing of the organ, as a result of which blood flow to the tubules of the kidneys is disturbed.

In case of blockage of the ureter due to a violation of the outflow of urine, the tubules expand, their epithelium becomes necrotic and desquamated.

This type of necrosis manifests itself with acute or gradual urinary retention, blood initially appears in the urine, and the frequency of urination per day decreases. Very often, patients feel discomfort and sharp pain in the lumbar region. The patient may have a fever. Such symptoms occur due to the development of a dangerous pathological condition with kidney dysfunction - renal failure.

Acute tubular necrosis of the kidneys - macropreparation

cortical

Necrosis of the cortical substance of the kidneys (cortical) is more common in newborns or in pregnant women.

Pathogenetically, necrosis of the cortex is due to increased intravascular coagulation locally in the kidneys or totally (in the bloodstream of the whole organism). The blood coagulates intensively due to a decrease in the level of fibrinogen and an increase in the concentration of thromboplastin and thrombin. There is a blockage of the blood-carrying (afferent) renal arterioles, which leads to disruption of the blood supply and shrinkage of the kidney.

As a result of criminal abortion under inappropriate conditions, bacteria enter the bloodstream and release toxins. A sharp intake of such toxins in large quantities into the blood provokes the development of a shock state (endotoxic shock).

In shock conditions, the blood flow becomes centralized, blood does not enter the cortical layer of the kidneys in a normal amount, and necrosis occurs.

Quite often, necrotic changes in the cortical layer end with the deposition of calcifications.

Symptoms for this type of pathology can be varied: there is urination with blood, the frequency of urination decreases until it is completely absent. There may be pain in the back (lower part), in the abdomen, vomiting and severe nausea, fever. If the process of intravascular coagulation is total, symptoms of damage to other organs join. Hemorrhages appear on the skin.

Cortical necrosis of the kidney

Papillary

The main etiological factor in the development of necrotic changes in the cells of the papillae of the kidneys is a bacterial infection. Bacteria can enter the pelvis from outside through the urinary tract, and are also transferred to the kidney with blood (hematogenous route). With an increase in urine pressure in the pelvis, bacteria spread to one or more papillae. As a result, cell lysis develops, blood flow to the kidney pyramids is disturbed.

The symptomatology is represented by a pronounced febrile state, pain syndrome, pronounced intoxication signs.

Papillary necrosis of the kidneys

Cheesy

Necrosis of the renal tissue of the caseous type usually develops at the site of growth and development of tuberculous or syphilitic granulomas (growths). Often the cause of this pathology can be a disease such as leprosy. Caseous areas resemble curdled mass on examination. Under the microscope, the homogeneous nature of the kidney tissue, destroyed cells and connective tissue fibers are noted.

Diagnosis of tuberculosis and syphilis by initial clinical manifestations is quite difficult. There may be periods of a significant rise in body temperature, for a long time leukocytes and erythrocytes can be detected in the urine in large quantities.

The diagnosis can be confirmed by laboratory and instrumental studies. The most informative diagnostic method is considered to be a puncture biopsy of the kidney.

Caseous nephrosis

Focal

Focal necrosis of the renal tissue is usually caused by bacterial flora (syphilis, tuberculosis, leprosy and some other diseases). Symptoms are similar to those in the above forms of kidney necrosis.

Treatment

The main principles of the treatment of kidney necrosis are to eliminate the root cause of the pathological process. For this, it is necessary to carry out a complete clinical and laboratory examination.

Therapeutic measures depending on the etiology and pathogenetic mechanisms of the development of the disease:

• Antibacterial therapy;
• Improvement of hemodynamics (anticoagulant therapy);
• Elimination of obstructive urinary tract syndrome (possible and formation of a nephrostomy).
• Elimination of signs of renal failure and elimination of toxic substances (using hemodialysis);
• To relieve pain, antispasmodics or non-narcotic / narcotic analgesics are prescribed.

Surgical interventions are carried out only in severe cases of the development of the disease. If necrosis covers almost the entire area of ​​\u200b\u200bthe kidney, then it is completely removed ().

If the cause of necrosis is vascular thrombosis, then thrombectomy and angioplasty with a balloon are widely used.

The prognosis for early detection of signs of ischemia of the renal tissue is quite favorable. Areas of necrosis as a result of timely and proper treatment are compacted and turn into a scar. And the surrounding active kidney cells compensate for their work.

Attention! In order to prevent necrosis of the renal tissue, it is recommended to be attentive to your health, to control the state of the cardiovascular, endocrine, and genitourinary systems. And when the slightest alarming symptoms appear, you should immediately consult a doctor!