Papillary necrosis of the kidneys. Kidney necrosis, symptoms, treatment, causes. Acute tubular necrosis

Very often, as a complication of various diseases of the renal tissue, a pathological condition develops, which is called papillary necrosis.

Papillary necrosis - what is it?

Papillary necrosis (necrotizing papillitis) is a degenerative-destructive change in the structure of the renal papilla for any specific reason. This disease affects the medulla of the kidneys and causes changes in the functional abilities of the urinary organs. Papillary necrosis is also called necrotizing papillitis, since the process is caused by inflammation of the renal papillae.

Causes

Most credible reason necrosis of the renal papillae is considered to be entering them coli, which provokes the development of the inflammatory process. Due to prolonged inflammation in tissues, cell degeneration occurs and scarring is possible, which significantly affects the function of the organ.

There are several precisely established causes and associated mechanisms for the development of necrotizing kidney papillitis:

Increased urine pressure in the renal pelvis. The pressure increases due to excessive accumulation of urinary fluid in the cavity of the pelvis and disruption of its outflow. The cause may be obstructive syndrome (tumor, ureteral stone). Also, a special role in the development of necrotizing papillitis is played by the backflow of urine into the renal pelvis and calyces for some reason. Thus, bacteria contained in the urine enter the renal papillae and provoke inflammation.
Disturbances in blood flow in the medulla of the kidneys or abnormalities in the structure of the renal vessels. If available atherosclerotic changes in the vessels or with the development of thrombosis, the blood flow to the papillary apparatus of the kidney is disrupted, this condition is called ischemia. Later, the ischemic stage is replaced by the necrotic stage.
Purulent processes in the kidney. Education purulent infiltrates or cavities filled with fluid can become one of the causes of impaired blood flow in the kidney and ischemia.
Blood pathology associated with changes in its qualitative composition and characteristics related to coagulation.
Uncontrolled use of painkillers can lead to changes in the vasa recta that supply blood to the renal papillae, thereby causing necrosis.
Sickle cell anemia.

Necrotic renal papillae are rejected and may cause occlusion urinary tract, can form coral-type stones over time.

Papillary necrosis

Signs and symptoms

Necrotizing papillitis clinical manifestations classified into two forms: acute and chronic.
Acute medullary necrosis is accompanied by high fever with chills, pain syndrome characteristic of renal colic and urination with a significant admixture of blood (gross hematuria). If you don't provide it on time medical care the patient rapidly develops severe renal failure.

The chronic form of necrotizing papillitis is accompanied by pain syndromes (as with colic) that occur with a certain frequency. Leukocyte cells and red blood cells, protein casts of the tubules are found in the urine. Often patients with this pathology complain of infections urinary tract which constantly recur.

The main and most reliable symptom of papillary necrosis is the separation of gray masses of dense consistency along with urine.

Diagnostics

To make a diagnosis of necrosis of the renal papillae, not only laboratory confirmation is necessary, but also data from instrumental research methods. Research methods using x-ray radiation. On examination, one can often detect sclerosis of the medullary substance of the kidney (has the outline of a pyramid). When performing excretory or retrograde urography, you can notice changes in the contours of the papillae themselves, the formation of ulcerative defects on them, rejection of necrotic areas and calcifications. Sometimes the contrast agent flows into the formed fistulous tracts, thus it is possible to study the extent of the destructive process in the kidney.

In this case, ultrasound diagnostics, and radioisotope methods research is uninformative.

Papillary necrosis according to the image

Treatment

For effective treatment of papillary necrosis, it is necessary to eliminate causal factors that caused the progression of the disease.

In the presence of purulent foci, antibacterial therapy should be prescribed; if an abscess or other neoplasms form that cause compression of the renal medulla - urgent surgery(impose a nephrostomy, excise the kidney capsule and many other operations). Nephrectomy surgery is rarely resorted to, since the process, in most cases, is bilateral.

Antiplatelet agents and anticoagulants are mandatory to improve blood rheology.

When the urinary tract is occluded by necrotic masses, it is necessary to restore the normal outflow of urine. If the cause of the disease is excessive use of analgesic drugs, stop taking them.

To prevent the development of medullary necrosis, it is necessary to be attentive to the state of your health, especially those who suffer from diabetes mellitus, sickle cell anemia, and systemic vasculitis. If any minor symptoms of renal dysfunction appear, you should immediately visit a doctor and undergo a full examination.

This is the destruction of the renal papillae caused by ischemia of the Malpighian pyramids. Appears in episodes renal colic, nagging pain in the lower back, hematuria, discharge of necrotic papillae. Diagnosed using general and bacteriological urine analysis, excretory urography, ureteropyeloscopy. For treatment, antibacterial therapy, peripheral vasodilators, anticoagulants, antiplatelet agents, membrane stabilizers, antioxidants, hemostatics, and venotonics are prescribed. If necessary, catheterization and stenting of the ureter, pelvis, kidney decapsulation, 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 30-40 years of age. 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 observational results, ischemic destruction of the upper part of the Malpighian pyramids is associated with diabetes mellitus and sickle cell anemia, but in last years increasingly occurs in other pathological conditions.

Causes

Necrotizing papillitis is a polyetiological disease that develops against the background of other pathological conditions or the intake of nephrotoxic substances. Features are considered a prerequisite for the occurrence of necrosis anatomical structure medullary substance - hypoxia of the renal papillae is promoted by the 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 identified several groups of causes causing papillary destruction:

Impaired blood supply to the medulla. Insufficient blood supply to the papillary apparatus is observed with changes vascular wall in patients with atherosclerosis, diabetes mellitus, vasculitis. Ischemia of papillary structures is provoked by diseases in which thrombosis of the renal microvessels is possible, most often necrotizing papillitis is complicated by sickle cell anemia, less often by coagulopathies, disseminated intravascular coagulation syndrome and other hypercoagulable conditions.
Increased intrapelvic pressure. With obstruction of the urinary tract, the outflow of urine is disrupted with its accumulation in the pelvic system. The resulting pyelorenal reflux contributes to the contamination of the renal papillae with bacteria contained in urine and the onset of an inflammatory reaction. In most cases, pelvic hypertension is formed due to obstruction of the ureter with a stone, neoplasm, accidental ligation during surgery, or the presence of a ureterovaginal fistula.
Purulent kidney diseases. Secondary inflammation of the apices of the renal pyramids complicates the course of severe purulent-destructive processes. The massive proliferation of infectious pathogens that secrete proteolytic exotoxins contributes to the formation of purulent infiltrates and melting of the kidney parenchyma, involving the papillae in the process of destruction. Papillary necrosis can develop against the background of pyelonephritis, apostematous nephritis, pyonephrosis, renal carbuncle, abscess.
Drug-induced nephropathy. Long-term uncontrolled use of certain over-the-counter analgesics and antipyretics leads to disruption of medullary blood flow, deterioration of perfusion of the cortex and medulla, and the development of analgesic nephropathy. In the most severe cases, against the background pronounced changes direct vessels feeding the renal papillae, their severe 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, vasocompression, infectious, which are often combined, leading to ischemic infarction of the medulla with its subsequent purulent melting and rejection of necrotic masses. A decrease in the lumen of the papillary arterioles due to thickening of the intima, thickening of the wall, compression by purulent foci or interstitium infiltrated by urine, and complete obstruction of their lumen by blood clots contribute to the occurrence of ischemia and tissue destruction.

The situation is aggravated by a narrowing of the diameter of the vessels supplying the papillae towards the apex, 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 the fatty tissue into which urine penetrates. An ischemic papilla may be subject to complete or partial destruction with damage to individual areas in the center or periphery. In severe cases, the entire Malpighian pyramid becomes necrotic; in case of multiple localization, the entire medullary layer of the affected kidney becomes necrotic. When an infection occurs, the necrotic process is complicated by an inflammatory reaction.

Classification

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 necrotizing 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-sclerotic changes in the parenchyma and renal sinus.

With initial damage to the papilla, they speak of a papillary form of destruction; with the primary formation of focal infarctions in the inner medullary zone with subsequent involvement of the apices of the Malpighian pyramids, they speak of a medullary form. Taking into account the characteristics of the flow, the following are distinguished:

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 papillitis that complicates pyelonephritis, other purulent nephrological diseases, nephrolithiasis.
Chronic papillary necrosis. Usually the symptoms are 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 signs, most of which are nonspecific. Often with papillary necrosis, renal colic occurs due to separation of the necrotic papilla, which may be accompanied by nausea, vomiting, and stool retention. Typical are constant nagging pain in the lumbar region and bleeding in the urine.

Patients experience intoxication syndrome of varying severity: low-grade or febrile fever, chills, headache, increased sweating, weakness. A pathognomonic sign of necrotizing papillitis, detected only at a late stage of the disease, is the excretion of dead areas in the urine renal parenchyma in the form of grayish masses with inclusions of lime salts. In a chronic course, laboratory symptoms may predominate with mild or absent clinical symptoms.

Complications

In the case of a bacterial infection, apostematous pyelonephritis occurs, manifested by the formation of small abscesses in the cortex of the kidney. With extensive damage, a clinical picture of acute renal failure is revealed - oliguria or anuria, increased levels 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 kidney stones with a high risk of developing coral stones. Massive papillary necrosis is often accompanied by profuse bleeding, which poses a danger to the patient’s life and requires emergency care.

Diagnostics

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

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

In a clinical blood test for papillary renal necrosis, signs of bacterial inflammation are determined: neutrophilic leukocytosis with an increase in the number of band cells, an increase in ESR. For a comprehensive assessment of the condition of the urinary system, ultrasound and CT scans 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 make it possible to identify associated pathological conditions- urolithiasis, pyelonephritis.

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

Treatment of renal papillary necrosis

Choice medical tactics determined by the causes and characteristics of the course of necrotizing papillitis. If possible, treatment should be etiopathogenetic, aimed at correcting the primary disorder, which is complicated by papillary necrosis, restoring normal hemoperfusion of the renal parenchyma, and combating uroinfection. At acute course important role plays a role in relieving the symptoms that have arisen - renal colic, occlusion of the pelvis and ureter by necrotic masses, bleeding from damaged papillae.

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

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 effects - 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 and antiplatelet agents. Auxiliary drugs are antioxidants and membrane stabilizers, which increase the ischemic resistance of papillary structures.
Hemostatic therapy. Drugs to stop bleeding are indicated when signs of severe and massive hematuria predominate in the clinical picture. Typically, fresh frozen or antihemophilic plasma, aminocaproic acid preparations, fibrinolysis inhibitors, and ethamsylate analogues are used. The use of hemostatic agents is limited for papillary necrosis caused by thrombosis.
Removal of necrotic masses. If sloughing papillary tissue causes occlusion of the renal pelvis and ureters, they are catheterized. Subsequent ureteral stenting can reduce pelvic hypertension and ensure normal urine passage. Necrotic masses can also be removed during ureteroscopy, retrograde or percutaneous nephroscopy (pyeloscopy).

When symptoms increase during conservative therapy, or when therapeutically resistant acute pyelonephritis, lasting more than 2-3 days, intractable profuse hematuria is recommended surgical treatment. In case of a bilateral necrotic process, organ-preserving interventions are preferred - nephrostomy, kidney decapsulation, 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 antibacterial therapy uroseptic antibiotics wide range actions, nitrofurans, sulfonamides. Antimicrobial agents are used for 4-6 months in 8-14 day courses with breaks, and 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, and venotonic agents from the rutoside group.

Prognosis and prevention

At early diagnosis and carrying out pathogenetic therapy, regeneration of the epithelium is possible 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 of timely treatment of infectious processes of the urinary system, nephrolithiasis, systemic vasculitis, toxic kidney damage, and justified prescription of NSAIDs. An important link in preventing the disease is clinical observation of patients at risk with careful drug control of diabetes mellitus and sickle cell anemia.

Kidney necrosis is a disease accompanied by a violation of the separation of cytoplasmic proteins. As a result, a characteristic process of cell destruction occurs. This disease is often observed when the blood supply is disrupted, as well as due to exposure to pathogens - bacteria or viruses.

What types of kidney necrosis are there, symptoms, causes? of this disease what are they? Let's talk about it today:

Classification of necrosis

There are the following types of this pathology:

Prerenal failure: this type of necrosis is characterized by a pronounced impairment of the functionality of the organ, due to a general disturbance of hemodynamics. This type often turns into renal failure, since impaired renal blood flow is the main cause of ischemia.

Renal failure: In this type, the functionality of the kidney is impaired due to damage to the organ tissue. Typically, renal failure occurs after warm ischemia or cold ischemia.

Postrenal failure: With this type, kidney function is usually not affected. Difficulty or lack of urine excretion occurs due to damage to the urinary tract. This type can become renal when the renal pelvis, overfilled with urine, compresses the kidney tissue, which contributes to the occurrence of ischemia.

Why does kidney necrosis occur? Causes of the condition

In children and infants, this disease can occur due to the penetration of bacteria into the blood, as well as due to dehydration (dehydration), or due to hemolytic-uremic syndrome (acute diarrhea). The cause of kidney necrosis in adults is often bacterial sepsis.

In pregnant women, pathology may develop due to sudden separation of the placenta, or due to its incorrect location. In addition, this pathology is diagnosed with severe uterine bleeding, when the artery fills amniotic fluid and etc.

Other reasons include: rejection of a transplanted kidney that has not taken root, kidney injuries, inflammatory diseases pancreas. The pathological process can be provoked by the bite of a poisonous snake, as well as arsenic poisoning.

Necrotizing papillitis or necrosis of the renal tubules often develops due to organic or functional disorders, which are characterized by destructive processes and changes in the medulla of the kidney.

Necrosis can be provoked by diseases such as diabetes mellitus, prolonged vasospasm, as well as thrombosis, atherosclerosis, anemia, urinary infection, etc. There is a high risk of developing acute tubular necrosis in patients who have suffered severe renal injuries, as well as in those who have suffered surgery dissecting aortic aneurysm.

How does kidney necrosis manifest? Symptoms of the disease

The main sign of developing necrosis is deterioration general condition occurring against the background of the underlying disease. Patients complain of strong lumbar pain, severe hyperthermia. There is high oliguria and other manifestations of acute renal failure. In this case, signs of serious leukocyturia, bacteriuria, and hematuria appear. Sometimes pieces of renal papillae are found in the urine.

If you consult a doctor in a timely manner, when timely treatment, the patient makes a full recovery. Otherwise, the disease may progress to a relapsing course with severe attacks of renal colic. A severe course without the necessary, timely treatment can result in death.

How is kidney necrosis corrected? state

The main thing in the treatment of this disease is diagnosis and elimination of the underlying pathology that caused necrosis. Carry out therapeutic measures aimed at improving and restoring blood microcirculation, eliminating bacteriuria, dehydration and arterial hypertension.

In the presence of complications, which often arise due to ureteral resistance with massive hematuria, the patient is subject to emergency hospitalization.

In order to restore and normalize the passage of urine, the patient is shown catheterization of the renal pelvis with the application of a nephrostomy. Medication consists of taking antibiotics. In case of acute renal failure, the patient undergoes hemodialysis. Patients with polyuria are advised to drink more and not limit salt intake.

Kidney necrosis, signs, therapy, the causes of which we discussed with you today - a pathology with very serious negative consequences. To prevent or reduce the risk of developing necrosis, diseases that may cause its occurrence should be promptly treated. Be healthy!

What types of kidney necrosis are there, symptoms, treatment, causes of this disease, what are they? Let's talk about it today:

Classification of necrosis

There are the following types of this pathology:

Renal failure: In this type, the functionality of the kidney is impaired due to damage to the organ tissue. Typically, renal failure occurs after warm ischemia or cold ischemia.

Why does kidney necrosis occur? Causes of the condition

In pregnant women, pathology may develop due to sudden separation of the placenta, or due to its incorrect location. In addition, this pathology is diagnosed when there is severe uterine bleeding, when the artery is filled with amniotic fluid, etc.

Other reasons include: rejection of a transplanted kidney that has not taken root, kidney injuries, inflammatory diseases of the pancreas. The pathological process can be provoked by the bite of a poisonous snake, as well as arsenic poisoning.

How does kidney necrosis manifest? Symptoms of the disease

The main sign of developing necrosis is a deterioration in the general condition that occurs against the background of the underlying disease. Patients complain of severe lumbar pain and severe hyperthermia. High oliguria and other manifestations of acute renal failure are observed. In this case, signs of serious leukocyturia, bacteriuria, and hematuria appear. Sometimes pieces of renal papillae are found in the urine.

If you consult a doctor in a timely manner and receive timely treatment, the patient will fully recover. Otherwise, the disease may progress to a relapsing course with severe attacks of renal colic. A severe course without the necessary, timely treatment can result in death.

How is kidney necrosis corrected? Treatment of the condition

The main thing in the treatment of this disease is diagnosis and elimination of the underlying pathology that caused necrosis. Therapeutic measures are carried out aimed at improving and restoring blood microcirculation, eliminating bacteriuria, treating dehydration and arterial hypertension.

In the presence of complications, which often arise due to ureteral resistance with massive hematuria, the patient is subject to emergency hospitalization.

In order to restore and normalize the passage of urine, the patient is shown catheterization of the renal pelvis with the application of a nephrostomy. Drug treatment consists of taking antibiotics. In case of acute renal failure, the patient undergoes hemodialysis. Patients with polyuria are advised to drink more and not limit salt intake.

Kidney necrosis, signs, therapy, the causes of which we discussed with you today is a pathology with very serious negative consequences. To prevent or reduce the risk of developing necrosis, diseases that may cause its occurrence should be promptly treated. Be healthy!

A large number of people are susceptible to diseases of the urinary system. Almost every second person has cystitis or pyelonephritis. But these are far from the most formidable processes that can occur. The complications of these diseases are much more severe.

One of them is kidney necrosis. This condition is characterized by a disruption of the normal structure cellular proteins, as a result of which the cells themselves begin to collapse.

Why is this happening?

Most often, renal necrosis develops for the following reasons:

bacteremia, or the entry of bacteria into the bloodstream due to general infectious processes;

severe dehydration, including acute diarrhea;

sublimate poisoning;

injury;

necrosis of the epithelium of the convoluted tubules of the kidney can develop in the presence of functional disorders in the functioning of the renal system;

urinary tract outflow disorders and infections Bladder;

kidney injuries.

Pregnant women should be placed in a separate group. In them, acute necrosis develops against the background of sudden placental abruption or with anomalies of attachment.

What types of necrosis are there?

All necrosis of renal tissues is divided into 3 types:

Prerenal failure. In this type, normal functioning is disrupted due to changes in hemodynamics. A decrease in blood flow leads to further development process.

Renal failure. The renal tubule is damaged due to ischemia. The functions of the organ will also be impaired.

Postrenal failure. With this type of necrosis, the functional component is not impaired. Destruction occurs due to damage to the walls of the bladder or ureters, as a result of which the outflow of urine is obstructed.

What will be the manifestations?

Next, the patient experiences paroxysmal pain in the lumbar region, which cannot be relieved with conventional painkillers. The amount of urine excreted is reduced to 50 ml per day. Clinical urine analysis reveals leukocytes in large quantities, bacteria, and sometimes even blood.

Cortical vascular necrosis

How to treat?

Treatment begins with identifying the underlying disease that led to the development of necrosis. The doctor carries out the necessary diagnostic tests, allowing us to determine the nature of the pathogen and the degree of damage to the tubules.

First of all, broad-spectrum antibiotics are prescribed. After receiving the results of a urine test, it is possible to replace it with a narrower drug.

If there has been damage to the ureters and bladder, then the causes that caused them are treated. If a stone is present, its destruction is carried out. In more severe cases, catheterization of the renal pelvis is performed to form a nephrostomy.

The acute process can be relieved by hemodialysis. But this method of removing toxins is best left as a last resort, since the clinic does not always have such a device, and unnecessary transportation of a patient in serious condition is not recommended.

In addition, the general condition of the body is corrected. Lost fluid is replenished, adaptogens and bed rest are prescribed.

From general recommendations You can also have a special diet and drinking regimen. Spicy and salty foods and smoked foods should be completely excluded from the diet. A diet low in salt and protein is prescribed. You need to drink at least 2 liters of fluid per day so that the amount does not decrease, as diuretics are used.

Kidney diseases are very serious pathologies that can lead to a significant deterioration in the patient’s quality of life. All urinary tract infections should be treated promptly. Bacterial carriage is also not allowed, since when the body’s immune defense is reduced for one reason or another, pathogens can become more active. Regular examinations and observations by your doctor will help prevent the development of serious complications and maintain health.

Kidney necrosis: symptoms and treatment

Factors causing pathology

Necrosis of the papillae with diabetes mellitus

IN childhood kidney necrosis occurs as a result of the introduction of bacteria and viruses into the blood, dehydration and acute diarrhea. In adults, it is often caused by bacterial sepsis. In 50% of cases, necrosis affects the kidneys of women due to sudden separation of the placenta, its incorrect location, uterine bleeding, etc. Rejection of a transplanted kidney, burns, inflammation in the pancreas, and previous injuries can lead to the development of the disease. Certain diseases also cause necrosis of the convoluted tubule epithelium. In this case, patients may not seek help from a specialist for a long time, mistaking the symptoms of the disease for manifestations of an existing disease. As a result, necrosis takes on an advanced form, which is much more difficult to treat.

Diseases that cause necrosis include diabetes mellitus, prolonged vasospasm, thrombosis, kidney damage, anemia and infection in the urine. Can provoke the development of the disease frequent use analgesics and actions aimed at dissolving and removing kidney stones. The risk group includes people who have previously received severe injuries and trauma, as well as those who have already undergone surgery for a dissecting aortic aneurysm.

Establishing diagnosis

Necrosis is characterized by gross hematuria, pain in the lower back, decreased diuresis, fever, impaired renal function in combination with arterial hypertension. However, it should be remembered that these symptoms can often be manifestations of an underlying disease. Various diagnostic methods help to recognize the disease.

MRA is one such method, the main advantage of which is the high accuracy of the results. MRA is performed without the administration of nephrotoxic contrast agents. However, the procedure is not without its drawbacks: it is time-consuming and can be difficult for critically ill patients.

CTA does not require much time, but is accompanied intravenous administration contrast, which may be nephrotoxic.

Isotope renography using diethylenetriaminepentacetinic acid allows you to see an enlarged kidney without obstruction to the outflow of urine with low or absent renal blood flow.

A kidney biopsy is necessary when there are no symptoms and a definitive diagnosis cannot be made. Such a study provides an accurate prognostic and diagnostic picture.

Blood and urine tests allow doctors to determine in which phase - acute or chronic - the development of the disease occurs.

Effective therapy

The treatment of convoluted tubule epithelial necrosis is based on eliminating the cause of this disease. In a state of remission, it is treated taking into account the symptoms that arise. Therapy promotes better microcirculation, elimination of bacteriuria, dehydration, and arterial hypertension. Due to polyuria, patients are advised to consume salt and water.

If complications associated with ureteral resistance or massive hematuria occur, the patient is urgently hospitalized. To restore the passage of urine, catheterization of the pelvis is performed and a nephrostomy is applied. The patient is prescribed antibiotics. In acute renal failure, hemodialysis is performed.

Prevention of the disease includes treatment of diseases that cause necrosis of the renal nipples, and rational use analgesics.

Kidney necrosis

Description of the pathology

With kidney necrosis, cytoplasmic proteins are damaged. As a result, organ cells are destroyed and tissue areas die. Pathology occurs in both adults and infants. The main causes of the disease are considered:

infections, sepsis;

sudden separation of the placenta in pregnant women;

injuries, bleeding;

rejection of a transplanted kidney;

complications of cardiovascular diseases;

chemical poisoning, snake bite.

There are the following types of necrosis:

Prerenal failure. As a result of circulatory disorders, the functional abilities of the kidney deteriorate. Since impaired blood flow leads to ischemia (death of a tissue area), this type of pathology develops into renal failure.

Renal failure. It is characterized by a malfunction of the kidney due to damage to its tissue. The main cause of the pathology is ischemia (warm or cold).

Postrenal failure. Kidney function is normal. Due to damage to the urinary tract, urination is difficult or absent. If compression of the kidney parenchyma occurs due to accumulated urine and bleeding occurs, this type of necrosis develops into renal failure.

Papillary necrosis (papillonecrosis)

Failure of blood circulation in the kidneys is one of the reasons for the death of organ cells.

The main causes of papillary necrosis are circulatory disorders and complications of pyelonephritis.

Papillary necrosis or necrotizing pyelonephritis is characterized by necrosis of the renal papillae and renal medulla. As a result, the functioning of the organ is disrupted; morphological changes. According to statistics, this pathology is observed in 3% of people suffering from pyelonephritis. This pathology is diagnosed in women 2 times more often than in men.

Causes of pathology:

Blood circulation in the brain is impaired.

The renal papillae are not sufficiently supplied with blood. This occurs due to compression of the vessels by edema, inflammatory processes, vascular sclerosis (blockage of the vessel bed with cholesterol plaque), regardless of their location (in the kidney or outside it).

Because of high pressure in the renal pelvis the outflow of urine is disrupted.

Foci of inflammation, ulcers in the brain part of the organ.

Poisoning of kidney tissue by toxins.

Violation of the blood picture.

With necrosis of the renal papillae, the symptoms differ depending on the form of the pathology:

Acute papillary necrosis is manifested by colic-like pain, severe fever and chills. There is blood in the urine. Acute renal failure develops within 3–5 days. In this case, little urine is excreted or urination stops.

Chronic necrosis of the renal papillae is manifested by the presence of blood and leukocytes in the urine. Mild pain appears periodically. Accompanied by repeated infectious diseases of the urinary tract and the formation of stones. With sickle cell anemia, there are no pathological symptoms.

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Cortical necrosis

The death of kidney cells can also be local, due to impaired blood circulation in certain areas of the organ.

As a result of blockage of the blood vessels through which nutrition is delivered to the renal cortex, outer part the organ dies. The functioning of the kidney is impaired and failure occurs. 30% of cases of this disease occur due to sepsis (blood poisoning). In addition, pathology is caused by rejection of a transplanted kidney, injuries and burns, and chemical poisoning.

Necrosis of the cortical layer develops as a result of circulatory disorders in the renal cortex and is complicated by acute renal failure.

Pathology can affect anyone, regardless of age. A tenth of cases of the disease are diagnosed in newborns. This is associated with premature placental abruption, sepsis, dehydration, shock, and infection. Together with the child, his mother often suffers. In women, half of the cases of this disease are a postpartum complication. Pathology develops due to early abruption or improper location of the placenta, uterine bleeding, infection introduced during childbirth, blockage of arteries with fluid from the amnion (the membrane in which the embryo is located).

Main symptoms of the disease:

urine turns red or brown (due to high content blood);

pain in the lumbar region;

increased body temperature;

demotion blood pressure;

disturbance or absence of urination.

Acute tubular necrosis

Tubular necrosis is damage to the renal tubules of a chemical and mechanical nature.

In tubular necrosis, the epithelial tissue of the renal tubules is affected. In this case, there are 2 types of disease, depending on the causes:

Ischemic necrosis is provoked by injuries, inflammatory processes, sepsis, shock, and low oxygen levels in the blood.

Nephrotoxic necrosis occurs as a result of poisoning of tissues and cells by toxins, heavy metals, antibiotics, etc.

Acute tubular necrosis means mechanical damage to the renal tubules due to “sloughing” of the epithelium. This pathology damages the tubular cells themselves and is accompanied by acute inflammatory process. The result is severe damage to the kidney tissue and changes in the structure of the organ, leading to kidney failure.

Symptoms of the pathology depend on the degree of organ damage. The most commonly observed signs are:

coma;

drowsiness;

delirium (damage to the nervous system by toxins);

swelling;

weak urination;

nausea, vomiting.

Complications and consequences

Only 20% of patients with kidney necrosis have a chance to survive.

Complications of each type of necrosis are reduced to the development of renal failure. In this case, severe intoxication is observed, as a result of which organs of other systems are affected. According to statistics, 70–80% of patients diagnosed with kidney necrosis die from blood poisoning, heart or kidney failure. If you have symptoms of this disease, especially if you have previously been diagnosed with kidney disease, you should urgently go to the hospital for diagnosis and treatment. If treatment is not started in time, the kidneys may be so damaged that a transplant will be required or the pathology will lead to death.

For correct setting Anamnesis is important for diagnosis. The doctor asks the patient about symptoms, existing kidney diseases and concomitant diseases, in particular diabetes mellitus, and the medications used. It is necessary to take into account possible injuries or contact with toxic substances. Then appointed laboratory analysis blood and urine. Since all types of necrosis cannot be determined using the same method, ultrasonography and x-ray.

If the patient has necrosis of the renal papillae, then dead papillae may be detected in the urine. The diagnosis is confirmed using radiography.

Cortical necrosis is determined by ultrasound.

Diagnosis of tubular necrosis requires maximum quantity information. A general and biochemical analysis blood and urine, ultrasound, x-ray, computed tomography.

Treatment methods

First of all, it is necessary to eliminate the causes of the disease as quickly as possible. Next, treatment is carried out depending on the type of pathology:

If necrosis of the renal papillae is diagnosed, antispasmodics are used to eliminate the cause. If the ureter is blocked, a catheter is inserted. Are used medications to restore blood circulation, strengthen the immune system, as well as broad-spectrum antibiotics. If drug treatment does not give results, the affected kidney is removed.

In the case of cortical necrosis, first of all, the blood supply to the brain tissue of the kidney is restored. The blood is purified using an artificial kidney machine (hemodialysis). Antibiotics are used to suppress infection.

If the tubules are damaged, the use of drugs that can cause intoxication is discontinued. To fight infection, antibacterial medications are prescribed, blood circulation in the organ is restored, and toxins are cleansed from the body. Apply necessary funds to relieve symptoms (nausea, vomiting).

General forecast

If treatment is started on time, the kidneys can be restored. However, according to statistics, most of cases requires transplantation. Dialysis is mandatory. This procedure cleanses the blood as well as the kidneys. Dialysis is mandatory for all patients with kidney failure. Unfortunately, if the visit to the hospital occurred in the last stages of the disease, there is a high probability fatal outcome. Therefore, if you have any symptoms indicating kidney disease, you should immediately consult a doctor.

Acute tubular and acute tubular necrosis

Acute tubular necrosis

Based on the morphology and physiology of the kidneys, they are a complex paired organ that promotes the removal of metabolic products from the body and the regulation of water and electrolyte balance. Acute tubular necrosis affects the epithelium of the renal tubules and is the cause of acute renal failure. This disease is divided into ischemic and toxic necrosis.

Ischemic acute tubular necrosis develops due to sharp decline blood pressure during shock, decreased circulating blood volume, placental abruption, postpartum hemorrhage. The cause of this type of pathology may be a narrowing of the renal artery, dissecting aortic aneurysm, or rupture of an abdominal aortic aneurysm. This is also facilitated by a large loss of fluid and electrolytes due to prolonged vomiting, diarrhea, burns, etc.

Sulfuric, hydrochloric, phosphoric, oxalic acids, organic solvents and drugs used for anesthesia are also among the common causes. There are known cases of necrosis after undergoing complex infections– cholera, typhoid fever, paratyphoid fever, sepsis. hemorrhagic fever with renal syndrome and leptospirosis. The kidneys are also sensitive to endogenous intoxication.

Intestinal obstruction, peritonitis, toxicosis during pregnancy, rapidly developing circulatory hepatic-renal failure become prerequisites for necrotizing phenomena. Under the influence of toxins, segmental or focal narrowing of the lumen of the tubules occurs, which leads to necrosis. Since a large volume of blood is purified by the kidneys, they are very vulnerable.

Most toxic substances affect the epithelium of the tubules due to the fact that it is there that primary urine is concentrated. In overly susceptible cells, cellular oxidation or metabolism is disrupted. The development of necrotic nephrosis is practically asymptomatic, but symptoms of acute renal failure may occur simultaneously. In this case, a decrease in the amount of urine excreted by the kidneys is often observed.

The diagnosis is confirmed if the plasma creatinine concentration exceeds the norm by 0.5 mg/dL per day after a decrease in blood pressure or exposure to a nephrotoxic agent. In tubular necrosis, the glomeruli and blood vessels may remain normal. The vast majority of patients with acute tubular necrosis are subject to the appearance of acute azotemia, acute and dangerous disturbances of water-salt metabolism.

Treatment of acute tubular necrosis is no different from the treatment of acute renal failure, which includes general measures aimed at eliminating specific causes.

It is imperative to maintain water and electrolyte balance, nutritional support, treatment of infectious complications and prevention. In the absence or improper treatment necrotic processes lead to the fact that the entire kidney is affected and hemodialysis or transplantation is indispensable. Other life-threatening conditions may include high blood pressure, strokes and myocardial infarctions.

Poisoning of the body with the toxins present leads to toxic damage to internal organs, the central nervous system and the gastrointestinal tract. At the first signs of discomfort, you should contact a nephrologist, who will prescribe blood and urine tests, and an ultrasound examination. For precise definition Biopsy is recommended for diagnosis.

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Acute tubular necrosis

Acute tubular necrosis of the kidneys damages the tubular cells. It means mechanical obstruction of the tubules by desquamated epithelium. The disease is characterized by acute immune inflammation. Often, such structural changes that cause acute renal failure progress rapidly when there is a lack of oxygen in the kidney tissues.

In the case of tubular necrosis, there is a decrease in consciousness.

Depending on the degree of the disease, coma may occur, delirium, drowsiness, decreased diuresis, edema, nausea and vomiting may occur. In practice, it has been proven that diabetes is accompanied by necrosis of this type. Acute necrosis may result from the influence of X-rays, the use of antifungal agents have a toxic effect on the kidneys.

The etiology of necrosis is based on toxic factors, the influence of infectious pathogens, and genetic defects. But the main reason lies in immunopathological mechanisms. Clinical symptoms manifested by feverish conditions, discharge of blood in the urine, detection of protein in the urine and the presence skin rashes. There is an increase in the size of the kidneys, swelling . The outcome of tubular necrosis depends on the cause of the disease and the duration of pathological changes.

The most common causes of acute tubuary necrosis- hypotension and nephrotoxins. The most common nephrotoxic agents include aminoglycoside antibacterials, amphotericin B, cisplatin, and radiocontrast agents. Large surgical interventions and long-term hepatobiliary pathology, poor perfusion and elderly age increase the risk of aminoglycoside toxicity. Less common causes include topic pigments, poisons, herbal and folk remedies. Certain drug combinations may be particularly nephrotoxic. Poisons cause focal and segmental occlusion of the tubular lumens by casts, cell decay products, or segmental tubular necrosis. ACC predominantly occurs in patients with creatinine clearance less than 47 ml/min, diabetes mellitus and hypovolemia or poor renal perfusion.

Prognosis of acute tubular necrosis good in patients without pathology of other organs and systems, when the etiological factor is eliminated; creatinine concentrations usually return to normal or nearly normal within 1 to 3 weeks. In weakened patients, even with moderate acute renal failure, the risk of complications and death increases; the prognosis is better in non-resuscitated patients compared to resuscitated patients. Risk factors for death include oliguria; high severity of the disease; myocardial infarction, stroke or seizure disorder; chronic immunosuppression; need for artificial ventilation. Usually the causes of death are infectious complications, the underlying pathology.

Supportive, includes early withdrawal of nephrotoxic drugs, support of euvolemia and parenteral nutrition. Diuretics are commonly used to maintain diuresis in oliguric acute insufficiency, but their effectiveness has not been proven.

Prevention of acute tubular necrosis includes support for euvolemia and renal perfusion in critically ill patients, avoidance of nephrotoxic drugs when possible, close monitoring of renal function when their use is necessary, and various measures to prevent contrast nephropathy. Ineffective and possibly harmful remedies include:

natriuretic peptides,

calcium channel blockers.

Acute tubular necrosis– damage to the kidney tubules as a result of a sudden disruption of the blood supply or direct damage to the kidney tissue by both ecto- and endogenous nephrotoxins. Thus, there are 2 forms of acute tubular necrosis:

Ischemic acute tubular necrosis (shock conditions, kidney injuries, septic conditions, hypoxia).

Nephrotoxic acute tubular necrosis (from exposure to various toxins: antibacterial agents, heavy metals, endogenous toxins, contrast agents, fluorinated anesthetics, organic solvents).

Acute tubular necrosis is one of possible reasons such a terrible condition as: acute renal failure (ARF). The clinical picture of acute tubular (tubular) necrosis includes symptoms of the underlying disease or pathological process leading to the development of acute renal failure, as well as the phenomenon of renal acute renal failure (ARF).

Acute tubular necrosis

Acute tubular necrosis is characterized by acute tubular cell damage and dysfunction causing renal failure. Frequent causes of acute tubular necrosis- hypotension causing insufficient renal perfusion, and nephrotoxic drugs. The disease is asymptomatic until renal failure develops. Diagnosis of acute tubular necrosis, suspected if azotemia occurs after a period of hypotension or exposure medicine and differs from prerenal azotemia in terms of blood and urine tests. Treatment of acute tubular necrosis symptomatic.

Symptoms diagnosis of acute tubular necrosis

OKN is usually asymptomatic, but may be accompanied by symptoms of acute renal failure, in which oliguria is common. The disease is suspected when the plasma creatinine concentration exceeds the normal range by 0.5 mg/dL per day after a period of hypotension or exposure to a nephrotoxic agent. Increases in creatinine concentrations may occur several days after exposure to some nephrotoxins. Criteria for distinguishing OKN from prerenal azotemia, important for determining treatment, are listed in Table. 236-1.

Prognosis, treatment and prevention of acute tubular necrosis

loop diuretics,

dopamine,

Symptoms of kidney disease

Kidney diseases are quite diverse in their origin, manifestations and consequences for the body. The most common are inflammatory kidney diseases, which usually occur in women (pyelonephritis, glomerulonephritis). Urolithiasis occurs equally often in both sexes over the age of 40 years. Children are characterized by pyelonephritis and congenital anomalies kidney

Causes and mechanism of development

There are a number of main reasons leading to certain diseases:

Autoimmune process. As a result of a failure in immune system antibodies are produced against kidney cells, which leads to the development of inflammation, resulting in glomerulonephritis.

Bacterial infection. Bacteria, entering the kidneys, begin to multiply there, this causes inflammation, which leads to pyelonephritis. In case of further progression of the disease and lack of treatment, ulcers appear (kidney abscess). The development of a bacterial infection is facilitated by impaired outflow of urine from the kidneys.

Intoxication of the body. Toxins circulating in the blood cause metabolic disorders in the kidneys, and toxic nephropathy develops. This is a reversible process that occurs after exposure to toxins ceases.

Disturbances in the metabolism and chemical composition of urine are the main cause of kidney stone disease. At the same time, stones form in the pelvis, which can disrupt the outflow of urine and injure the mucous membrane of the kidneys and ureters. This contributes to the addition of a secondary bacterial infection and pyelonephritis.

Hemolysis is a condition in which red blood cells are destroyed and hemoglobin is released into the blood. It settles in the glomeruli of the kidneys and makes it difficult for them to work. As a result, it develops dangerous condition– acute renal failure.

Impaired blood flow in the vessels of the kidneys. The presence of atherosclerotic plaques reduces the diameter of the vessel and leads to insufficient blood flow to the kidney cells, and metabolic nephropathy develops. This process can last for years without any symptoms.

Low blood pressure. Systolic pressure is below 70 mm Hg. Art. causes cessation of the process of filtration of blood plasma in the renal glomeruli and their necrosis (death).

Impaired kidney maturation in the prenatal period leads to the formation of anomalies in shape (horseshoe-shaped, bifurcated kidney), position (prolapsed kidney) or number (one or, conversely, an additional kidney). The fusion of kidney tubules to form cysts is called atresia.

Traumatic factors. Bruise, puncture or cut wounds cause damage to renal tissue with disruption of its function.

Symptoms of kidney disease

Manifestations of kidney diseases can be divided into local and general. Local symptoms include those whose occurrence is directly related to the kidneys:

Pain in the lumbar region. It happens with pyelonephritis (on one side) and glomerulonephritis (on both sides). Intense paroxysmal pain is characteristic of kidney stones, more often in men (renal colic).

Decreased urine output (decreased daily diuresis). Oligouria is a symptom of impaired renal function, is a manifestation of acute renal failure (urine may be completely absent - anuria), severe glomerulonephritis, blockage of the renal tubules due to hemolysis of the blood.

The appearance of blood in the urine is the result of bleeding due to kidney injuries, kidney stones and a tumor process.

Change in urine color. Turbid urine with a greenish tint indicates a purulent process in the kidney (kidney abscess due to pyelonephritis); urine the color of “meat slop” occurs with hemolysis and partial release of free hemoglobin in the urine.

Common symptoms that may appear with kidney disease are:

increased body temperature, general weakness, headache and joint aches are the result of intoxication (toxins entering the blood) due to bacterial inflammation of the kidneys, pyelonephritis;
increase in systemic blood pressure above 140/90 mm Hg. Art. – a symptom of renal malnutrition in the presence of atherosclerotic plaque in their vessels; in response, kidney cells produce angiotensin, a substance that causes vasospasm;
the appearance of “bags” under the eyes, swelling of facial tissues after sleep are the first signs of kidney disease, especially common in initial stages development of glomerulonephritis.

Diagnostics

To most accurately determine kidney disease, additional laboratory and instrumental diagnostics which includes:

Clinical blood test - indicates the inflammatory nature of the disease due to an increase in the number of leukocytes and erythrocyte sedimentation rate (ESR).
Immunological blood test. An increase in the titer of antibodies to the renal glomeruli and the appearance C-reactive protein(CRP) are specific markers of glomerulonephritis.
Clinical urine analysis is a universal test that helps diagnose kidney disease. Protein is detected in the urine (appears with glomerulonephritis), its specific gravity(decreases in case of development of renal failure). Under a microscope, the number of leukocytes (increased with pyelonephritis) and erythrocytes (nephrolithiasis, glomerulonephritis) in the field of view is determined. Bacterial kidney inflammation is characterized by the appearance of bacteria in the urine. The formation of kidney stones is manifested by the presence of salt crystals in the sediment.
Ultrasound examination (ultrasound) of the kidneys – instrumental method diagnostics, allowing you to see changes in the shape and position of the kidneys (developmental anomalies), the presence of stones in kidney stones and various tumors.
Computed tomography is a modern x-ray diagnostic method that allows you to see even small structural changes in the kidneys in layer-by-layer images.
Antegrade radiography of the kidneys. A contrast agent is injected into the blood, which, together with the plasma, is filtered in the glomeruli of the kidneys and excreted in the urine. This method allows you to see obstacles to the outflow of urine, their localization in case of kidney stones or a tumor process.

Only on the basis of research results and symptoms of the disease can a doctor make a final conclusion. Knowing the incidence of various kidney diseases depending on age also helps in determining them.

The most common kidney diseases in adults are:

pyelonephritis - more often in women;
kidney stones - in people over 40 years of age;
tumor diseases (frequency increases over the age of 60 years);
metabolic nephropathy.

Common kidney diseases in children:

Pathological anatomy of the kidneys

Kidney atrophy in pure form rarely occurs. More often it is associated with circulatory disorders and chronic inflammation in the kidneys. Kidney atrophy occurs due to senility and starvation. With atrophy, the kidney is macroscopically reduced, with single cysts. Vacat hypertrophy of the perirenal tissue is sharply expressed, which makes it possible to distinguish atrophy from hypoplasia. Microscopically, there is desolation of nephrons with glomerular sclerosis and proliferation connective tissue, very rich cellular elements in the renal cortex. The medulla often has areas of hyalinosis. Atrophy is often a consequence of hydronephrosis. Kidney hypertrophy most often has a compensatory nature and is associated with a change or absence of the second kidney.

Dystrophic kidney disorders occur with various metabolic disorders.

Protein metabolism disorders are accompanied by the development of a picture of cloudy swelling or granular degeneration of the kidneys (see Dystrophy of cells and tissues). The kidney is enlarged, with a wide swollen cortical layer; the capsule slides off easily when incised. Microscopically, the epithelium of the convoluted tubules shows a weak granularity; a spherical transformation of mitochondria in epithelial cells is noted. Hyaline droplet dystrophy is observed in diphtheria, infectious polypeptidemia, and tuberculosis.

Violations fat metabolism are expressed in the appearance of fat droplets in the epithelium of the convoluted tubules. Infiltrative obesity of the kidneys occurs with pathology of the endocrine glands (for example, lipemia in diabetes mellitus), with poisoning with chloroform, arsenic, and phosphorus. Hypoxemic kidney obesity is observed with pernicious anemia, high altitude sickness, diffuse thyrotoxic goiter. A special type is the so-called fatty infarction of the renal papillae, associated with severe disorders of cholesterol metabolism (hypercholesterolemia). Macroscopically, in the papillae there are extensive whitish-yellow fields, matte in appearance on a section, usually clearly demarcated from the surrounding tissue, wedge-shaped. Microscopically, in the interstitial tissue and the proper membrane of the straight tubules and collecting ducts there are massive deposits of cholesterol.

Impaired carbohydrate metabolism is expressed in the development of so-called glycogen nephrosis in diabetes mellitus, when an abundance of glycogen is observed in the epithelium of the convoluted tubules, loop of Henle and collecting ducts. With Gierke's glycogenosis, the kidney doubles in size and lumps of glycogen occupy both the glomeruli and the tubular epithelium throughout the nephron.

Disturbances in salt metabolism lead to the formation of kidney stones or local calcification processes of the dystrophic type (with necrotic nephrosis). Abundant leaching of lime into the blood, observed with bone tumors (primary or metastatic in the skeletal system) or with Recklinghausen's disease, is accompanied by calcareous metastases in the kidney as an organ that secretes acidic valences. In old age, calcium is deposited in the form of grains in the hyalinized interstitial tissue of the kidneys and the proper membrane of the collecting ducts, sometimes combined with a fatty infarction. The macroscopic appearance of this calcification has given rise to the term “calcareous infarction.” The deposition of uric acid salts causes a picture of uric acid infarction.

Disorders of pigment metabolism are expressed in the picture of pigmentary nephrosis. Hemosiderosis of the kidneys is a particular manifestation of widespread hemosiderosis.

Disorders of water metabolism are closely related to a violation of the colloidal state of the convoluted tubule epithelium and give a picture of the so-called hydropic nephrosis.

Rice. 1. Cystic kidney. Rice. 2. Kidney tuberculosis. Rice. 3. Solitary renal carbuncle. Rice. 4. Stagnant kidney.

Circulatory disorders in the kidneys are most often expressed in hyperemia (arterial and venous, see color Fig. 4), ischemia, heart attacks and hemorrhages.

Anemia (ischemia) of the kidneys is a particular manifestation of general anemia or local violation patency of the renal artery (trauma, atherosclerosis, inflammatory changes). Microscopically, large multinucleated cells can be observed in the epithelium of convoluted tubules, protruding into the lumen of the tubule and considered as a kind of regeneration of renal epithelial cells under conditions of oxygen starvation.

Kidney infarctions can be arterial, venous or traumatic. Arterial are associated with the closure of the lumen of the renal artery or its smaller branches. They are always ischemic. Venous infarctions, usually hemorrhagic, are associated with impaired venous outflow, which is caused by stasis and thrombosis of the branches of the renal vein. Thrombosis of the renal veins is not always accompanied by the development of a heart attack: with terminal thrombosis it does not have time to develop; with slow thrombosis, wide collaterals are formed, however, secondary thrombosis of the renal arteries and the appearance of ischemic-hemorrhagic renal infarction are possible. Thrombotic infarction is based on vasospasm, which occurs reflexively in response to the action of a traumatic agent. Its leading role is evidenced by the appearance of contralateral infarction in wounds. Traumatic heart attacks are rare. Small infarctions are observed in periarteritis nodosa or obliterating endarteritis with localization of the process in the kidneys. Hemorrhages into the parenchyma are observed when hemorrhagic diathesis, intoxications (meningococcemia, diphtheria, etc.). In hemorrhagic nephrosonephritis, bilateral massive hemorrhages into the stroma of the pyramids often involve the entire Malpighian pyramids and renal pelvis, accompanied by hematuria and impaired urination up to anuria.

Kidney inflammation can be acute or chronic. Acute inflammation(usually purulent) are associated with hematogenous, lymphogenous, urogenic and interstitial spread of infection. Of the limited purulent processes, abscesses (single or multiple) are most common. Single ones are localized either in the cortex or in the medulla, multiple are scattered throughout the kidney. They are greenish-yellowish with a red rim, clearly demarcated from the intact parenchyma. Merging, the abscesses form a kidney carbuncle (tsvetn. Fig. 3), which is a massive node, fluctuating, purple-bluish in color. Its chronic course can be complicated by purulent paranephritis. Lymphogenous spread of infection leads to the so-called lymphogenous necrosis of the kidneys. In this case, the kidney is sharply enlarged, swollen, hyperemic, with isolated small abscesses. Microscopically, in the cortical and medulla layers there are extensive fields of necrosis with leukocyte infiltration around them. Renal lymphangitis can be complicated by the development of secondary purulent panarteritis and panphlebitis with further apostematous nephritis.

Chronic kidney inflammation may be nonspecific [ chronic pyelonephritis, (see)] and specific (tuberculosis, syphilis, etc.). Acute miliary tuberculosis of the kidneys develops through hematogenous generalization and is clinically asymptomatic. It does not affect kidney function. The surface of the kidney is dotted with small millet-like tubercles against a background of hyperemia. Microscopically, these are typical tuberculous tubercles. As miliary tuberculosis is eliminated, no noticeable traces remain in the kidneys. With hematogenous dissemination, chronic renal tuberculosis occurs, which has a distinct clinical picture. In the cortical and medulla layers of the kidneys, large grayish-white nodes with yellow fields in the center are macroscopically determined - the so-called focal, or nodular, form. With a positive immunological reaction of the body, the microscopic picture indicates the predominantly productive nature of the process, which tends to be limited. However, more often it has an exudative character with massive melting of cheesy foci, breakthrough of caseous masses into the pelvis and the formation of caverns - cavernous-ulcerative tuberculosis (printing Fig. 2). Microscopically, in the cavity wall, along with fields of exudative inflammation, tubercles are identified in different stages development - from fresh to scarring. If the scar fields extend to the pelvis, narrowing of the ureteric orifices may occur, and the so-called hydronephrotic form of renal tuberculosis develops. In this case, the kidney resembles a thin-walled sac filled with greenish-yellowish pus mixed with curdled masses (tuberculous pyonephrosis). With extremely rare chronic tuberculosis of the kidneys, there are no tubercles, necrosis and cavities, but there is a picture of diffuse infiltration of the stroma with epithelioid and lymphoid cells - the so-called interstitial nephritis, or Koch's nephrocirrhosis (fibro-indurative form of renal tuberculosis). Its specific nature is indicated by the detection of tuberculosis bacillus in the interstitium when stained with Ziehl. Renal tuberculoma is a single node that involves the medulla and cortex, prone to encapsulation and subsequent calcification.

With secondary syphilis, syphilitic interstitial fibrous nephritis may develop. The kidneys are enlarged, light brown in color, with no boundaries between the cortical and medulla layers. Microscopically, there is a picture of interstitial edema with focal infiltration of it by lymphoid, plasma cells and fibroblasts. The outcome of the process is nephrocirrhosis. Tertiary syphilis leads to the formation of gummas (solitary and miliary) in the kidneys, located in the cortical and medulla layers, resulting in scarring disfigurement of the kidneys.

Actinomycosis occurs when the process transfers to the kidneys from the intestines. In rare cases, it can be complicated by purulent paranephritis.

With Wegener's granulomatosis, granulomatous periglomerulitis, which is a periarteritis-like inflammation of the afferent vessels of the glomerulus, can develop in the kidneys. With renal cytomegaly, giant cells with nuclear inclusions appear in the epithelium of convoluted tubules and glomeruli with very mild signs of focal interstitial inflammation.

Benign tumors in the kidneys include adenomas, fibromas, lipomas, fibroids, angiomas, teratomas, chondromas, osteomas, myxomas, neurofibromas, and papillomas. They can be single or multiple, located in the cortical (adenoma) and medulla (fibroma) layers, usually clearly defined, dense in consistency, color from yellowish (adenoma) to dark red (hemangioma). Renal teratomas are divided into simple cystic formations type of dermoid cyst (tsvetn. Fig. 1), hamartomas and embryonic tumors of mesenchymal origin. All benign tumors can recur after removal.

Malignant kidney tumors can be primary or secondary. Of the primary ones, the most common is hypernephroid kidney cancer, followed by cancers that develop in the form of a whitish node without clear boundaries with yellowish fields of necrosis. Histologically, they have the character of solid cancer, adenocarcinoma (usually cystopapillary) or squamous cell carcinoma (keratinizing or non-keratinizing) if the tumor originates from the pelvis. Sarcoma is rare and usually reaches very large sizes, involves both the cortex and medulla; microscopically, the tumor most often has the structure of a fibrosarcoma. Mixed tumor- the so-called embryonal nephroma (see Wilms tumor) - occurs in children. Secondary kidney tumors arise through hematogenous, less often lymphogenous, metastasis. These are cancer, sarcoma, melanoma, chorionepithelioma. They can be in the form of multiple or single nodes, clearly demarcated from the surrounding parenchyma of the kidney. Leukemic infiltration of renal tissue in leukemia is only a manifestation general illness body.

Changes in the kidney under the influence of therapy. Mercuzal, mersaline, preparations of silver, gold, bismuth, chromium salts, foreign blood, antibiotics directly act on kidney tissue. Other drugs increase sensitization of the kidneys, causing allergic changes in its parenchyma. Excessive use of diuretics (such as Mercusal and Mersaline) causes dramatic changes in the epithelium of convoluted and straight tubules from granular dystrophy to coagulative necrosis up to calcification of dead masses of the epithelium. The prevalence of the process depends on the frequency of use of drugs and their dosage. Silver preparations can lead to kidney arthrosis. At the same time, the kidneys are enlarged, with small dark specks in the cortex and silver infarcts in the papillae. Microscopically, along the vascular loops of the glomeruli and the basement membranes of the tubules, a narrow border consisting of black dots is determined. Silver infarcts are the deposition of clumps of silver into the stroma of the papillae. The use of gold preparations can be complicated by chrysiasis - the deposition of gray to bluish-violet pigment into the stroma of the kidneys; depending on the amount of pigment, secondary phenomena of circulation disturbances in the organ occur. Bismuth, chromium salts, phosphorus, and choline group drugs cause dystrophic processes in the epithelium of convoluted tubules from fatty degeneration to necrosis.

In terms of the frequency of toxic reactions during sulfonamide therapy, streptocide is in first place, followed by sulfidine and norsulfazole. Predisposing points are acid reaction urine and decreased diuresis. Kidney damage can be of two types. In one case, the kidneys are enlarged, swollen, with a pale yellow cortex. Microscopically - cloudy swelling of the convoluted tubule epithelium, fatty degeneration it up to focal necrosis, there is an abundance of red blood cells in the tubules, hemorrhages into the pelvis. Another type of poisoning is manifested by a sharp dilation of the pelvis and ureters with their filling with whitish sulfidine crystals mixed with blood and amorphous masses, impeding the outflow of urine and, in a bilateral process, giving a picture of acute uremia. The degree of kidney changes depends on the individual sensitivity of the body to sulfonamide drugs. Changes under the influence of transfusion of blood of a different group give a classic picture of nephrosis of the lower nephron.

Among antibiotics, penicillin can have a direct toxic effect on the kidneys, causing changes in the lysosomes of the convoluted tubule epithelium. The latter stick together to form lumps, releasing a mass of hydrolytic enzymes leading to necrosis of the renal epithelium. Neomycin may also cause cloudy swelling, vacuolation, and necrosis of the convoluted tubule epithelium. Tetracycline has the ability to block redox enzymes of the convoluted tubule epithelium, suppressing the reabsorption function of the proximal nephron.

Drugs that cause allergic changes in the kidneys include amidopyrine, barbiturates, camphor, and salicylates. With individual intolerance to these drugs, a picture of fibrinoid necrosis develops in the renal vessels with perivascular infiltration like periarteritis nodosa with secondary necrosis and hemorrhages into the parenchyma. The kidneys are enlarged, their surface is dark red, smooth, when cut, the tissue is variegated (yellow areas alternate with dark red ones), and there are hemorrhages in the pelvis. The process may result in acute uremia. Camphor preparations can cause widespread spasm of the renal artery, resulting in massive necrosis in the kidneys.

With increased pressure inside the pelvis (hydronephrosis, retrograde pyelography, hyperkinesis of the urinary tract), so-called pelvic-renal reflux (see), clinically expressed in hematuria, occurs. In this case, ruptures of the renal vaults and penetration of urine into the renal sinuses are observed. The kidney is enlarged, pale, there are areas of hemorrhage in the papillae, and blood in the calyces and pelvis. Microscopically, in places of ruptures there are foci of hemorrhage and necrosis. See also Nephritis, Nephrotic syndrome.