What is kidney necrosis: symptoms and treatment. Papillary and cortical necrosis of the kidneys in children

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, treatment, causes of this disease what are they? Let's talk about it today:

Classification of necrosis

Distinguish 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 general violation 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 output occurs due to damage 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 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. provoke pathological process can be a poisonous snake bite, 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 vascular spasm, 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 undergone surgery for a 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. 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.

At timely application see a doctor, with timely treatment, the patient recovers completely. Otherwise, the disease may progress to a relapsing course with severe attacks of renal colic. Severe course without the necessary, timely treatment, it can be fatal.

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 - 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!

Acute tubular necrosis is characterized by acute injury tubular cells and dysfunction causing. Frequent causes of acute tubular necrosis- hypotension causing insufficient renal perfusion, and nephrotoxic drugs. The disease is asymptomatic until renal failure develops. The diagnosis of acute tubular necrosis is suspected if azotemia occurs after a period of hypotension or drug exposure and is distinguished from prerenal azotemia by blood and urine test results.

symptomatic. The most common reasons 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 combinations medicines

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 and hypovolemia or poor renal perfusion.

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 Prognosis of acute tubular necrosis good in patients without pathology of other organs and systems, when etiological factor eliminated; creatinine concentrations usually return to normal or nearly normal within 1 to 3 weeks. In weakened patients, even with moderate acute, 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; myocardium, or convulsive syndrome; chronic immunosuppression; need for artificial ventilation. Usually the causes of death are infectious complications, the underlying pathology.

Treatment of acute tubular necrosis 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. Ineffective and possibly harmful remedies include:

• loop diuretics,
• dopamine,
• natriuretic peptides,
• calcium channel blockers.

A condition in which there is chaotic death cellular elements of the paired urinary organ is called necrosis of the kidney. This severe structural and functional pathology is characterized by the rate of progression and the development of irreversible changes leading to renal failure.

As necrosis develops, it decreases functional activity paired organ and a clinical picture of general intoxication of the body develops, which is caused by the accumulation of toxins and metabolic products in the systemic bloodstream. If necrotic changes in the kidneys are not detected in a timely manner, the person’s condition will rapidly deteriorate and lead to death.

If we talk in detail about what kidney necrosis is, then this condition can be characterized as structural damage to the proteins of the cytoplasm of the cells of a paired organ, as a result of which the death of individual areas is observed renal tissue.

This condition occurs with equal frequency in both adult patients and newborns. Potential factors for the development of necrotic changes include:

• Generalized spread of infection throughout the body (sepsis);
• Traumatic injury to the kidney area;
• Rejection by the body of a previously transplanted kidney;
• Placental abruption in a pregnant woman;
• Bites from poisonous snakes and insects;
• Poisoning by toxic components and chemical compounds;
• Complications of existing vascular and heart diseases.

Classification

Depending on the location of necrotic changes and the processes occurring in the paired organ, the following types of renal necrosis are distinguished:

• Tubular (acute) necrosis. IN in this case, necrotic changes affect the epithelium of the renal tubules. The disease itself is divided into nephrotoxic and ischemic necrosis. Nephrotoxic necrosis is triggered by toxic and chemical compounds entering the paired organ. Ischemic necrosis usually occurs when states of shock, with sepsis, as well as against the background traumatic injuries. Tubular necrosis is characterized by an intense inflammatory process, under the influence of which the tissue of the paired organ is damaged, its structure changes and failure is formed.
• Cortical necrosis or mercuric bud. This pathology occurs with partial or complete obstruction (blockage) blood vessels, feeding the paired organ. When there is insufficient blood supply, the functional state kidneys and its failure develops. In no less than 35% of cases of diagnosed cortical necrosis, the pathology arose against the background of septic damage to the body. In addition to sepsis, the disease can be triggered by intoxication with chemical compounds, burns, transplantation procedures and injuries. In newborns, cortical renal necrosis occurs if a pregnant woman is faced with the problem of placental abruption.
• Papillonecrosis. The papillary form of this disease is characterized by the involvement of the renal medulla and renal papillae in the necrotic process. At least 3% of people who have previously had pyelonephritis experience complications in the form of papillary necrosis. Female patients are 2 times more likely to experience this disease.

Symptoms

The clinical manifestations of renal necrosis directly depend on the form of the disease.

At acute form papillary necrosis, the patient is concerned about acute pain syndrome, severe chills and fever. In addition, when the bladder is emptied, fragments of blood are visible in the urine. If the patient is not provided with timely assistance, then within 3-5 days he will develop acute failure renal activity. The chronic form of papillary necrosis is manifested by moderate pain in the lumbar region, leukocytosis in the urine, as well as signs of sickle cell anemia.

When a mercuric bud forms, the following clinical symptoms come to the fore:

• Partial or complete absence the act of emptying the bladder;
• Pain in the area of ​​​​the projection of the kidneys;
• The appearance of blood fragments in urine, as a result of which it acquires characteristic color urine with renal necrosis: brown or red;
• Decrease in blood pressure;
• Increase in body temperature.

The tubular form of renal necrosis is characterized by the following clinical manifestations:

• Swelling in the face, neck and lower extremities;
• Drowsiness;
• Nausea and vomiting;
• Decreased volume of urine excreted;
• Severe damage to the central nervous system, which manifests itself in the form of confusion, even coma.

It is important to remember that failure to provide timely assistance to a person with signs of one or another type of renal necrosis will lead to death in a short period of time.

Diagnostics

To correctly formulate a diagnosis, the doctor collects the patient’s medical history and analyzes his complaints. Important has a list of medications used, as well as the presence of diseases such as diabetes and heart failure.

It is also important to take into account information about possible contact with poisonous, toxic and other chemical compounds. Confirm clinical diagnosis The following laboratory and instrumental examination options will help:

Treatment

The primary task when diagnosing renal necrosis is to eliminate the cause that provoked this serious complication.

If the patient has been diagnosed with a papillary form of necrosis, then he is prescribed antispasmodic drugs and catheterization of the bladder is performed. In addition, they are appointed antibacterial agents wide range actions, drugs that improve blood circulation, as well as immunostimulants. If conservative treatment is ineffective, the issue of removing the damaged organ is decided.

When necrotic changes develop in the area of ​​the cortex of the paired organ, measures are taken to restore normal blood supply to the kidney, the blood is cleansed of toxic elements using the hemodialysis procedure, and a course of antibacterial therapy is prescribed.

If necrosis has affected the kidney tubules, a set of measures is implemented to eliminate general intoxication of the body. Appointed infusion therapy, a course of antibiotic treatment, antiemetics and antispasmodics. IN severe cases, patients undergo hemodialysis.

Complications and prognosis

The only possible complication for each form of renal necrosis is functional renal failure. This condition is characterized by severe intoxication of the whole body, heart failure and septic complications. The only way to save a person's life is timely diagnosis and proper treatment.

With timely treatment, it is possible to preserve the paired organ and restore its functional state. Despite this, statistics indicate that 70% of patients with a similar problem require an organ transplant. For patients with diagnosed necrosis, hemodialysis is vital. In especially severe cases, if treatment is not timely, death is likely.

This is the destruction of the renal papillae caused by ischemia of the Malpighian pyramids. It manifests itself as episodes of renal colic, nagging pain in the lower back, hematuria, and discharge of necrotic papillae. Diagnosed using general and bacteriological analysis urine, 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.

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. Half the time 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. A prerequisite for the occurrence of necrosis is considered to be the peculiarities of the anatomical structure of the medullary substance - hypoxia of the renal papillae is promoted by a combination of relatively poor vascularization 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 intake blood 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 pelvis system. The resulting pyelorenal reflux contributes to the contamination of the renal papillae with bacteria contained in urine, and the onset of 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 mechanism development of renal papillary necrosis - angiopathic, vasocompression, infectious, which are often combined with each other, leading to ischemic infarction 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 forms of papillary necrosis takes into account the mechanism and dynamics of the development of the disease, severity 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.

When the papilla is initially damaged, they speak of papillary form destruction, with the primary formation of focal infarctions in the inner medullary zone with subsequent involvement of the apices of the Malpighian pyramids - about the medullary. 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 complicated 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. Constants are typical nagging pain in the lumbar region, bleeding in the urine.

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

Complications

In case of joining bacterial infection Apostematous pyelonephritis occurs, manifested by the formation of small abscesses in the cortex of the kidney. At 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 high risk formation of 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 tissue gray oblong or triangular in 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. Characteristic sign total necrosis - flow of contrast into the kidney parenchyma (symptom of “fire flame”).
• Ureteropyeloscopy. To perform nephroscopy, a flexible endoscope is used, which is inserted retrograde (through the urethra) or antegrade (through abdominal wall), which allows you to assess the condition of the ureters and pyelocaliceal system of the kidneys. With papillitis, multiple destructions of the renal papillae are observed, which is often accompanied by bleeding from the fornical zone.

IN clinical analysis blood with 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 relief of symptoms plays an important role - 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 such 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 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 there is a predominance of clinical picture signs of severe and massive hematuria. 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).

If symptoms increase during treatment, conservative therapy, the emergence of 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 with broad-spectrum uroseptic antibiotics, nitrofurans, and sulfonamides. Antimicrobial agents are used for 4-6 months in 8-14 day courses with breaks, and it is recommended to prescribe at least two drugs various groups taking into account data on the sensitivity of 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 involves timely treatment infectious processes urinary system, nephrolithiasis, systemic vasculitis, toxic lesions kidneys, 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.

As a result of complications of certain diseases, injuries, and blood poisoning, kidney necrosis may occur. This dangerous pathology, causing kidney failure. In this case, the death of kidney tissue cells is observed. The functioning of the organ deteriorates, and signs of poisoning appear. If you do not go to the hospital in time, the disease will lead to kidney loss or death.

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;
• poisoning chemicals, snake bite.

There are the following types of necrosis:

1. 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.
2. 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).
3. 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)

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, and morphological changes occur in it. According to statistics, this pathology is observed in 3% of people suffering from pyelonephritis. Among women this pathology diagnosed 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 blood vessels by edema, inflammatory processes, vascular sclerosis (blockage of the vessel bed cholesterol plaque), regardless of their location (in or outside the kidney).
• Because of high pressure V 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. Within 3-5 days, acute renal failure develops, with little urine being 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 urinary tract, stone formation. With sickle cell anemia, there are no pathological symptoms.

Cortical necrosis

As a result of blockage of the blood vessels through which nutrition is delivered to the kidney cortex, the outer part of 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. It's connected with premature detachment placenta, sepsis, dehydration, shock, infection. Together with the child, his mother often suffers. In women, half of the cases of this disease are postpartum complication. The pathology develops due to early abruption or incorrect location of the placenta, uterine bleeding, infection introduced during childbirth, blockage of the 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;
• lowering blood pressure;
• disturbance or absence of urination.

Acute tubular necrosis

In tubular necrosis, it affects epithelial tissue renal tubules. 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 an acute inflammatory process. As a result, there arises serious damage kidney tissue and changes in the structure of the organ, which leads 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

Complications of each type of necrosis are reduced to the development of renal failure. At the same time, it is observed severe intoxication, 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.

Diagnostics

For a correct diagnosis, taking an anamnesis is important. The doctor asks the patient about symptoms, existing kidney diseases and concomitant diseases, in particular diabetes mellitus, and the medications used. Need 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, ultrasound and x-rays are performed.

• 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 the maximum amount of information. A general and biochemical blood and urine test, ultrasound, x-ray, and computed tomography are performed.

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. Prescribed to fight infection antibacterial drugs, restore blood circulation in the organ, cleanse the body of toxins. The necessary means are used 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 a visit to the hospital occurred in the last stages of the disease, there is a high probability of death. Therefore, if you have any symptoms indicating kidney disease, you should immediately consult a doctor.