Necrotic changes in the animal's kidneys. What is kidney necrosis and its symptoms

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

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

RENAL NECROSIS (Papillonecrosis) - clinical picture. Main clinical signs are acute onset with worsening general condition against the background of the underlying disease ( diabetes mellitus and etc.), severe pain V lumbar region, high fever, chills, oliguria and other symptoms of acute renal failure. Severe leukocyturia and bacteriuria, hematuria, and sometimes pieces of renal papillae in the urine are observed. Possible recovery death, as well as a transition to a recurrent course, characterized by attacks of pain in the abdomen, lower back, in the area of the affected kidney and ureter. Relapses usually occur with exacerbation of the underlying disease and under the influence of other factors (overwork, infections, etc.). During this period, ESR is increased, leukocytosis, limitation of tubular functions and glomerular filtration in some patients. At excretory urography deformation of the cups is revealed, in late stages- picture of severed papillae.

RENAL NECROSIS (Papillonecrosis) - diagnosis. Based on sudden appearance septic condition and signs of acute renal failure in the presence of severe urinary syndrome.

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

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

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

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

RENAL NECROSIS (Cortical). Treatment. Elimination of signs of acute renal failure with conservative measures and hemodialysis, as well as antibacterial and symptomatic therapy(diuretic and antihypertensive drugs, etc.).

Causes of necrosis

Necrosis is the irreversible cessation of the vital activity of cells, tissues or organs in a living organism, caused by the influence of pathogenic microbes. The cause of necrosis can be tissue destruction by a mechanical, thermal, chemical, infectious or toxic agent. This phenomenon occurs due to an allergic reaction, disruption of innervation and blood circulation. The severity of necrosis depends on the general condition of the body and unfavorable local factors.

The development of necrosis is facilitated by the presence pathogenic microorganisms, fungi, viruses. Also negative impact has cooling in the area where there is poor circulation; under such conditions, vascular spasm intensifies and blood circulation is further disrupted. Excessive overheating affects the increase in metabolism and with a lack of blood circulation, necrotic processes appear.

Symptoms of necrosis

Numbness and lack of sensitivity are the very first symptoms that should be a reason to visit a doctor. There is pallor skin as a result of improper blood circulation, the skin color gradually becomes bluish, then black or dark green. If necrosis occurs in lower limbs, then at first it manifests itself as rapid fatigue when walking, a feeling of cold, the appearance of lameness, after which non-healing lesions form trophic ulcers, necrotic over time.

Deterioration of the general condition of the body occurs from dysfunctions of the central nervous system, blood circulation, respiratory system, kidneys, liver. In this case, there is a decrease in immunity due to the appearance of concomitant blood diseases and. Metabolic disorder, exhaustion, hypovitaminosis and overwork occur.

Types of necrosis

Depending on what changes occur in the tissues, two forms of necrosis are distinguished.

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. 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 zone. Specialists in the field of modern urology and nephrology have identified several groups of causes causing papillary destruction:

Impaired blood supply 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 urinary tract the outflow of urine is disrupted with its accumulation in pelvic 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 of pronounced changes in the vasa recta feeding the renal papillae, their severe ischemic destruction occurs. NSAIDs also have direct toxic effect on the renal medulla, which aggravates papillary necrotic processes.

Pathogenesis

There are three main pathogenetic mechanisms for the development of renal papillary necrosis - angiopathic, vasocompressive, infectious, which are often combined, 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 Inflammation and venous hyperemia of the fatty tissue into which urine penetrates become aggravating ischemic processes during obstruction of the urinary organs. The ischemic papilla may be subject to complete or partial destruction with damage individual areas at the center or periphery. In severe cases, the entire Malpighian pyramid becomes necrotic, with multiple localization- medullary layer of the affected kidney throughout. When an infection occurs, the necrotic process is complicated by an inflammatory reaction.

Classification

The systematization of the forms of papillary necrosis takes into account the mechanism and dynamics of the development of the disease, the severity 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 primary formation 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 thorough examination 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 may prevail laboratory symptoms 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 kidney stones With high risk education 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 disease is often difficult to diagnose. Difficulties in diagnosis are also due to hidden development renal papillary necrosis against the background of another pathology 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. In the later stages, necrotic masses are found in the form of pieces of tissue. gray oblong or triangular in shape. The method is complemented bacteriological research urine with the determination of the sensitivity of the flora.
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 are determined bacterial inflammation: neutrophilic leukocytosis with an increase in the number of band cells, an increase in ESR. For comprehensive assessment conditions 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 concomitant 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 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 that increase the ischemic resistance of papillary structures.
Hemostatic therapy. Means to stop bleeding are indicated with 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 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 occurrence 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 uroseptic antibiotics wide range actions, nitrofurans, sulfonamides. Antimicrobials 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 conducting pathogenetic therapy regeneration of the epithelium is possible with 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 was 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 disease prevention is dispensary observation for patients at risk with careful drug control of diabetes mellitus and sickle cell anemia.

(synonyms: papillonecrosis, necrotizing pyelonephritis).

Papillonecrosis. Etiology and pathogenesis. Most often it occurs as a complication of various diseases (pyelonephritis, diabetes mellitus, nephrolithiasis, etc.), more rarely - as primary kidney damage. In adults, a common cause of papillonecrosis is analgesic nephropathy, which occurs as a result of long-term use of analgesics. The leading role in the development of the disease belongs to Escherichia coli, which penetrates the kidney papillae more often by contact (from the mucous membrane of the pelvis), and in some patients - by hematogenous route. The development of the disease is facilitated by an increase in pressure in the pelvis, followed by a disorder of blood circulation in the pyramids of the kidneys, which can also be observed with hypertensive pathology, thrombosis, etc. Papillary necrosis can be unilateral or bilateral, accompanied by damage to one or a number of papillae, which are characterized by sharp pallor and clearly demarcated from the adjacent tissue.

They often contain abscesses and an ulcerative-necrotic process with rejection of the affected areas. Morphologically, significant neutrophil infiltration is noted in the affected papillae, and with a protracted course of the pathology, sclerosis is observed.

Clinical picture. The main clinical signs are o. start with deterioration of general condition against the background of the underlying disease (diabetes mellitus, etc.), strong painful sensations in the lumbar region, high hyperthermia, chills, oliguria and other signs of acute renal failure. Severe leukocyturia and bacteriuria, hematuria, and at times small pieces of renal papillae in the urine are observed. Possible recovery fatal outcome, and transition to a recurrent course, characterized by attacks of colic in the abdomen, lower back, in the area of the affected kidney and ureter. Relapses usually occur during exacerbation of the underlying disease and under the influence of other factors (overwork, infections, etc.). During this period, ESR is increased, leukocytosis, limitation of tubular functions and glomerular filtration are noted in some patients. Excretory urography reveals deformation of the cups, and in the later stages - a picture of chopped off papillae.

Diagnosis. It is based on the sudden appearance of a septic condition and symptoms of acute renal failure in the presence of a pronounced urinary symptom complex.

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

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

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

Clinical picture. Clinical manifestations and outcome of cortical necrosis depend on the extent of the necrotic process. Signs of acute renal failure (oligoanuria, hyperazotemia, electrolyte disorders), hematuria are leading in focal and total necrosis, which usually ends in death. With focal cortical necrosis, renal failure and recovery are likely to reverse. In such patients, excretory urography for several months often reveals calcifications at the site of foci of necrosis.

Treatment. Elimination of symptoms of acute renal failure using conservative measures and hemodialysis, both symptomatic and antibacterial therapy(diuretic and antihypertensive drugs and etc.).

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

kidney necrosis

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

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

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

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

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

Kinds

Necrosis of epithelial cells of convoluted tubules

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

In the role toxic substances may act:

Pesticides included in various toxic substances or detergents;
Connections heavy metals, often mercury, lead and arsenic;
Ethylene glycol is a representative of organic solvents.

The photo shows necrotic changes in the epithelial cells of the convoluted tubules of the kidneys or acute tubular necrosis - microscopic specimen

A.- Nucleated cells; B. - Preserved nuclei in the cells of the loop of Henle; B. The vessels are filled with blood and dilated.
Also possible reason Acute tubular necrosis can result from an injury consisting of severe compression of the organ, resulting in disruption of blood flow to the kidney tubules.

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

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

Acute tubular necrosis of the kidneys - macropreparation

cortical

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

Pathogenetically, cortical necrosis is caused by increased intravascular blood coagulation locally in the kidneys or totally (in the bloodstream of the whole body). Blood clots intensely due to a decrease in fibrinogen levels and an increase in the concentration of thromboplastin and thrombin. There is a blockage of the blood-bearing (afferent) renal arterioles, which leads to impaired blood supply and shrinkage of the kidney.

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

At states of shock blood flow becomes centralized, blood does not enter the cortical layer of the kidneys normal quantity and necrosis occurs.

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

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

Cortical necrosis of the kidney

Papillary

Main etiological factor the development of necrotic changes in the cells of the renal papillae is bacterial infection. Bacteria can enter the pelvis from outside urinary tract, and are also transferred to the kidney with the blood (hematogenous route). When urine pressure increases in the pelvis, bacteria spread to one or more papillae. As a result, cell lysis develops and blood flow to the kidney pyramids is disrupted.

Symptoms are represented by pronounced feverish state, pain syndrome, pronounced signs of intoxication.

Papillary necrosis of the kidneys

Cheesy

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

Diagnosis of tuberculosis and syphilis according to initial clinical manifestations quite complicated. There may be periods of significant rise in body temperature, long time leukocytes and red blood cells are found in the urine in large quantities.

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

Caseous nephrosis

Focal

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

Treatment

The main principles of treating renal necrosis are to eliminate the root cause pathological process. To do this, it is necessary to carry out a complete clinical and laboratory examination.

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

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

Surgical interventions are performed only in severe cases of the disease. If necrosis covers almost the entire area of the kidney, then it is completely removed ().

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

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

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