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What is tubulointerstitial nephritis? Clinical guidelines for the diagnosis of tubulointerstitial nephritis Tubulointerstitial nephritis in children, prognosis.

18.02.2021

Among urological pathologies, a special place is occupied by tubulointerstitial nephritis (TIN), a primary inflammatory process that affects the entire kidney as it develops. Given the specificity of the pathology, treatment involves the elimination of intoxication and the restoration of the functions of the urinary system. In the absence of the necessary treatment, dangerous complications may develop, for example, pulmonary edema.

Infections and allergic reactions to drugs are responsible for 95% of cases of tubulointerstitial nephritis.

general information

This type of nephritis is primary, that is, it is not preceded by another disease. The inflammation affects the interstitium - the connective tissue that is the framework of the kidney, as well as the tubules, but not inside, but outside. In fact, the tissue that protects the tubules becomes inflamed. Edema of the interstitium develops, which negatively affects blood filtration. The epithelial layer of the tubules swells, then tissue degeneration and necrosis develops. Kidney function is impaired. Pathology is of an allergic, toxic and infectious nature.

Causes of occurrence

The disease develops under the influence of a certain stimulus, but its pathogenesis is still unknown. In some cases, pathology is considered as the result of an individual's hypersensitivity. There are several factors that most often provoke tubulointerstitial kidney damage:

Taking medications. The acute form of pathology occurs as a result of the use of antibiotics, non-steroidal anti-inflammatory drugs, diuretics and antihistamines, herbs with a laxative effect. Often the pathology develops due to uncontrolled intake of pills for pain in the head and back.
Infections, viruses. This type of nephritis occurs due to the action of cytomegalovirus, syphilis, mycoplasma, diphtheria, legionella.
The effect of household or industrial toxic substances (heavy metals, ethanol).
Radiation exposure.

The main symptoms

In chronic tubulointerstitial nephritis, symptoms are usually absent.

Within a month, after the cause of the pathology began to have an effect on the body, the symptoms of nephritis appear:

thirst;
profuse urination;
rash in the form of papules or spots;
temperature increase;
pain in the kidney area;
swelling (rare);
lack of urination (rare).

If the factor of occurrence of tubulointerstitial nephritis is unspecified, the pathology is called idiopathic.

The formation of edema and anuria (a decrease in the volume of excreted urine until the complete cessation of urination) is characteristic of a disease caused by the use of non-steroidal anti-inflammatory drugs. In this case, laboratory analysis detects protein in the urine. Based on the existing signs of pathology, it is impossible to establish a diagnosis without consulting a doctor. You should go to the hospital and undergo the prescribed examination.

Tubulointerstitial nephritis in children has an immunoallergic etiology and often develops in the presence of a baby. The disease manifests itself in pain, intoxication, changes in blood pressure, dysuria, rash. Blood is detected in the urine, an insignificant content of protein, leukocytes appear over time. In 9% of young patients, the pathology has signs of renal failure.

Forms of tubulointerstitial nephritis

Depending on the cause and severity of the course of the disease, the following forms of TIN are distinguished:

hereditary;
acute;
chronic.

Hereditary (Alport syndrome)

The genetic basis of the disease is a mutation in the gene.

The disease is inherited and is diagnosed in childhood. It is accompanied by deafness and vision problems. Kidney function is significantly reduced, blood is detected in the urine. Edema occurs with subsequent dissection of glomerular membranes. Renal develops gradually failure. The disease is rare. Among 100 thousand children, this type of nephritis is diagnosed in 17 babies.

Acute TIN

Acute tubulointerstitial nephritis affects the lymphatic and circulatory vessels... There is edema of the interstitium, inflammation of the cortex and medulla of the kidney, necrosis of the tubules. It is the most severe form and occurs regardless of the person's age, including in newborn babies. The main reason is the body's reaction to certain medications.

Chronic

This type of pathology develops in a latent form for some time before the manifestation of symptoms. An inflammatory process develops in the interstitial (interstitial) tissue of the kidneys, in the tubules, blood and lymphatic vessels of the organ. The reason is considered metabolic failure, the influence of infections, the use of drugs. It is often diagnosed accidentally during a routine examination or when pronounced signs of another disease occur. To make a diagnosis, the doctor collects an anamnesis and prescribes an examination for the patient, which includes:

General and biochemical blood test. TIN is distinguished by low hemoglobin, increased leukocyte count and ESR. A high level of urea and creatinine in the blood indicates damage to the renal parenchyma.
A general urinalysis detects blood, protein, and casts in urine at low urine density.
Ultrasound. The kidneys are visible of normal or enlarged size.
Nephrobiopsy. It is carried out at the discretion of the doctor to identify inflammation and necrosis of the renal parenchyma.

The kidneys are an organ that ensures the constancy of homeostasis in the body, which helps to maintain the volume of circulating blood and other fluids of the internal environment, ensures the constancy of the concentration of osmotically active substances and individual ions in them, the pH of the blood, and the excretion of foreign substances. The endocrine function of the kidneys is associated with their role in the renewal of the protein composition of the blood, the production of glucose, erythropoietin, renin, prostaglandins, and active forms of vitamin D 3.

The number of nephrons in young children is the same as in adults, but they are smaller in size, the degree of their development is not the same: juxtamedullary nephrons are better developed, cortical and isocortical are worse. The epithelium of the basement membrane of the glomerulus is high, cylindrical, which leads to a decrease in the filtration surface and a higher resistance at the same time. Decreased glomerular filtration is a predisposing factor for edema in children. The tubules in young children, especially in newborns, are narrow, short, the loop of Henle is also shorter, and the distance between the descending and ascending knees is greater, which contributes to a low reabsorption capacity. At the same time, the differentiation of the epithelium of the tubules, the loop of Henle and the collecting ducts after birth is not yet complete, which explains the increased excretion of amino acids, bicarbonates, phosphates. Reduced excretion of hydrogen ions can explain the tendency of children to metabolic acidosis. Thus, glomerulocanalis imbalance in children indicates an excess of the filtration capacity over the reabsorption capacity of the tubules, which, under certain conditions, will invariably lead to changes in urine analysis. The juxtaglomerular apparatus in young children is also not yet formed, while the vasoactive systems (renin-angiotensin-aldosterone system - RAAS, intrarenal adenosine) are active and easily stimulated by hypoxia. Despite the fact that the morphological maturation of the kidney as a whole ends by school age (by the age of 3-6), children of any age are at risk of kidney damage due to one or another effect on the body. The following risk factors for kidney damage in childhood can be distinguished:

intrauterine growth and development retardation (IUGR), morphological and functional immaturity;
ante- and intranatal hypoxia, asphyxia;
postnatal hypoxia (respiratory distress syndrome, pneumonia);
hypovolemia and hypoperfusion, including congenital heart disease, shock;
disseminated intravascular coagulation syndrome (disseminated intravascular coagulation syndrome);
renal vascular thrombosis;
chemicals (drugs, hyperbilirubinemia);
metabolic and electrolyte shifts;
malformations of the kidneys, dysplasia of the renal tissue;
infections.

The nature of kidney damage during infections is diverse and is primarily due to the properties of the infectious agent and the state of the macroorganism. Depending on the clinical and laboratory changes, there are:

functional disorders of the nephron;
transient (transient) urinary syndrome;
interstitial nephritis (IN);
acute and chronic glomerulonephritis;
nephrotic syndrome (NS);
acute renal failure (ARF), hemolytic uremic syndrome (HUS);
urinary tract infection, pyelonephritis;
secondary metabolic disorders.

When analyzing the nature of kidney damage in infectious diseases, it is important for a doctor to distinguish whether kidney pathology is:

manifestation of the underlying disease;
its complication, possible, but not necessary for the underlying pathology;
exacerbation of nephro-urological pathology, provoked by non-renal disease.

Kidney pathology as a manifestation of the main infectious disease is represented by rather rare diseases, such as:

hemorrhagic fever with renal syndrome (HFRS);
leptospirosis;
yellow fever;
lassa fever, etc.

Diagnosis of these diseases is based, among other things, on a clinical and laboratory study of kidney damage, and, as a rule, there are no difficulties in their interpretation.

If we talk about the complications of infectious diseases, it is necessary to dwell on only some of them. So, the most common complication in childhood is IN.

Remarkable is the fact that IN was first described in 1898 by Kaunsilman in patients who had undergone diphtheria and scarlet fever. However, for a very long time, IN was identified exclusively with pyelonephritis. The term "chronic interstitial nephritis" for a long time corresponded to the modern understanding of kidney damage in hypertension - nephroangiosclerosis, primary shriveled kidney, that is, it designated those types of kidney pathology, which are based on vascular lesions. In parallel, in the first half of the twentieth century, there was the term "tubulointerstitial nephritis" (TIN) to denote acute renal failure.

Today, TIN is understood as an inflammatory (more often immuno-inflammatory) kidney disease, occurring with a predominant lesion of the interstitial tissue and tubules. In this case, the term "interstitial nephritis" is identified with tubulointerstitial, since it is difficult to imagine the defeat of the interstitium without damage to the tubules. According to ICD-10, headings N10, 11 include acute and chronic infectious TIN.

Acute TIN (ATIN) is an acute inflammation of the interstitium and tubules, often combined with minimal involvement of glomeruli and blood vessels in the process. Clinically, ATIN is often manifested by acute renal failure, less often by tubular disorders and changes in urinary sediment.

Chronic TIN (CTIN) is an irreversible process characterized by a progressive decline in kidney function with the development of chronic renal failure.

Primary TIN is inflammation (usually of an immune nature) of the interstitial tissue and tubules directly without the involvement of glomeruli or vessels in the process.

Secondary TIN - inflammation of the interstitial tissue and tubules, which developed against the background of another nephropathy (usually glomerulonephritis), or tubulointerstitial nephritis, concomitant (associated) with glomerulonephritis or other nephropathies.

Significant difficulties in everyday practice arise for the doctor in the differential diagnosis of TIN of infectious and drug origin, since therapy directed against the microorganism is usually intense, aggressive, long-term and can cause damage to the renal tissue. The following are just a few of the antimicrobial and antiviral drugs used in pediatric practice that can lead to kidney damage.

Antibacterial and antiviral drugs that promote TIN

Penicillins (methicillin, ampicillin, oxacillin, carbenicillin).
Cephalosporins.
Sulfanilamide.
Rifampicin.
Polymyxin.
Tetracycline.
Vancomycin.
Erythromycin.
Aminoglycosides (gentamicin, amikacin).
Kanamycin.
Ciprofloxacin.
Interferon alfa, acyclovir, tenofovir.

The clinical symptoms of TIN are varied and, in some cases, disguise themselves as symptoms of the underlying disease or come to the fore. Both in many infectious diseases and in TIN, general intoxication symptoms such as fever, headache, weakness, weight loss, pallor of the skin, mucous membranes, and arthralgia may prevail in the clinic. Nausea, abdominal pain, diarrhea, and lymphadenopathy are more often associated with infection, but often occur as a result of kidney damage. And only back pain, polyuria, polydipsia force the doctor to exclude the involvement of the kidneys in the pathological process.

The laboratory findings of this involvement are nonspecific and intermittent. In particular, in blood tests, changes may be observed in the form of anemia, leukocytosis, eosinophilia, increased ESR, increased levels of urea and creatinine, metabolic acidosis, increased levels of IgG and IgE. In the study of urinary sediment, aminoaciduria, bicarbonaturia, leukocyturia, eosinophiluria\u003e 1% (more often with drug etiology), glucosuria, hematuria (usually microhematuria), phosphaturia, proteinuria (up to 1 g / day), cylindruria (hyaline, leukocytic) can be detected. In many respects, the clinical and laboratory picture is determined by the site of tubular disturbance (Table 2), and its most severe manifestation will be the development of Fanconi's syndrome in a patient. Perhaps, only a decrease in the specific gravity of urine, regardless of the rate of diuresis and impaired reabsorption of beta2-microglobulin, will allow the doctor to speak with confidence about the development of acute TIN.

The differential diagnosis of ATIN is carried out primarily with acute glomerulonephritis. The absence of nephritic syndrome (edema, arterial hypertension, hematuria), erythrocyte casts, hypocomplementemia, cyclic flow will allow to exclude acute post-infectious glomerulonephritis.

The absence of diagnostically significant bacteriuria, ultrasound and X-ray signs of obstruction, deformation of the calyx-pelvic system will allow to reject the diagnosis of pyelonephritis.

The absence of staging of the process, the dependence of azotemia on the rate of decrease in diuresis, necronephrosis will be distinguished from OPN TIN. TIN is not characterized by DIC, such electrolyte changes as hyperkalemia, which accompanies ARF. Already at the beginning of TIN, azotemia and polyuria are possible, which should alert the doctor and help in the differential diagnosis.

In acute respiratory viral infections in children, damage to the urinary system is the second most frequent complication, and is manifested either by transient urinary syndrome or ATIN. Such a representation is valid if:

1) the appearance of symptoms of nephropathy against the background of an acute period of a viral infection (on days 2-5 of the disease) and their presence for 2-3 weeks, it is on these days that viruria appears and the maximum accumulation of viruses in the parenchymal organs is noted;
2) the absence of true bacteriuria, which can indirectly confirm the viral nature of the lesion;
3) changes in the urinary tract, mainly in the first year of life, characterized by an increase in ARVI, which indicates the epidemic nature of the pathology and further confirms the viral etiology of the process occurring in the urinary system;
4) the benign nature of the course of nephritis.

Glomerulonephritis is another fairly common complication of infectious diseases. To date, this category includes a heterogeneous group of diseases of immunoinflammatory genesis with a predominant lesion of the glomerular apparatus of the kidneys with a different clinical and morphological picture, course and prognosis. The variety of diseases and pathogens that lead to damage to the glomeruli are presented in table. 3.

The mechanisms of glomerular lesions are associated with a direct cytopathic effect, the participation of an infectious agent in the formation of immune complexes, and the involvement of glomeruli in autoimmune mechanisms. In some diseases, viral antigens are found in biopsies of kidney tissue in children with glomerulonephritis.

Manifestations correspond to the main clinical and laboratory syndromes, such as nephritic, nephrotic (pure or mixed), hematuric. Extrarenal symptoms include headache due to arterial hypertension, peripheral edema. Renal - pain in the lumbar region due to an increase in the size of the kidneys, oliguria associated with a decrease in the glomerular filtration rate, and urinary syndrome. The latter can be in the form of proteinuria and / or hematuria, the degree of which will determine the leading syndrome. During the examination, it is necessary to determine the kidney function by measuring the level of serum creatinine and urea. An increase in humoral activity, immunological changes (an increase in circulating immune complexes (CIC), levels of immunoglobulins, complement) will help to establish the immuno-inflammatory genesis of the disease. Hypercoagulable shifts (acceleration of APTT (activated partial thromboplastin time), increase in soluble fibrin-monomer complexes (RFMK), D-dimers), as a rule, accompany this kidney injury.

The most frequent infections that significantly damage the glomerular apparatus of the kidneys are viral hepatitis. Moreover, the type of kidney damage, the course and prognosis depends on its type. So, kidney damage usually develops against the background of chronic persistent or active hepatitis B. Men get sick more often; among the patients there are many injection drug addicts and other persons with a high risk of hepatitis B. The latter is complicated by membranous nephropathy (membranous glomerulonephritis. MemGN), MCGN, IgA-nephropathy. The most common occurrence is MemHN, in which in endemic areas (for example, countries in Asia and Africa) HBsAg is detected in 80-100% of children and 30-45% of adults. Immune complexes are formed locally after the antigen settles or are formed in the bloodstream and only then settle in the glomeruli. The prognosis for MemHN in children is favorable: within 3 years, 2/3 of them recover without treatment. In adults, the prognosis is worse: within 5 years, 30% develop chronic renal failure (CRF), in 10% of cases - end-stage CRF.

In hepatitis C, the most common morphological variants of glomerulonephritis are MPGN, MCGN, MemGN. At the same time, changes in urinary sediment are found in 30% of those infected with the hepatitis C virus. Against the background of changes typical for MCGN, deposits in the glomeruli of IgG, IgM, C 3 are found. Most patients have NS and microhematuria (sometimes erythrocyte casts). Against this background, the activity of liver enzymes is usually increased, the CZ level is reduced, and antibodies to the virus and viral RNA are present in the blood.

In recent years, in children's practice, much attention has been paid to cytomegalovirus infection (CMV), in the congenital or acquired form of which nephropathy with NS can develop. With nephrobiopsy, membranous nephropathy, FSGS can be detected. CMV is an etiological factor in the development of hormone-resistant NS, which largely determines the course of the disease and the prognosis for renal survival.

Syphilis can be complicated by NS, and secondary - in 0.3%, and congenital in 8% of cases. A typical morphological picture is membranous nephropathy, sometimes in combination with proliferation of the mesangium and endothelium. Immunofluorescence staining detects IgG and IgM deposits and antigens Treponema pallidum... In congenital syphilis, the levels of C 3 and C 4 complement are reduced. The standard therapy for syphilis is penicillins; in most cases, no specific treatment for glomerulonephritis is required.

In recent years, HIV infection has attracted great interest among practicing doctors. Scant evidence suggests that this infection can cause FSGS, MPGN (including IgA nephropathy), MCGN, and membranous nephropathy. However, the most characteristic FSGS, called HIV nephropathy, which may even be the first manifestation of HIV infection. HIV nephropathy occurs in all groups at risk of HIV infection, including children born to HIV-infected mothers, but it is most common among blacks and injecting drug users and to a lesser extent among homosexuals. The mechanism of development of HIV nephropathy is not exactly known, especially given the presence of such opportunistic infections as hepatitis, CMV, long-term, highly active antiretroviral therapy in this category of patients. In some studies, viral DNA was found in the kidneys of these patients, but it is also found in HIV-infected people without nephropathy. Probably, for the development of nephropathy, some additional factors are needed. HIV nephropathy manifests itself as severe mixed NA, and end-stage CRF may develop in a few weeks or months.

ARF is a clinical and laboratory syndrome characterized by a rapid decrease in renal productivity, which leads to an increase in the concentration of nitrogenous wastes in the blood serum and a decrease in urine output. This complication can accompany any infectious process, due to the variety of reasons that lead to its development. All these reasons are presented in the classification of J. Amburge, dated 1968, and subsequently supplemented. Thus, today the following forms of arrester and the reasons are distinguished:

prerenal: acute dehydration, shock, hypovolemia, thrombosis of the renal vessels, ascending thrombosis of the inferior vena cava;
renal (parenchymal):
- underlying kidney disease: diseases of the glomeruli, interstitium or blood vessels;
- ARF due to damage to the renal tubules (acute tubular necrosis): circulatory (ischemic) and nephrotoxic;
postrenal: megaureter, congenital anomalies of the ureters, bladder, ureterolithiasis, tumor obstruction.

Currently, in practical work, the following main criteria for diagnosing ARF are used:

1) absence of chronic renal failure;
2) increased serum creatinine levels;
3) increased serum urea;
4) a decrease in the rate of urination.

According to the ADQI (2004) recommendations and the AKIN (2005) consensus definition, ARF in adults is a rapid increase in plasma creatinine concentration of at least 3 times compared to the initial values \u200b\u200bor a creatinine level of at least ≈360 μmol / L (4 mg / dL ) as a result of a recent, rapid increase of at least ≈45 μmol / L (0.5 mg / dL) with or without concomitant oligo-, anuria. At these forums, the main stages and their criteria (RIFLE) in kidney damage were developed and presented (Table 4).

In recent years, the term "acute renal injury" (AKI) has become firmly established in the practice of a doctor; a consensus conference of major nephrological societies and leading experts on the problem of acute renal failure (AKIN, Amsterdam, 2005) defines it as a complex polyetiological syndrome, which is clinically characterized by a rapid increase in creatinine concentration : from slightly increased values \u200b\u200bto the actual arrester.

AKI is a sharp, in less than 48 hours, increase in plasma creatinine of more than 26.5 μmol / L (0.3 mg / dL) (absolute values) or 50% (relative values); and / or objectively marked oliguria (decrease in urine output to values \u200b\u200bof less than 0.5 ml / kg / h for more than 6 hours) (Table 5). These characteristics of acute kidney injury are applicable in older children.

Taking into account the peculiarities of the formation of kidney function in children, Akcan-Arikan et al. in 2007, the pediatric classification of RIFLE was proposed, which meets the requirements of pediatricians, pediatric resuscitators (Table 6).

Thus, we can talk about the multifaceted nature of kidney damage in children, against the background of acute or chronic infection. The clinical picture of these injuries can complicate the diagnosis of the underlying disease, often predetermines the management tactics for this category of patients and affects the prognosis for life.

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S. A. Loskutova,
E. I. Krasnova, doctor of Medical Sciences, Professor
S. V. Danchenko

NSMU, Novosibirsk

Tubulointerstitial nephritis is an ailment from the group of primary nonspecific kidney pathologies. The inflammatory process occurs in the renal tubules and interstitium, and then spreads to the rest of the tissue structures in the kidneys. The disease is characterized by an allergic, toxic or infectious origin and impairs renal function.

According to ICD-10 1995, several forms of the disease are distinguished, depending on the degree of damage. The commonality of pyelonephritis and interstitial nephritis is manifested in the similarity of the nature of morphological pathologies and the type of tubular lesions. However, the different etiology, as well as the nature of the pathogenesis, do not allow considering these two diseases as two forms of one disease.

Causes of occurrence

The disease is accompanied by inflammation of the interstitial tissue of the kidney, followed by its infiltration (up to 80% of the number of cells), granulomas or leukocytes of the nuclear polymorphic type. The epithelium of the tubules first swells, then dystrophy is observed in its cells, which is replaced by necrosis. Inclusions of immunoglobulins during research, as a rule, are not detected.

To date, the number of cases of nephritis caused by infections is decreasing, although acute tubulointerstitial nephritis very often begins to develop after infectious diseases suffered by a person (up to 95% of cases). Other causes of the onset of the disease include:

(bacterial kidney damage);
cancerous growths (leukemia, tumors);
hereditary diseases;
intoxication with medicines, chemical compounds;
nephropathy in various forms;
immune diseases.

Symptoms

The course of the disease directly depends on its form. The main symptoms of the disease include:

increased body temperature;
fever;
urticaria rash ();
pain during urination;
an increase in the size of both kidneys;
detection of purulent discharge in the urine;
the presence of pain in the lumbar region and in the side;
general weakness;
decreased activity due to excessively rapid fatigue;
decreased appetite.

Sometimes the symptoms over a long period of time are latent or subtle, which makes it possible to identify the disease only with a medical examination, which will show the presence of renal failure.

Chronic tubulointerstitial nephritis has nonspecific symptoms, so the patient does not pay attention to the signs of the development of pathology for a long time, or simply confuses them with symptoms of other ailments. In some cases, the body can retain fluid. The acute form of the disease is characterized by thirst, the presence of frequent urination.

Tubulointerstitial nephritis occurs in children with a frequency of 1.5% to 5%, according to renal biopsy. Experts are inclined to believe that the etiology of the disease is immunoallergic. Quite often, the disease begins to progress if the child has dysmetabolic nephropathy (about 15% of cases). To prevent the appearance of pathology, the parents of the child need to consult a doctor when symptoms appear, to treat immune, allergic and other diseases, as well as metabolic pathologies, in time and to the end.

Forms of the disease

There are three main forms of the disease:

hereditary. Other name - . This tubulointerstitial nephritis in children is inherited and is a non-immune form of glomerulopathy. Sometimes hematuria manifests itself, renal function is significantly reduced, which causes kidney failure. Often accompanied by vision problems and deafness. With disease, glomerular membranes increase in size and begin to exfoliate. The disease is caused by a mutation in the type 4 collagen gene, and its severity depends on the degree of gene expression. The incidence of the disease is 17 cases per 100 thousand children;
sharp. Acute tubulointerstitial nephritis is an abacterial form of inflammation in the renal tissue. The tubules, blood and lymph vessels in the renal stroma are also involved in the inflammatory process. This toxic subspecies of the disease can manifest itself at any age, including in newborns. It is considered the most severe form of the disease, which mainly occurs due to the body's reaction to the introduction of certain medications.

Drugs that can cause illness are penicillin, gentamicin, analgin, as well as various barbiturates and non-steroidal medicines. In addition, a reaction in the body can occur due to the ingress of large amounts of lithium, gold, lead, mercury there, as well as when exposed to radiation. In this case, it is not so important the number of drugs in the body that is important, but how long they were taken and what is the body's sensitivity to them. After the medication enters the patient's body, an allergic edema develops in the kidneys. The acute form of nephritis is also observed with, and various burns.

chronic. Chronic tubulointerstitial nephritis is a polyetiological type of disease. It manifests itself through abacterial inflammation of the interstitial renal tissue together with the tubules, lymphatic, and also blood vessels in the stroma of the kidneys. The disease develops as a result of metabolic disorders, previous infections (hepatitis, tuberculosis), taking medications or vitamins. The chronic form of the disease in children is found more often than acute. The manifestation of signs of the disease is preceded by a long latent stage. This often leads to an accidental diagnosis of the disease (when taking urine tests after, for example, past illnesses). The chronic form can occur due to a hypoimmune state, deviations in the development of the organs of the urinary system, or due to dysembryogenesis of the tissue of the affected organ.

Diagnostics

For the diagnosis of the disease, as well as its subsequent treatment, the patient should consult a nephrologist. He will be able to make a preliminary diagnosis based on:

analysis of the patient's history;
patient complaints of pain, problems with urination and other characteristic symptoms;
information obtained through physical research. In urine tests, a reduced amount of protein can be detected as well. At the same time, urine has a reduced density and contains sodium in small amounts;
tests from the laboratory;
x-ray examination of the kidneys;
magnetic resonance imaging (MRI);
kidney biopsy.

Treatment

Treatment guidelines for a disorder such as tubulointerstitial nephritis include:

elimination of the cause of the development of pathology. If the patient has an acute form of the disease, the first stage of treatment is to identify and stop taking medications that caused the allergic reaction. But it should be noted that this will not help to eliminate the already incipient renal fibrosis, which in some cases is irreversible. Also, if the disease is caused by an allergy, the patient may be prescribed corticosteroids. They will help speed up the healing process;
organization of the patient's life regimen, which provides for a decrease in the functional load on the kidney tissue;
a diet that minimizes the burden on the kidneys;
elimination of metabolic disorders;
restoration of renal functions;
elimination of sclerosis of renal tissue;
taking antibacterial, antifungal medicines, as well as uroseptics;
physiotherapy procedures.

To carry out detoxification in the body, the patient is prescribed infusion treatment. Drugs are prescribed based on urine culture and antibiotic susceptibility tests. In addition, the list of drugs includes the use of immune stimulants.

The success of treatment directly depends on the stage of the identified disease and whether irreversible tissue fibrosis has begun as a result of the inflammatory process. Given that many genetic and other factors of the disease cannot be corrected, the patient may develop end-stage renal failure.

Visible results of treatment are already noted within 2 months after its start, although characteristic residual scars may form on the kidney tissue. The patient may not fully recover with azotemia above the normal level. Changes in histology are often reversible if the doctor recognizes and eliminates their cause in time. At the same time, kidney failure, diffuse infiltration indicate an irreversible disruption of the organ. The prognosis for the treatment of the chronic form of the disease depends on whether the doctor detects and prevents the onset in time.

As for nutrition in case of illness, the food eaten should not be fatty, spicy, sour, fried. It is strictly forbidden to consume alcoholic beverages. At the same time, it is recommended to include in the diet boiled, steamed vegetables and meat, as well as greens, fruits and dairy products. You also need to consume enough vitamins and minerals. To draw up the correct individual diet, you need to contact your doctor.

Traditional medicine also has many recommendations for curing the disease, but it is worth remembering the accuracy of using folk remedies. Before you start taking any folk remedy, you need to consult a doctor. If he approves of the use of the tool, you can start using it.

The most popular folk remedies include:

medicinal herbal preparations. Mixtures of leaves of nettle, birch, parsley and other medicinal plants are used. They help relieve symptoms and get rid of toxins in the body. There are a dozen fees that are used for nephritis in both children and adults. In particular, according to some popular recipes, nephritis is treated with the help of bearberry tincture. It is worth knowing that this herb is not used by pregnant women;
taking berries. Lingonberries and strawberries are widely used. They are recommended to be consumed in a 1: 1 ratio with sugar. If you boil strawberry leaves, a decoction of them is also suitable for use in small quantities;
receiving pumpkin. It is recommended to bake it in the oven with sugar in a 1: 1 ratio and consume it throughout the day;
the use of quince. The broth includes both seeds and leaves of the fruit, and the remedy itself is recommended to be consumed 4 times a day in a tablespoon.

Prevention

Acute tubulointerstitial nephritis can be prevented by:

control over the intake of medicines. You do not need to self-medicate, take medications in high doses, without consulting your doctor;
rejection of bad habits that have a detrimental effect on kidney function (smoking, drinking alcohol);
a healthy and balanced diet, containing all the necessary vitamins, microelements.

Acute tubulointerstitial nephritis (TIN) is non-specific. If measures are not taken in time, the passages (tubules) of the kidneys gradually atrophy, and the kidneys themselves cease to function normally. Due to the violation of the blood filtration process, all body systems suffer. The nature of tubulointerstitial nephritis can be hidden in metabolic or immune changes, external exposure to infection and chemicals. Inflammation of all structures of the kidney tissue and the duct passages of the kidneys occurs.

In the CIS countries, the disease is not widespread, according to statistics, 1.7% of the population have TIN. Such patients must undergo hemodialysis (extrarenal cleansing of the blood) annually.

There are several criteria by which TIN is divided:

by the nature of the flow;
due to the occurrence;
by pathogenesis;
by the nature of the tubular disorder.

The nature of the tubular disorder can be of three types:

Endocrine dysfunctions.
Partial violations.
Disruption of the tubules.

The form of the course of the disease is acute and chronic.

The disease can be hereditary, then it is called Alport syndrome. A baby is born with glomerulopathy or hematuria, which lowers kidney function and results in. Tubulointerstitial nephritis in children is accompanied by visual and hearing impairment.

The sudden onset of renal failure is the main symptom of the acute form. This occurs as a result of damage to the renal tubules and tissues.

Chronic tubulointerstitial nephritis appears after damage to the same structures of a larger scale. The most common cause is long-term or uncontrolled medication, the influence of another kidney disease.

Tubulointerstitial nephritis is primary and secondary. The primary leads to a harmful agent, for example, chemicals, infections, toxins, metabolic failure. Secondary tubulointerstitial nephritis appears if the body already has chronic kidney disease, namely radiation nephritis, amyloidosis, nephroangiosclerosis,.

The following classification by the nature of the damaging factor:

infectious;
drug;
immune;
metabolic disorders.

The reasons for the development of the disease

Unspecified acute tubulointerstitial nephritis occurs when the body is exposed to harmful factors. The main harmful agents are infections, medicines and allergens.

What substances most affect the tissues and tubules of the kidneys:

analgesics of non-narcotic origin;

antibiotics;
sulfonamides;
immunosuppressants;
substances for chemotherapy;
iodine, lithium;
biological toxins, pesticides;
heavy metals;
medicinal herbs, herbicides;
alcohol.

TIN develops as a result of metabolic disorders, namely:

clogging of blood vessels with cholesterol;
high levels of uric acid in the blood.

The kidneys are affected by the following systemic diseases:

hepatitis;
oncological diseases;
diseases of the lymphatic system;
anemia;
myeloma;
diseases of the genitourinary system;
vasculitis;
sarcoidosis;
sjogren's syndrome.

Manifestations of vasculitis in the neck and chest

Infections that have a negative effect on the kidneys:

The above factors negatively affect human kidneys only with increased sensitivity to certain components. If the patient is at risk, then it is almost impossible to protect yourself from the problem.

Chronic tubulointerstitial nephritis appears in a person with an untimely visit to a doctor or with an incorrectly chosen treatment strategy. The more common cause is severe intoxication, exposure to radiation, immune or metabolic disorders, and nephropathy. The most susceptible to the disease are patients suffering from cirrhosis of the liver, diabetes, abuse of caffeine, analgesics and antibiotics, with heart disease.

Diabetes mellitus is one of the possible causes of tubulointerstitial nephritis

Symptoms

The disease develops at least 30 days after exposure to a harmful factor. At the beginning of the development of the acute phase, the patient's pressure rises, the blood flows through the tubules more slowly, the quality of filtration decreases. Due to the decrease in water reabsorption, the amount of urine increases. Symptoms can be confused with inflammatory kidney disease. Therefore, the patient must undergo a laboratory test. As the disease progresses, the amount of fluid in the body increases, kidney stones and protein in the urine appear.

Depending on the form, the disease has different symptoms. The acute form is characterized by the following features:

increased body temperature;
backache;
enlargement of the kidneys, which can be detected during palpation or ultrasound;
painful urination;
discharge of pus in the urine;
rashes on the body.

Some patients experience no symptoms or they are mild. Renal failure is detected during a routine blood test.

In chronic forms of tubulointerstitial nephritis, symptoms initially also appear mildly, gradually increasing the effect. The patient has:

general weakness of the body;
decreased appetite;
increased fatigue.

Despite the water retention in the body, the limbs do not swell. The more kidneys are affected, the more acute nephritis symptoms appear. Added to these are dry mouth, frequent urination.

Symptoms often appear several weeks after exposure to a toxic substance. Some patients only begin to feel sick after repeated exposure. If the cause of TIN is the use of non-steroidal anti-inflammatory drugs, then the disease begins to actively develop after a year and a half.

Edema appears after the development of renal failure. Along with this, or polyuria appears. If renal function is impaired, then the symptoms of renal failure become pronounced.

Diagnostic methods

Determining the presence of tubulointerstitial nephritis is not easy, there is no single analysis that will surely show the problem. The patient needs to undergo a comprehensive examination. In the presence of a TIN, the following inconsistencies will be identified:

increased amounts of protein, white and red blood cells in the urine;
alkaline urine reaction;
decreased urine density;
hemoglobin level less than 100 units;
increased levels of eosinophils and sodium in the blood.

A general analysis of urine and blood is examined in comparison before and after certain loads.

Before starting treatment, the doctor must exclude the presence of prostatitis, urolithiasis, nephroptosis, tumors. The above problems give symptoms similar to those of TIN.

An ultrasound of the kidneys is mandatory. In the presence of TIN in the acute phase, the organs will be edematous and enlarged; in the chronic form, the size of the kidneys is normal. Kidney tubules are enlarged, cysts are found. Computed tomography provides more reliable information about the condition of the kidneys. MRI, CT, radiography provide information about the size of organs, the shape of the edge, the degree of calcification.

Additional information will be shown by urine culture and renal biopsy.

Treatment

The goals of drug therapy:

relieving symptoms;
restoration of the filtration process;
stabilization of the state of the body;
exclusion of the development of renal failure.

Treatment of tubulointerstitial nephritis begins after the removal of the harmful factor. For this, the patient's history is studied. If the reason is long-term use of medications, then it is replaced with another.

A patient with tubulointerstitial nephritis is prescribed a diet, especially in the acute phase of the disease. Salt, seasonings, spicy and smoked foods are excluded, abundant drinking is recommended. The amount of protein in the diet decreases, coffee and tea are replaced by herbal infusions. Lingonberry leaves, bearberry, flax seeds are useful.

The patient, if possible, should exclude stressful situations, physical and intellectual stress, hypothermia.

TIN of a viral nature is treated with antiviral drugs, bacterial - with antibiotics. If medications have led to a violation of blood clotting, anticoagulants are prescribed, the danger is the increased density of the blood, which causes blood clots. Antifungal drugs, uroseptics, immunostimulants can be prescribed.

Drug therapy includes taking such drugs:

Isoniazid.
Omeprazole.
Fluoroquinolone.
Sulfanilamide.
Ranitilin.

Depending on the results of the analysis, the following can be assigned:

Pyridoxine.
Cholestyramine.
Calcium lactate.

Forecast

The genetic, toxic and metabolic type of the disease is not amenable to correction, end-stage renal failure occurs. A neglected disease can cause pulmonary edema.

With chronic tubulointerstitial nephritis of the stage of the disease, as well as the continuation of exposure to the body of a harmful agent, there is a risk of prescribing lifelong hemodialysis.

After the end of treatment, renal fibrosis remains, the functions themselves are restored, the prognosis is favorable.

Tubulointerstitial nephritis is a disease characterized by damage to the renal tubules and interstitial tissue. The painful process tends to spread to all parts of the organ. There are acute and chronic forms. Consider the main factors in the development of this pathology, its characteristic manifestations and methods of treatment.

Causes

The causes of this disease are very diverse. However, most urologists associate its occurrence with the use of a number of medications - antibiotics. Penicillin antibiotics (aminoglycoside derivatives, Rifampicin, etc.) are especially harmful to the kidneys.

Quite often, tubulointerstitial nephritis forms after taking such medications:

sulfa drugs, because they have a toxic effect on kidney tissue;
non-steroidal anti-inflammatory drugs (Indomethacin, Brufen and their analogues, in case of improper and excessive use, have a toxic effect on the kidneys);
pain relievers;
drugs that suppress the immune system;
diuretic drugs;
barbiturates.

Tubulointerstitial nephritis is the result of a high sensitivity of the organs to certain chemicals, in particular, ethylene glycol and ethyl alcohol.

Chronic tubulointerstitial nephritis develops as a result of a poorly treated acute process. It often happens that it is preceded by prolonged poisoning with poisonous substances, immune disorders, and medication.

Pathogenesis

Acute tubulointerstitial nephritis is a specific disease, its pathogenesis has not yet been elucidated. The autoimmune nature of renal tubular damage is discussed. In the course of immune interactions of antigens with antibodies, inflammation and morphological changes occur in the kidney tissue. Due to vasospasm, edema develops in the interstitial tissue.

Edema often leads to a gradual decrease in the glomerular filtration rate. The defeat of the tubules, in turn, further aggravates the picture of kidney damage. Reduced water reabsorption, which leads to polyuria, hypostenuria. Prolonged compression of the tubular capillaries is the cause of proteinuria and tubular acidosis.

Prolonged action of toxic nephrotoxic substances, taking medications gradually lead to the fact that the tubules do not cope with their function. Of great importance is the negative effect of one or another medication on the protein that makes up the renal tissue. The development of symptoms in chronic tubulointerstitial nephritis is noticeably slower.

Symptoms

The vast majority of patients experience symptoms such as pronounced weakness, profuse sweating, and headache. In the lumbar region, weak aching pains are recorded. Loss of appetite is characteristic, a feeling of nausea appears.

These signs are combined with chills and fever, aches and severe muscle pain. Patients are worried about polyarthralgia. In some cases, short and small rashes appear on the skin, pressure is not expressed and increases for a short time. Acute tubulointerstitial nephritis is characterized by the absence of edema. Dysuric phenomena, as a rule, are not observed. Moreover, already starting from the first days of the disease, the patient notes a sharp increase in the amount of urine excreted with a reduced density. This phenomenon is called hypostenuria.

In severe episodes of the acute course of the disease, oliguria develops - a decrease in the amount of daily urine.

Chronic tubulointerstitial nephritis is characterized by less pronounced symptoms. Its manifestations develop very slowly; often patients do not pay attention to them. However, with the progression of kidney damage, they cannot fail to notice the following signs:

general weakness and malaise;
growing weakness, including muscle weakness;
drop in performance;
thirst;
increased urge to urinate;
dryness in the mouth.

Pediatric pathology

Tubulointerstitial nephritis in children is considered a fairly common pathology. Most doctors are inclined to believe that such a pathology in children is of an immune or allergic nature. Usually, the disease develops in those children and adolescents who have a tendency to nephropathies caused by metabolic disorders.

There are frequent cases of the development of this disease in children who are taking sulfonamides and antibiotics uncontrollably. The latter include Cefazolin, Ampicillin or Penicillin. That is why, when prescribing such medications, a preliminary test for compatibility with the kidneys is important.

The clinical manifestations of this disease in children are similar to those in adults. Medical measures also do not differ from the generally accepted ones. It is important to use short courses of glucocorticosteroid drugs in appropriate dosages or cytostatics. Children are prescribed procedures aimed at treating violations of the water-salt balance. In severe renal failure, dialysis or kidney transplant is prescribed.

Diagnostics

In order for the doctor to be able to make an accurate diagnosis, on which the effectiveness of subsequent treatment will depend, the patient must undergo the following studies:

General and biochemical blood tests (indicators such as leukocytosis, erythrocyte sedimentation rate, creatinine and urea levels are important).
General urine analysis (indicators of hematuria, proteinuria, urine density are important).
The level of protein in the urine per day.
Urine tests according to Zimnitsky and Nechiporenko.
Ultrasound examination of the kidneys and internal organs.
Bacterial urine culture.
Biochemistry of urine.
Immunological tests (important indicators - IgE, IgA).
Biopsy.

Treatment

First of all, it is necessary to cancel the drug that caused the cause of nephritis. If the cause of the disease is an infection, then therapeutic measures should be aimed at eliminating it. In most cases, it is necessary to refrain from taking glucocorticosteroid drugs. Their appointment is justified only in cases where kidney failure persists for more than a week after their cancellation. It is preferable to prescribe treatment with Prednisolone, in short courses.

In periods when a pronounced clinical picture of diseases is observed, a sparing regimen is necessary, preferably bed. At least it should last at least seven days from the onset of nephritis or exacerbation of a chronic form. During periods of remission of the disease, diet therapy, limitation of physical activity and exclusion of exposure to cold (especially drafts) are indicated.

Acute kidney failure caused by this disease requires urgent treatment. Elimination of water-salt imbalance is carried out (with the help of infusion treatment). Provided that the immune causes of the disease are proven, special desensitizing drugs are prescribed.

When choosing a diet, it is very important to limit salt and seasonings. If nephritis has caused the development of chronic kidney failure, then the amount of protein in the daily diet is limited.

Acute tubulointerstitial nephritis caused by microbes and viruses requires appropriate treatment. So, with the viral nature of inflammation, antiviral drugs are prescribed - Metisazon, Acyclovir, Remantadin, etc. In the presence of a bacterial infection, antibiotic treatment is indicated. The range of drugs used is quite wide, and the doctor has the ability to prescribe the necessary drug, based on each individual case. The course of taking such drugs lasts until the temperature drops to normal and the kidney function normalizes.

In the case of toxic renal damage, glucocorticosteroids and antihistamines are indicated. Glucocorticosteroids are preferred for autoimmune disorders. In case of intoxication, specific antidotes and hemosorption are used to quickly remove the toxic substance from the body. In case of collapse or shock, anti-shock measures are used.