Interstitial nephritis is clinically manifested. What is interstitial nephritis

Interstitial nephritis is a disease characterized by inflammation in the areolar connective tissue of the kidneys. Women at various stages of pregnancy and children are most susceptible. Interstitial nephritis in children often occurs against the background of allergic diathesis, drug poisoning, excess salts in the urine and leads to growth retardation.

Causes

The causes of interstitial nephritis are varied. The most common is prolonged use of certain drugs, among which the most dangerous are:

antibiotics;
immunosuppressants;
analgesics;
non-steroidal anti-inflammatory drugs;
sulfonamides.

Interstitial nephritis in children often appears against the background of disembryogenesis of renal tissue, difficulty in the metabolism of urates and oxalates, and abnormalities of the urinary tract. However, the mechanism of disease formation has not been fully studied.

The main provoking factor today is considered to be the effect of toxins and antibiotics on kidney tissue. When etiological factors enter the kidneys with the blood, they are released into the glomerular filter, from where they enter the lumen of the tubules and are reabsorbed. Then complete antigens are formed, which interact with antibodies, forming immune complexes. The latter are deposited in the interstitium, resulting in inflammation.

Other reasons include:

urinary tract obstruction;
vesicoureteral reflux;
prolonged intoxication with heavy metals;
immune diseases;
granulomatous diseases;
oncology;
radiation;
infections;
systemic pathologies of connective tissue.

Classification

There are several classifications of interstitial nephritis, based on the nature of the course, development, causes, and clinical picture. Due to the characteristics of the course, acute and chronic forms of the disease are distinguished. Acute interstitial nephritis develops rapidly:

body temperature rises;
urine formation increases;
Blood begins to be released in the urine.

In advanced cases, renal failure may develop, but in general the prognosis for patients is favorable. Chronic interstitial nephritis is a serious disease, accompanied by the appearance of scars on the connective tissue of the kidneys and the death of the tubules. In later stages, glomerular damage develops. Nephrosclerosis often occurs, in which the kidneys literally shrink. Due to the death of kidney cells, chronic renal failure is formed. These changes become irreversible.

Based on the mechanism of development, two types of the disease are also distinguished: primary and secondary. Primary is not preceded by any renal pathologies. Secondary is complicated by existing ailments, the most common of which are:

leukemia;
diabetes;
gout.

Another classification is based on the etiological factor. Depending on the underlying causes, the following types of interstitial nephritis are distinguished:

Toxic-allergic form - develops as a result of prolonged intoxication with chemicals and drugs, as well as as a result of the administration of vaccines and serums.
Post-infectious - occurs against the background or as a result of exposure to viral or bacterial infections.
Autoimmune - develops due to dysfunction of the immune system.
Factors influencing the appearance of the idiopathic form of the disease are unknown.

The classification is based on the clinical picture and includes the following forms:

expanded;
heavy;
“abortive”;
"focal".

In the advanced form, all the symptoms of the disease are observed, in the severe form, the signs of acute renal failure appear more strongly than others. The “abortive” form is accompanied by the absence of urine, but the prognosis is favorable: rapid normalization of organ functions is possible. The “focal” type of the disease is characterized by an increase in urine volume, all other signs appear rather weakly.

Characteristic symptoms of the pathology

Interstitial nephritis does not have specific symptoms that can be easily diagnosed by a layperson. Symptoms of the disease are also typical for other renal pathologies, among them are:

headache;
lethargy;
muscle aches;
aching pain in the lower back;
fever;
drowsiness;
general malaise;
increased sweating;
loss of appetite;
temperature increase;
nausea;
hypertension;
increase or decrease in urine production.

Among the initial symptoms, polyuria is often observed - the release of more than 1800–2000 ml of urine per day, but when complications arise, this volume decreases sharply. In most cases, swelling is not observed.

Symptoms may vary depending on the form of the disease. Thus, the main symptom of acute interstitial nephritis is prolonged anuria and an increase in the concentration of creatinine in the blood.

Among the signs of the “abortive” form of interstitial nephritis are early polyuria and short-term azotemia. In some cases, extensive necrosis of the renal tissue develops from the very beginning, especially in the cortex. The main symptom of this condition is acute uremia. Death occurs after 2–3 weeks.

In the idiopathic form of the disease, there are no specific signs. In rare cases, inflammation of the eye vessels and brain symptoms are observed.

Acute interstitial nephritis is characterized by a rapid increase in symptoms. Inflammatory processes are mainly observed.

Symptoms of the chronic form of the pathology are often completely absent. However, in some cases, anemia or minor changes in urine, arterial hypertension, dull back pain, lethargy, and decreased performance are observed.

Primary chronic interstitial nephritis develops very slowly and can progress for years without showing significant symptoms.

The secondary form of the disease occurs in different ways, depending on the severity of the underlying pathology. Possible polyuria, stone deposits, muscle weakness, hypotension. Symptoms are caused by the fact that the kidney loses its ability to normally concentrate salt, as a result of which it is washed out of the body in the urine.

Diagnostic methods

Before treating interstitial nephritis, it is important to make a proper diagnosis. Various methods are used for this:

anamnesis;
blood analysis;
biochemistry of urine;
Zimnitsky and Reberg samples;
serological studies;
urine culture;
renal biopsy.

A general blood test reveals leukocytosis in the patient, as well as eosinophilia and signs of an inflammatory process. In addition, an imbalance of proteins, creatinines and urea is recorded.

Making a diagnosis in the early stages is based on changes in partial kidney function if the patient has dealt with pesticides or medications.

A urine test for biochemical parameters reveals an increase in the concentration of proteins in the urine, leukocyturia, microhematuria and eosinophiluria. A characteristic sign of the disease is a decrease in the density of urine.

Other tests help evaluate various kidney functions. However, the most informative is a biopsy. During which a small piece is taken from the organ and examined under a microscope.

Treatment options

Treatment of interstitial nephritis begins with the abolition of medications that provoked the disease. Then it is necessary to speed up the elimination of this drug from the body. At the same time, symptomatic treatment is carried out. With the “abortive” form, it is usually enough to take a course of calcium gluconate, rutin and vitamin C.

The patient must be treated inpatiently, strictly observing bed rest. In addition to basic therapy, it is important to maintain normal electrolyte levels and monitor the acid-base balance.

If the disease is severe, it is necessary to reduce swelling as soon as possible. For this purpose, glucocorticoids and antihistamines are prescribed. Sometimes drug overdoses and intoxications occur. In such cases, the medicine is quickly eliminated from the body using one of the available methods:

hemosorption;
antidotes;
hemodialysis.

Treatment of chronic interstitial nephritis is primarily aimed at eliminating the causes that provoked the disease. The patient is prescribed restorative therapy, medications and vitamins. For necrosis, special medications are used:

Trental;
salurtiki;
Heparin;
antibiotics.

If treatment does not produce results within two days, the patient is prescribed glucocorticosteroids - hormonal drugs. It is important for the patient to ensure high-quality hydration: increase the volume of water and liquid injected into the vein with increased urination, and reduce with decreased urination.

Possible complications

The most serious consequences of interstitial nephritis are:

Chronic form of the disease - in the absence of qualified therapy, the acute course of the pathology becomes chronic.
Renal failure - the acute form is expressed in a sharp deterioration in kidney function, and the chronic form is expressed in irreversible impairment of organ functionality due to the death of nephrons.
Arterial hypertension - the patient has constantly elevated blood pressure - from 140/90 mm Hg. Art.

Interstitial nephritis in children often causes a complication in the form of “kidneys losing salt” syndrome. All salt begins to be washed out of the body in the urine, after which salt depletion and hypotension develop. The risk of collapse increases.

Disease Prevention

In order to maintain kidney health after treatment, it is necessary to follow preventive measures:

To drink a lot of water.
Do not abuse medications, including painkillers.
There are foods with B vitamins.
Limit salt in your diet.
Have your urine tested regularly.
Treat foci of chronic infections.
Avoid hypothermia.
Dose physical activity.

The interstitial form of nephritis requires immediate contact with a specialist and initiation of treatment. The patient will temporarily lose his ability to work (for 3-4 months), but in the future this will allow him to recover and fully recover.

Interstitial nephritis is a common disease characterized by acute or chronic abacterial inflammation of the interstitial tissue and kidney tubules. The disease is an independent nosological form. Its symptoms are in many ways similar to those of pyelonephritis, but there are also significant differences.

Thus, with interstitial nephritis, organ tissues are not destroyed. The inflammation covers exclusively the connective tissue, which forms a kind of “framework” of the organ, without further spreading to the renal pelvis and calyces.

Interstitial nephritis develops in people from various age groups, in particular in young children. But most often it affects people of working age - from 20 to 50 years.

Forms

According to the nature of the course in medicine, the following forms of interstitial nephritis are distinguished:

acute interstitial nephritis. It is characterized by an acute onset - the temperature rises sharply, the amount of urine excreted by a person increases and blood appears in it (hematuria), pain occurs in the lower back. In more severe cases, it may develop. If you experience one or more of these symptoms, it is recommended that you consult a qualified physician without delay. The prognosis for acute interstitial nephritis in most clinical situations is positive;
chronic interstitial nephritis. If the disease develops into this form, then the patient develops fibrosis of the tissue that forms the stroma of this parenchymal organ. The tubules also die. The last stage of development of chronic interstitial nephritis is damage to the glomeruli (this is the functional part of the kidneys in which blood filtration occurs). If the patient is not provided with qualified medical care. help, then he will develop nephrosclerosis - this syndrome of impaired renal function is irreversible and life-threatening.

According to the development mechanism, the following forms are distinguished:

primary. In this case, the pathological process develops in the renal tissue independently, and not against the background of another disease;
secondary. It develops against the background of an existing kidney disease and significantly complicates its course. It can also develop due to the presence of other diseases in the body.

According to the etiology of occurrence, the following forms of interstitial nephritis are distinguished:

autoimmune. The disease occurs due to a previously occurring malfunction of the human immune system;
toxic-allergic. This form occurs due to prolonged exposure to toxic chemicals. substances on the body, as well as when administering protein preparations;
idiopathic. In this case, the etiology of interstitial nephritis is not established;
post-infectious.

According to clinical manifestations, there are:

expanded form. All clinical symptoms of interstitial nephritis are pronounced;
severe form. In this case, symptoms of prolonged anuria and acute renal failure are pronounced. If they are detected, it is necessary to urgently perform hemodialysis on the patient. If this procedure is not carried out, it can lead to death;
"abortive" form. The patient has no anuria, kidney function is quickly restored. The course of this form of the disease is favorable and does not pose a threat to the patient’s life;
"focal" form. The symptoms of interstitial nephritis are rather mild. Polyuria is noted. The patient is recovering quickly.

Etiology

Interstitial nephritis can be the result of a fairly wide range of pathological conditions.

Factors contributing to the development of acute interstitial nephritis:

the presence of infectious processes in the body;
lymphoproliferative pathologies;
diathesis of an allergic nature;
introduction of protein preparations into the body;
chemical intoxication of the body. substances;
diseases that affect connective tissue.

Factors contributing to the occurrence of chronic interstitial nephritis:

autoimmune diseases:
chronic intoxication of the body;
diseases during which granulomatous inflammation develops. For example, or ;
disturbances in the development of kidney tissue;
taking painkillers and non-preventive medications for a long period of time;
various anomalies of the urinary system;
congenital disorders of oxalate and urate metabolism.

Symptoms

Interstitial nephritis has no symptoms that are unique to it. It has the same symptoms as other kidney diseases:

a sharp increase in temperature to high numbers;
decrease in the volume of urine excreted (in severe clinical cases);
headache, dizziness;
sweating Some patients complain of chills;
lower back pain;
drowsiness;
there is no swelling in the limbs;
aches in the muscles of the trunk and limbs;
loss of appetite or complete refusal to eat;
polyuria;
The patient develops arterial hypertension.

Diagnostics

a thorough analysis of the patient’s complaints, as well as the disease itself, will help the doctor determine when the first symptoms appeared, how severe they were, and so on. Based on the data obtained, a further examination plan is drawn up;
. It shows leukocytosis, an increase, and in some cases a decrease in the amount;
. Elevated levels of creatinine and urea are noted;
biochemistry of urine. One of the most informative diagnostic methods. The analysis reveals proteinuria, microhematuria, eosinophiluria;
Rehberg's test. This method makes it possible to assess the excretory capacity of the kidneys and allows you to check the ability of the tubules to absorb and excrete certain substances;
Zimnitsky's test. Allows the doctor to evaluate the ability of the kidneys to concentrate urine;
urine culture. This method is necessary to check if there are bacteria in the urine;
kidney biopsy.

Treatment

Treatment of interstitial nephritis must begin after the cause of its development in the human body has been established.

Considering the fact that the disease most often develops while taking certain synthetic medications, in this case the only method of treatment is to identify and stop taking the drug that triggered the development of the disease. If there is no effect within 3 days, it is indicated to take glucocorticosteroids.

It is important to provide the patient with the most optimal hydration regimen. If the amount of urine he excretes increases, then the volume of fluid he receives intravenously or consumes independently also increases accordingly. If the volume of urine decreases, the amount of fluid administered also decreases.

If a patient develops acute renal failure, hemodialysis must be performed urgently.

During treatment, it is important that the patient receives sufficient amounts of vitamins, proteins and carbohydrates, so doctors prescribe him a special diet.

Diet

If the patient has no symptoms of the chronic course of the disease, then he is prescribed a physiologically complete diet. The diet will be structured so that the human body receives all the substances it needs - fats, vitamins, proteins, carbohydrates. It is important to limit your consumption of table salt. This is especially true if the patient has high blood pressure.

Diet for chronic disease has other nuances. Its action is aimed at correcting oxalate-calcium metabolism. Doctors, as a rule, prescribe a cabbage-potato diet to patients.

Be sure to exclude from the diet foods that can negatively affect the tubular apparatus of the kidneys - citrus fruits, spicy, fatty and smoked foods. Spices are also excluded.

The diet will help restore normal kidney function. But it is also important to drink at least two liters of fluid per day. It's better if it's just purified water.

Features of the course of the disease in children

Interstitial nephritis occurs quite often in children. It can even occur in newborns who are diagnosed with nephropathies. In most clinical cases, the diagnosis was confirmed in premature babies. As a rule, their illness develops as a reaction of the body to a toxic or hypoxic effect.

In children, the first sign of the disease is the appearance of edema. Polyuria then develops. There is an increase in creatinine and urea levels in the blood. In almost all cases, the disease in children is diagnosed in the acute period. But there have been cases when the disease took a chronic course. This was due to incorrect and untimely treatment.

Prevention

You need to drink at least two liters of fluid daily;
exclude strong physical activity;
prevent hypothermia of the body;
Do not take synthetic medications for a long time. This is especially true for drugs that help eliminate pain;
sanitation of foci of infection in the body.

Is everything in the article correct from a medical point of view?

Answer only if you have proven medical knowledge

Interstitial nephritis is an abacterial inflammatory disease of the intermediate tissue of the kidneys with damage to the tubules and blood vessels of the organ and the subsequent spread of the inflammatory process to all structures of the kidney tissue.

Acute and chronic interstitial nephritis is caused by various etiological factors and pathogenetic mechanisms, and accordingly affects the choice of treatment approaches. Kidney diseases affecting exclusively the tubules and interstitium account for 20-40% of cases of chronic kidney disease and 10-25% of acute renal failure.

Now the generally accepted name in the world is not “interstitial nephritis”, but “tubulointerstitial nephropathy”. The choice of this name is explained by the fact that the interstitium does not play a major role in the pathogenesis of the disease, the inflammatory process only begins from it, and the disease is based on tubular dysfunction. Changes in blood vessels and glomeruli occur later. This is mainly glomerulosclerosis, which leads to an increase in azotemia. In turn, the interstitium can be affected by GN, vasculitis, and systemic connective tissue diseases, which leads to their progression.

Etiology

Patients with acute interstitial nephritis make up 76% of people who have had acute renal failure.

Causes of acute interstitial nephritis:

1. Drugs (in order of decreasing nephrotoxic effect):

a) antibiotics: penicillins, cephalosporins, gentamicin, tetracyclines, rifampicin, doxycycline, lincomycin, etc.).
b) sulfonamides
c) non-steroidal anti-inflammatory drugs
d) anticonvulsants
e) anticoagulants (warfarin)
e) diuretics: thiazides, furosemide, triamterene
g) immunosuppressants: azathioprine, sandimune
h) others: allopurinol, captopril, clofibrate, acetylsalicylic acid.

2. Infections:

a) direct damaging effect: B-hemolytic streptococcus, leptospirosis, brucellosis, candidiasis
b) indirect damaging effect: sepsis of any etiology.

3. Systemic diseases:

a) immune diseases (SLE, transplant rejection crisis, Sjogren's syndrome, mixed cryoglobulinemia, Begener's granulomatosis)
b) metabolic changes (increased concentrations of urates, oxalates, calcium, potassium in the blood)
c) intoxication with heavy metals, ethylene glycol, acetic acid, aniline
d) lymphoproliferative diseases and plasma cell dyscrasias
e) intoxication: hepatotoxins (poison of the toadstool), formaldehyde, chlorinated hydrocarbons.

4. Idiopathic acute interstitial nephritis.

In 30% of patients with chronic interstitial nephritis, congenital anatomical abnormalities of the kidney structure are found. Among the causes of chronic interstitial nephritis, 20% is the use of analgesics, 11% is uric acid diathesis. Many patients with benign arterial hypertension show changes in the interstitium; in 7% of patients the causes are different, including radiation damage. In some patients the cause is unknown.

Causes of chronic interstitial nephritis:

1. Immunosuppressive diseases: SLE, transplant rejection crisis, cryoglobulinemia, Sjogren's syndrome, Goodpasture syndrome, IgA nephropathy.

2. Medicines: analgesics, non-steroidal anti-inflammatory drugs, sandimune, lithium.

3. Infections: bacterial, viral, mycobacterial.

4. Obstructive uropathy: vesicoureteral reflux, mechanical obstruction.

5. Diseases of hematopoiesis: hemoglobinopathies, lymphoproliferative diseases, plasma cell dysplasia.

6. Heavy metals: cadmium, mercury.

7. Metabolic changes: hyperuricemia, hyperoxalemia, cystinosis, hypercalcemia.

8. Wegener's granulomatosis, sarcoidosis, tuberculosis, candidiasis.

9. Vasculitis: inflammatory, sclerotic, embolic.

10. Congenital diseases: congenital nephritis, “spongy” renal medulla, medullary cyst disease, polycystic disease.

11. Endemic diseases: Balkan nephropathy.

12. Idiopathic chronic interstitial nephritis.

Pathogenesis of interstitial nephritis

The leading role in the pathogenesis of acute interstitial nephritis is played by immune mechanisms: immunocomplex (with IgE) and antibody (antibodies against the tubular basement membrane). The first occurs with SLE, lymphoproliferative diseases, and the use of NSAIDs, the second occurs with intoxication with penicillin antibiotics and a crisis of transplant rejection.

During the course of the disease, inflammatory swelling of the interstitial tissue of the kidneys occurs, vascular spasm and mechanical compression, and kidney ischemia develop. The intratubular pressure increases and the effective renal plasma flow and CP rate decrease, the creatinine content increases. Severe ischemia can lead to papillary necrosis with massive hematuria. Interstitial edema and tubular lesions lead to decreased water reabsorption (polyuria, hyposthenuria, despite decreased GFR). In the interstitium of the renal medulla, as a consequence of the inflammatory process, cellular infiltration occurs, which causes depolymerization of acidic mucopolysaccharides, disrupting their ability to bind osmotically active substances.

All these changes cause long-term disturbances in urine concentration. Gradually, interstitial edema decreases, effective renal plasma flow is resumed, and the rate of CF is normalized.

The pathogenesis of acute interstitial nephritis varies depending on the etiology. For example, acetylsalicylic acid in the cytoplasm of cells inhibits the penetration of amino acids into cellular proteins and reduces amino acid phosphorylation.

There are 5 mechanisms of nephrotoxicity in acute interstitial nephritis:

1) redistribution of renal blood flow and its decrease

2) ischemic damage to the glomerular and tubular basement membranes

3) delayed hypersensitivity reaction

4) direct damage to tubular cells by enzymes under anoxic conditions

5) selective accumulation of the drug in the kidneys.

The nature of the dysfunction of the tubules varies greatly depending on the location of the lesion.

The pathogenesis of chronic interstitial nephritis, associated with bacterial or viral infections or the use of the above-mentioned drugs, has an immunocellular mechanism of development. The role of Tamm-Horsfall protein, a surface membrane glycoprotein in the ascending limb of the nephron loop and distal tubules, is debated. Less commonly, the genesis of interstitial nephritis is associated with antibodies to the tubular basement membrane (in Goodpasture syndrome, transplant rejection crisis, methicillin therapy). When antitubular-basal membrane antibody deposits are deposited, chemotactic factors of macrophages are released. These cells and T lymphocytes disrupt the structure of the tubules, cause proteolysis of their basement membrane and the formation of free radicals. Lymphocytes stimulate fibroblast proliferation and collagen synthesis. Even less commonly, the genesis of interstitial nephritis is immunocomplex (with lupus nephritis, Sjögren's syndrome). Most often this happens with secondary interstitial nephritis caused by primary damage to the glomeruli. There are many hypotheses regarding how glomerular lesions may affect the interstitium.

Mechanism I - the formation of cross-reacting antibodies to their glomeruli and interstitium.
II mechanism - circulating immune complexes contain exogenous antigen (for example, with streptococcal GN).
III mechanism - under the condition of primary damage to the glomeruli, autoantigens can be produced that stimulate cross-reactive humoral immunity aimed at normal determinants of the interstitium.

Heredity plays a major role in the development of the disease, causing an autosomal recessive transmission route. The inheritance defect concerns abnormal contrasuppression and is associated with chromosome X.

The morphology of acute interstitial nephritis consists of initial swelling of the interstitium followed by its infiltration with plasma cells and eosinophils. Occasionally, infiltrates of large mononuclear cells form around the tubules; the epithelium of the tubules is vacuolated.

On the 10th day, the morphological picture becomes bright. Multiple diffuse infiltrates are dominated by mononuclear cells, small lymphocytes and plasma cells. The older the infiltrates, the more lymphocytes they contain. The degree of cellular infiltration of the interstitium correlates with a decrease in the rate of CF and an increase in azotemia. In the epithelium of the tubules there is vacuolar degeneration, protein inclusions are found, the tubular basement membrane is torn in places. In 20% of patients, electron microscopy reveals destruction of small podocyte sprouts, and swelling of mitochondria and fragmentation of cristae are observed in the tubular epithelium. Changes in the glomeruli are irregular and secondary.

V.V. Serov (1983) understands the tubulointerstitial component of GN as widespread atrophy of the epithelium of the distal tubules in combination with severe stromal sclerosis. The tubulointerstitial component is natural during the fibroplastic transformation of GN, but it also occurs in other morphological forms of the disease - membranous, mesangiocapillary, proliferative GN. In the first case, the occurrence of changes in the tubules and interstitium is associated with the desolation of nephrons, which is caused by glomerular sclerosis. In other types of GN, changes in the tubules and stroma have a different genesis. They are determined by hypoxia of the tubular epithelium and an increased intake of excess filtered protein reabsorbed by the tubules into the stroma. The importance of these factors is supported by the frequency of the tubulointerstitial component in chronic GN with HC in the hypertensive stage. Similar changes in the renal interstitium occur in chronic renal failure, renal nephrocalcinosis, and primary nephrosclerosis.

Morphological signs of chronic interstitial nephritis are infiltration of the interstitium of the kidneys by lymphocytes and plasmacytes, tubular atrophy, fibrosis, areas of tubular atrophy and dilatation, the presence of colloidal masses in the lumen of the tubules with the formation of a picture of a thyroid-like kidney. The main cells of the infiltrate are T lymphocytes, some of them are activated, up to 20% of the cells are plasmacytes. Scarring occurs diffusely or in patches; vessels in areas of active inflammation are affected, while those outside them remain unchanged.

In lupus nephritis, DNA deposits can be observed along the tubular basement membrane, in the peritubular spaces, and interstitium. Tamm-Horsfall protein deposits are present in the interstitium of the ascending limb of the nephron loop and distal tubules; they are associated with mononuclear infiltrates, plasma cells, and occasionally with multinucleated giant cells. In the case of chronic interstitial nephritis, the rate of decline in CP levels correlates with the severity of interstitial fibrosis. The expansion of the interstitium and its cellular infiltration have virtually no effect on the rate of CF and are not dependent on it. A well-known condition, which, however, is assessed differently, is infectious-toxic kidney (for example, with influenza). In the epithelium of the tubules, granular degeneration is found, sometimes moderate edema of the stroma, vessels and glomeruli - without pathology.

During the course of the disease, changes develop in the area of the renal papillae, which then spread to the entire parenchyma.

The development of papillary sclerosis is typical. Papillary lesions can cause the development of capal atrophy and chronic inflammation of the interstitium. Heredity plays a major role in the development of the disease.

Classification of acute interstitial nephritis

1. Clinical

1) primary acute interstitial nephritis (occurs in the intact kidney)

2) secondary acute interstitial nephritis (occurs against the background of any renal disease).

2. Pathogenetic:

1) mainly from the humoral - immune mechanism of kidney damage

2) with cellular immune reactions caused by autologous and exogenous antibodies.

There is no generally accepted classification of chronic interstitial nephritis, but primary and secondary chronic interstitial nephritis are distinguished. Primary interstitial nephritis occurs in an intact kidney, secondary is associated with the formation of interstitial changes against the background of any pre-existing kidney disease.

Clinical symptoms of interstitial nephritis

The first signs of acute interstitial nephritis appear on the 2-3rd day after the prescription of the above-mentioned groups of medications or the action of the above-mentioned factors: lower back pain, adynamia, loss of appetite, headache, nausea. There may be fever (70% of cases), itchy skin (50%), rash - macules or papules (25%), arthralgia (15 - 20%). Edema is usually not observed.

Clinical variants of the course:

1) expanded form (the most common and typical)

2) “banal” form of acute interstitial nephritis (long-term anuria with increased creatininemia)

3) nephritis due to another renal disease

4) “abortive” form (polyuria appears early, azotemia is low, short-term, renal concentration function is restored after 1.5-2 months)

5) “focal” form with erased symptoms (hypercreatininemia is absent, polyuria quickly appears, a decrease in urine GV is the only manifestations of the disease).

In some cases, from the very beginning, the disease can progress with the development of massive necrosis of kidney tissue, especially the renal cortex - necronephrosis. Clinically, this is manifested by acute uremia and death of the patient in the next 2-3 weeks.

Some authors identify idiopathic interstitial nephritis, which accounts for 10-20% of reversible AKI with biopsy-proven interstitial edema and infiltration of mononuclear cells. There are no generalized manifestations, uveitis is occasionally observed, and sometimes bone marrow symptoms are observed.

Acute interstitial nephritis may end with recovery or transition to chronic interstitial nephritis.

Clinical manifestations of chronic interstitial nephritis are sometimes very subtle or absent altogether. The course of the disease can sometimes be asymptomatic or accompanied by arterial hypertension, anemia and (or) minor changes in urine; As a rule, there is no swelling. Sometimes patients complain of weakness, fatigue, dull pain in the lower back; arterial hypertension is usually benign.

Polyuria with low urine VG, renal tubular acidosis, and “kidney that loses salt” syndrome (the kidney is not able to concentrate urine normally) are also characteristic. This condition is called nephrogenic diabetes. The development of renal tubular acidosis and loss of calcium in the urine lead to muscle weakness, stone formation, and osteodystrophy. Some patients exhibit glucosuria and aminoaciduria. Hypotension may occur due to loss of salt in the urine.

Primary chronic interstitial nephritis has a long-term course with slow progression, gradual development of arterial hypertension, slow formation of chronic renal failure, secondary - proceeds depending on the severity and speed of development of the underlying disease.

Completion is the development of nephrosclerosis, the clinical equivalent of which is renal failure.

Diagnosis

Erythrocyturia is observed in almost 100% of cases; in most patients, slight proteinuria is observed - no more than 1.5-3.0 g per day, which is due to insufficient protein reabsorption in the tubules. In 1/3 of cases there is no oliguria phase. Changes in urinary sediment are variable. There is a slight leukocyturia, cylindruria, oxalate or calcium crystals are found. A decrease in urinary GV usually leads to the development of azotemia and lasts several months. Preserved kidney function is impaired early - the concentration of urea and creatinine increases, and the levels of these substances are very variable. All of the above phenomena are reversible; in case of adequate treatment, acute renal failure disappears after 2 - 3 weeks. There remains a slight leukocytosis with a moderate shift to the left, eosinophilia, an increase in ESR, an increase in the level of aglobulins, immunoglobulin E, and occasionally a decrease in complement levels. Acidosis and hypokalemia are also characteristic.

The effectiveness of X-ray and radionuclide research methods is very low due to a decrease in the concentrating ability of the kidneys, but sometimes radionuclide renography in people with acute interstitial nephritis reveals a predominant decrease in the evacuation rate and, less often, a decrease in the ratio of the height of the secretory segment to the height of the vascular segment.

In the initial stage of the disease, the diagnosis is based on changes in partial kidney function in persons who have been in contact with pesticides or the already mentioned medications. A definitive diagnosis can only be made with a needle biopsy of the kidney. Most often it is necessary to distinguish acute interstitial nephritis from acute diffuse GN and acute renal failure. Anamnesis is of great importance.

In the case of chronic interstitial nephritis, minor changes in the urine are observed. Low urine VH, polyuria, leukocytes and erythrocyturia in the sediment are also characteristic. Proteinuria rarely exceeds 3 g per day. Hyponatremia and hypokalemia are common. X-ray examination often does not reveal any abnormalities unless there is papillary necrosis. Papillary necrosis most often develops with the abuse of analgesics, clinically manifested by periodic lower back pain (often colic-type), fever, hematuria and leukocyturia, recurrent severe urinary tract infection, often with stones.

Necrotic masses are found in the urine of papillary necrosis. On a survey image, it is sometimes possible to find in the projection of the kidney the shadow of calcifications of the necrotic masses of the renal papilla and the shadow of a triangular-shaped calculus with areas of rarefaction in the center. An excretory urogram and a retrograde pyelogram reveal ulcers of the papillae in the area of their apexes, fistulas with contrast leakage into the renal tissue, rejection of the papilla or its calcification, ring-shaped shadows, and cavities.

When differential diagnosis, one should take into account anamnesis, chronic undulating course, detection of high concentrations of uric acid, and benign hypertension.

The differential diagnosis of chronic interstitial nephritis and PN is very difficult - immunofluorescence studies and counting the number of neutrophils in biopsy specimens are necessary. In the case of culture of a biopsy sample in the presence of a clinical and morphological picture of PN, there will be no microbial growth, despite bacteriuria.

We also need differential diagnosis with alcoholic “necronephrosis” and kidney damage in infectious mononucleosis. The final question of diagnosis is determined by the results of intravital morphological examination of renal tissue.

Treatment of interstitial nephritis

Treatment of acute interstitial nephritis consists of withdrawal and removal from the body of the drug that caused the disease, desensitization for a disease of immune origin, and symptomatic treatment.

Treatment can only be carried out in a specialized hospital with bed rest. An important factor is maintaining electrolyte and acid-base balance.

The medications that caused the disease should be stopped immediately. In the case of abortive and focal forms, you can limit yourself to prescribing calcium gluconate (up to 3 g per day), ascorbic acid (0.2 g 3 times a day), rutin (0.02-0.05 g 2-3 times a day).

In severe cases of the disease, it is necessary to quickly reduce the swelling of the interstitium. For this purpose, glucocorticoids are prescribed (prednisolone 40 - 60 mg per day for 1-2 weeks), antihistamines (tavegil 0.001 3 times a day, diphenhydramine 0.05 g 3 times a day). In cases of drug overdose, in cases of obvious poisoning or accumulation, hemosorption, hemodialysis, and antidotes are used to quickly eliminate the drug and its metabolites.

Experiments have already proven the possibility of preventing or reducing the nephrotoxic effect of certain drugs that inhibit microsomal enzymes that metabolize these substances.

For nephrotic and lupus syndromes, prednisolone is usually used, often together with anticoagulants and antiplatelet agents.

For timely diagnosis of renal failure in the case of lesions of an allergic nature or the use of nephrotoxic drugs, it is necessary to monitor daily diuresis in the first days of the disease and monitor renal function in case of prolonged acute interstitial nephritis. The occurrence of oliguria should be regarded as the beginning of acute renal failure, which requires monitoring of water balance and the level of kalemia. Vasodilators, anticoagulants, and antiplatelet agents are also prescribed. The duration of active therapy depends on the severity of the disease and the effect of the treatment.

Premature return to work and active work can lead to chronicity of the inflammatory process in the kidneys. It is necessary to monitor patients in a specialized hospital (nephrologist’s office) with release from work for at least 3-4 months. The performance of patients who have fully recovered is completely restored.

Treatment of chronic interstitial nephritis consists primarily of eliminating the causes that led to the disease. General strengthening measures, the use of drugs that support renal plasma flow, and vitamin preparations are important. In the case of papillary necrosis, trental, heparin, saluretics, leukocyturia - antibiotics are used (depending on the results of bacteriological analysis of urine).

Prevention of interstitial nephritis consists of excluding and early identifying the causes of acute interstitial nephritis, its careful treatment, and health education among the population to prevent overdose of analthetics, especially phenacetin.

Labor expertise

The patient’s performance is determined by the functional state of the kidneys, as well as in the presence of a primary disease. If the course of the disease is benign, the patients’ ability to work remains for a long time.

Dispensary observation is carried out to establish the nature of the course of the disease (stable, progressive) on the basis of periodic (twice a year) examinations of the patient, urine and blood tests, and determination of the functional state of the kidneys. It is imperative to examine and examine the patient after respiratory infections, injuries, hypothermia, etc. Patients are contraindicated from working in harmful conditions. In the case of chronic renal failure, the frequency of examinations of the patient increases to 4 - 6 times a year.

Chronic interstitial nephritis is an analgesic-induced kidney disease. Other names for this disease are analgesic nephropathy and phenacetin kidney.

Interstitial nephritis is a non-bacterial inflammation of the interstitial tissue of the kidneys. Unlike pyelonephritis, with this disease there is no destruction (destruction) of connective tissue caused by the local action of microbes. Interstitial nephritis occurs most often after taking various medications (antibiotics, sulfonamides), after vaccination, infection and some other conditions.

Symptoms

Headache.
Depression.
Decreased performance.
Bluish-grayish complexion.

The first symptoms seem harmless: a headache begins, mental disorders appear, performance decreases, and depression sets in. Anemia is often detected, the face acquires a bluish-grayish color. The duration of the disease is up to 20 years. Symptoms of kidney degeneration appear, the papillae of the medulla of the kidneys are destroyed. In the final stage of the disease, kidney function is impaired, or they do not function at all.

Causes

The kidneys, like the liver, play a major role in the metabolism and elimination of various toxic and medicinal substances from the body, therefore the concentration of these substances in the kidney tissue is much higher than in the blood. The cause of the development of interstitial nephritis is immune-allergic processes. Most drugs are relatively simple chemical compounds compared to proteins. In immunological terms, they are inferior antigens - haptens. A strong bond with protein makes drugs full-fledged antigens, and they begin to have sensitizing ability. The body's immune response is directed against the protein part of such a compound. Allergic reactions to penicillin are observed in 1-3% of patients, to sulfonamides - in 5%, to streptomycin - in 9%, to insulin - in 14%, etc.

Responses can occur acutely, within 30-60 minutes after administration of the drug, or subacutely - after 1-24 hours, or delayed - after 1 day and even after several weeks. The shorter the latent period, the greater the threat the response poses to the body.

In the mid-20th century, doctors noticed that there was a connection between interstitial nephritis and painkillers that included phenacetin. Phenacetin is an antipyretic, analgesic, mildly euphoric active substance found in many medications (for example, citramone). Currently, the composition of citramon has been changed and is suitable for use. Later it turned out that with long-term use, aspirin has a similar effect, although weaker. Sometimes paracetamol can also cause this disease.

Acute interstitial nephritis can develop at any age. It often occurs with symptoms of acute renal failure 2-3 days after starting medication. The patient exhibits oligoanuria, sometimes, on the contrary, polyuria with low urine density and hyposthenuria. Symptoms of adynamia, drowsiness develop, headaches, nausea, and vomiting appear. Kidney function declines rapidly and azotemia increases. These phenomena usually last 2-3 weeks. Complete restoration of kidney function occurs only after 3-4 months.

Long-term use of analgesics, in particular those containing phenacetin, can lead to the development of chronic interstitial nephritis. Kidney damage can occur in approximately 50% of people using analgesics for 1-3 years, 1 g per day.

The complaints of patients in the initial period of the disease are not very characteristic and correspond to the process for which painkillers are taken. When the kidneys are damaged, polyuria occurs, which may be accompanied by thirst, weakness, and fatigue. The skin becomes grayish-brown in color, bleeding from the gastrointestinal tract may occur, anemia appears early, the liver and spleen become enlarged, and blood pressure rises.

Low density, slight proteinuria (up to 1-3 g/day), moderate erythrocyturia and leukocyturia are detected in the urine. Glomerular filtration gradually decreases, azotemia increases, and after 3-4 years chronic renal failure develops.

Treatment

When analgesic nephropathy occurs, you must first stop taking the painkillers that caused it. Unfortunately, sometimes this is not easy, the fact is that some patients feel a morbid attraction to such drugs and think that they cannot live without them. The use of other medications depends on the degree and stage of kidney damage. If renal failure occurs (the functionality of the kidneys is impaired or they are completely unable to produce urine), the patient is prescribed hemodialysis (blood purification using a special device) and (or) prepared for a kidney transplant operation.

The only effective remedy is to stop taking the medications. In general, painkillers should be taken with particular caution and only as prescribed by a doctor.

If drug dependence occurs, the patient should consult a doctor. Being at this stage of the disease, it is relatively easy to refuse analgesics; kidney damage can also still be treated. However, if the patient notices (with long-term use of any medication) that he has developed nervous disorders, decreased performance, often has a headache, or is tormented by depression, then contacting a doctor is mandatory. A symptom of analgesic nephropathy is increasingly progressive cyanosis. In case of cyanosis, you should immediately consult a doctor.

First of all, the doctor will try to convince the patient to stop abusing medications. In severe cases, he may invite a psychiatrist or psychotherapist. If a patient cannot live without painkillers due to constant chronic pain, the doctor will try to see if the patient can do without medications that include phenacetin or acetylsalicylic acid (aspirin). Treatment depends on the severity of the kidney damage. When the disease is advanced, the patient requires hemodialysis or is being prepared for a kidney transplant.

In the final stage of the disease, renal failure occurs. If left untreated, interstitial nephritis is life-threatening.

Prevention

Prevention of interstitial nephritis consists of reasonable prescription of various medications and testing of the patient's sensitivity to antibiotics. If there is a tendency to allergic reactions, simultaneous administration of desensitizing agents (diphenhydramine, calcium gluconate, etc.) with antibiotics is indicated. The medicine must be discontinued if its nephrotoxic effect appears. To prevent the chronic form of the disease, it is necessary to avoid long-term use of analgesics.

Acute interstitial nephritis is treated with corticosteroids (40-80 mg/day); in the oligoanuria phase, large doses of furosemide are prescribed, electrolyte disturbances and acid-base status are corrected. In severe cases, hemodialysis is indicated.

For chronic interstitial nephritis, sufficient fluid and salt intake is recommended, the diet includes the physiological norm of protein (1 g/kg body weight), vitamins B and C, anabolic drugs, and, if necessary, corticosteroids.

Medicines that contain phenacetin are harmless when used for short periods of time. Long-term use may damage the kidneys, hematopoietic system, and central nervous system. When taking 1 g of phenacetin daily for a year, analgesic nephropathy appears.

Inflammatory diseases of the urinary system affect all structures of the kidneys and lead to loss of their functionality. Interstitial nephritis involves the connective tissue and tubules of organs. The disease has no characteristic symptoms, so it is often diagnosed in a chronic form. With timely treatment, it is possible to restore the normal state of the kidneys.

Interstitial nephritis is an inflammatory process in the kidney tissues that develops asymptomatically.

Definition and forms of the disease

An inflammatory focus of non-infectious origin, covering the renal connective tissue, blood-carrying vessels and nephron tubules is called interstitial nephritis. The disease resembles pyelonephritis in its symptoms, but it does not destroy kidney tissue and does not spread to the pelvis and calyces. The pathology is often diagnosed in young children, and among adults it affects people from 20 to 50 years old. The table shows the forms of the disease depending on the severity and manifestations in the clinical picture.

Classification	Form	Peculiarities
With the flow	Acute	Abrupt onset and vivid symptoms
With the flow	Chronic	Consequences of untimely acute treatment
According to the development mechanism	Primary	Independent pathology
According to the development mechanism	Secondary	Manifests against the background of other diseases and pathologies of the urinary system
By origin	Autoimmune	Failure of immune defense
	Toxic-allergic	Long-term exposure to toxins, allergens
	Post-infectious	Appears after an infection
	Idiopathic	Etiology unknown
According to clinical manifestations	Expanded	All symptoms are clearly presented
	Heavy	Dangerous to the patient's life and requires
	Abortive	Favorable course and quick recovery
	Focal	Mild symptoms, the patient recovers in a short time

The modern definition of the disease is tubulointerstitial nephropathy, since the inflammation originates in the interstitial tissue, and the main impact falls on the renal tubules.

Causes of inflammation

Interstitial nephritis can occur due to unfavorable ecology, long-term use of medications, or poisoning.

Interstitial nephritis is provoked by many factors that cause swelling of the connective tissue of the kidneys. Spasmed or compressed vessels do not allow adequate blood flow to the affected organs and their ischemia develops. The functioning of the tubules deteriorates, which leads to an increase in the volume of urine and the appearance of blood and creatinine in it. Causes of the disease:

congenital kidney anomalies;
long-term use of nephrotoxic medications - analgesics, antibiotics, non-steroidal anti-inflammatory drugs;
infectious agents - streptococcus, candida;
autoimmune diseases;
disorders of mineral metabolism;
toxic poisoning;
urinary tract obstruction;
effect of radiation.

Symptoms that should alert you

The disease does not have specific symptoms, which requires a competent differential diagnosis from the doctor. The pathological process can be hidden for a long time and become apparent after it has become chronic. Thus, the interstitial type of nephritis often manifests itself in children, since the first weak signals of the disease are rarely associated with renal dysfunction. The intensity of manifestations depends on the activity of inflammation and the level of intoxication of the body. Acute interstitial nephritis has the following symptoms:

Interstitial nephritis is a source of headaches, exhaustion, and anuria.

increased body temperature;
headache;
weakness and drowsiness;
lack of appetite;
nausea and vomiting;
pale skin with itchy rashes;
pain in the joints and lumbar area;
sometimes - an increase in the volume of urination (polyuria), in severe cases - a decrease to complete absence (anuria).

If inflammation of the kidney tissue is provoked by taking nephrotoxic medications, then the first signs of the disease appear after 2-3 days of use. Symptoms of the disease in chronic form are erased or absent. The pathology may be accompanied by slight arterial hypertension, anemia, and changes in the composition of urine. Swelling is not typical. There are minor signs of intoxication.

List of diagnostic measures

It is not easy to notice the development of the inflammatory process due to the lack of distinctive symptoms and similarity with other renal pathologies. A detailed survey will allow the doctor to find out when the first manifestations appeared, their strength and duration. Then he will refer the patient for diagnostic tests:

general blood analysis;
biochemistry of blood and urine;
assesses the excretory capacity of the kidneys and the degree of tubular damage;
Zimnitsky's test will show the ability of the kidneys to concentrate urine;
bacteriological urine culture;
kidney tissue biopsy;
An ultrasound will show changes in the structure of the kidneys.

Treatment: features of treatment of acute and chronic forms

Treatment of interstitial nephritis is carried out comprehensively: pills, diet, folk therapy.

Acute and chronic interstitial nephritis requires an integrated approach to therapy. First of all, it is necessary to eliminate the influence of the factor that provoked the disease, and then resume normal kidney function. Treatment must be carried out in a hospital. Drug therapy is combined with folk remedies and diet. If the patient is in serious condition, hemosorption and hemodialysis are indicated.

Drug assistance for interstitial nephritis

To treat the disease in acute form, you first need to stop taking nephrotoxic drugs. For mild cases of the disease, calcium gluconate, vitamin C and rutin are prescribed. To eliminate severe swelling of interstitial tissue within 1-2 weeks, use:

Glucocorticoids:
- "Prednisolone."
Antihistamines:
- "Tavegil";
- "Diphenhydramine."

To restore blood flow to the kidneys, medications to dilate blood vessels, anticoagulants, and antiplatelet agents (Heparin) are needed. If bacteria are found in the urine, antibiotics are used. When manifestations occur, diuretics are used: “Hypothiazide”, “Uregit”. Excretion of large volumes of urine and severe intoxication dehydrate the body. To replenish fluid reserves, injection of a glucose solution, “Reopoliglucin”, into a vein is indicated. To restore the disturbed balance of sodium and potassium, the medicinal complex “Asparkam” is used.