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Interstitial nephritis (tubulointerstitial nephritis)
Last reviewed: 23.04.2024
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Interstitial nephritis (tubulointerstitial nephritis) in children - acute or chronic nonspecific, abacterial, nondestructive inflammation of the interstitial tissue of the kidneys, accompanied by involvement of the tubules, blood and lymph vessels of the renal stroma in the pathological process.
The importance of the problem of tubulointerstitial nephritis in children is determined by the fact that the absence of pathognomonic clinical syndromes, the similarity with other nephropathies is the reason for its rare diagnosis, especially acute tubulointerstitial nephritis.
According to ICD-10 (1995), pyelonephritis belongs to the group of tubulointerstitial nephritis, which is considered as a bacterial (infectious) version of tubulointerstitial nephritis. Such a combination of pyelonephritis and tubulointerstitial nephritis is based on the generality of morphological changes with the predominant involvement of tubules and interstitium. However, the etiology of these diseases is different, each of them has its own features of pathogenesis, which determines a fundamentally different approach to therapy. Moreover, with pyelonephritis, in addition to tubulointerstitia, lesions of the pelvis and the fornal apparatus of the kidney are noted. These differences do not allow treating tubulointerstitial nephritis and pyelonephritis as variants of a single disease.
Epidemiology of interstitial nephritis in children
The prevalence of interstitial nephritis has not been accurately determined, which is largely due to the rare carrying out of a kidney biopsy. According to autopsy data, the frequency of tubulointerstitial nephritis ranges from 1.47 to 5%. In kidney biopsy in children with nephropathies tubulointerstitial nephritis is detected in 5-7% of cases, and in children with acute renal failure - in 2%. According to a number of morphologists, tubulo-interstitial diseases are much more common (4.6%) than glomerular diseases (0.46%). There are also indications that tubulointerstitial nephritis is noted in 14% of children with nephropathy on dispensary records.
According to some data, tubulointerstitial nephritis is not clinically diagnosed in more than 30% of cases, but only in the course of a morphological study of kidney biopsy. Thus, there is no doubt that tubulointerstitial nephritis is more common than diagnosed.
Causes of interstitial nephritis in children
The etiology of tubulointerstitial nephritis is diverse. Acute tubulointerstitial nephritis can develop with various infections, as a result of the use of certain drugs, poisoning, burns, trauma, acute hemolysis, acute circulatory disorders (shock, collapse), as a complication of vaccination, etc.
Chronic tubulointerstitial nephritis also represents a heterogeneous polyethological group of diseases in which, in addition to the above factors, hereditary predisposition and renal dysembryogenesis, metabolic disorders, chronic infection and intoxication, immunologic diseases, adverse environmental factors (heavy metal salts, radionuclides ), etc. Chronic tubulointerstitial nephritis can develop as a continuation of acute.
Pathogenesis of interstitial nephritis in children
The diversity of etiological factors makes the pathogenesis of tubulointerstitial nephritis ambiguous
The development of postinfection tubulointerstitial nephritis is associated with the exposure of microorganism toxins and their antigens to the endothelium of the capillary interstitium and the basal membrane of the tubules. This leads to direct damage to cells, excessive penetration of capillaries, the inclusion of nonspecific factors of inflammation. In addition to direct toxic effects, immunologically mediated damage to the endothelium and tubules develops.
Chemicals, heavy metal salts, drugs, kidney-edged can also have a direct damaging effect on the tubular epithelium. However, the main importance for the development and maintenance of inflammation, especially with medicinal tubulointerstitial nephritis, will be the development of immune reactions in which drugs play the role of allergens or haptens.
Symptoms of interstitial nephritis in children
Symptoms of interstitial nephritis are nonspecific and are often less than symptomatic, which determines the difficulties of its diagnosis. In acute tubulointerstitial nephritis, the clinic of the main disease predominates (acute respiratory viral infection, sepsis, shock, hemolysis, etc.), against which oliguria, hypostenuria, moderate tubular proteinuria (up to 1 g / l), hematuria, which is often treated as acute renal failure.
Diagnosis of interstitial nephritis in children
The tubular dysfunction syndrome manifests itself in a decrease in titrated acidity, a decrease in ammonia excretion and a concentration ability. Possible disruption of the processes of reabsorption and transport in tubules (aminoaciduria, glucosuria, acidosis, hyposthenia, hypokalemia, hyponatremia, hypomagnesemia).
The study of enzymes - markers of mitochondrial activity - reveals mitochondrial dysfunction. The study of urine enzymes in the active phase of acute tubulointerstitial nephritis shows, first of all, an increase in γ-glutamyltransferase, alkaline phosphatase, as well as beta-galactosidase, N-acetyl-O-glucosaminidase and cholinesterase, which emphasizes the interest in the pathological process of the glomerular apparatus.
According to ultrasound and DG, half of patients with acute tubulointerstitial nephritis have an increase in echogenicity of the renal parenchyma, and 20% have an increase in their size. In the CDC regime, there are no signs of a violation of the intra-arterial blood flow. Pulse dopplerometry in 30% of patients shows a decrease in indices of resistance at the level of interlobar and arterial arteries.
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Treatment of interstitial nephritis in children
The polyethological nature of tubulointerstitial nephritis suggests a differentiated approach to its therapy in each specific case. Nevertheless, it is possible to single out the general principles of therapy of tubulointerstitial nephritis, which should include:
- termination of the influence of the etiological factor (chemical, physical, infectious, autoimmune, toxic-allergic, etc.) on interstitial renal tissue;
- organization of general and motor regimes aimed at reducing the functional load on the kidney tissue;
- rational, sparing diet therapy, the purpose of which is to reduce the metabolic load on the kidney tissue;
- elimination of abacterial inflammation in the kidney tissue;
- elimination of exchange disturbances;
- prevention of sclerosing interstitium;
- recovery of kidney function.
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