Medical expert of the article
New publications
Chronic interstitial nephritis
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Chronic interstitial nephritis is a polyethological disease, the main manifestation of which is the abacterial nondestructive inflammation of the interstitial tissue of the medullary layer of the kidneys involving the tubules, blood and lymph vessels of the renal stroma.
Causes of development of chronic interstitial nephritis:
- Metabolic (any metabolic disorder, accompanied by increased excretion of metabolites with urine).
- Infections - tuberculosis, leptospirosis, iersiniosis, chronic active hepatitis.
- Long-term use of drugs such as analgin, acetylsalicylic acid, phenacetin, indomethacin; drugs used for epilepsy, tuberculosis.
Chronic interstitial nephritis in children is more common than acute. Before the detection of changes in the urine often takes a long latent period. In most cases, it is diagnosed accidentally during a urine test as a control after the transferred diseases or when registered in a children's institution. The following predisposing factors contribute to the formation of chronic interstitial nephritis:
- Dysembryogenesis of the renal tissue.
- Anomalies of the urinary system.
- Hypoimmune conditions.
- Violation of the elimination function of the macrophagal-phagocytizing system.
- Violation of renal hemo- and urodynamics (increased mobility of the kidneys, abnormalities of the kidney vessels).
- Salts of heavy metals - lead, cadmium, mercury, radiation intoxication.
- Introduction of serums, vaccines.
It matters not so much the dose of the drug as the duration of its administration and the sensitivity to it. It is established that in the interstitial tissue of the medulla of the kidney develops immune inflammation, allergic edema.
According to its origin, morphological manifestations and outcomes, interstitial nephritis is divided into acute and chronic.
Pathogenesis of chronic interstitial nephritis . At the heart of the pathological process is progressive sclerosis interstitium, compression and atrophy of the tubules, secondary lesion of the glomeruli. More important in pathogenesis are metabolic disorders, toxic effects than immune.
Establish a chronic interstitial nephritis can only morphologically.
Symptoms of chronic interstitial nephritis . In the beginning, the symptoms are meager. As the development of pathological processes in the kidneys appear symptoms of intoxication, pallor, abdominal pain and lumbar region. Complaints of weakness, fatigue. Polyuria is characteristic. In the study of urine - moderate proteinuria, microhematuria, abacterial leukocyturia. With dismetabolic chronic interstitial nephritis - in the urine crystalluria. The disease progresses slowly. There is anemia and mild labile hypertension. There is an aggravation of violations of tubular functions of the kidneys. Reduction of the optical density of urine, a violation of the concentration function of the kidneys, an increase in the level of beta 2- microglobulin; reduction of secretory and excretory functions, reduction of titrated acidity, excretion of ammonia in urine.
There is a violation of osmotic concentration. Dysfunction of tubules can be manifested by a decrease in reabsorption, which causes loss of salt. Glomerular filtration is preserved. The disease has been going on for many years.
Further, the clinic is determined by progressive tubular disorders. Strengthen the inability of the kidney to normally concentrate the urine. This condition is sometimes called nephrogenic diabetes, since increased urination results in polydipsia, kidney tubular acidosis and associated calcium loss increase. Clinically, this leads to the development of muscle weakness, osteodystrophy, growth retardation. A syndrome of "salt-losing kidney" can develop - salt depletion, hypotension and a vascular collapse, reminiscent of the adrenal insufficiency, is possible. Further progression increases the decrease in kidney function and the development of chronic renal failure.
Chronic kidney failure in children appears in tens of years, but with an analgesic kidney may appear earlier, 5-7 years after the first signs of the disease.
Diagnosis of chronic interstitial nephritis . Prolonged latent period before the detection of urinary syndrome, lymphocytic character of leukocyturia, polyuria, hypostenuria, increased excretion of beta 2- microglobulin.
Clinical symptoms are sometimes meager. Minor changes in urine, anemia, mild hypertension, labile. Edema, as a rule, does not happen. Sometimes there may be an increase in the level of urea in the blood serum.
Complaints remain on weakness, fatigue, dull pain in the lumbar region. Characterized by polyuria with a low relative density of urine. The urinary syndrome is moderately pronounced. Protein in urine is no more than 1,0-3,0 g / day, microhematuria and small leukocyturia. Expressed leukocyturia, as a rule, does not happen.
For the diagnosis of chronic interstitial nephritis of metabolic genesis, the presence of allergic diathesis, often excessive body mass, dysuric disorders not accompanied by changes in urinary sediment, high urine optical density, oxalate-calcium crystallium, and enhanced excretion of oxalates or urates is important.
Chronic interstitial nephritis on the background of renal dysplasia is characterized by an earlier development of hypertension and impaired renal function.
Chronic interstitial nephritis due to tuberculosis infection develops against the background of tuberculous intoxication, positive Mantoux reaction is noted, the neutrophil defectiveness index during incubation with tuberculin rises to 0.15; there are no extrarenal manifestations. In the study of urine - the largest proteinuria, microhematuria. In cytomasks from urine, the amount of lymphocytes and monocytes in total is more than 75 %. The absence of mycobacteria in the urine during the study of bacterioscopy and sowing on the Levenshtein-Jensen phase. Children sick and infected with tuberculosis, especially for three or more years, should be screened for possible chronic interstitial nephritis.
Chronic interstitial nephritis in the background of chronic glomerulo- or pyelonephritis is the most difficult for diagnosis, since the emerging changes are considered as an aggravation of the course of the underlying disease. At the same time, timely detection of interstitial nephritis in nephropathies is extremely important; its occurrence indicates iatrogenic kidney damage, which requires cancellation, rather than strengthening therapy. Morphological confirmation is of great importance in diagnosis. In pyelonephritis, tubulo-interstitial nephritis often develops against the background of acute respiratory infection and the administration of antibiotics. The process proceeds as neoliguric renal failure. A special feature is the preservation of interstitial inflammation with a decrease in the degree of creatinemia.
In patients with chronic glomerulonephritis, tubulo-interstitial nephritis often also occurs against the background of acute respiratory viral infection and the administration of antibiotics.
The peculiarity is the reversibility of neoliguric renal failure, but with a certain decrease in the concentration function of the kidneys and after the elimination of the severity of the process; the absence of complete reversibility, a reliable test for detecting the initial manifestations of interstitial nephritis is the determination of beta 2- microglobulin, the excretion of which with urine grows already in the first days of the disease and decreases with the reverse development of the process.
Treatment of chronic interstitial nephritis.
It is important to reduce or completely stop the influence of factors that cause and maintain inflammation in the stroma of the kidneys.
The diet should take into account metabolic disorders. To correct the oxalate-calcium metabolism, a potato-cabbage diet is prescribed. If you have a history of food allergies - hypoallergenic.
With any etiology of chronic interstitial nephritis, foods that irritate the kidney tubular apparatus are excluded from consumption: obligate allergens, spices, marinades, smoked products; herbs that have a sharp taste (garlic, onion, coriander). The liquid is not less than 1 l / m 2 of the body surface. With alkaline urine reaction, dyeing madder (1-2 tablets a day before meals for a month). Improvement of microcirculation - trental, curantil, theonikol.
The prognosis for acute interstitial nephritis is favorable. In chronic interstitial nephritis depends on the cause. Clinical follow-up in acute interstitial nephritis is performed during the year with urinalysis every month, freeing from preventive vaccinations, injections of gamma globulin. Nephrotoxic drugs are excluded. In chronic interstitial nephritis dispensary observation of a pediatrician and a nephrologist up to 18 years with subsequent transfer to an adult network.
Prevention of interstitial nephritis. Analysis of the pedigree when the doctor visits the newborn. With burdened heredity for dysmetabolic nephropathies, the preparation of a plan for preventive measures. Purpose of a rational diet and sufficient drinking regime. Urine examination for each intercurrent disease, before and after preventive vaccinations. Conducting courses of membrane-stabilizing agents and activators of intracellular metabolism, sanation of chronic foci of infection, elimination of hypothermia and excessive physical exertion.
Where does it hurt?
What's bothering you?
What do need to examine?
What tests are needed?
Использованная литература