Chronic interstitial nephritis

Chronic interstitial nephritis is a polyetiological disease, the main manifestation of which is abacterial non-destructive inflammation of the interstitial tissue of the renal medulla with involvement of the tubules, blood and lymphatic vessels of the renal stroma in the process.

Causes of development of chronic interstitial nephritis:

1. Metabolic (any metabolic disorder accompanied by increased excretion of metabolites in the urine).
2. Infections - tuberculosis, leptospirosis, yersiniosis, chronic active hepatitis.
3. Long-term use of medications such as analgin, acetylsalicylic acid, phenacetin, indomethacin; medications taken for epilepsy, tuberculosis.

Chronic interstitial nephritis in children is more common than acute nephritis. There is often a long latent period before changes in urine are detected. In most cases, it is diagnosed accidentally during a urine test as a control after illnesses or when enrolling in a children's institution. The following predisposing factors contribute to the development of chronic interstitial nephritis:

1. Dysembryogenesis of renal tissue.
2. Anomalies of the urinary system.
3. Hypoimmune conditions.
4. Violation of the eliminating function of the macrophage-phagocytic system.
5. Impaired renal hemo- and urodynamics (increased mobility of the kidneys, renal vascular anomalies).
6. Heavy metal salts - lead, cadmium, mercury, radiation intoxication.
7. Introduction of serums, vaccines.

It is not so much the dose of the drug that matters, but the duration of its use and increased sensitivity to it. It has been established that immune inflammation and allergic edema develop in the interstitial tissue of the renal medulla.

Based on its origin, morphological manifestations and outcomes, interstitial nephritis is divided into acute and chronic.

Pathogenesis of chronic interstitial nephritis .The pathological process is based on progressive interstitial sclerosis, compression and atrophy of the tubules, and secondary glomerular damage. Metabolic disorders and toxic effects are more important in the pathogenesis than immune ones.

Chronic interstitial nephritis can only be established morphologically.

Symptoms of chronic interstitial nephritis .At first, the symptoms are scanty. As the pathological processes in the kidneys develop, symptoms of intoxication, pallor, pain in the abdomen and lumbar region appear. Complaints of weakness, fatigue. Polyuria is characteristic. Urine examination reveals moderate proteinuria, microhematuria, abacterial leukocyturia. In dysmetabolic chronic interstitial nephritis, there is crystalluria in the urine. The disease progresses slowly. Anemia and moderate labile hypertension appear. There is an aggravation of the renal tubular functions. Decreased optical density of urine, impaired renal concentrating function, increased beta ₂ -microglobulin levels; decreased secretory and excretory functions, decreased titratable acidity, and ammonia excretion with urine.

Osmotic concentration is impaired. Tubular dysfunction may manifest itself as decreased reabsorption, causing salt loss. Glomerular filtration is preserved. The disease lasts for many years.

Further clinical picture is determined by progressive tubular disorders. Increased inability of the kidney to concentrate urine normally. This condition is sometimes called nephrogenic diabetes, as increased urine output leads to polydipsia, renal tubular acidosis and associated calcium loss increase. Clinically, this leads to the development of muscle weakness, osteodystrophy, growth retardation. The syndrome of "salt-losing kidney" may develop - salt depletion, hypotension and possible vascular collapse, resembling the picture of adrenal insufficiency. Further progression intensifies the decline in kidney function and the development of chronic renal failure.

Chronic renal failure in children appears after decades, but with analgesic kidney it can appear earlier, 5-7 years after the first signs of the disease.

Diagnosis of chronic interstitial nephritis .Long latent period before detection of urinary syndrome, lymphocytic nature of leukocyturia, polyuria, hyposthenuria, increased excretion of beta ₂ -microglobulin.

Clinical symptoms are sometimes scanty. Minor changes in urine, anemia, moderate, labile hypertension. Edema is usually absent. Sometimes there may be an increase in the level of urea in the blood serum.

Complaints of weakness, fatigue, and dull pain in the lumbar region persist. Polyuria with low relative density of urine is characteristic. Urinary syndrome is moderately expressed. Protein in urine is no more than 1.0-3.0 g/day, microhematuria and slight leukocyturia. Expressed leukocyturia, as a rule, does not occur.

For the diagnosis of chronic interstitial nephritis of metabolic genesis, the presence of allergic diathesis, often excess body weight, dysuric disorders not initially accompanied by changes in urinary sediment, high optical density of urine, oxalate-calcium crystalluria and increased excretion of oxalates or urates is important.

Chronic interstitial nephritis against the background of renal dysplasia is characterized by earlier development of hypertension and impaired renal function.

Chronic interstitial nephritis caused by tuberculosis infection develops against the background of tuberculosis intoxication, a positive Mantoux reaction is noted, the neutrophil damage index during incubation with tuberculin increases to 0.15; there are no extrarenal manifestations. When examining urine, the greatest proteinuria, microhematuria. In cytosmears from urine, the number of lymphocytes and monocytes in total is more than 75 %. The absence of mycobacteria in urine during bacterioscopy and sowing for the Lowenstein-Jensen phase. Children sick and infected with tuberculosis, especially for three or more years, should be examined to detect possible chronic interstitial nephritis.

Chronic interstitial nephritis against the background of chronic glomerulo- or pyelonephritis is the most difficult to diagnose, since the emerging changes are considered as an aggravation of the underlying disease. At the same time, timely detection of interstitial nephritis in nephropathies is extremely important; its occurrence indicates iatrogenic kidney damage, requiring the cancellation, rather than intensification of therapy. Morphological confirmation is of great importance in diagnostics. In pyelonephritis, tubulointerstitial nephritis most often develops against the background of an acute respiratory infection and antibiotic use. The process occurs as non-oliguric renal failure. A feature is the preservation of interstitial inflammation with a decrease in the degree of creatinemia.

In patients with chronic glomerulonephritis, tubulointerstitial nephritis also often occurs against the background of acute respiratory viral infections and the use of antibiotics.

The peculiarities are the reversibility of non-oliguric renal failure, however, with the preservation of some decrease in the concentration function of the kidneys and after the elimination of the acuteness 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 increases 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 renal stroma.

The diet should take into account metabolic disorders. To correct oxalate-calcium metabolism, a potato-cabbage diet is prescribed. If there is a history of food allergies, a hypoallergenic diet is prescribed.

For any etiology of chronic interstitial nephritis, products that irritate the renal tubular apparatus are excluded from consumption: obligatory allergens, spices, marinades, smoked foods; herbs with a pungent taste (garlic, onion, cilantro). Liquid at least 1 l / m ² of body surface. For alkaline urine, madder (1-2 tablets per day before meals for a month). Improvement of microcirculation - trental, curantil, theonikol.

Forecastin acute interstitial nephritis, favorable. In chronic interstitial nephritis, it depends on the underlying cause. Outpatient observation in acute interstitial nephritis is carried out for a year with monthly urine testing, exemption from preventive vaccinations, gamma globulin injections. Nephrotoxic drugs are excluded. In chronic interstitial nephritis, outpatient observation by a pediatrician and nephrologist until the age of 18, with subsequent transfer to the adult network.

Prevention of interstitial nephritis. Analysis of the pedigree during the first visit to the newborn. In case of a burdened heredity for dysmetabolic nephropathy, drawing up a plan of preventive measures. Prescribing a rational diet and sufficient drinking regime. Urine analysis for each intercurrent disease, before and after preventive vaccinations. Conducting courses of membrane stabilizing agents and activators of intracellular metabolism, sanitation of chronic foci of infection, eliminating hypothermia and excessive physical activity.

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