Acute interstitial nephritis

Acute interstitial nephritis is a non-bacterial non-specific inflammation in the interstitial tissue of the kidneys with secondary involvement of the tubules, blood and lymphatic vessels of the renal stroma.

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Epidemiology

Interstitial nephritis can manifest itself at any age, including neonatal age.

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Causes acute interstitial nephritis

Most specialists consider interstitial nephritis to be the most severe renal reaction in the chain of general reactions of the body to the administration of drugs. Among the drugs that are important for the development of acute interstitial nephritis are: antibiotics (penicillin, ampicillin, gentamicin, cephalosporins); sulfonamides; non-steroidal anti-inflammatory drugs; barbiturates; analgesics (analgin, amidopyrine); drugs containing lithium, gold; cytostatics (azathioprine, cyclosporine); salts of heavy metals - lead, cadmium, mercury; radiation intoxication; administration of serums, vaccines.

What matters is not so much the dose of the drug as 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.

Acute interstitial nephritis can also be observed in infections such as hepatitis, leptospirosis, infectious mononucleosis, diphtheria, as well as shock and burns.

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Pathogenesis

The development of acute interstitial nephritis is associated with the entry of a toxic product or bacterial toxin into the blood, which, being reabsorbed by the tubules, damages the tubular basement membrane. After reabsorption, antigenic substances cause an immunological reaction with the fixation of immune complexes in the interstitial tissue and the tubular wall. Immune inflammation and allergic edema in the interstitium develop. The inflammatory process in the interstitium leads to compression of the tubules and vessels. Intratubular pressure increases and, as a consequence, the effective filtration pressure in the glomeruli of the kidneys drops.

Reflex vascular spasm and renal tissue ischemia develop, and renal blood flow decreases. The glomerular apparatus is initially relatively intact. As a result of decreased intraglomerular blood flow, glomerular filtration decreases, which causes an increase in the concentration of creatinine in the blood serum. Interstitial edema and tubular damage, leading to a decrease in water reabsorption, cause polyuria and hyposthenuria, despite a decrease in glomerular filtrate. Impaired tubular function leads to electrolyte shifts, the development of tubular acidosis, and impaired protein reabsorption, manifested by proteinuria.

Morphology of interstitial nephritis. Light microscopy depends on the severity of the process. Three stages of development are distinguished - edematous, cellular infiltration and tubulonecrotic.

The edematous stage is characterized by interstitial edema with minor cellular infiltration. At the cellular stage - pronounced infiltration of the renal stroma by lymphocytes and macrophages, less often a variant with a predominance of plasma cells and eosinophils. In the 3rd stage, necrotic changes in the tubular epithelium are determined.

The distal part of the nephron and collecting ducts are mainly affected. The peculiarities of the morphological picture in children include a significant frequency of signs of glomerular immaturity, their hyalinosis and insufficient differentiation of the tubules.

Electron microscopy reveals non-specific changes in the tubular apparatus. Research using monoclonal serums allows one to identify CD4 and CD8 T-lymphocytes.

In some patients, severe ischemia of the papillary zone can provoke the development of papillary necrosis with massive hematuria.

Electrolyte disturbances in acute interstitial nephritis are reduced to increased excretion of sodium and potassium. Functional disorders of the kidneys are characterized by a decrease in the secretory and excretory function of the tubules, a decrease in the optical density of urine, titratable acidity, and excretion of ammonia with urine.

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Symptoms acute interstitial nephritis

The development of the process in acute interstitial nephritis is characterized by cyclicity:

• oliguria, if it occurs, is expressed for 2-3 days;
• normalization of creatinine occurs on the 5th-10th day;
• urinary syndrome persists for 2-4 weeks, and polyuria up to 2 months;
• The concentration function of the kidneys is restored much later - by 4-6 months.

The wave-like, progressive course of acute interstitial nephritis is usually observed in cases where the cause of its development is various congenital and hereditary factors (impaired stability of cytomembranes, metabolic disorders, hypoimmune state, renal dysplasia, etc.).

Symptoms of acute interstitial nephritis have a clearly defined onset and, as a rule, a cyclic course. On the 2nd-3rd day after an antibiotic injection or taking a drug prescribed for acute respiratory viral infection, tonsillitis or other infectious diseases, the first non-specific signs of acute interstitial nephritis appear: pain in the lumbar region, headache, drowsiness, adynamia, nausea, loss of appetite. Then a moderate urinary syndrome is detected: proteinuria (does not exceed 1 g / day), hematuria (up to 10-15 erythrocytes in the field of vision, less often more), leukocyturia (up to 10-15 in the field of vision), cylindruria. Changes in urine are transient, scanty. Edema, as a rule, does not occur. Blood pressure can sometimes be slightly elevated. The renal nitrogen-excreting function is impaired early (increased concentration of creatinine, urea, residual nitrogen in the blood plasma). Oliguria, as a rule, does not occur; on the contrary, more often from the very onset of the disease, a lot of urine is excreted against the background of hyperazotemia. Polyuria persists for a long time (up to several months) and is combined with hyposthenuria. However, in severe cases of acute interstitial nephritis, oliguria may be observed for several days. The severity of uremia can vary widely - from insignificant to severe, requiring hemodialysis. However, these phenomena are reversible and the symptoms of acute renal failure in most cases disappear after 2-3 weeks. As a rule, renal failure is not accompanied by hyperkalemia. In 100%, there is a violation of the renal concentration function and a violation of the reabsorption of beta2-microglobulin, an increase in its level in the urine and blood serum. In the blood - hypergammaglobulinemia.

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Forms

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

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Diagnostics acute interstitial nephritis

For the diagnosis of acute interstitial nephritis the following is important:

1. Acute development of renal failure against the background of taking medications and in connection with infection.
2. Early development of hyposthenuria regardless of the amount of diuresis.
3. Absence of a period of oliguria in most cases.
4. Creatininemia in the initial period of the disease (often against the background of polyuria).
5. Azotemia to oliguria (if present) or against the background of polyuria.

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Differential diagnosis

Unlike acute glomerulonephritis, acute interstitial nephritis has no edema, hypertension, or pronounced hematuria; azotemia in acute interstitial nephritis increases to oliguria, often against the background of polyuria. In glomerulonephritis, at the onset of the disease, the optical density of urine is high, and there is no hyposthenuria. Acute interstitial nephritis is characterized by hyposthenuria. In acute interstitial nephritis, blood pressure increases in the first 2-3 days of the disease; in acute interstitial nephritis, hypertension, if it appears, does not appear immediately, and, once it appears, it persists for a long time.

Unlike pyelonephritis, acute interstitial nephritis does not have bacteriuria; urine culture is sterile; there are no radiographic findings characteristic of pyelonephritis. Unlike usual acute renal failure, acute interstitial nephritis does not have the usual periods of the course; in the latter, azotemia increases after oliguria has set in, whereas in acute interstitial nephritis, azotemia appears before the development of acute interstitial nephritis or, more often, it is expressed against the background of polyuria.

Treatment acute interstitial nephritis

Bed rest. Immediately stop exposure to the suspected etiologic factor. Withdrawal of the drug quickly leads to the disappearance of all symptoms.

To improve renal hemodynamics - heparin, euphyllin, persantine, trentil, nicotinic acid, rutin. Antioxidant - vitamin E, unitiol, dimephosphone, essentiale. To reduce interstitial edema, large doses of lasix up to 500 mg or more, with the lowest possible filtration - prednisolone. Antihistamines - tavegil, diazolin, diphenhydramine, claritin, etc. To improve metabolic processes - ATP, cocarboxylase. Correction of dyselectrolytemia. In severe cases with high azotemia, oliguria and no effect from the therapy - hemodialysis.