Acute interstitial nephritis

Acute interstitial nephritis is an abacterial nonspecific inflammation in the interstitial tissue of the kidneys with secondary involvement of the tubules, blood and lymph vessels of the renal stroma in the process.

[1], [2], [3], [4], [5], [6]

Epidemiology

Interstitial nephritis can occur in any age, including neonatal.

[7], [8], [9], [10], [11], [12], [13], [14]

Causes of the acute interstitial nephritis

Most specialists consider interstitial nephritis as the most severe renal reaction in the chain of general reactions of the body to the administration of drugs. Among drugs for the development of acute interstitial nephritis are important: antibiotics (penicillin, ampicillin, gentamicin, cephalosporins); sulfanilamide preparations; non-steroidal anti-inflammatory drugs; barbiturates; analgesics (analgin, amidopyrine); preparations containing lithium, gold; cytostatics (azathioprine, cyclosporine); 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.

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

[15], [16],

Pathogenesis

The development of acute interstitial nephritis is associated with the entry into the bloodstream of a toxic product or bacterial toxin, which, reabsorbed by tubules, damages the tubular basal membrane. After reabsorption, antigenic substances cause an immunological reaction with fixation of immune complexes in the interstitial tissue and the tubular wall. Developed immune inflammation, allergic edema in the interstitium. Inflammatory process in the interstitium leads to compression of tubules and vessels. The intrachannel pressure rises and as a result - the effective filtration pressure drops in the glomerulus of the kidneys.

Reflex spasm of the vessels and ischemia of the renal tissue develops, the renal blood flow decreases. The glomerular apparatus is initially relatively in-tact. As a result of a decrease in intra-cerebral blood flow, a drop in glomerular filtration occurs, which causes an increase in the serum creatinine concentration. Edema interstitium and tubular lesions, leading to a decrease in water reabsorption, causes polyuria and hypostenuria, despite the decrease in glomerular filtrate. Violation of the function of the tubules leads to electrolyte shifts, tubular acidosis development, disruption of protein reabsorption, manifested by proteinuria.

Morphology of interstitial nephritis. Light microscopy depends on the severity of the process. There are three stages of development - edematous, cellular infiltration and tubulo-necrotic.

For the edematous stage, edema is interstitial with insignificant cellular infiltration. At a cellular stage - the expressed infiltration of a stroma of kidneys by lymphocytes and macrophages, less often a variant with prevalence of plasma cells and eosinophils. In the third stage, necrotic changes in the epithelium of the tubules are determined.

The distal part of the nephron and the collecting tubes are mostly affected. The features of the morphological picture in children include a significant frequency of signs of immaturity of the glomeruli, their hyalinosis and insufficient differentiation of the tubules.

With electron microscopy, nonspecific changes in the tubular apparatus are revealed. The study using monoclonal sera allows the detection of T-lymphocytes of CD4 and CD8.

In a number of 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, titrated acidity and excretion of ammonia in the urine.

[17], [18], [19], [20], [21],

Symptoms of the acute interstitial nephritis

The cyclicity of the development of the process with acute interstitial nephritis is characteristic:

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

Wavy, progressive course of acute interstitial nephritis is usually observed in cases when the cause of its development is various congenital and hereditary factors (disruption of the stability of cytomebranes, metabolic disorders, hypoimmune condition, renal dysplasia, etc.).

Symptoms of acute interstitial nephritis have a well-defined beginning and, as a rule, a cyclic course. The first non-specific signs of acute interstitial nephritis appear on the 2-3rd day after the injection of an antibiotic or medication prescribed for ARVI, angina or other infectious diseases: pain in the lumbar region, headache, drowsiness, adynamia, nausea, loss of appetite . Then there is a moderate urinary syndrome: proteinuria (not exceeding 1 g / day), hematuria (up to 10-15 erythrocytes in the field of vision, rarely more), leukocyturia (up to 10-15 in the field of vision), cylindruria. Changes in the urine are transient, meager. Edema, as a rule, does not happen. Blood pressure can sometimes be slightly increased. The nitrogen excretory function of the kidneys (an increase in the concentration of creatinine, urea, residual nitrogen in the blood plasma) is disturbed early. Oliguria, as a rule, does not happen, on the contrary, more often from the very beginning of the disease against a background of hyperaemia, a lot of urine is allocated. Polyuria persists for a long time (up to several months) and is combined with hypostenuria. However, in severe cases of acute interstitial nephritis, oliguria can be observed for several days. The severity of uremia can vary widely - from minor 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 concentration function of the kidneys and a violation of reabsorption of beta2-microglobulin, an increase in its level in urine and in blood serum. In the blood there is hypergammaglobulinemia.

[22], [23],

Forms

According to its origin, morphological manifestations and outcomes, interstitial nephritis is divided into acute and chronic.

[24], [25], [26], [27], [28]

Diagnostics of the acute interstitial nephritis

For the diagnosis of acute interstitial nephritis matters:

1. Acute development of renal failure against the background of taking medications and in connection with infection.
2. Early development of hypostenuria, regardless of the magnitude of diuresis.
3. Absence in most cases of the oliguria period.
4. Creatinine in the initial period of the disease (often against the backdrop of polyuria).
5. Azotemia to oliguria (if it is present) or against polyuria.

[29], [30], [31]

Differential diagnosis

Unlike acute glomerulonephritis in acute interstitial nephritis there is no edema, hypertension, severe hematuria; Azotemia with acute interstitial nephritis grows to oliguria, often against polyuria. With glomerulonephritis at the beginning of the disease, the optical density of urine is high, and there is no hypostenuria. For acute interstitial nephritis hypostenuria is characteristic. In acute interstitial nephritis, blood pressure rises in the first 2-3 days of the disease, with acute interstitial nephritis hypertension, if it appears, it does not immediately, and, having appeared, persists for a long time.

Unlike pyelonephritis, there is no bacteriuria in acute interstitial nephritis; the culture of urine is sterile; there are no X-ray data typical for pyelonephritis. Unlike usual acute renal failure in acute interstitial nephritis, there are no usual periods of flow; with the latter azotemia increases after the oliguria, 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 of the acute interstitial nephritis

The regime is bedding. Immediately stop the effect of the alleged etiologic factor. The abolition of the drug quickly leads to the disappearance of all symptoms.

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