Symptoms of interstitial nephritis

The clinical picture of tubulointerstitial nephritis is non-specific and often asymptomatic, which determines the difficulties of its diagnosis. In acute tubulointerstitial nephritis, the clinical picture of the underlying disease (ARI, sepsis, shock, hemolysis, etc.) dominates, against the background of which oliguria, hyposthenuria, moderate tubular proteinuria (up to 1 g/l), hematuria are detected, which is often interpreted as acute renal failure.

Symptoms of acute tubulointerstitial nephritis appear on the 2nd-3rd day of exposure to etiologic factors. The first signs are a short-term increase in temperature, symptoms of intoxication, the appearance of recurrent pain in the lumbar region, in the abdomen, headache, lethargy, drowsiness, nausea, loss of appetite, sometimes - puffiness of the eyelids, face, moderate thirst, a tendency to polyuria and quite often - a change in the color of urine (from pink to dark). In addition, patients show signs of allergy (skin rashes, arthralgia) and lymphadenopathy of the cervical, tonsillar lymph nodes, a tendency to a decrease in blood pressure. Development of acute renal failure is possible.

Chronic tubulointerstitial nephritis is usually characterized by a low-symptom course, although in the active stage there are signs of intoxication, pain in the abdomen and lumbar region. The disease progresses slowly with the development of anemia and moderate labile hypertension.

Urinary syndrome is characterized by moderate proteinuria, hematuria of varying severity, and abacterial mononuclear (less often eosinophilic) leukocyturia.

Tubulointerstitial nephritis-uveitis syndrome

First described by R. Dobrin in 1975. It is a combination of acute tubulointerstitial nephritis with uveitis or without any other signs of systemic pathology. The pathogenesis of the disease is unclear, it is assumed that the basis of the disease is a violation of immunological regulation with a decrease in the ratio of CD4 / CD8 lymphocytes. Teenage girls are affected, less often - adult women.

In the midst of complete health, non-specific symptoms appear: fatigue, weakness, weight loss, myalgia, abdominal pain, lower back pain, joint pain, skin rashes, fever. Many patients have a history of allergic diseases. After several weeks, the clinical picture of acute tubulointerstitial nephritis develops with dysfunction of the proximal and/or distal tubules. Uveitis (usually anterior, less often posterior) is detected simultaneously with the onset of tubulointerstitial nephritis or soon after it and is recurrent. Hypergammaglobulinemia is characteristic. tubulointerstitial nephritis-uveitis syndrome responds well to treatment with corticosteroids.

Endemic Balkan nephropathy

Chronic nephropathy with histological signs of tubulointerstitial nephritis, characteristic of some areas of the Balkan Peninsula (Romania, Serbia, Bulgaria, Croatia, Bosnia). The cause of the disease is unknown. The disease is not familial, is not accompanied by hearing and vision impairment. The role of heavy metals, the effects of viruses, bacteria, fungal and plant toxins is assumed, genetic factors are being studied.

The disease begins in the age range of 30 to 60 years, is rarely detected in adolescents and young adults, and those who leave endemic areas in their youth do not develop the disease.

The onset of the disease is never acute and is detected during a routine examination by the presence of slight proteinuria or symptoms of chronic renal failure. A characteristic symptom is persistent severe anemia. There is no edema, hypertension rarely develops. The disease progresses slowly, reaching the terminal stage 15-20 years after the first symptoms appear. Malignant tumors of the urinary tract are detected in 1/3 of patients.

Non-specificity, low clinical manifestations, and often latent course of tubulointerstitial nephritis cause difficulties in its diagnosis. More than half of patients with tubulointerstitial nephritis are examined and treated with an incorrect diagnosis. Thus, 32% are diagnosed with glomerulonephritis, 19% with pyelonephritis, 8% with metabolic nephropathy, 4% with hematuria of unknown genesis, and 2% with nephroptosis. Only 1/3 of patients are diagnosed with chronic tubulointerstitial nephritis.

The problem of early and differential diagnostics of chronic tubulointerstitial nephritis in children is extremely complex. For these purposes, clinical and laboratory signs most frequently encountered in children with chronic tubulointerstitial nephritis are identified.

Characteristic symptoms: age over 7 years, minor developmental anomalies, symptoms of endogenous intoxication, arterial hypotension, proteinuria, erythrocyturia, decreased excretion of titratable acids.

Confirmatory symptoms: manifestation at the age of over 7 years, accidental detection, frequent acute respiratory viral infections, acute respiratory infections, chronic pathology of ENT organs, hyperoxaluria, nocturia, decreased excretion of ammonia, aminoaciduria, lipiduria.

Additional symptoms: gestosis of the 1st and 2nd half of pregnancy, metabolic pathology in the family tree, gastrointestinal pathology in the family tree, pain in the lumbar region, recurrent abdominal pain, vegetative dystonia, gastrointestinal pathology, food and drug allergies, retinal angiopathy, bone anomalies, deformation and increased mobility of the kidneys, decreased concentration function of the kidneys, increased optical density of urine, abacterial leukocyturia, increased excretion of urates and lipid peroxides in the urine.

Associated symptoms: association of the disease onset with acute respiratory viral infection, medication intake, kidney pathology in the family tree, thyroid pathology, cardiovascular pathology, CNS pathology, subfebrile condition, dysuric phenomena, increased blood pressure, episodes of microhematuria, doubling of the renal pelvis, increased creatinine at the onset of the disease, hypercalciuria.

Differential diagnosis of tubulointerstitial nephritis is carried out primarily with the hematuric form of glomerulonephritis, pyelonephritis and hereditary nephritis, other congenital and acquired nephropathies.

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Classification of tubulointerstitial nephritis in children

Nature of the flow

• Spicy
• Chronic:
  • manifest
  • wavy
  • latent

Kidney function

• Saved
• Decreased tubular function
• Partial decrease in tubular and glomerular functions
• Chronic renal failure
• Acute renal failure

Stage of the disease

• Active
  • 1st degree
  • II degree
  • III degree
• Inactive (clinical and laboratory remission)

Variants of tubulointerstitial nephritis

• toxic-allergic
• metabolic
• post-viral
• in renal tissue dysembryogenesis
• for microelement deficiencies
• radiation
• circulatory
• autoimmune
• idiomatic

The toxic-allergic variant of tubulointerstitial nephritis is observed as a result of exposure to bacterial infections, drugs, vaccines and serums, tuberculosis, acute hemolysis, and increased protein breakdown.

Metabolic tubulointerstitial nephritis is detected in cases of metabolic disorders of urates, oxalates, cystine, potassium, sodium, calcium, etc.

The post-viral variant develops as a result of exposure to viruses (enteroviruses, influenza, parainfluenza, adenovirus).

Tubulointerstitial nephritis in microelementoses develops under the influence of metals such as lead, mercury, gold, lithium, cadmium, etc.

Circulatory tubulointerstitial nephritis is associated with acute and chronic (anomalies in the number and position of the kidneys, pathological mobility, anomalies of the renal vessels) hemodynamic disorders.

The idiopathic variant of tubulointerstitial nephritis is established when, as a result of examining the child, it is not possible to identify any cause of the disease.

The degree of activity of tubulointerstitial nephritis is determined by the severity of clinical and laboratory signs of the disease:

• Grade I - with isolated urinary syndrome;
• II degree - with urinary syndrome and metabolic disorders, symptoms of intoxication;
• Grade III - in the presence of extrarenal changes.

Clinical and laboratory remission should be considered the absence of clinical and laboratory signs of tubulointerstitial nephritis.

Any variant of tubulointerstitial nephritis may have an acute or chronic course, but the acute course is more often observed in toxic-allergic, postviral and autoimmune tubulointerstitial nephritis, whereas in dysembryogenesis, metabolic and circulatory disorders of tubulointerstitial nephritis, a chronic latent course occurs. The acute course is characterized by a clearly defined onset of the disease, vivid clinical symptoms and most often rapid reverse development, restoration of the tubular structure and renal functions. In the chronic course of tubulointerstitial nephritis, the processes of tubulointerstitium sclerosis develop with gradual involvement of glomeruli. Chronic tubulointerstitial nephritis often has a latent course (randomly occurring urinary syndrome in the absence of a clinical picture) or a wave-like course with periods of exacerbation and remission.

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