Symptoms of 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If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The clinic of tubulointerstitial nephritis is non-specific and is often less than symptomatic, which determines the difficulties of its diagnosis. In acute tubulointerstitial nephritis, the clinic of the main disease predominates (acute respiratory viral infection, sepsis, shock, hemolysis, etc.), against which oliguria, hypostenuria, moderate tubular proteinuria (up to 1 g / l), hematuria, which is often treated as acute renal failure.
Symptoms of acute tubulointerstitial nephritis appear on day 2-3 of the effect of etiological factors. The first signs are a short-term rise in temperature, symptoms of intoxication, the appearance of relapsing pain in the lumbar region, in the abdomen, headache, lethargy, drowsiness, nausea, decreased appetite, sometimes - eyelid pastness, facial, moderate thirst, a tendency to polyuria and quite often - color of urine (from pink to dark). In addition, allergy symptoms (skin rashes, arthralgia) and lymphadenopathy from cervical, tonsillar lymph nodes, a tendency to decrease blood pressure are revealed in patients. It is possible to develop renal failure in an acute period.
Chronic tubulointerstitial nephritis is characterized, as a rule, by a low-symptom course, although signs of intoxication, abdominal pain and lumbar region are observed in the active stage. The disease progresses slowly with the development of anemia and mild labile hypertension.
Urinary syndrome is characterized by moderate proteinuria, hematuria of varying severity, abacterial mononuclear (less often eosinophilic) leukocyturia.
Tubulointerstitial nephritis-uveitis syndrome
It was first described by R. Dobrin in 1975. It is a combination of acute tubulointerstitial nephritis with uveitis or with no other signs of systemic pathology. The pathogenesis of the disease is not clear, it is assumed that the disease is based on a violation of immunological regulation with a decrease in the ratio of CD4 / CD8 lymphocytes. Girls of teenage age are ill, less often - adult women.
Among full health nonspecific symptoms appear: fatigue, weakness, weight loss, may be myalgia, abdominal pain, lower back, joints, skin rashes, fever. Many patients have allergic diseases in the anamnesis. A few weeks later, a clinic of acute tubulointerstitial nephritis develops with a disruption of the function of the proximal and / or distal tubules. Uveitis (often anterior, less often - posterior) is detected simultaneously with the onset of tubulointerstitial nephritis or soon after it and has a recurrent character. Hypergammaglobulinemia is characteristic. Tubulointerstitial nephritis-uveitis syndrome is well treatable with corticosteroids.
Endemic Balkan Nephropathy
Chronic nephropathy with histological signs of tubulointerstitial nephritis is characteristic for some areas of the Balkan Peninsula (Romania, Serbia, Bulgaria, Croatia, Bosnia). The cause of the disease is unknown. The disease is not of a family nature, is not accompanied by hearing and visual impairment. The role of heavy metals, the impact of viruses, bacteria, fungal and plant toxins is assumed, genetic factors are studied.
The disease begins in the age range from 30 to 60 years, is rarely detected in adolescents and young people, and those who leave endemic areas in their youth do not fall ill.
The onset of the disease is never acute and the disease is detected by routine examination due to the presence of small proteinuria or symptoms of chronic kidney failure. A characteristic feature is persistent severe anemia. Edema is absent, hypertension develops rarely. The disease progresses slowly, reaching the terminal stage 15-20 years after the appearance of the first signs. In one third of patients, malignant tumors of the urinary tract are detected.
Nonspecific, low severity of clinical manifestations, often the latent course of tubulointerstitial nephritis, makes it difficult to diagnose it. More than half of patients with tubulointerstitial nephritis are on examination and treatment with an incorrect diagnosis. Thus, 32% have glomerulonephritis, 19% have pyelonephritis, 8% have metabolic nephropathies, 4% have hematuria of unknown origin, and 2% have nephroptosis. Only one third of patients are diagnosed with chronic tubulointerstitial nephritis.
The problem of early and differential diagnosis of chronic tubulointerstitial nephritis in children is extremely complicated. For these purposes, clinical and laboratory signs, most common in children with chronic tubulointerstitial nephritis, have been identified.
Characteristic symptoms: age over 7 years, small developmental anomalies, symptoms of endogenous intoxication, arterial hypotension, proteinuria, erythrocyturia, decreased excretion of titrated acids.
Confirming symptoms: manifestation over the age of 7 years, accidental detection, frequent acute respiratory viral infection, acute respiratory disease, chronic pathology of ENT organs, hyperoxaluria, nocturia, decreased ammonia excretion, aminoaciduria, lipiduria.
Additional symptoms: gestosis 1 and 2 half of pregnancy, metabolic pathology in the pedigree, pathology of the gastrointestinal tract in the pedigree, pain in the lumbar region, recurrent abdominal pain, autonomic dystonia, gastrointestinal pathology, food and drug allergies, retinal angiopathy, bone anomalies, deformity and increased the mobility of the kidneys, a decrease in the concentration function of the kidneys, an increase in the optical density of urine, abacterial leukocyturia, an increase in the excretion of urates and lipo peroxides in the urine.
Concomitant symptoms: the connection of the debut of the disease with ARVI, the taking of medications, the pathology of the kidneys in the pedigree, the pathology of the thyroid gland, the pathology of the cardiovascular system, the pathology of the central nervous system, the subfebrile condition, dysuric phenomena, increased blood pressure, episodes of microhematuria, doubling of the bowel system, in the debut 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.
Classification of tubulointerstitial nephritis in children
Flow pattern
- Acute
- Chronic:
- manifest
- wavelike
- latent
Kidney function
- Saved
- Decrease of tubular functions
- Partial decrease in tubular and glomerular functions
- Chronic renal failure
- Acute kidney failure
Stage of the disease
- Active
- I degree
- II degree
- III degree
- Inactive (clinical and laboratory remission)
Variants of tubulointerstitial nephritis
- toxic-allergic
- metabolic
- post-virus
- with dysembryogenesis of renal tissue
- with microelements
- radiation
- circulatory
- autoimmune
- idiomatic
Toxico-allergic variant of tubulointerstitial nephritis is noted as a result of exposure to bacterial infections, drugs, vaccines and serums, with tuberculosis, acute hemolysis, increased protein breakdown.
Metabolic tubulointerstitial nephritis is revealed in violation of the exchange of urates, oxalates, cystine, potassium, sodium, calcium, etc.
The post-virus 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, abnormalities of the kidney vessels) by hemodynamic disorders.
An idiopathic version of tubulointerstitial nephritis is established when, as a result of a child's examination, it is not possible to identify any cause of the disease.
The degree of activity of tubulointerstitial nephritis is determined by the severity of clinico-laboratory signs of the disease:
- I degree - with isolated urinary syndrome;
- II degree - with urinary syndrome and metabolic disorders, symptoms of intoxication;
- III degree - in the presence of extrarenal changes.
Clinical and laboratory remission should be considered the absence of clinical and laboratory signs of tubulointerstitial nephritis.
Any of the variants of tubulointerstitial nephritis can have acute or chronic course, however, acute course is more often observed in toxic-allergic, post-virus and autoimmune tubulointerstitial nephritis, whereas in dysembryogenesis, metabolic disorders and circulation of tubulointerstitial nephritis, there is a chronic latent flow. The acute course is characterized by a clearly delineated onset of the disease, a vivid clinic and most often by rapid reverse development, restoration of tubular structure and renal functions. In the chronic course of tubulointerstitial nephritis, the processes of sclerosing tubulointerstitia develop with the gradual involvement of the glomerulus. Chronic tubulointerstitial nephritis often has a latent course (accidental urinary syndrome in the absence of a clinical picture) or a wave flow with periods of exacerbation and remissions.