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Diagnosis of interstitial nephritis

 
, medical expert
Last reviewed: 06.07.2025
 
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In patients with acute tubulointerstitial nephritis, the urinary syndrome is characterized by hematuria (macro- and micro-), abacterial leukocyturia, moderate proteinuria (0.03-0.09%) and cylindruria. Lymphocytes and eosinophils are detected in the morphology of the urinary sediment.

Tubular dysfunction syndrome is manifested by decreased titratable acidity, decreased excretion of ammonia and concentration capacity. Possible disruption of reabsorption and transport processes in the tubules (aminoaciduria, glucosuria, acidosis, hyposthenuria, hypokalemia, hyponatremia, hypomagnesemia).

The study of enzymes - markers of mitochondrial activity - reveals mitochondrial dysfunction. The study of urine enzymes in the active phase of acute tubulointerstitial nephritis shows, first of all, an increase in y-glutamyl transferase, alkaline phosphatase, as well as beta-galactosidase, N-acetyl-O-glucosaminidase and cholinesterase, which emphasizes the interest in the pathological process of the glomerular apparatus.

According to ultrasound and DG data, half of the patients with acute tubulointerstitial nephritis show increased echogenicity of the renal parenchyma, and 20% show an increase in their size. In the CDC mode, no signs of intra-arterial blood flow disturbance are detected. Pulse Doppler imaging reveals a decrease in the resistance index at the level of the interlobar and arcuate arteries in 30% of patients.

Functional disorders in chronic tubulointerstitial nephritis are characterized by a fairly rapid decrease in the secretory and excretory capacity of the tubules, manifested by a decrease in the relative density of urine, ammonia levels and titratable acidity, aminoaciduria, increased excretion of sodium and potassium, and other tubular dysfunctions. Glomerular filtration remains intact for a long time.

Ultrasound of the kidneys in patients with chronic tubulointerstitial nephritis in 50% of cases reveals a violation of differentiation of the parenchyma into the cortex and medulla, an increase in the echogenicity of the renal cortex in 38% of children. The results of pulsed Doppler show a significant violation of intrarenal hemodynamics at the level of the arcuate artery in patients with chronic tubulointerstitial nephritis.

Diagnosis of tubulointerstitial nephritis is very complex and requires consideration of all anamnestic, genealogical and clinical laboratory data, however, in most cases only a morphological examination of a renal biopsy allows a final diagnosis to be made.

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