Classification and pathomorphology
The disease is divided into acute (focal inflammation) and chronic (sclerotic changes) courses.
According to pathogenesis, obstructive (against the background of anatomical anomalies disrupting urine flow) and non-obstructive (most commonly associated with vesicoureteral reflux) variants are distinguished.
- Acute phase: characterized by pronounced exudation. Edema and massive neutrophil infiltration occur in the interstitium (especially in the medulla and around blood vessels). Epithelial dystrophy and necrosis are observed in the tubules. The pelvic mucosa is hyperemic. Inflammation starts as serous, but in the presence of urinary outflow obstruction, it rapidly turns into purulent with tissue melting.
- Chronic phase: lymphocytes and histiocytes begin to predominate in the cellular composition. Connective tissue gradually proliferates, forming scars. The lumen of dilated tubules is filled with colloid masses. In the final stage, renal tissue is replaced by fibrous tissue, peritubular sclerosis develops, glomeruli are destroyed, and the kidney shrinks.
Symptoms of acute pyelonephritis
In older children, the classic clinical picture consists of three main syndromes:
- Intoxication syndrome: febrile fever, severe chills followed by a sharp drop in temperature and profuse sweating. The child is lethargic, pale, complains of a headache, and has no appetite (anorexia).
- Pain syndrome: pain is localized in the lower back (worsens with physical exertion) or has a diffuse character throughout the abdomen. Examination reveals abdominal tenderness and a positive costovertebral angle tenderness sign (Pasternatsky's sign).
- Dysuric disorders: depend on the cause. If obstruction is present, urination becomes less frequent, up to acute urinary retention. With combined inflammation of the lower urinary tract, frequent urges (pollakiuria), pain, and incontinence occur.
Features of the course in children under 1 year of age
In infants, inflammation has a high tendency toward generalized infection. Systemic extrarenal manifestations completely overshadow local symptoms:
- Systemic response: onset is acute and turbulent. Initial agitation is quickly replaced by adynamia and lethargy. High risk of developing neurotoxicosis. Meanwhile, in 5–7% of children under two years of age, the infection may be atypical — without fever.
- Dyspepsia: is much more pronounced than difficult-to-assess dysuria. The child suffers from persistent regurgitation, vomiting, and diarrhea.
- Metabolic disorders: toxicosis with exicosis (dehydration) rapidly increases, leading to weight loss. Transient pseudohypoaldosteronism is possible.
Laboratory diagnostics
To confirm the diagnosis, it is necessary to identify markers of inflammation and assess the functional state of the kidneys.
- Urinalysis: urine is visibly turbid. The sediment reveals neutrophilic leukocyturia, bacteriuria, and numerous desquamated epithelial cells. Leukocyte casts, microhematuria, and mild proteinuria may occur. The marker of tubular damage, N-acetyl-β-glucosaminidase, increases.
- Blood test: characterized by neutrophilic leukocytosis with a left shift, accelerated ESR, positive C-reactive protein, and elevated procalcitonin (as a marker of bacterial infection). Moderate anemia may be registered against the background of inflammation.
- Renal function: in an acute process, Zimnitsky test may show transient hyposthenuria (decreased urine specific gravity). In a chronic obstructive course, persistent chronic renal failure (CRF) develops — concentrating function drops, urea and creatinine increase, and electrolyte balance is disturbed.
Principles of initial therapy
Treatment of an acute episode usually takes 10 to 14 days (the course may be prolonged in case of obstruction). Drugs of first choice are two groups of antibiotics active against Enterobacteriaceae:
- Third-generation cephalosporins: resistant to β-lactamases, accumulate in the kidneys. Orally (for children older than 6 months), ceftibuten (9 mg/kg/day) or cefixime (8 mg/kg/day) are prescribed. Parenterally (from any age) — cefotaxime or ceftazidime.
- Inhibitor-protected aminopenicillins: amoxicillin + clavulanic acid (40–60 mg/kg/day). Approved for patients of any age.
Important: Young children with pronounced intoxication, refusal to eat/drink, and vomiting require immediate hospitalization. Due to the inability to take medications orally, therapy begins with parenteral administration of antibiotics in a hospital setting.
In older children, pyelonephritis manifests as the classic UTI triad: Intoxication, Pain, Dysuria. In infants, dysuria is difficult to assess, so the triad transforms into: Intoxication, Restlessness (equivalent to pain), Dyspepsia.
Class and exam questions
What forms can chronic pyelonephritis take?
In two variants: recurrent (alternating remissions and exacerbations, often triggered by acute respiratory infections) and latent (scant clinical presentation with asthenia, diagnosed based on isolated urinary syndrome).
What is the main factor in the transition of acute pyelonephritis to chronic?
The main factor in the chronization of the process is the presence of urodynamic disorders (urine outflow).
What purulent-destructive complications can develop with obstruction?
The rapid transition to the purulent stage threatens urosepsis, apostematous nephritis, abscess, renal carbuncle, or papillary necrosis.
What else to study on this topic
- Mechanisms of vesicoureteral reflux formation
- Differential diagnosis of pyelonephritis and urosepsis in children under 1 year of age
- Features of transient pseudohypoaldosteronism
- Guidelines and interpretation of the Zimnitsky test
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