Nephrology for Family Doctors - O.I. Bakaliuk 2003
Pediatric Nephrology
Pyelonephritis in Children
In children, a clear distinction should be made between the terms "Pyelonephritis" and "Urinary Tract infection".
The term "urinary tract infection" refers to the infection of a child's Urinary System without specifying its exact level. The latter may occur in the presence of gestational pyelonephritis or maternal Kidney disease prior to Pregnancy, manifesting as so-called "asymptomatic" bacteriuria (affecting 1% of full-term, apparently healthy newborns, regardless of gender). As children grow older, this "asymptomatic" bacteriuria begins to prevail in girls (4.5:1). To define microbial-inflammatory lesions of the renal pelvis and interstitium in pediatric practice, the term "bacterial tubulointerstitial nephritis" is more commonly used as a synonym for pyelonephritis.
Thus, the following types of urinary tract infections are identified in children (D. Ivanov, 2001): asymptomatic bacteriuria, lower urinary tract infection (urethral syndrome, cystitis), and upper urinary tract infection (pyelonephritis).
Asymptomatic bacteriuria is diagnosed when there are 10,000 or more microbial bodies per 1 mL of urine. This bacteriuria may progress in the following ways: spontaneous resolution (70–80% of cases), transient manifestation (10–20% of cases), or progression to pyelonephritis (5–10% of cases).
An absolute indication for antibacterial therapy in this condition is The Development of neutrophilic leukocyturia accompanied by signs of dysmetabolic nephropathy (3-, 7-, or 10-day courses of Antibiotics, Ribomunyl, Broncho-Vaxom, autovaccines, etc.).
Urethral syndrome is diagnosed in the presence of dysuria with urinary urgency, febrile Temperature, and neutrophilic leukocyturia (exceeding 50% neutrophils).
Cystitis is characterized by similar dysuric Complaints, pain in the projection area of the Urinary Bladder, and bacteriuria.
The onset of pyelonephritis in children is directly linked to dysmetabolic nephropathies, renal dysplasias, and obstructive uropathies.
The causative agents are most frequently uropathogenic strains of Escherichia coli (O6, O8, O17, O83, O117; V.I. Kirillov et al., 1997), white and golden staphylococci, and Proteus. In newborns, the infection typically spreads via a hematogenous route, whereas later on, it spreads via an ascending urinogenous route.
In children with pyelonephritis, as in adults, METABOLISM/2.html">THE CONCEPT OF L-form microorganisms remains relevant. These L-forms are detected in 17–20% of cases. In addition to these, Mycoplasmas play a significant role in the development of "abacterial" pyelonephritis in children, with infection rates reaching 45–71% (E.S. Maltseva et al., 1996).
A certain role is also attributed to the premorbid Background, immune system dysfunction, and refluxes (Scheme 3).
Class="center">
The Diagnosis of pyelonephritis in children primarily relies on a detailed analysis of clinical symptoms, functional test data, radiocontrast, isotopic, and ultrasound imaging techniques.
Below are the differential diagnostic criteria for urinary tract infection, pyelonephritis, and abacterial (interstitial) pyelonephritis (Tables 9 and 10).
Differential diagnostic table for urinary tract infection, pyelonephritis, and abacterial (interstitial) pyelonephritis in children (M.S. Ignatova et al., 1982)
|
Clinical, laboratory, and instrumental sign |
Urinary tract infection |
Pyelonephritis |
Interstitial nephritis |
|
Leukocyturia |
+ |
+ |
+ |
|
Neutrophilic leukocyturia |
+ |
+ |
- |
|
Lymphocytic leukocyturia |
+ |
+,- |
+ |
|
Proteinuria |
- |
+,- |
+ |
|
+,- |
+,- |
+ |
|
|
Bacteriuria |
+ |
+ |
- |
|
Edema |
- |
- |
+ ,- |
|
Arterial Hypertension |
- |
+,- |
- |
|
Dysuric manifestations |
+ |
+,- |
- |
|
Pain syndrome (abdominal or lumbar pain) |
+ |
+ |
+ ,- |
|
Antibody titer against E. coli |
Low |
High |
Normal |
|
Changes in protein and Lipid Metabolism parameters |
- |
Moderate |
Pronounced |
|
Changes on excretory urography |
- |
Asymmetric |
Symmetric |
|
Changes on isotope renography |
- |
Asymmetric |
Symmetric |
|
Changes in Doppler parameters |
- |
Venous congestion |
Venous congestion |
|
Impaired renal Functions |
- |
Tubular type |
Tubular type |
Let us briefly outline the individual Clinical forms of pyelonephritis in children.
Neonatal pyelonephritis. Its Pathogenesis is primarily associated with umbilical infections and Sepsis. The development of neonatal pyelonephritis is frequently driven by intrauterine infections, birth trauma, asphyxia, and maternal gestational pyelonephritis.
In fact, this is a localized manifestation of acute neonatal sepsis, most commonly of staphylococcal origin. The disease typically manifests with endogenous Intoxication syndrome—fever, anorexia, vomiting, regurgitation, weight loss, dry and pale Skin, and urinary disturbances.
Pyelonephritis in infants rarely has an acute onset (it may possibly originate during the neonatal period) and, due to its latent course, is mainly characterized by extrarenal symptoms, such as poorly localized abdominal pain, decreased skin turgor, dry skin, thirst, tachycardia, and convulsions.
Pyelonephritis in young children most frequently develops against the background of urinary tract obstruction at various levels. At the renal level, these may include congenital stenosis of the pelviureteric junction, Polycystic Kidney Disease, or renal dystopia; at the ureteral level—strictures or achalasia; and at the bladder level—neck strictures.
Functional obstructions include vesicoureteral reflux and neurogenic bladder. It should be noted that such pyelonephritis is resistant to Treatment, requiring a therapeutic complex aimed at restoring normal urine flow. Despite the lack of strictly specific signs for this type of pyelonephritis, renal symptoms play a leading role in the clinical picture: lumbar and abdominal pain, dysuria, facial edema, Urinary Incontinence, and arterial hypertension. R.F. Yezersky (1997) distinguishes Influenza-like, asthenic, dysuric, and dyspeptic variants of this pyelonephritis.
Distinguishing pyelonephritis in girls as a separate nosological entity is justified by the fact that it occurs much more frequently in them (80–90% of all cases) than in boys. Beginning in childhood, such pyelonephritis often persists, leading to the development of end-stage renal failure at a young age.
Risk factors include the specific Water/140.html">Anatomical Structure of the urinary system in females (short Urethra, close proximity of the external urethral meatus and the hymen, tendency to secrete mucus), imperfect neural regulation of urination, frequent development of vulvovaginitis, congenital and acquired urethral strictures, bladder sphincter spasm that impedes normal urination and promotes bladder atony, and the combination of urinogenous pathogenic factors with others (extra-urinogenous foci of chronic infection).
The clinical picture is dominated by dysuria and endogenous intoxication syndromes.
When treating renal failure in children, the core principles remain the same as in adults: eliminating the inflammatory process, correcting Metabolic Disorders and restoring renal function, ensuring normal urine flow when obstructed, stimulating the body's immune defenses and renal tissue regeneration, preventing the fibrosis of kidney structures, and providing anti-relapse therapy.
The diet includes: kefir with sugar syrup, stewed potatoes, cereal coffee, sweet tea, white and black bread with butter and cheese, fresh vegetable salads, vegetarian soups, boiled meat goulash, porridges, baked potatoes, lemons with sugar, tomato juice, fruit morses, pancakes with jam, cabbage cutlets, and cottage cheese casserole. It is also recommended to include (in the absence of oxaluria, uraturia, etc.) eggplants, zucchini, carrots, beets, turnips, pumpkins, watermelons, and melons.
Citing D. Ivanov (2001), we outline specific principles for treating renal failure in children. In ACUTE RENAL FAILURE or an Exacerbation of chronic renal failure, two consecutive pairs of antibiotics and uroantiseptics are used, such as a cephalosporin + biseptol, or an aminoglycoside + furazolidone. It is considered mandatory to administer one agent from the first pair intravenously during the febrile period, and the second intramuscularly (or both intravenously until bacteriuria is eradicated). The early prescription of bactericidal drugs is recommended, with the duration of a single agent usually lasting 7-10 days. Cefepime (a fourth-generation cephalosporin) is effective for eliminating hospital-acquired bacterial strains. Macrolides (with the exception of erythromycin and rovamycin due to their low concentration in the urinary tract) and azalides can also be used. The administration of Probiotics (e.g., biosporin) or prebiotics (fructose, lactose) is deemed appropriate. To relieve dysuria in children aged 12 and older, phenazopyridine or detrusitol are used; for neurogenic bladder, oxibutynin (driptan); and for enuresis, desmopressin (vasopressin), lamotrigine (lamictal), or imipramine (melipramine).
If renal failure develops against the background of polycystic kidney disease, the administration of biseptol, metronidazole, clindamycin, ceftriaxone, and vancomycin is generally recommended.
Medicinal herbs used include horsetail, bearberry, stinging nettle, yarrow, rose hips, common barley, St. John's wort, red clover, and European centaury.
Below is a general scheme for using various groups of medications depending on the degree of renal failure activity in children (Table 11).
V.I. Kirillov (1990) and G.A. Makovetskaya et al. (2000) recommend the widespread Use of immunomodulators—such as T-activin, thymalin, sodium nucleinate, and lycopid—in the Treatment of renal failure. In some cases of latent disease progression, these serve as an alternative to antibacterial therapy.
Last update: 08/08/2026
Editorial and Educational Adaptation: This material has been compiled based on the primary/original source text. The project team performed an editorial review, corrected technical inaccuracies, structured sections, and adapted the content for an educational format.
What was processed:
- elimination of formatting defects (OCR errors, structural breaks, corrupted characters);
- editorial organization of content;
- standardization of terminology in accordance with academic sources;
- verification of factual statements against the original source text.
All mentions of the author, publication year, and origin of the primary text have been preserved in accordance with the source.