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Kidney diseases in children 2023.ppt
1. Federal State Budgetary Educational Institution of Higher
Education "Bashkir State Medical University"
of the Ministry of Healthcare of the Russian Federation
Department of Children's Diseases
«Kidney diseases in children»
Lecture for 3rd year students of the Faculty of Dentistry
2022-2023 academic year
2. Prevalence
• In the structure of the overall morbidity in
Russia, kidney and urinary tract diseases take
the 8th place in children and the 7th place in
adolescents.
• Prevalence: 29 per 1 thousand children.
• In 50% of children, the disease is mild or
asymptomatic.
3. Structure
• Pyelonephritis 18:1000;
• Glomerulonephritis 3.3:1000;
• Dysmetabolic nephropathy 1,4:1000;
• Anomalies of the urinary system organs
1,3:1000;
• Tubulointerstitial nephritis 1:1000.
4. Factors that damage the kidneys:
• hereditary and teratogenic factors (cause
parenchymal dysembriogenesis);
• factors causing hypoxic-ischemic damage to
the renal tissue;
• intrauterine and intranatal infections
5. Risk factors
• presence of a nephrological patient in the family;
• presence of metabolic pathology in the family;
• pathological course of pregnancy, diseases during
pregnancy;
• occupational hazards and bad habits;
• violation of neurohumoral regulation of the pituitary-
hypothalamic-adrenal system;
6. Risk factors
• deficiency of certain hemostatic factors (von
Willebrand factor);
• allergic diathesis;
• the presence of familial instability of cytomembranes
(crystalluria);
• anomalies of the structure of the urinary system,
parenchymal dysembriogenesis;
• hypersensitivity to infections;
• hypovitaminosis, helminthosis.
7. Major renal syndromes
I. Urinary syndrome
1. Hematuric variant (more than 4 red blood cells in
the field of vision in the general analysis of urine):
• - extrarenal,
• - renal,
• - as a result of pathology of the urethra.
2. Hemoglobinuric variant includes free
hemoglobin in the urine.
8. Urinary syndrome
3. Proteinuria:
• physiological - (up to 2 g of protein in daily urine)
its types:
- orthostatic,
- caused by physical stress,
- during fever, stagnant.
• pathological:
- prerenal is a result of increased synthesis of low-
molecular proteins (paraproteins), protein breakdown in
tissues during intravascular hemolysis of red blood cells
and rhabdomyolysis;
9. Urinary syndrome
3. Proteinuria: pathological:
• renal:
• as a result of violation of the integrity of the basement
membrane with the filtration of plasma proteins (albumin,
transferrin, β2-globulin, γ-globulin);
• disorders of tubular reabsorption (in the proximal tubules
due to congenital or acquired enzymatic insufficiency);
• in a combined lesion (glomerular-tubular);
• postrenal (extrarenal or false)
• - as a result of ingestion of inflammatory exudate rich in
protein in the urine during diseases of the urinary system.
10. Proteinuria
• According to the amount of protein released,
proteinuria is divided into:
• a) microalbuminuria – up to 300 mg of protein in the
daily urine;
• b) low proteinuria – up to 1 g of protein in the daily
urine;
• c) moderate proteinuria – up to 3 g of protein in the
daily urine;
• d) high (nephrotic) proteinuria – more than 3 g of
protein in the daily urine
11. Urinary syndrome
4. Cylindrical version
• The basis of the cylinder is Tamm-Horsfall
uroprotein, synthesized by the epithelium of
the convoluted tubules, on which red blood
cells and the exfoliated epithelium are
layered.
• The presence of cylinders in the urine is an
indicator of severity of kidney damage.
12. Urinary syndrome
5. Pyuric variant
• a. Leukocyturia - more than 4 white blood cells in the field
of vision; more than 1 thousand in 1 ml of urine in the de
Nechiporenko analysis method;
• - more than 1 million in the urine analysis according to the
Addis-Kakovsky test in boys, girls have normal indicators 2
times higher.
• b. Bacteriuria - more than 10х4 microbial bodies (CFU –
colony-forming units) in 1 ml of an average portion of freshly
released urine collected during free urination in sterile dishes
after the toilet of the external genitals
• For staphylococci – 10х3 CFU / ml.
13. Urinary syndrome
• 6. Crystalluria
• the crystals are based on salts formed by calcium
ions with residues of oxalic, acetic, uric acid, and
triple phosphates.
14. II Hypertension syndrome
- persistent, increased blood pressure above the 95th
percentile for a specific age and sex of the child.
The basis of renovascular hypertension includes:
• hypervolemia (violation of the excretion of sodium and
water);
• activation of the renin-angiotensin-aldosterone system,
• activation of the sympathetic nervous system
• endothelial dysfunction
• metabolic syndrome.
15. II Hypertension syndrome
• The level of normal blood pressure (BP) in
children can also be determined by the
formulas:
• Systolic blood pressure (SBP) = 80 + n, where n
is the number of months to 1 year;
• SBP = 90 + 2n, where n is the years after 1 year.
• Diastolic blood pressure (DBP) = ½ SBP + 5 mm
Hg.
16. III Edematous syndrome:
• nephrotic variant:
high proteinuria, hyperlipidemia, widespread
peripheral edema, activation of the coagulation system,
hypoalbuminemia.
• the nephritic variant:
moderate proteinuria, local peripheral edema (eyes,
brain, lumbar region, shins, feet)
• non-edematous nephrotic (incomplete) variant
high proteinuria, hypoalbuminemia.
17. Major renal syndromes
IV Dysuric disorders:
• dysuria,
• oligo -, poly -, anuria.
V Pain syndrome:
- Abdominal
- Lumbar
VI Syndrome of small anomalies (stigmata of
dysembriogenesis):
1) external stigmata of dysembriogenesis (gothic sky,
wide nose bridge, blue sclera, etc.)
18. Major renal syndromes
VI Syndrome of small anomalies (stigmata of
dysembriogenesis):
• 2) somatic stigmata (doubling of the calyx-pelvic system,
lengthening or shortening of the ureters, kidney
dystopia, etc.) -they are detected during instrumental
examination
VII. Delayed physical development syndrome
VIII. Azotemia syndrome (increase in urea and
creatinine in the blood).
19. Acute glomerulonephritis
• It is acquired polyethological immuno-
inflammatory bilateral kidney disease with
a predominant initial lesion of the
glomeruli and possible involvement of any
component of the renal tissue in the
pathological process.
• ICD-10 N03.0- N03.7
21. Acute glomerulonephritis
• Primary GN occurs as a result of the impact on
the renal tissue of various infectious and non-
infectious (for example, allergic) factors after
1-3 weeks.
• Secondary GN occurs in systemic connective
tissue diseases (systemic lupus
erythematosus, Henoch-Schonlein purpura),
hypertension, etc.).
22. Morbidity rate
• Acute glomerulonephritis (AGN) is 0.4-0.5 per 1000
children.
• Boys are more likely to get sick than girls (1.5-2.0:1), rural
residents are more likely to get sick than urban residents.
• Among the closest relatives, AGN is observed 2-2. 5 times
more often. AGN is widespread everywhere, but more
often in countries with cold and humid climates.
• The disease is seasonal.
• School age prevails (7-12 years), children under the age
of 2 years rarely get sick
23. Etiology
I. Infectious agents:
• Streptococci - beta-hemolytic streptococcus of group A
(nephritogenic strains – 4, 12, 25, 49, 55, 57, 60).
• Staphylococci
• Malarial plasmodium
• Viruses - influenza, parainfluenza, adenoviruses, Coxsackie B-
4, CMV, herpes simplex virus, Epstein-Barr virus, hepatitis B
and C, HIV.
24. Etiology
II. Toxic substances (alcohol, mercury, heavy metal
salts, etc.)
III. Exogenous (repeated vaccinations, snake bites,
bee stings) and endogenous (uric acid, tumor, DNA)
antigens.
IV. Cooling, injuries
25. Pathogenesis
• In patients with the presence of risk factors and damaging
factors, streptococcal infection causes excessive synthesis
of antibodies, and excessive formation of nephritogenic CIC
(circulating immune complexes) occurs.
• Since this child's kidneys were still imperfect before the
present disease, they are not able to remove all the CIC
formed in the body in large quantities through the
glomerula.
• Immune complexes (IC) are deposited in the glomerular
endothelium, the basement membrane, and the
mesangium
26. Pathogenesis
• As a result, there is a spasm of the glomerular capillaries,
peeling and proliferation of their endothelium, stasis inside
the glomerular capillaries, loosening and thickening of the
basement membrane, increasing its permeability and the
appearance of the first signs of urinary syndrome in the form
of proteinuria, hematuria.
• IC activate the complement system, which initiates an
intensive migration of immune inflammatory cells
(macrophages, lymphocytes, plasmocytes, neutrophils, etc.)
towards the glomerular elements, into the thickness of the
basement membrane.
27. Pathogenesis
• Immune inflammatory cells produce cytokines that аct on
the vessels of the glomeruli, which leads to an increase in
the vascular permeability of the glomeruli and the
development of urinary syndrome (proteinuria, hematuria
and leukocyturia)
• Activates the complement system (complements C 5-9)
and leads to the formation of a membrane attack complex
(MAC)
• As chemoattractants, cytokines attract a new flow of
immune inflammatory cells and a new release of cytokines
to the inflammatory site, forming a vicious circle.
28. Pathogenesis
• MAC activates:
• thromboplastin, which leads to the activation of the
fibrin coagulation system
• Platelets, thromboxanes, serotonin
• macrophages that are rich in phospholipids
• Mesangial cells, neutrophils
• Lysosomal enzymes and free radicals are released
29. Pathogenesis
• Arachidonic acid, phospholipase, and leukotrienes are
released, which leads to the release of free radicals
• Primary damage to glomerular structural elements,
microobstruction, decreased glomerular filtration
• There is a depolymerization of the protein component of
the basement membrane and overgrowth of connective
tissue
• Oliguria, retention of nitrogenous waste,
• Increase in circulating blood volume
30. Pathogenesis
• Hypervolemia develops, which leads to the
development of arterial hypertension and the
development of edematous syndrome.
• Systemic hemodynamic disorders develop:
changes in the fundus of the eye, cardiovascular
and central nervous systems, and in the renal
glomeruli.
• The renin-angiotensin system is activated.
31. Pathogenesis
• Hyperperfusion of the renal glomeruli
develops, proteinuria and metabolic disorders
progress.
• Severe and prolonged proteinuria has a toxic
effect, tubulointerstitial inflammation develops,
then sclerosis renal tissue hardens.
• Increasing loss of renal function and acute renal
failure develop.
33. Clinical picture
• Develops 3-4 weeks after a streptococcal infection.
• The initial period is 4-6 weeks.
• Extrarenal symptoms predominate: signs of intoxication
(non-specific symptoms: weakness, headache, fever,
drowsiness, anorexia, general pallor), subfebrile fever.
• Arterial hypertension
• Edematous syndrome
• The renal group of symptoms includes pain in the lower back
(due to stretching of the renal capsule), abdominal pain,
dysuric syndrome: oliguria, a decrease in daily diuresis, a
change in the color of urine (the color of meat slops), urinary
syndrome (hematuria, proteinuria, cylindruria)
34. Clinical picture
• Period II of expanded clinical manifestations: there is an
increase in the symptoms of the initial period.
• Arterial hypertension progresses (changes in the fundus of
the eye, cardiovascular system, and central nervous
system).
• Changes in the central nervous system - lethargy, weakness,
nausea, insomnia, headache, associated with intoxication
and the development of acidosis, convulsions.
• Changes in the CVS - an increase in the size of the heart,
muffled heart sounds, the appearance of systolic murmur,
bradycardia, ECG changes in the form of
myocardiodystrophy.
35. Clinical picture
• Signs of renal insufficiency develop (decreased
glomerular filtration in the form of oliguria, azotemia
syndrome, impaired water and sodium excretion,
electrolyte imbalance, hypervolemia and edematous
syndrome).
• The nephritic form is manifested by local peripheral
edema, moderate hypertension, hematuria,
proteinuria — 2 g/day or more.
36. Clinical picture
• Nephrotic (edematous-albuminuric) form of glomerulonephritis
• The clinical picture develops gradually: increasing edema (face,
eyelids, lower back), may be anasarca (ascites, hydrothorax),
significant hepatomegaly.
• Blood pressure may be normal.
• Characterized by massive proteinuria (more than 50 mg / kg /
day), hypoalbuminemia, hyperlipidemia (cholesterol level is
above 6.5 mmol/l).
• The urea level is normal, the content of potassium and sodium is
reduced.
• The ESR is sharply increased (up to 50-70 mm / h).
• Oliguria (urine specific gravity is 1025-1030-1040.)
• Nephrotic syndrome usually has a wave-like course, aggravation
can be caused by acute respiratory viral infections or cooling .
37. Clinical picture
• Mixed form of glomerulonephritis is characterized by
increasing edema, intoxication, pallor, persistent
hypertension, hypoproteinemia, anemia.
• The urine tests show advanced proteinuria, polyuria,
isostenuria.
• High levels of fibrinogen and fibrin degradation products
are detected in the urine and blood.
• Isolated urinary syndrome is confirmed by biopsy
extremely rarely, more often hereditary or tubulo-
interstitial variants of nephritis are revealed.
38. Clinical picture
• Period III - reverse development of symptoms (from 1-3
months to 1-1.5 years).
• The prolonged course of acute glomerulonephritis can be
stated with a duration of symptoms of more than 6 months.
• Period IV – complete clinical and laboratory remission.
• With its duration of more than 5 years, one can state
recovery.
• If the symptoms persist for more than 1 year, the transition to
a chronic form takes place (in 5-15% of cases of AGN).
39. Rapidly progressive glomerulonephritis
(subacute, malignant)
• It is rarely observed, develops after streptococcal and viral
infections.
• It is characterized by early (after 1-2 weeks) development
of oligoanuria with inhibition of renal functions, edema,
high hypertension, significant proteinuria and hematuria,
and increasing hyperazotemia.
• After 6-12 months from the onset of the disease, with its
natural course, there is a fatal outcome from chronic renal
failure in many patients.
40. Berger's disease
• IgA-nephropathy can be an independent disease or a symptom
in diseases of the liver or gastrointestinal tract (celiac disease,
Crohn's disease)
• The reasons for the development of IgA-nephropathy are
associated with a hereditary violation of IgA synthesis in the
form of switching of IgM synthesis to IgA synthesis in B-
lymphocytes
• Berger's disease is clinically manifested by macrohematuria,
attacks of which are associated with infectious diseases of the
upper respiratory airway
• An unfavorable prognostic symptom is the addition of
proteinuria to hematuria.
41. Chronic glomerulonephritis (CGN)
• It is bilateral diffuse inflammation of the
glomeruli of the kidneys of immune origin.
• The disease often has a progressive course
with a gradual involvement in the process of
all parts of the nephron, the development of
nephrosclerosis and chronic renal failure (CRF)
42. Etiology of CGN
• viral and bacterial agents
• irrational drug therapy
• actively functioning foci of chronic infection
• persistent viral infections
• excessive antigenic loads (combined
infections, improperly received preventive
vaccinations),
• violations in dietary treatment, etc.
43. Clinical picture
• Hematuric form: urinary syndrome in the form of macro-
or microhematuria with a small proteinuria (up to 1-2
g/l). Hypertension and edema are usually absent
• Nephrotic form (edematous-proteinuric) is observed
mainly in preschoolers, has a recurrent course,
characterized by pronounced edema and massive
proteinuria (more than 3 g/day); hypo - and
dysproteinemia, hyperlipidemia develop.
• Filtration function of the kidneys remains normal for a
long time.
44. Clinical picture
• The mixed form is detected mainly in schoolchildren, less
often in preschoolers.
• It is clinically characterized by a combination of nephrotic
and hematuric syndrome (prognostically more favorable
option) or a combination of these syndromes with
hypertension (unfavorable prognosis).
• Early development of glomerular filtration restriction and
concentration function, anemia is observed.
• Edema is less pronounced, but more persistent.
• Proteinuria - from 3-4 to 10 g/l, hematuria is almost
constantly detected.
45. Diagnostics
• General blood test
• General urine test
• Urine analysis according to Zimnitsky, according to
Nechiporenko
• Biochemical blood test
• Electrocardiography (ECG)
• Immunological examination
• Ultrasound of the abdominal cavity organs and kidneys
• Plain radiography
• Nephroscintigraphy
• Biopsy
• CT, MRI
46. Complications
1. Complications associated with the underlying disease:
a) eclampsia (angiospastic, hypertensive encephalopathy)
b) acute cardiovascular insufficiency
c) acute renal failure (ARF)
d) abdominal crisis.
2. Treatment-related complications:
a) Cushing's syndrome,
b) acute adrenal insufficiency,
c) mental disorders,
d) acute pancreatitis,
e) shingles.
3. Complications related to the disease itself and its treatment:
a) thrombosis, b) purulent complications.
47. Treatment
• Bed rest is prescribed until the elimination of edema,
hypertension, macrohematuria for 2-4 weeks
• Diet includes limited intake of salt and water.
• In azotemia, protein and fat are reduced. By the end of the
second week of treatment, the physiological norms of
protein and fat should be taken.
• Loop diuretics (furosemide 1.5-2 mg / kg of body weight
per day) should be taken until the complete restoration of
diuresis, the disappearance of edema and the relief of
azotemia
• Antibacterial therapy includes semi-synthetic penicillins
(ampicillin, oxacillin, amoxicillin), cephalosporins of the III-
IV generation, macrolides - for 7-10 days
48. Treatment
• In order to increase renal blood flow, curantil or trental are
prescribed.
• Calcium channel blockers and ACE inhibitors (captopril,
enalapril) are prescribed for the correction of hypertension.
• To suppress immune inflammation, a patient should take
prednisolone by mouth, in the form of pulse therapy
(metipred by drop infusion, intravenous).
• Combination of glucocorticoids with cytostatics
(cyclophosphamide, chlorbutin)
• Cyclosporine A (sandimmun), Tacrolimus, Mycophenolate
mofetil (MMF), Rituximab
• Plasmapheresis
• Hypolipidemic drugs
• Syndromic therapy is performed
49. Follow-up care
• Follow-up is carried out before the transition of
patients to an adult polyclinic.
• Examinations with the measurement of blood
pressure are carried out 1 time per month by a
pediatrician.
• Urine tests are taken 1-2 times a month.
• Regular conservative treatment of chronic foci of
infection and dehelmintization.
50. Acute pyelonephritis (PN)
• this is a non-specific microbial-inflammatory kidney
disease with a predominant lesion of the tubulo-
interstitial tissue and its calices-pelvis system.
• In women, it occurs 5 times more often, except for
the age of up to 1 year.
• In the Russian Federation, the prevalence of urinary
tract infection among children is 18-22:1000,
pyelonephritis - from 0.3% to 4.0%
• ICD-10 N10- N13.6
51. Acute pyelonephritis
• Primary (uncomplicated) PN develops as an independent
disease.
• Secondary (complicated) PN:
• obstructive
• affected by a violation of the passage of urine due to organic
(congenital, hereditary or acquired pathology)
• or functional uropathy (more often, vesicoureteral-pelvic
reflux and neurogenic dysfunction of the bladder)
• non- obstructive
• Affected by metabolic disorders (metabolic) involving oxalic
acid, uric acid, calcium, cystine, etc., immunodeficiency states,
endocrinopathy.
52. Etiology
• Bacteria (bacteria of the family
Enterobacteriaceae, the basis of which (up to
80 %) is Escherichia coli, enterococci, Proteus,
Klebsiella, Pseudomonas aeruginosa,
staphylococci, ureoplasma).
• Viruses
• Mixed-flora
53. Properties of E. coli
• it has superficial O-antigens and capsular K-antigens;
• on the outer cell membrane of Escherichia coli, there are
adhesive molecules (adhesins) to the receptors of the
uroepithelium of the urinary tract (UT);
• the endotoxic effect of O–antigen is associated with lipid
A, causes the induction of inflammation, increased
adhesion,
• lipid A affects the smooth muscle of the UT, which leads
to obstruction with subsequent pressure increase and the
development of reflux;
54. Properties of E. coli
• E. coli stimulates the synthesis of adrenomedulline,
which promotes relaxation of the smooth muscles of the
UT, which disrupts the passage of urine;
• K-antigens prevent phagocytosis of microorganisms by
macrophages on the mucosa of the UT;
• E. coli secretes aerobactin or colicine, which inhibits the
growth of other microorganisms, ensuring the stability of
the colonies;
• E. coli secretes ά-hemolysin, which causes massive death
of red blood cells with the release of free Fe, which is
necessary for its own growth.
55. Pathways of pathogen penetration into the
kidney
• Hematogenic variant occurs as a result of
pyelovenous reflux, the microbe enters the general
bloodstream, then, returning through the arterial
system to the same kidney, causes inflammation in it.
• Urinogenic (ascending) variant occurs in
vesicoureteral and pyelorenal refluxes
• Lymphogenic way
• Translocation of microbes from the intestine is
considered as an endogenous infection
56. Pathogenesis
• Features of E. coli:
• isolation of Lipid-A (endotoxin)
• paralytic effect on ureteral peristalsis - functional obstruction
• pyelorenal reflux (violation of intra - and extrarenal
urodynamics)
• microbes enter the tubules, where they attach to the
uroepithelial receptors with their adhesive molecules.
• During the first 24 hours, the uroepithelium remains virtually
unchanged, and the bacteria multiply intensively, doubling
their number every 20 minutes.
• The presence of bacteria, their growth and the release of
toxins contribute to the activation of local and humoral
immunity
57. Pathogenesis
• An inflammatory reaction develops in the form of migration to
the renal interstitium of inflammatory cells
(polymorphonuclear leukocytes, neutrophils, macrophages,
monocytes, etc.)
• In the focus of inflammation, the activation of these cells
causes the release of various pro-inflammatory cytokines:
tumor necrosis factor ά, IL-1, 2, 6, 8; interferons.
• Activation of phagocytosis leads to a "respiratory explosion"
with a massive release of free radicals, lysosomal enzymes,
numerous inflammatory mediators (leukotrienes,
prostaglandins, etc.), and nitric oxide.
58. Pathogenesis
• Not only the bacterium is damaged, but also
the host's own kidney tissue.
• Metabolic disorders lead to changes in the
urine osmolarity, in which microbes migrate to
the medullar layer of the kidney, where
microorganisms find a protective environment
and are able to exist for a long time
(persistence).
59. Clinical picture
• Intoxication syndrome: acute onset, high (up to 40 °C)
temperature, general feeling of being unwell, thirst,
shaking multiple chills, followed by heavy sweat;
adynamy, headache, nausea, vomiting.
• Pain syndrome includes pain in the lumbar region; it is
acute, located on the side of the affected kidney;
tension of the anterior abdominal wall, sharp soreness
in the costovertebral angle, with radiation to the
anterior abdominal wall, it can simulate acute surgical
pathology.
60. Clinical picture
• Urinary syndrome (proteinuria, leukocyturia,
bacteriuria)
• Dysuric syndrome (pollakiuria, pain and
cutting sensation when urinating, frequent
urination, enuresis, change in the amount of
urine released)
• Arterial hypertension-intermittent
61. Clinical picture
• Symptoms of urinary tract infection in children, depending on
age:
• Newborns
• - dyspeptic disorders
• - lack of weight gain, vomiting, diarrhea, jaundice
• 1 month – 3 years
• - dysuric disorders;
• - "unmotivated" temperature rises, intoxication;
• - urinary syndrome.
• Over 4 years old
• - pain syndrome (pain is localized in the side or lower back);
• - enuresis;
• - classical picture (fever, intoxication, dysuria, urinary syndrome).
62. Classification
Clinical forms:
• Latent form includes recurrent or persistent bacteruria.
• Low-manifestation.
• With pronounced symptoms.
According to activity:
• active stage,
• partial clinical and laboratory remission,
• complete clinical and laboratory remission.
According to the safety of renal function:
• preserved
• impaired
• acute renal failure
63. Chronic pyelonephritis
• Chronic pyelonephritis is a consequence of incurable
acute PN
• The development of primary chronic PN is associated
with a genetically determined infection-mediated
immune inflammation of the renal tissue, mainly the
interstitium of the kidneys, with a subsequent recurrent
course, involvement of all kidney structures in the
pathological process and eventual nephrosclerosis
• Complications of PN: nephrolithiasis, pyonephrosis,
necrosis of the renal papillae.
64. Chronic pyelonephritis
• In 1 / 3 patients, the usual examination fails to detect
signs of pyelonephritis.
• Periods of unexplained fever
• Unilateral chronic PN is characterized by dull persistent
pain in the lumbar region on the side of the affected
kidney
• In the urine sediment, predominance of white blood cells
over other shaped elements of urine is determined
• Bacteriuria
• Arterial hypertension
• Chronic renal insufficiency
66. Diagnostics
• General blood test
• General urine test
• Urine analysis according to Zimnitsky, according to Nechiporenko
• Biochemical blood test
• Electrocardiography (ECG)
• Immunological examination
• Ultrasound of the abdominal cavity organs and kidneys
• Plain radiography
• Excretory urography
• Voiding cystourethrogram
• Chromocytoscopy (violation of the passage of urine through the
upper urinary tract)
• Dynamic nephroscintigraphy
• CT, MRI
67. Treatment
• Diet:
• In acute PN for 7-10 days, a dairy-vegetable diet with
moderate restriction of protein (1.5-2.0 g/kg of body
weight), salt (up to 2-3 g per day), and increased fruit
juices and fruit drinks is used.
• In chronic PN, slightly alkaline mineral waters (such as
Slavyanovskaya, Smirnovskaya) at the rate of 2-3 ml/kg of
weight are taken for 20 days, 2 courses per year
• The schedule of regular urination is urinating every 2-3
hours, depending on the age.
68. Treatment
• Daily hygiene measures include shower, bath, wiping,
depending on the condition of the child.
• Physical therapy is performed lying or sitting, depending on
the condition of the child.
• Antibacterial therapy should take place until the suppression
of the activity of the pathogen for 3 weeks with a change of
the drug every 7-10-14 days (protected penicillins,
cephalosporins of the III-IV generation, macrolides,
aminoglycosides)
• In severe PN, combined antibacterial therapy is used.
70. Treatment
• Herbal medicine - in remission - (leaf and fruit of
clusterberry, cranberries, field horsetail, etc., Kanefron,
Phytolysin)
• In obstructive pyelonephritis, the decision on the possibility
of surgical correction should be taken
• Vaccination of children with pyelonephritis is carried out
after reaching remission with mandatory preliminary
laboratory control of blood and urine tests, according to an
individual schedule
• Sanatorium-resort therapy is carried out during the period
of acute PN subsiding (3 months after the beginning of the
disease activity)
73. Prevention
• antenatal prevention of kidney diseases in pregnant
women;
• teaching personal hygiene skills from childhood;
• improving social conditions of life;
• mass preventive examinations, screenings;
• prevention of hospital uroinfection;
• timely diagnosis and treatment of kidney diseases in
children
• early correction of urological diseases;
• sanation of chronic foci of infection.
