Lecturer,

associate professor
Jemoityak V. A.
• New nephrons cannot be formed after birth,
• Progressive loss of nephrons may lead to renal
insufficiency.
 Theglomeruliareverysmall,important
structuresinthekidneysthatsupply
bloodflowtothekidney

• The glomerular network of specialized

capillaries serves as the filtering mechanism
of the kidney, that filter the excess and waste
fluids from the body.
The glomerular basement membrane (GBM) forms a continuous
layer between the endothelial and mesangial cells on one side and
the epithelial cells on the other.
The membrane has 3 layers: a central electron-dense lamina densa;
the lamina rara interna, which lies between the lamina densa and
the endothelial cells; and the lamina rara externa, which lies
between the lamina densa and the epithelial cells.
The visceral epithelial cells cover the capillary and project
cytoplasmic “foot processes,” which attach to the lamina rara
externa. Between the foot processes are spaces or filtration slits.
• (mesangial cells and matrix) lies between the
glomerular capillaries on the endothelial cell side of
the GBM and forms the medial part of the capillary
wall.
• The mesangium may serve as a supporting structure
for the glomerular capillaries and probably has a
role in the regulation of glomerular blood flow and
filtration and in the removal of macromolecules (such
as immune complexes) from the glomerulus, either
through intracellular phagocytosis or by transport
through intercellular channels to the juxtaglomerular
region.
which surrounds the glomerulus, is composed of
a basement membrane, which is continuous with
the basement membranes of the glomerular
capillaries and the proximal tubules, and the
parietal epithelial cells, which are continuous
with the visceral epithelial cells.
The kidneys carry out the detoxification
process in the body by filtering the
blood and eliminating waste from the
body.

Problems arise when the glomeruli become

inflamed.
the glomeruli become inflamed and impair the
kidney's ability to filter urine.
 Glomerulonephritis (GN)

– is an acquired
polyetiologic kidney disease,
characterized by
immune inflammation of glomeruli.
Children between ages 2 to 12 are more
prone to glomerulonephritis and is
more common in boys.
Glomerulonephritis can be acute
(sudden)
or chronic (gradual).
• Primary glomerulonephritis (GN) occurs as primary process.
• Secondary glomerulonephritis means that it is caused by
another disease, such as lupus or diabetes.
So, secondary GN appears as a clinical syndrome of systemic
connective tissue diseases, systemic vasculitis or chronic
infections.
Etiology:
Immunologic injury is the most common
cause and results in glomerulonephritis.
 There appear to be 2 major mechanisms of
immunologic injury: (1) glomerular
deposition of circulating antigen-antibody
immune complexes and
(2) interaction of antibody with local antigen
in situ.
• Glomerulonephritis usually occurs more than one week after
an infection. This is often referred to as acute
poststreptococcal glomerulonephritis or APSGN.
1) Infectious agents: Β-hemolytic Streptococcus group A,
types 4 and 12 causing pharyngitis and type 49 causing
pyoderma (nephritogenic strains) or Staphylococcus
(sore throat, tonsillitis, upper respiratory tract
diseases);
Viruses (Hepatitis B, herpes, rubella, adenoviruces).
2) Repeated vaccination, or serum, insect poisons,
medicines;
 Secondaryglomerulonephritisarecausedbyseveral
differentdiseasestates,includingthefollowing:
• Systemic immune diseases, like systemic lupus erythematosus
(SLE), Goodpasture’s syndrome and IgA nephropathy),
• Other systemic diseases may include:
◦ Polyarteritis nodosa - an inflammatory disease of the arteries.
◦ Wegener vasculitis. A progressive disease that leads to
widespread inflammation of all of the organs in the body.
◦ Henoch-Schönlein purpura (HSP). A disease usually seen in
children that is associated with purpura (small or large purple
lesions on the skin and internally on the organs) and involves
multiple organ systems.
• GN can also result from a gene on the X
chromosome passed from carrier mothers who have
no features, or minimal features of GN, to their sons,
who are affected with the disorder in 50 percent of
the cases.
• A form of inherited glomerulonephritis called
Alport syndrome, which affects both men and
women; men are more likely to have kidney
problems. Treatment focuses on preventing and
treating high blood pressure and preventing kidney
damage.
• History of cancer, blood or lymphatic system disorders,
and exposure to hydrocarbon solvents and diabetes
may increase the patient’s chances of getting
glomerulonephritis.
 pathophysiology

In most circumstances, glomerular inflammation

begins with an antigen-antibody reaction,
either direct antibody binding to an antigen
expressed or trapped in the glomerulus, or the
localization of a circulating complex in the
kidney.
• The inflammation is marked by proliferation of resident glomerular
cells and infiltration by lymphocytes or neutrophils.
• and expansion impairs the microcirculation, reducing
the glomerular filtration rate (GFR) and usually
resulting in an increase in BUN and creatinine. This
reduction in GFR, in turn, leads to the retention of
salt and water, causing fluid overload.

• The degree of fluid overload in AGN can vary

considerably. In severe situations, it can be manifest
by life-threatening hypertension and pulmonary
edema.
 Etiologic factors:
Β-hemolytic Streptococcus group A, Staphylococcus,
serum, insect poisons, medicines

Immune complexes formation in glomerulus and

vessels
Glomerular membrane antigen penetration into the
bloodstream and contact with immune cells

Autoantibodies formation to own basal membrane of

glomeruli

Immune pathologic process and increase basal

membrane permeability
Inflammatory mediators (complement) activation
take place, which neutrophyls attract in locus of
involvement. Lysosomes of neutrophyls excretes
enzymes, which damage basal membrane
endothelium.
Complement activates Hageman’s factor (factor XII),
trombocytes aggregation, and blood coagulation and
fibrin deposition in glomeruli capillaries take place.

Proteinuria, hematuria, decrease of filtrative kidney

function
 Glomerulonephritis may be a temporary and
reversible condition, or it may progress and lead
to complications and/or chronic kidney failure.
 Signs and symptoms of
glomerular disease include
various degrees of renal failure,
edema, oliguria, hypertension,
and anemia out of proportion to
the degree of renal failure.
• Fatigue
• Nausea and vomiting
• Headache
• Pale skin color
• Fluid accumulation in the tissues (edema)
• High blood pressure
• Less frequent urination
• Dark brown-colored urine (from blood and protein)
• Sore throat
• Increased breathing effort
• Lethargy
• Seizures (may occur as a result of high blood pressure)
• weight loss
• Joint pain
• Rash appearance, especially on the legs and buttocks
• Foamy urine
It is next important to ascertain any symptoms suggestive
of complications of the AGN. These might include
shortness of breath or exercise intolerance from fluid
overload or headaches, visual disturbances, or alteration
in mental status from hypertension.
 HistoryandPhysicalExamination

Most typically, the child with AGN will be seen

because of the sudden development of change in
urine color.
On occasion, however, the presenting complaint may
relate to a complication of the disease: hypertensive
seizures, edema, and so forth.
• Hematuria in children with AGN is typically described as
“coke,” “tea,” or “smoky” colored. True bright red blood in
the urine is more likely a consequence of anatomic problems
such as urolithiasis, than glomerulonephritis.
• Urine color in AGN is uniform throughout the stream.
• The gross hematuria of AGN is virtually always painless;
dysuria accompanying gross hematuria points to acute
hemorrhagic cystitis rather than renal disease.
• A history of previous such episodes would point to an
exacerbation of a chronic process such as IgA nephropathy.
Although a history of a recent documented streptococcal
infection would be consistent with poststreptococcal AGN.
• Pathologic proteinuria – is a condition, when the
quantity of protein in daily urine is higher than 30-60
mg.
Selective proteinuria – molecular weight of protein
with urinal excretion <85000: albumin, seromucoid.
Non-selective proteinuria – molecular weight >85000:
γ- and α2-macroglobulins.
•Leucocyturia inconstant, 40-50% of cases.
•Cilindruria – hyaline, erythrocytic, leucocytic,
granular.
Edematous
Hypertensive
Urinary
Hematuria is present (micro- and macrohematuria).

Hematuria may be isolated or accompanied with

proteinuria, leucocyturia, cilindruria.
Hematuria in GN appears because of increase
permeability of glomerular capillaries, or
hemarrhagies in glomeruli result in capillaries
ruptures.
Hypertensivesyndrome:
Characterized by regular increase of systolic and
diastolic blood pressure. Take place in 60-70% of cases.

Great role in blood pressure and water-salt regulation

the renin-angiotensin-aldosteron system take place.
• Since AGN may be the presenting complaint of a
multisystem illness, a complete review of systems is
vital.
• Particular attention should be paid to rash, joint
discomfort, recent weight change, fatigue, appetite
changes, respiratory complaints, and recent
medication exposure.
The physical examination begins with a careful assessment of
vital signs, particularly blood pressure. Blood pressures 5 
mm above the 99th percentile for the child’s age, sex, and
height, especially if accompanied by any alteration in mental
status, demand prompt attention. Tachycardia and tachypnea
point toward symptomatic fluid overload. Careful examination
of the nose and throat may provide evidence of bleeding,
suggesting the possibility of one of the ANCA-positive
vasculitides such as Wegner’s granulomatosis
• Cervical lymphadenopathy may be the residua of a recent
streptococcal pharyngitis.
• The abdominal examination is particularly important:
• Ascites may be present if there is a nephrotic component to
the AGN.
• Hepato- or splenomegaly may point to a systemic disorder.
• Significant abdominal pain may accompany HSP.
• Scrotal edema may occur in nephrotic syndrome as well, and
orchitis is an occasional finding in HSP.
• In AGN a very careful examination of the skin is important
The rash of HSP may initially be subtle and limited to the
buttocks or the dorsa of the feet.
• Some peripheral edema from salt and water retention is seen in
AGN, but this tends to be a more subtle “brawny” edema than
the pitting edema characteristic of nephrotic syndrome.
• Joint involvement occurs in some multisystem disorders with
AGN. Small joint (e.g., fingers) is more typical of SLE, while
or knee involvement is seen with HSP.
• Urinalysis is the first order in assessing a child with suspected
AGN.
• The presence of red blood cell casts,
while not invariably seen, is diagnostic of glomerulonephritis if
present.
 Pyuriaandbacteriuriainapatientwithaurinarytract
infection.Asimplestainwasaddedtothewetmountofspunurine.
Althoughthereareepithelialcellspresent,theculturedemonstrateda
trueurinarytractinfection(UTI)andnotmerelycontaminatedurine.
• AGN is an inflammatory process, so it is not at all
unusual to see white blood cells in nephritic urine.
Unfortunately, this occasionally leads to an
inappropriate diagnosis of urinary tract infection.
• Proteinuria is also nearly invariant in AGN although
any cause of gross hematuria can lead to some
urinary protein. If the urine is not grossly bloody,
however, the combined presence of hematuria and
proteinuria always means glomerulonephritis.
• Assessing renal function and electrolytes is an important first
step, as is obtaining a hemogram.
• A mild degree of anemia is frequently seen with AGN and
likely is dilutional; more significant anemia would be evidence
that the process may be more chronic.
• There are typically no important changes in the white blood
cell count or platelet count in most causes of AGN. A normal
platelet count in the presence of purpura is the usual finding in
HSP.
• A serum albumin is usually included; a slight degree of
hypoalbuminemia is typical of many inflammatory processes
such as HSP, but values <20 g/L are quite unusual in
straightforward AGN and point to a process with a nephrotic
syndrome component.
• By far, the most important test to obtain initially is an
assessment of the complement system. This generally means
obtaining a serum C3 and C4.
• Poststreptococcal AGN is characterized by a very low C3,
sometimes with minimal decreases in C4.
• In addition may be recommend the following diagnostic tests:
• Throat culture
• Electrocardiogram (ECG or EKG). A test that records the electrical activity
of the heart, shows abnormal rhythms (arrhythmias or dysrhythmias), and
detects heart muscle damage.
• Renal ultrasound (also called sonography). The test is used to determine the
size and shape of the kidney and to detect a mass, kidney stone, cyst, or
other obstruction or abnormalities.
• Chest X-ray.
• Renal biopsy. A procedure during which a small sample of tissue is taken
from the kidney through a needle. The tissue is sent for special testing to
determine the specific disease.
 Forms of GN Activity Kidney functions

Acute:
● With nephritic ● Period of initial mani - ● Normal (without
(hematuric) syndrome festations (2-4 weeks) kidney function
● With nephrotic ● Period of sharp mani- disorders)
syndrome festations (2-4 weeks) ● With kidney function
● Isolating urinary ● Period of decreased disorders
syndrome manifestations (2-3 months)● Acute renal failure
● With nephrotic ● Transformation into
syndrome, hematuria chronic glomerulo-
and hypertension nephritis
 Forms of Activity Kidney functions
GN
Chronic :
● Hematuric ● Exacerbation ● Without kidney
form ● Partial clinical and function disorders
● Nephrotic laboratory remission ● With kidney function
form ● Complete remission disorders
● Mixed form ● Chronic renal failure

Subacute ● With kidney function

(malignant) disorders
● Chronic renal failure
Morphologicclassificationofprimary
glomerulilesions:
oMild glomeruli lesions
oFocal or (and) segmental lesions

oDiffuse GN:
●Membranous GN
●Diffuse proliferative GN

Pathogenetic treatment of GN depends on

morphologic changes in kidneys.
In hematuric form of GN often diagnosed:
Membranous GN
Mesangioproliferative GN
In nephrotic form of chronic GN often diagnosed:
Minimal membranous changes
Membranous proliferative changes
In mixed form of chronic GN:
Proliferative and fibroplastic changes
Focal and segmental glomerulosclerosis
[A] A normal glomerulus.
Note the open capillary
loops and the thinness of
their walls—‘should look as
if you could cut yourself on
them'.
 C.Clipslide

NORMALGLOMERULUS

Thenormalglomerulusofthekidneyathighpower
hasthin,delicatecapillaryloopsandthemesangium
isnotprominent.
[B| Focal segmental
glomerulosclerosis. The
portion of the glomerulus
at 2 o’clock shows loss of
capillary loops and cells,
which are replaced by
matrix,
[C] Focal necrotising
glomerulonephritis. The portion of the
glomerulus at 6 o'clock is replaced by
bright pink material with some 'nuclear
dust’. Neutrophils may be seen
elsewhere in the glomerulus. There is
surrounding interstitial inflammation.
Disease of this type is most commonly
associated with small-vessel vasculitis
and may progress to crescentic nephritis
(see [Е]).
[D] Membranous
nephropathy. The capillary
loops are thickened
(compare with the normal
glomerulus) and there is
expansion of the mesangial
regions by matrix
deposition. However, there
is no gross cellular
proliferation or excess of
inflammatory cells.
[E] Crescentic
glomerulonephritis. The
lower part of Bowman's
space is occupied by a
semicircular formation
('crescent') of large pale
cells, compressing the
glomerular tuft. This is
usually seen in
aggressive inflammatory
ECrescenticglomerulonephritis
types of
glomerulonephritis.
• [F] Granular deposits of
IgG along the basement
membrane in a
subepithelial pattern,
typical of membranous
nephropathy,
• [G] IgA deposits
In the mesangium,
as seen in IgA
nephropathy
[h] Ribbon-like linear deposits of anti-
GBM antibodies along the GBM in
Goodpasture's disease Glomerular structure
is well preserved in all of these examples.
 Diagnosed usually in children older than 5 years and
characterized by:
Macrohematuria (red color of urine);
Moderate proteinuria (till 1-3gr);
Moderate edema of the face and lower extremities;
Increase blood pressure;
Common blood count: anemia, moderate leucocytosis,
eosinophyllia, moderate increase of ESR;
Biochemical blood analysis: dysproteinemia, increase α2- and
γ-globulins, hyperazothemia, normocholesterolemia.
 Basis: the increase vascular permeability in case of increase
hydrostatic pressure and increase level of angiotensin and
aldosteron.
• Membranoproliferative
glomerulonephritis: may be undistinguishable
from post-streptococcal glomerulonephritis at disease
onset. However, complement C3 levels remain
persistentlylow beyond 8 weeks following the disease onset,
indicating chronic immune complex deposition.
• Lupus nephritis—Distinguished by the systemic
manifestations and the persistently low complement
C3 and C4. Positive anti double stranded DNA
antibodies and/or anti Smith antibodies confirms the
diagnosis. Renal biopsy reveals glomerular deposition
ofimmu noglobulins, C3 and Clq (Full house
immunofluorescence).
• IgA nephropathy—Gross hematuria tends to
occur concurrenntly
• with upper respiratory infections (In contrast, post-
 Diagnosed usually in pre-school age children and
characterized by:
o Severe edemas to ascitis and anasarca, sometimes
hydrothorax is present;
o Normal or decrease blood pressure;
o Common blood count: severe increase of ESR (to 50
mm/hour and more);
o Urinary syndrome: oliguria and increase relative density of
urine, severe selective proteinuria (6-20g/day);
o Biochemical blood analysis: hypoproteinemia,
hypoalbuminemia, hyper-α2-globulinemia, hyperlipidemia.
◦ proteinuria,
◦ hypoalbuminemia (serum albumin <30
mg/L),
◦ edema,
◦ end hyperlipidemia.

Prognosis is largely dependent on the glomerular

etiology of the proteinuria. Minimal change
disease is by far the most common etiology of
nephrotic syndrome in childhood
Can be different in severity (from mild edemas to
anasarca)
Usually appear on the face, then spread on the body
and extremities (ascit, hydrothorax)
More severe at the morning
Regular weight is very important for edemas
estimation
Edemas appear in 2-3 days after disease start, and
usually least less than 2 weeks

There are different mechanisms of edemas in case of

nephritic and nephrotic syndromes
 Glomeruli membranes lesions, the increase of
glomerular permeability, the increase of
hyaluronidase activity, renal blood and lymph flow
changes

Proteinuria, the increase of vascular permeability,

the decrease of glomerular filtration rate and
reabsorption in canaliculi, protein synthesis and
metabolism disorders
 Hypoproteinemia, hypovolemia

The decrease of oncotic, osmotic and intravascular

pressure

Hypersecretion of ADH, aldosterone, secondary

aldosteronism, activity of rennin-angiotensin system
increase
Increase sodium and water reabsorption in renal
canaliculi

Increase volume of blood circulation

Water retention and its displacement into the

extracellular space
• Primary/Idiopathic.
◦ Minimal change disease.
◦ Focal segmental glomerulosclerosis—To be considers when renal
function is not normal. Steroid resistant. Diagnosis made
histologically.
• Most glomerulonephritic disorders can have
associate nephrotic syndrome.
• IgA nephropathy.
• Post-streptococcal glomerulonephritis.
• Systemic lupus erythematosus.
• Infection can have associated nephrosis.
• Hepatitis B and C.
• Syphilis
• Malignancy - Very rare cause of nephrotic syndrome.
• Congenital nephrotic syndrome.
• Should be considered in all patients under 1 year of age.
• Etiology most often is a genetic defect leading to absence of a structural
protein important in podocyte function.
 Diagnosed in all age periods and characterized by:
• Proteinuria (1g/l);
o Micro- and macrohematuria;
o Abacterial leucocyturia;
o Extrarenal symptoms are absent;
This is a classic example of the acute nephritic syndrome characterized by the
sudden onset of gross hematuria, edema, hypertension, and renal insufficiency.
Acute poststreptococcal glomerulonephritis is one of the most common
glomerular causes of gross hematuria in children, surpassed only by IgA
nephropathy.
ETIOLOGY AND EPIDEMIOLOGY.
Acute poststreptococcal glomerulonephritis follows infection of the throat or skin by
certain “nephritogenic” strains of group A β-hemolytic streptococci. The factors that
allow only certain strains of streptococci to be nephritogenic remain unclear.
Poststreptococcal glomerulonephritis commonly follows streptococcal pharyngitis
during cold weather months and streptococcal skin infections or pyoderma during
warm weather months.
PATHOLOGY.
The kidneys appear symmetrically enlarged. All glomeruli appear enlarged and
relatively bloodless and show diffuse mesangial cell proliferation with an increase in
mesangial matrix. Polymorphonuclear leukocytes are common in glomeruli during
the early stage of the disease. Crescents and interstitial inflammation may be seen in
severe cases. Immunofluorescence microscopy reveals lumpy-bumpy deposits of
immunoglobulin and complement on the glomerular basement membrane (GBM)
and in the mesangium. On electron microscopy, electron-dense deposits, or
“humps,” are observed on the epithelial side of the GBM.
• Poststreptococcal glomerulonephritis is most common in
children aged 5–12 yr and uncommon before the age of 3 yr.
The typical patient develops an acute nephritic syndrome 1–2
wk after an antecedent streptococcal pharyngitis or 3–6 wk
after a streptococcal pyoderma.
The severity of renal involvement varies from asymptomatic
microscopic hematuria with normal renal function to acute renal
failure. Patients may develop various degrees of edema, hypertension,
and oliguria. Patients may develop encephalopathy and/or heart
failure owing to hypertension or hypervolemia. Encephalopathy may
also possibly result from the direct toxic effects of the streptococcal
bacteria on the central nervous system.

Edema typically results from salt and water retention; nephrotic

syndrome may develop in 10–20% of cases. Nonspecific symptoms
such as malaise, lethargy, abdominal or flank pain, and fever are
common. The acute phase generally resolves within 6–8 wk. Although
urinary protein excretion and hypertension usually normalize by 4–6
wk after onset, persistent microscopic hematuria may persist for 1–2
yr after the initial presentation.
Poststreptococcal glomerulonephritis is quite likely in a child
presenting with acute nephritic syndrome, evidence of recent
streptococcal infection, and a low C3 level.
However, it is important to consider other diagnoses such as
systemic lupus erythematosus and an acute exacerbation of
chronic glomerulonephritis.
Renal biopsy should be considered only in the
presence of acute renal failure, nephrotic syndrome,
absence of evidence of streptococcal infection, or
normal complement levels.
• Management is directed at treating the acute effects of renal
insufficiency and hypertension. Although a 10-day course of
systemic antibiotic therapy with penicillin is recommended to
limit the spread of the nephritogenic organisms, antibiotic
therapy does not affect the natural history of
glomerulonephritis. Sodium restriction,
• Diuretics - usually with intravenous Lasix, and
pharmacotherapy with calcium channel antagonists,
vasodilators, or angiotensin-converting enzyme inhibitors
are standard therapies used to treat hypertension.
o Acute renal failure
o Eclampsia
o DIC syndrome
o Pulmonary edema
• Fortunately, most cases of AGN in children are either
self-limited or amenable to therapy although there
may be devastating complications of the illness
during the acute phase. Less commonly, what begins
as an apparent AGN may presage the development of
a chronic process, which ultimately may progress into
irreversible end-stage renal disease (ESRD).
o Acute GN nephrotic syndrome – favorable prognosis
(recovery – 80-85%);

o Acute GN nephritic syndrome and acute GN

nephrotic syndrome with hematuria and
hypertension – transformation in chronic GN;
develops over several years, and is marked by
progressive inflammation of the glomeruli. As kidneys
fail to filter blood properly, excess fluid and
electrolytes pass from the bloodstream to urine. Even
proteins and blood might pass into the urine.
Presence of blood or protein in urine
Confusion
Drowsiness
Lack of concentration
Lethargy or sleepiness
The patient may start having lowered sensation in limbs and other areas
Easy bleeding
Malaise
High blood pressure
Edema
Less urination than normal
Itching
Muscle twitching
Cramps
Seizures
Nausea or vomiting
Clinical and laboratory remission absence during 6
months;
Two and more exacerbations of pathologic process
during 6 months after the first episode of GN;
Severe leucocyturia;
Decrease functions of renal canaliculi longer than 6
months after the first episode of GN;
Extrarenal symptoms presents more than 1
month;
Combination of hematuria and proteinuria,
recurrence of macrohematuria during 3 months.
Arterial hypertension – in 1 week
Hyperazotemia – in 1.5 weeks
Edemas – 2 weeks
Proteinuria – 4 weeks
Hematuria – 5 weeks
ESR – in 5-6 weeks and more
Acute pyelonephritis
Hereditary nephritis
Interstitial nephritis
Urolithiasis
Renal tuberculosis
Different forms of chronic GN and malignant GN
• Specific treatment for glomerulonephritis will be based on:
◦ child's age, overall health, and medical history
◦ The extent of the disease
◦ child's tolerance for specific medications, procedures, or therapies
◦ Expectations for the course of the disease
• If glomerulonephritis is caused by a streptococcal infection, then treatment
will be focused on curing the infection and treating the symptoms
associated with the infection. Treatment will depend on the underlying
cause.
• Therefore, treatments focus on slowing the progression of the disease
and preventing complications.
• Treatment for glomerulonephritis may include:
◦ Fluid restriction
◦ Decreased protein diet
◦ Decreased salt and potassium diet
◦ Medication, such as:
• Diuretics
• Blood pressure medications
• Phosphate binders. Medications to decrease the amount of the mineral
phosphorus in the blood.
• Immunosuppressive agents
◦ Dialysis. A medical treatment to remove wastes and additional fluid
from the blood after the kidneys have stopped functioning. Dialysis may
be required for short-term or long-term therapy.
 Basic therapy:
● Regimen
● Diet
● Antibacterial therapy
 Symptomatic therapy:
Diuretics:
Indications:
● Severe edemas
● Oliguria
● Hypertension
o Furosemide (Lasix) 1-2mg/kg/d tid in 7.00 and 13.00
o Verospirone (Spironolactone) 2-5mg/kg/d tid in 15.00
21.00
o Best scheme:
• 8.00 – Furosemide
• 10.00 – Hypothiazide (0.5-1mg/kg)
• 16.00 – Verospirone
o Hypotensive drugs (ACE inhibitors):
● Captopril (Capoten), Angiopril (tab.
0,025; 0,05), Tensiominum (tab. 0,05;
0,1), Acetenum (tab. 0,025), Catopil
(tab. 0,025; 0,05; 0,1) – 1-2 mg/kg/day.
orally
Captopril 0.3-1.0 mg/kg/d
 o Chophytol
o Lespenephril
o Carbolen
o Calcium-D3-Nycomed 1t/d during using of
corticosteroids
o Antacids: during using of
corticosteroids
Drugs, which improve (increase) renal blood
circulation:
o Euphylline 0.15 tab in dose 5-7 mg/kg/d
o Sol. Euphyllini 2,4%-10,0 in dose 1.0 ml/year of life
IV
o Pathogenic therapy:
● Antiaggregants
● Anticoagulants
● Glucocorticoids
● Cytostatics;
● Membranostabilizing drugs
● 4-amino-quinolonic drugs
Curantil (Dipiridamol, Persantil) in dose 2-5 mg/kg/d
during 2-3 months – decrease of thrombocytes
aggregation

Trental (Pentoxyphyllin) 1.5-5.0 mg/kg/d

 Direct anticoagulants (heparin 150 –250 IU/kg
subcutaneously 4 times, 2-4-6 weeks):

Indications:
● Hypercoagulation
● DIC syndrome
● Severe edematous syndrome
● Severe hyperlipidemia
 Glucocorticoids Prednisolon 2 mg/kg/d
Full dose during 4-8 weeks, than alternating using (in
day) with gradual drug withdrawal in 6-24 months.
Indications:
● Acute GN nephrotic syndrome
● Exacerbation of nephrotic form of chronic GN
● Sub-acute, malignant GN
Contraindications:
● Severe kidney function disorders in case of chronic GN
● Disposition to azotemia
● Constant hypertension
● Chronic renal failure
Hormone-sensitivity
Hormone-dependence
Hormone-toxicity
o Cytostatics
Indications:
● Hormone-resistance in nephrotic form of chronic GN
● Frequent recurrences of nephrotic form of chronic GN
● Mixed form of chronic GN
Contraindications:
● Chronic renal failure
● Anemia
● Leucopenia
● Thrombocytopenia
Chlorbutin 0.2-0.25 mg/kg/d during
6 weeks, than – ½ of full dose during
6 months
Azathioprin (Cyclophosphamid) 2-4
mg/kg/d during 6 weeks, than - ½ of
full dose during 6 months
Decrease leucocytes level less than
3x109/l
Decrease thrombocyte level less than
100x109/l
Decrease erythrocytes level less than
2.5x1012/l
o Membranostabilizing drugs and
antioxydants:
● Dimephosphon
● Essentiale forte
● Retinoli acetas
● Tocoferoli acetas
 4-amino-quinolonic drugs
Oculist consultations every month because of
cornea and retina lesions
Indications: urinary syndrome without extrarenal
symptoms
Delagil 5-10 mg/kg/d 3-6-12 months
Placvenil 5-10 mg/kg/d 3-6-12 months
Resochin
Cyclosporin C