CHRONIC GLOMERULONEPHRITIS
Chronic GN — heterogeneous group of chronic glomerulopathies, with
predominant immune complex mechanism of glomerular lesion, different clinical
and morphological presentation, course and outcome.
Etiology: rarely develops as evolution of APGN. More common is a primary
chronic course, i.e. without acute attack.
Four main groups of etiological factors are described:
– infections (bacterial, viral);
– mechanic and physical factors (traumas, cold weather, sun exposure);
– allergic toxins (food, chemical substances, drug abuse, medicines);
– vaccines.
Morphological classification.
Not proliferative (non inflammatory):
– minimal changes nephropathy;
– membranous nephropathy;
– focal-segmental glomerulosclerosis.
Proliferative (inflammatory):
– mesangial proliferative GN;
– mesangiocapillary GN;
– fibroplastic GN.
Minimal changes nephropathy (lipoid nephrosis, small foot processes of
podocytes disease, idiopathic nephrotic syndrome, minimal changes nephrotic
syndrome) — the leading cause of nephrotic syndrome in childhood.
Boys : girls ratio 2 : 1.
Onset after upper respiratory tract infection, allergic reaction is common.
Atopy can be predisposing factor. Nephrotic syndrome is usually steroid sensitive,
arterial hypertension and hematuria are not characteristic for this condition.
Although there can be relapses of nephrotic syndrome, kidney function however
remains normal for a long time. In general, prognosis is favorable.
Morphology.
Light microscopy: glomeruli appear normal (figure 7).
Fig. 7. Light microscopy — normal glomerulus. H&E stain, ×400
, Immunofluorescence: absence of immune deposits.
Electron microscopy: normal podocytes (figure 8, a) and diffuse effacement
of podocytes foot processes (figure 8, b).
a b
Fig. 8. Electron microscopy:
а — normal podocytes foot processes; b — diffuse effacement of podocytes foot processes
Nephrotic syndrome includes 4 main criteria:
– massive proteinuria, mainly albuminuria (over 50 mg/kg/day);
– low serum protein level (low albumin, increased α2- and decreased γ-
globulins);
– high blood cholesterol level (> 5,2 mmol/l);
– severe edema (the consequence of reduced oncotic pressure due to low
serum protein).
Pathology:
– minimal changes nephrotic syndrome;
– focal-segmental glomerulosclerosis;
– membranous GN;
– mesangiocapillary GN.
Treatment:
1. Standard protocol — oral prednisolone 60 mg/m2/24 h (2 mg/kg, max
80 mg per day), for 4 weeks (up to 6 weeks), than switch to alternate-day
administration:
– 60 mg/m2/48 h — 8 weeks;
– 45 mg/m2/48 h — 2 weeks;
– 30 mg/m2/48h — 2 weeks;
– 15 mg/m2/48h — 2 weeks.
Treatment duration from 4 to 5 months.
2. Proton pump inhibitors — omeprazole 1 mg/kg/day for children older than
5 years, almagel, gefal — for younger children.
3. Calcium, vit. D (osteoporosis prophylaxis).
4. Albumin i.v. (if serum albumin level is lower 20 g/l and or ascites is
present).
Chronic GN — heterogeneous group of chronic glomerulopathies, with
predominant immune complex mechanism of glomerular lesion, different clinical
and morphological presentation, course and outcome.
Etiology: rarely develops as evolution of APGN. More common is a primary
chronic course, i.e. without acute attack.
Four main groups of etiological factors are described:
– infections (bacterial, viral);
– mechanic and physical factors (traumas, cold weather, sun exposure);
– allergic toxins (food, chemical substances, drug abuse, medicines);
– vaccines.
Morphological classification.
Not proliferative (non inflammatory):
– minimal changes nephropathy;
– membranous nephropathy;
– focal-segmental glomerulosclerosis.
Proliferative (inflammatory):
– mesangial proliferative GN;
– mesangiocapillary GN;
– fibroplastic GN.
Minimal changes nephropathy (lipoid nephrosis, small foot processes of
podocytes disease, idiopathic nephrotic syndrome, minimal changes nephrotic
syndrome) — the leading cause of nephrotic syndrome in childhood.
Boys : girls ratio 2 : 1.
Onset after upper respiratory tract infection, allergic reaction is common.
Atopy can be predisposing factor. Nephrotic syndrome is usually steroid sensitive,
arterial hypertension and hematuria are not characteristic for this condition.
Although there can be relapses of nephrotic syndrome, kidney function however
remains normal for a long time. In general, prognosis is favorable.
Morphology.
Light microscopy: glomeruli appear normal (figure 7).
Fig. 7. Light microscopy — normal glomerulus. H&E stain, ×400
, Immunofluorescence: absence of immune deposits.
Electron microscopy: normal podocytes (figure 8, a) and diffuse effacement
of podocytes foot processes (figure 8, b).
a b
Fig. 8. Electron microscopy:
а — normal podocytes foot processes; b — diffuse effacement of podocytes foot processes
Nephrotic syndrome includes 4 main criteria:
– massive proteinuria, mainly albuminuria (over 50 mg/kg/day);
– low serum protein level (low albumin, increased α2- and decreased γ-
globulins);
– high blood cholesterol level (> 5,2 mmol/l);
– severe edema (the consequence of reduced oncotic pressure due to low
serum protein).
Pathology:
– minimal changes nephrotic syndrome;
– focal-segmental glomerulosclerosis;
– membranous GN;
– mesangiocapillary GN.
Treatment:
1. Standard protocol — oral prednisolone 60 mg/m2/24 h (2 mg/kg, max
80 mg per day), for 4 weeks (up to 6 weeks), than switch to alternate-day
administration:
– 60 mg/m2/48 h — 8 weeks;
– 45 mg/m2/48 h — 2 weeks;
– 30 mg/m2/48h — 2 weeks;
– 15 mg/m2/48h — 2 weeks.
Treatment duration from 4 to 5 months.
2. Proton pump inhibitors — omeprazole 1 mg/kg/day for children older than
5 years, almagel, gefal — for younger children.
3. Calcium, vit. D (osteoporosis prophylaxis).
4. Albumin i.v. (if serum albumin level is lower 20 g/l and or ascites is
present).
