Diagnosis of acute glomerulonephritis

Clinical examination of acute glomerulonephritis in children

The diagnosis of acute poststreptococcal glomerulonephritis is established on the basis of a history of streptococcal infection (2-4 weeks after tonsillitis or exacerbation of chronic tonsillitis, 3-6 weeks after impetigo), a characteristic clinical picture of the disease with the development of nephritic syndrome and reversible sequential resolution of glomerulonephritis manifestations with restoration of renal function.

Laboratory diagnostics

The diagnosis of acute poststreptococcal glomerulonephritis is confirmed by:

• a decrease in the concentration of the _C3 component of the complement system in the blood with a normal concentration of the _C4 component in the 1st week of the disease;
• increase in the ASLO titer over time (over 2-3 weeks);
• detection of group A beta-hemolytic streptococcus during bacteriological examination of a throat swab.

Instrumental methods

During ultrasound, the kidneys are of normal size, although there may be a slight increase in volume with increased echogenicity.

Radioisotope studies for the diagnosis of poststreptococcal glomerulonephritis are uninformative and reflect only the degree of impairment of the functional state of the kidneys.

In the event of development of manifestations not typical for poststreptococcal glomerulonephritis, a puncture biopsy of the kidneys is performed in order to determine the morphological variant of glomerulopathy, prescribe adequate treatment and assess the prognosis of the disease. Indications for kidney biopsy:

• decrease in glomerular filtration rate (GFR) to less than 50% of the age norm;
• prolonged decrease in the concentration of the _C3 component of the complement system in the blood, persisting for more than 3 months;
• persistent macrohematuria for more than 3 months;
• development of nephrotic syndrome.

Morphologically, acute poststreptococcal glomerulonephritis is an exudative-proliferative endocapillary glomerulonephritis with proliferation of endothelial and mesangial cells. In some cases, extracapillary crescents are observed in the Bowman-Shumlyansky capsule. Electron microscopy (EM) reveals deposits of immune complexes subendothelially, subepithelially, and in the mesangium. Immunofluorescence reveals granular luminescence of IgG and C3 _- component of complement, localized along the walls of glomerular capillaries, more often above the mesangial zone.

Diagnostic criteria for acute glomerulonephritis in children:

• presence of previous streptococcal infection;
• latent period after infection is 2-3 weeks;
• acute onset, characteristic clinical and laboratory picture of nephritic syndrome (edema, hypertension, hematuria);
• short-term renal dysfunction in the acute period;
• detection of CIC in the blood serum, low levels of complement fraction C3;
• endocapillary diffuse proliferative glomerulonephritis, “humps” on the epithelial side of the capillary basement membrane (IgG and C3 complement fraction).

Criteria for the activity of acute glomerulonephritis:

• increased titers of streptococcal antibodies (antistreptolysin, antistreptokinase);
• decrease in complement fractions C3, C5; increase in the level of CIC;
• increased levels of C-reactive protein; leukocytosis, neutrophilia, increased ESR in the blood;
• activation of the hemostasis system (platelet hyperaggregation, hypercoagulation shifts);
• persistent lymphocyturia;
• enzymuria - excretion of transaminidase in urine;
• increased level of urinary excretion of chemotactic factors.

Possible complications of the acute phase of post-streptococcal nephritis:

• acute renal failure, anuria is rare;
• renal eclampsia in older children - high arterial hypertension, increasing headache, nausea, vomiting, bradycardia, followed by motor restlessness, loss of consciousness, tonic and clonic convulsions, coma; occurs more often in adolescence.
• Acute heart failure and pulmonary edema are rare in children.

Differential diagnostics

IgA nephropathy (Berger's disease)

Characterized by torpid microhematuria and persistent macrohematuria against the background of acute respiratory viral infection. Differential diagnostics can only be performed by renal biopsy with light microscopy and immunofluorescence. IgA nephropathy is characterized by granular fixation of IgA deposits in the mesangium against the background of mesangiocyte proliferation.

Membranoproliferative glomerulonephritis (MPGN) (mesangiocapillary)

It occurs with nephritic syndrome, but is accompanied by more pronounced edema, arterial hypertension and proteinuria, as well as a significant increase in the concentration of creatinine in the blood. With MPGN, a long-term (>6 weeks) decrease in the concentration of the C3 _component of complement in the blood is noted, in contrast to the transient decrease in the C3 _component of complement in acute poststreptococcal GN. To diagnose MPGN, a nephrobiopsy is necessary.

Thin basement membrane disease

It is characterized by torpid microhematuria of a familial nature against the background of preserved renal functions. Biopsy reveals typical changes in the renal tissue in the form of diffuse uniform thinning of the glomerular basement membrane (<200-250 nm in more than 50% of glomerular capillaries). In case of extrarenal manifestations of pathology, it is necessary to exclude kidney damage against the background of systemic diseases and hemorrhagic vasculitis. To exclude systemic pathology, blood is examined for the presence of markers: LE cells, antibodies to DNA, ANF, lupus anticoagulant, antineutrophil cytoplasmic antibodies (ANCA), antiphospholipid and anticardiolipin antibodies. The concentration of cryoprecipitates is also determined.

Hereditary nephritis

It may first appear after an acute respiratory viral infection or streptococcal infection, including in the form of macrohematuria. However, with hereditary nephritis, the development of nephritic syndrome is not typical, and hematuria is persistent. In addition, families of patients usually have similar kidney diseases, cases of chronic renal failure, and sensorineural hearing loss. The most common type of inheritance of hereditary nephritis is the X-linked dominant type, autosomal recessive and autosomal dominant variants are less common. A presumptive diagnosis is made based on a pedigree analysis. To diagnose hereditary nephritis, 3 of 5 signs must be present:

• hematuria in several family members;
• patients with chronic renal failure in the family;
• thinning and/or disruption of the structure (splitting) of the glomerular basement membrane (GBM) during electron microscopy of a nephrobiopsy specimen;
• bilateral sensorineural hearing loss determined by audiometry;
• congenital visual pathology in the form of anterior lenticonus.

In hereditary nephritis, especially in boys, proteinuria progresses during the disease, arterial hypertension appears and the SCF decreases. This is not typical for acute poststreptococcal glomerulonephritis, which proceeds with the sequential disappearance of the urinary syndrome and restoration of kidney function.

The detection of a mutation in the type 4 collagen gene (COL4A3 and COL4A4) confirms the diagnosis of hereditary nephritis with the corresponding symptom complex of the disease.

Rapidly progressive glomerulonephritis

In the development of renal failure against the background of acute poststreptococcal glomerulonephritis, it is necessary to exclude rapidly progressive glomerulonephritis (RPGN), which is manifested by a progressive increase in the concentration of creatinine in the blood over a short period of time and nephrotic syndrome. In acute poststreptococcal glomerulonephritis, acute renal failure is short-term and renal function is quickly restored. RPGN associated with microscopic polyangiitis is characterized by signs of systemic pathology and ANCA in the blood.

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