Diagnosis of acute glomerulonephritis

Clinical examination for acute glomerulonephritis in children

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

Laboratory diagnostics

The diagnosis of acute poststreptococcal glomerulonephritis is confirmed by:

• decrease in the concentration of the C ₃ -component of the complement system in the blood at a normal concentration of the C _4- component on the 1st week of the disease;
• an increase in the ASLO titer in dynamics (within 2-3 weeks);
• detection of a smear from the throat of beta-hemolytic group A streptococcus in bacteriological studies.

Instrumental methods

With ultrasound of the kidneys of normal size, there may be a slight increase in volume with an increase in echogenicity.

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

When developing non-typical for poststreptococcal glomerulonephritis, the manifestations perform a puncture biopsy of the kidneys in order to determine the morphological variant of glomerulopathy, the appointment of adequate treatment and the evaluation of the disease prognosis. Indications for kidney biopsy:

• decrease in the glomerular filtration rate (GFR) is less than 50% of the age norm;
• long-term decrease in the concentration of the C ₃ -component of the complement system in the blood, which lasts 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 semiluns are observed in the Bowman-Shumlyansky capsule. With the electron microscopy (EM) subendothelial, subepithelial and mesangium, the deposits of immune complexes are found. By immunofluorescence detected granular glow IgG and C ₃ -component complement localized along glomerular capillary walls, often over mesangial area.

Criteria for diagnosis of acute glomerulonephritis in children:

• presence of a prior streptococcal infection;
• latent period after infection 2-3 weeks;
• acute onset, characteristic clinical and laboratory picture of nephritic syndrome (edema, hypertension, hematuria);
• short-term renal dysfunction in acute period;
• detection in the blood serum of the CEC, low level of the NW of the complement fraction;
• endocapillary diffuse proliferative glomerulonephritis, "humps" on the epithelial side of the basement membrane of the capillaries (IgG and S3 complement fraction).

Criteria for the activity of acute glomerulonephritis:

• increased titres of streptococcal antibodies (anti-streptolysin, antistreptokinase);
• reduction of complement fractions of S3, C5; raising the level of the CEC;
• increase in the content of C-reactive protein; in the blood leukocytosis, neutrophilia, increased ESR;
• activation of the hemostatic system (platelet hyperaggregation, hypercoagulable shifts);
• resistant lymphocyturia;
• fermentia - urinary excretion of transaminidase;
• increased 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, then comes motor anxiety, loss of consciousness, tonic and clonic convulsions, a coma develops; occurs more often in adolescence.
• Acute congestive heart failure and pulmonary edema in children are rare.

Differential diagnostics

IgA nephropathy (Berger's disease)

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

Membranoproliferative glomerulonephritis (MPGH) (mesangiocapillary)

It flows with nephritic syndrome, but is accompanied by more pronounced edema, arterial hypertension and proteinuria, and a significant increase in the concentration of creatinine in the blood. For IGCP, there is a long (> 6 weeks) decrease in the concentration of the C ₃ complement component in the blood, in contrast to the transient decrease in the C ₃ complement component for acute poststreptococcal GH. For the diagnosis of IGOS, nephrobiopsy is necessary.

Disease of thin basal membranes

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

Hereditary nephritis

It may first appear after SARS or streptococcal infection, including in the form of macrohematuria. However, with hereditary nephritis is not typical development of nephritic syndrome, and hematuria is of a persistent nature. In addition, families of patients usually have the same type of kidney disease, cases of chronic renal failure, neurosensory hearing loss. The most common X-linked dominant type inheritance of hereditary nephritis, autosomal recessive and autosomal dominant variants are less common. Presumptive diagnosis is based on the analysis of the pedigree. For the diagnosis of hereditary nephritis, 3 of 5 symptoms are necessary:

• hematuria among several family members;
• patients with chronic kidney failure in the family;
• thinning and / or disruption of the structure (cleavage) of the glomerular basement membrane (GBM) with electron microscopy of the nephrobioptate;
• bilateral neurosensory hearing loss, determined with audiometry;
• Congenital pathology of vision in the form of anterior lenticone.

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

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

Rapidly progressive glomerulonephritis

With the development of renal failure against a background of acute poststreptococcal glomerulonephritis, it is necessary to exclude the rapidly progressive glomerulonephritis (PGGN), manifested by a progressive increase in the creatinine concentration in the blood in a short period of time and nephrotic syndrome. In acute poststreptococcal glomerulonephritis, acute renal failure has a short-term character and renal function is rapidly restored. For TGP associated with microscopic polyangiitis, features of systemic pathology and ANCA in the blood are characteristic.

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