Symptoms of chronic glomerulonephritis

Chronic glomerulonephritis most often has a primarily chronic course, less often it occurs as a consequence of acute glomerulonephritis. Glomerulonephritis is characterized by a triad of syndromes: urinary, edematous (nephritic or nephrotic type) and arterial hypertension. Depending on the combination of these 3 main syndromes, the following clinical forms of chronic glomerulonephritis are distinguished: hematuric, nephrotic and mixed.

Nephrotic syndrome is a symptom complex characterized by:

• proteinuria more than 3 g per day (50 mg/kg per day);
• hypoalbuminemia less than 25 g/l;
• dysproteinemia (decreased levels of gamma globulins, increased levels of alpha ₂ globulins);
• hypercholesterolemia and hyperlipidemia;
• swelling.

Features of the clinical picture and course of various morphological variants of chronic glomerulonephritis

Minimal changes are the most common cause of nephrotic syndrome in children (in boys 2 times more often than in girls). The disease often occurs after an upper respiratory tract infection, allergic reactions, and is combined with atopic diseases. NSMI is characterized by the development of SNNS and the absence of arterial hypertension, hematuria; kidney function remains intact for a long time.

FSGS is usually characterized by the development of SRNS in more than 80% of patients. In less than 1/3 of patients, the disease is accompanied by microhematuria and arterial hypertension.

In most patients, membranous nephropathy manifests itself as nephrotic syndrome, less often persistent proteinuria, microhematuria and arterial hypertension.

MPGN in children, unlike in adults, is usually primary. Clinical manifestations of MPGN include the development of nephritic syndrome at the onset of the disease with subsequent development of nephrotic syndrome, often with hematuria and arterial hypertension. A decrease in the concentration of C3 _and C4 _complement fractions in the blood is characteristic.

MzPGN is manifested by persistent hematuria, increasing to the degree of macrohematuria against the background of acute respiratory viral infections, and is characterized by slowly progressive treatment.

IgA nephropathy. Its clinical manifestations can vary widely from symptomatic torpid isolated microhematuria (in most cases) to the development of RPGN with the formation of chronic renal failure (extremely rare). With IgA nephropathy, 5 clinical syndromes may develop:

• asymptomatic microhematuria and minor proteinuria are the most common manifestations of the disease, they are detected in 62% of patients;
• episodes of macrohematuria, mainly against the background of or immediately after acute respiratory viral infections, occurring in 27% of patients;
• acute nephritic syndrome in the form of hematuria, proteinuria and arterial hypertension, it is typical for 12% of patients;
• nephrotic syndrome - observed in 10-12% of patients;
• In rare cases, IgA nephropathy may debut as RPGN with severe proteinuria, arterial hypertension, and decreased SCF.

RPGN. The leading syndrome is a rapid decline in renal function (doubling of the initial blood creatinine level within a period of several weeks to 3 months), accompanied by nephrotic syndrome and/or proteinuria, hematuria and arterial hypertension.

Often, RPGN is a manifestation of systemic pathology (systemic lupus erythematosus, systemic vasculitis, essential mixed cryoglobulinemia, etc.). The spectrum of RPGN forms includes glomerulonephritis associated with antibodies to GBM (Goodpasture's syndrome - with the development of hemorrhagic alveolitis with pulmonary hemorrhage and respiratory failure) and with ANCA (Wegener's granulomatosis, nodular periarteritis, microscopic polyangiitis and other vasculitis).

Criteria of activity and signs of exacerbation of chronic glomerulonephritis.

• edema with increasing proteinuria;
• hypertension;
• hematuria (during an exacerbation, an increase in erythrocyturia by 10 times or more compared to a long-standing stable level);
• rapid decline in kidney function;
• persistent lymphocyturia;
• dysproteinuria with increased ESR, hypercoagulation;
• detection of organ-specific enzymes in urine;
• increase in anti-renal antibodies;
• IL-8 as a chemotactic factor for neutrophils and their migration to the site of inflammation.

The period of clinical and laboratory remission of chronic glomerulonephritis is determined by the absence of clinical symptoms of the disease, normalization of biochemical blood parameters, restoration of renal function and normalization or minor changes in urine tests.

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Factors in the progression of chronic glomerulonephritis.

• Age (12-14 years).
• Frequency of relapses of nephrotic syndrome.
• Combination of nephrotic syndrome and hypertension.
• Adjacent tubulointerstitial lesion.
• Damaging effect of antibodies to the glomerular basement membrane of the kidneys.
• Autoimmune variant of chronic glomerulonephritis.
• Persistence of the etiological factor, constant supply of antigen.
• Inefficiency, insufficiency of systemic and local phagocytosis.
• Lymphocyte cytotoxicity.
• Activation of the hemostasis system.
• The damaging effect of proteinuria on the tubular apparatus and interstitium of the kidney.
• Uncontrolled hypertension.
• Lipid metabolism disorder.
• Hyperfiltration as a cause of renal tissue sclerosis.
• Indicators of tubulointerstitial damage (decreased optical density of urine; osmotic concentration functions; presence of hypertrophied renal pyramids; resistance to pathogenetic therapy; increased excretion of fibronectin in urine).

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