Symptoms of chronic glomerulonephritis

Chronic glomerulonephritis most often has a primary chronic course, rarely 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 symptomatic complex characterized by:

• proteinuria more than 3 g per day (50 mg / kg per day);
• hypoalbuminemia less than 25 g / l;
• dysproteinemia (decrease in the level of y-globulins, increase in the level 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 (boys are 2 times more likely than girls). The disease often occurs after infection of the upper respiratory tract, allergic reactions, combined with atopic diseases. NSMI is characterized by the development of SSHNS and the absence of arterial hypertension, hematuria; the kidney function remains intact for a long time.

FSSS, as a rule, is characterized by the development of SRNS in more than 80% of patients. Less than in 1/3 of patients, the disease is accompanied by microhematuria and arterial hypertension.

Membranous nephropathy in most patients manifests a nephrotic syndrome, less often persistent proteinuria, microhematuria and arterial hypertension.

IGNA in children, as opposed to adults, is usually the primary. Clinical manifestations of IGOS include the development of nephritic syndrome in the onset of the disease with the subsequent development of nephrotic syndrome, often with hematuria and hypertension. Characteristic decrease in the concentration of C ₃ - and C ₄ -fractions of complement in the blood.

MZPGN is manifested by persistent hematuria, which increases to the degree of macrohematuria against the background of acute respiratory viral infection, is characterized by a slow progressing course.

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

• asymptomatic microhematuria and insignificant proteinuria - the most common manifestations of the disease, they are detected in 62% of patients;
• episodes of macrohematuria mainly on the background or immediately after ARVI, 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 - noted in 10-12% of patients;
• In rare cases, IgA-nephropathy can make its debut in the form of GIPH with pronounced proteinuria, arterial hypertension, and a decrease in GFR.

The BCPA. The leading syndrome is a rapid decrease in renal function (doubling the input level of blood creatinine in the period from several weeks to 3 months), accompanied by nephrotic syndrome and / or proteinuria, hematuria and hypertension.

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

Criteria of activity and signs of exacerbation of chronic glomerulonephritis.

• swelling with increasing proteinuria;
• hypertension;
• hematuria (exacerbation of erythrocyturia is 10 times or more in comparison with the long-term stable level);
• rapid decrease in kidney function;
• resistant lymphocyturia;
• disproteinuria with an increase in ESR, hypercoagulation;
• detection in the urine of organ-specific enzymes;
• growth of contra-antibodies;
• IL-8 as a chemotactic factor for neutrophils and their migration to the inflammatory focus.

The period of clinico-laboratory remission of chronic glomerulonephritis is established in the absence of clinical symptoms of the disease, normalization of biochemical parameters of blood, restoration of renal functions and normalization or minor changes in urinalysis.

[1], [2], [3], [4], [5], [6]

Factors of progression of chronic glomerulonephritis.

• Age (12-14 years).
• Frequency of recurrences of nephrotic syndrome.
• Combination of nephrotic syndrome and hypertension.
• Attachment of tubulointerstitial lesion.
• Damaging effect of antibodies to the basal membrane of the glomerular buds.
• Autoimmune variant of chronic glomerulonephritis.
• Persistence of the etiologic factor, a constant supply of antigen.
• Inefficiency, insufficiency of systemic and local phagocytosis.
• Cytotoxicity of lymphocytes.
• Activation of the hemostasis system.
• Damaging effect of proteinuria on the tubular apparatus and interstitium of the kidney.
• Uncontrolled hypertension.
• Violation of lipid metabolism.
• Hyperfiltration as a cause of sclerosis of the renal tissue.
• Indicators of tubulointerstitial lesion (decrease in the optical density of urine, osmotic concentration function, the presence of hypertrophic renal pyramids, resistance to pathogenetic therapy, increased urinary excretion of fibronectin).

[7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17]