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Mesangiocapillary (membranoproliferative) glomerulonephritis
Last reviewed: 04.07.2025
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Epidemiology
Morphologically, the proliferation of mesangial cells is characteristic, creating lobularity of the glomeruli ("lobular nephritis"), and thickening or double-contour of the capillary wall - due to penetration into them (interposition) of mesangial cells. According to the location and nature of electron-dense deposits, three (sometimes four) types of mesangiocapillary nephritis are distinguished, which are identical clinically and differ slightly in laboratory data and transplantation results. Types I and II are more common. In type I, immune deposits are localized under the endothelium and in the mesangial region of the glomeruli (subendothelial or classic mesangiocapillary glomerulonephritis), in type II ("dense deposit diseases") special osmiophilic electron-dense deposits of unclear nature are located inside the basement membrane.
The incidence among other types of glomerulonephritis in the 1970s was 10-20%; in recent years, mesangiocapillary glomerulonephritis has become less common in Europe and North America (5-6%).
Causes mesangiocapillary (membranoproliferative) glomerulonephritis
The causes of mesangiocapillary glomerulonephritis are divided into viral and bacterial infections. Often, mesangiocapillary glomerulonephritis type I develops with HBV infection, but recently special attention has been paid to the relationship of mesangiocapillary glomerulonephritis type I with HCV. Cryoglobulins are detected in 50-60% of patients with mesangiocapillary glomerulonephritis type I infected with HCV. Cases associated with streptococcal infection, infective endocarditis, as well as with the development of mesangiocapillary glomerulonephritis in schistosomiasis, pulmonary tuberculosis, malaria have been described.
Along with the idiopathic form, mesangiocapillary glomerulonephritis is detected in systemic lupus erythematosus, mixed cryoglobulinemia, Sjogren's syndrome, nonspecific ulcerative colitis, sarcoidosis, lymphomas, neoplasms, etc.
Genetic factors may play a role in the development of mesangiocapillary glomerulonephritis. Familial cases of the disease in siblings and in several generations have been described.
A characteristic feature of mesangiocapillary glomerulonephritis is hypocomplementemia with a decrease in the level of C3 and/or C4 components, which is especially often detected in type II. Hypocomplementemia is caused by a violation of the synthesis and catabolism of complement, as well as the presence in the blood serum of a special immunoglobulin - C3-nephritic factor, directed against C3-convertase.
Mesangiocapillary glomerulonephritis (usually type II) is sometimes combined with partial lipodystrophy (a disease that also occurs with hypocomplementemia).
Young men and children (younger age for type I) are slightly more likely to get sick. It is rare in the elderly.
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Symptoms mesangiocapillary (membranoproliferative) glomerulonephritis
The symptoms of mesangiocapillary (membranoproliferative) glomerulonephritis are the same for all morphological variants: hematuria is characteristic (in 10-20% transient macrohematuria), pronounced proteinuria and nephrotic syndrome (often with elements of acute nephritic syndrome), decreased renal function. Mesangiocapillary glomerulonephritis is the cause of 10% of cases of nephrotic syndrome in adults and 5% in children. Arterial hypertension is observed frequently, sometimes it is severe.
The combination of nephrotic syndrome with hematuria and hypertension should always raise concerns about the possibility of mesangiocapillary nephritis. Anemia is possible (associated with the presence of activated complement on the surface of red blood cells). In type II, a peculiar retinopathy is described (diffuse bilateral symmetrical yellow lesions).
Mesangiocapillary (membranoproliferative) glomerulonephritis often begins with acute nephritic syndrome with sudden development of hematuria, severe proteinuria, edema and hypertension; in this case, acute nephritis is erroneously diagnosed. In almost 1/3 of patients, the disease may manifest itself as rapidly progressing renal failure with the presence of "crescents" in the renal biopsy.
Due to the frequent combination of mesangiocapillary glomerulonephritis with infections and systemic diseases, a thorough search for concomitant pathology is necessary in each case.
The course of the process is steadily progressive, spontaneous remissions are rare. Mesangiocapillary glomerulonephritis is one of the most unfavorable forms; in the absence of treatment, terminal renal failure develops after 10 years in almost 50%, after 20 years - in 90% of patients. According to J.St. Cameron et al. (1983), 10-year survival of patients with nephrotic syndrome was 40%, patients without nephrotic syndrome - 85%. A special feature of the course of mesangiocapillary glomerulonephritis is the "stepwise" progression and relatively sudden deterioration of renal function in some patients. Clinically poor prognostic signs are the presence of nephrotic syndrome, diastolic hypertension, decreased renal function and the detection of serological signs of HCV and HBV infection. Complement levels have no prognostic value. Mesangiocapillary glomerulonephritis, especially type II, often recurs in the transplant.
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Treatment mesangiocapillary (membranoproliferative) glomerulonephritis
Treatment of mesangiocapillary glomerulonephritis is still insufficiently developed. A number of proposed approaches are not sufficiently substantiated and are considered controversial by many authors. Unfavorable prognostic signs are the presence of nephrotic syndrome and renal dysfunction from the very beginning of the disease. In patients with nephrotic syndrome, 10-year renal survival is no more than 50%.
It is necessary to remember about the possibility of secondary forms of mesangiocapillary glomerulonephritis, which require other therapeutic approaches: this is mesangiocapillary glomerulonephritis in chronic infections (including HBV and HCV viral infections), cryoglobulinemia, and various forms of plasma cell dyscrasias. Antibacterial therapy, alpha interferon, plasmapheresis or chemotherapy may be indicated for these diseases.
In the remaining patients, if idiopathic mesangiocapillary glomerulonephritis is confirmed, the following approaches are recommended.
Treatment of mesangiocapillary glomerulonephritis without nephrotic syndrome
Patients with proteinuria less than 3 g/day and normal CF do not require active treatment; in arterial hypertension, strict control of blood pressure is important, preferably with ACE inhibitors; in case of high proteinuria and decreasing CF, prednisolone and cytostatics or a combination of aspirin and dipyridamole can be used.
Treatment of mesangiocapillary glomerulonephritis with nephrotic syndrome
Corticosteroids / corticosteroids and cytostatics
At the first attack of nephrotic syndrome and normal renal function, corticosteroids can be started [1 mg/(kg x day) for 2 months]. However, the results are better in children who have accumulated the most experience with long-term steroid therapy.
When corticosteroids are combined with cytostatics, the results are better. R. Faedda et al. (1994) in the treatment of 19 patients with glucocorticoids (initially with methylprednisolone pulses, then oral prednisolone) and cyclophosphamide for an average of 10 years with subsequent observation (7.5 years) noted remission in 15 of 19 patients (while 40% of patients developed gonadal failure); some patients had relapses, which were also inferior to combined therapy. In our group of 28 patients with mesangiocapillary glomerulonephritis who received cytostatics (cyclophosphamide, chlorbutin, or azathioprine) in combination with prednisolone, the 10-year renal survival was 71%, which is significantly higher than is usually observed in untreated nephrotics with mesangiocapillary glomerulonephritis. In another study of 9 seriously ill patients with mesangiocapillary glomerulonephritis treated with cyclophosphamide pulses, the best results (100% renal survival after 7 years) were recorded in 4 patients with a high morphological activity index (>4) who received at least 6 g of the drug over 6 months. At the same time, in 5 patients with the same activity index, but less actively treated (who received less than 6 g of the drug), the renal survival was less than 50%.
In this regard, in case of severe nephrotic syndrome or nephrotic syndrome with declining renal function, it is better to immediately start with a combination of corticosteroids and cytostatics (the latter can be in the form of cyclophosphamide pulses).
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Cytostatics, anticoagulants and antiplatelet agents
In uncontrolled studies, a combination of cytostatics, anticoagulants, and antiplatelet agents gave good results. In a controlled study that assessed the effect of cyclophosphamide, dipyridamole, and warfarin, no significant effect on proteinuria or progression of renal failure was found. In another controlled study in patients with type I mesangiocapillary glomerulonephritis, dipyridamole (225 mg/day) and aspirin (975 mg/day) slowed the rate of progression during the first 4 years, but by the 10th year these differences between treated and untreated patients were erased (renal survival, respectively, 49 and 41%).
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Cyclosporine
Data on the use of cyclosporine in mesangiocapillary glomerulonephritis are very limited. In uncontrolled studies, cyclosporine [4-6 mg/(kg x day)] in combination with low doses of prednisolone caused a moderate decrease in proteinuria. However, due to potential nephrotoxicity and increased hypertension, cyclosporine is currently not widely used in patients with mesangiocapillary glomerulonephritis.
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