Systemic lupus erythematosus (SLE)
In systemic lupus erythematosus, renal involvement is characterized by a variety of clinical and morphological forms. Patients often present with recurrent microhematuria or macrohematuria. The pathology may manifest as acute nephritis or overt nephrotic syndrome. Disease progression naturally leads to persistent arterial hypertension and chronic kidney disease.
Histologically, four main variants of glomerular changes are distinguished in lupus nephritis:
- Mesangial lupus nephritis.
- Focal glomerulonephritis.
- Diffuse proliferative glomerulonephritis.
- Diffuse membranous glomerulonephritis.
Henoch-Schönlein purpura
The disease is characterized by a classic clinical triad of extrarenal manifestations. First, there is involvement of the skin and extensor muscles on the upper and lower extremities, as well as the buttocks. Morphologically, subepidermal hemorrhages and necrotizing vasculitis of small dermal vessels are detected in the skin. Second, abdominal syndrome originating from the gastrointestinal tract, including severe abdominal pain, vomiting, and gastrointestinal bleeding. Third, joint involvement in the form of non-migratory arthralgia.
Renal involvement occurs in one-third of patients and presents with macro- and microhematuria, proteinuria, and nephrotic syndrome. The histological picture is variable: ranging from mesangioproliferative changes to membranoproliferative glomerulonephritis. Some adult patients are diagnosed with severe glomerulonephritis with crescent formation. It is important to note: unlike the prominent vascular lesions of the skin and gastrointestinal tract, vasculitis directly in the kidneys occurs extremely rarely.
Fluorescence microscopy is used for diagnostics. A key sign is the deposition of IgA deposits (sometimes along with IgG and the C3 complement fraction) in the glomerular mesangium. This distribution of deposits is completely identical to the picture in IgA nephropathy, which gave rise to the hypothesis that they are the same disease.
Bacterial endocarditis
Renal involvement in bacterial endocarditis is pathogenetically a type of immune complex glomerulonephritis. Glomerular injury is initiated by circulating bacterial antigen-antibody complexes.
The clinical picture is most characteristically marked by hematuria and proteinuria of varying severity. At the same time, the development of classic acute nephritis is atypical for this pathology, and rapidly progressive glomerulonephritis is rare.
Morphological changes in the kidneys directly depend on the severity of the process:
- In mild cases, focal or segmental necrotizing glomerulonephritis develops.
- In more severe cases, diffuse proliferative glomerulonephritis develops.
- With the development of rapidly progressive glomerulonephritis, multiple crescents are observed in the glomeruli.
Briefly: answers to topical questions
What classes of lupus nephritis are distinguished according to the modern ISN/RPS morphological classification?
According to the modern ISN/RPS morphological classification, six classes of lupus nephritis are distinguished.
- Class I — minimal mesangial alterations.
- Class II — mesangial proliferative lupus nephritis.
- Class III — focal lupus nephritis (affecting <50% of glomeruli).
- Class IV — diffuse lupus nephritis (affecting 50% or more of glomeruli).
- Class V — membranous lupus nephritis (thickening of the glomerular basement membrane).
- Class VI — advanced sclerosis lupus nephritis (90% or more sclerotic glomeruli).
What changes are detected in the renal glomeruli in systemic lupus erythematosus according to electron microscopy?
According to electron microscopy, immune deposits and specific inclusions are detected in the renal glomeruli in systemic lupus erythematosus.
- Immune deposits — located in the mesangium and on the glomerular basement membrane (subendothelial, subepithelial, and intramembranous).
- Virus-like inclusions — found in the capillary endothelium.
The localization of deposits in a specific zone of the basement membrane determines the clinical and morphological form of glomerulonephritis.
From which components do cellular crescents form in the glomeruli in rapidly progressive glomerulonephritis?
Cellular crescents in the glomeruli in rapidly progressive glomerulonephritis are formed from inflammatory infiltrate cells and elements of the capsule. The crescents consist of:
- Proliferating epithelium — cells of the parietal layer of Bowman's capsule (podocytes and parietal epithelial cells).
- Macrophages — cells migrating to the focus of inflammation.
- Fibrin strands — protein structures emerging through capillary ruptures.
- Fibroblasts — join the cellular component with further progression of the process.
What specific morphological changes (types of glomerulosclerosis) develop in the kidneys in diabetes mellitus?
In diabetes mellitus, diabetic intracapillary glomerulosclerosis (Kimmelstiel-Wilson syndrome) develops in the kidneys. The following types of microscopic glomerular changes are distinguished:
- Nodular glomerulosclerosis — proliferation of mesangial cells with the production of membrane-like substance and the formation of homogeneous eosinophilic PAS-positive rounded structures.
- Diffuse glomerulosclerosis — diffuse thickening of capillary basement membranes and proliferation of the glomerular mesangium (the most frequent variant).
- Mixed diabetic glomerulosclerosis — a combination of nodular and diffuse changes.
Thickening of the capillary basement membrane is also an obligatory component.
To remember the clinical picture of Henoch–Schönlein purpura, use the rule «SJA + Kidneys»: Skin (vasculitis and hemorrhages), Joints (non-migrating arthralgia), Abdomen (abdominal syndrome). And remember that in 1/3 of patients, this triad is joined by kidney involvement.
Class and exam questions
Which systemic diseases are most frequently accompanied by severe glomerular damage?
Glomerular involvement can accompany many congenital, metabolic, and immunological pathologies. However, it is in systemic lupus erythematosus (SLE) and diabetes mellitus that renal injury is one of the leading clinical manifestations that determine the prognosis.
What is the paradox of vascular lesions in Henoch-Schönlein purpura?
The paradox is that despite the presence of pronounced necrotizing vasculitis of small dermal vessels and gastrointestinal hemorrhages, true vasculitis in the kidneys themselves is extremely rare in this disease.
How can fluorescence microscopy be used to confirm renal involvement in Henoch-Schönlein purpura?
A key diagnostic sign is the detection of immunoglobulin A (IgA) deposits in the glomerular mesangium. Sometimes they precipitate along with IgG and the C3 complement component. This picture is completely identical to isolated IgA nephropathy.
What is the renal morphology in infective endocarditis depending on the severity of the clinical course?
In mild endocarditis, focal or segmental necrotizing glomerulonephritis is observed in the kidneys. In more severe cases, it transforms into diffuse proliferative glomerulonephritis, and with a rapidly progressive course, multiple crescents are formed.
What else to study on this topic
- Pathogenesis of the formation of antigen-antibody immune complexes in bacterial endocarditis.
- Comparative characteristics of Henoch-Schönlein purpura and isolated IgA nephropathy: arguments for a single disease.
- Morphological differences of the four histological variants of lupus nephritis in SLE.
- Mechanisms of cellular crescent formation in rapidly progressive glomerulonephritis.
- Features of renal glomerular involvement in diabetes mellitus (diabetic nephropathy).
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