Etiology and development dynamics
Nephrosclerosis is a natural outcome of various glomerulopathies. The classic dynamics of the pathological process is as follows: acute glomerulonephritis transitions into a chronic form, which eventually culminates in nephrosclerosis.
The rate of progression directly depends on the primary disease:
- Rapid development: characteristic of focal segmental glomerulosclerosis and rapidly progressive glomerulonephritis (if the patient survives the acute episode).
- Slow development: observed in membranous nephropathy, IgA nephropathy, and membranoproliferative glomerulonephritis.
- Asymptomatic course: sometimes preceding glomerulonephritis is latent, making it impossible to establish its specific form, and the disease manifests only at the uremic stage.
Benign nephrosclerosis
Arteriolosclerotic (benign) nephrosclerosis develops against the background of benign arterial hypertension. The pathogenesis is based on arteriolar hyalinosis, which causes microfocal parenchymal ischemia and subsequent sclerosis.
Macroscopic picture: the kidneys retain normal size or are moderately reduced (weight decreases to 110–130 g). A mildly granular surface forms under the capsule. Cross-section reveals narrowing of the cortical layer to 0.5–0.6 cm (normal is 0.7–0.8 cm).
Microscopic changes:
- Vessels: narrowing of the lumen of small arteries and arterioles due to thickening and hyalinosis of their walls. In larger vessels (interlobular and arcuate arteries), fibroelastic hyperplasia occurs—doubling of the elastic lamina and proliferation of fibrous tissue in the tunica media.
- Parenchyma: foci of ischemic tubular atrophy alternate with areas of interstitial fibrosis.
- Glomeruli: collapse of the glomerular basement membrane, collagen deposition within the capsule, and periglomerular or total sclerosis are observed.
Malignant nephrosclerosis
This form is associated with the malignant (accelerated) phase of arterial hypertension. It is rare (in 1–5% of individuals with high BP), most commonly affecting young men. The mechanism of development is associated with high levels of renin, angiotensin, and aldosterone. Hyperreninemia causes generalized vasospasm, a sharp jump in blood pressure, and tissue necrosis.
Macroscopically: kidney sizes vary. A specific sign is small petechial hemorrhages on the cortical surface, resembling "flea bites". They occur due to ruptures of arterioles or glomerular capillaries.
Microscopically, severe damage to the vascular bed is revealed:
- Fibrinoid necrosis of arterioles: vessel walls are impregnated with fibrin (eosinophilic granular changes), often accompanied by an inflammatory infiltrate, indicating necrotizing arteriolitis.
- Concentric arteriolitis: "onion-skin" thickening of the intima of interlobular arteries due to concentric proliferation of smooth muscle cells and collagen.
- Necrotizing glomerulonephritis: glomeruli are necrotic, capillaries are thrombosed, and neutrophil infiltration is present.
Extrarenal manifestations and dialysis changes
Patients with nephrosclerosis develop systemic complications due to uremia. The cardiovascular system (uremic pericarditis, left ventricular hypertrophy), gastrointestinal tract (uremic gastroenteritis), respiratory system (uremic pneumonitis), and bone-endocrine system (secondary hyperparathyroidism, nephrocalcinosis, renal osteodystrophy) are affected.
If a patient undergoes long-term hemodialysis, specific changes develop in the kidneys that are unrelated to the primary disease:
- Thickening of the arterial intima due to an accumulation of smooth muscle cells and proteoglycans.
- Calcification of glomeruli and tubular basement membranes.
- Pronounced crystalluria (calcium oxalate precipitation).
- Development of acquired cystic disease.
- Increased risk of renal adenomas and adenocarcinomas.
Briefly: answers to topical questions
What is the difference between a primary and a secondary contracted kidney in terms of etiology and pathogenesis?
- Primary contracted kidney (arteriolosclerotic nephrosclerosis, benign nephrosclerosis) is the outcome of benign essential hypertension (renal form), where the contraction process is primary relative to vascular pathology. The morphological substrate consists of arteriolosclerosis of the afferent glomerular vessels followed by glomerulosclerosis and loss of a portion of nephrons.
- Secondary contracted kidney forms as the outcome of a primary inflammatory lesion of the glomeruli—glomerulonephritis, where immune inflammatory glomerular damage is primary, and vascular changes are secondary.
What histological stains are used for the differential diagnosis of sclerosis, hyalinosis, and amyloidosis of renal tissue?
- Sclerosis (connective tissue): van Gieson's picrofuchsin special stain is used, which selectively stains collagen fibers.
- Hyalinosis: characterized by the formation of acellular eosinophilic PAS-positive masses, detected using the PAS reaction.
- Amyloidosis: the specific diagnostic method is histochemical staining with Congo red (Congo red), in which amyloid stains brick-red and exhibits characteristic apple-green birefringence under polarized light (apple-green birefringence).
To memorize the macroscopic picture of malignant nephrosclerosis, use the "angry flea" association: malignant hypertension causes vascular ruptures, leaving petechiae on the kidneys in the form of "flea bites".
Class and exam questions
How does benign nephrosclerosis macroscopically differ from malignant nephrosclerosis?
In benign nephrosclerosis, the kidney surface is finely granular, and the organs themselves are moderately reduced. In malignant nephrosclerosis, sizes are variable, but a characteristic sign is punctate hemorrhages ("flea bites").
What masses are found in the glomeruli during their obliteration?
Sclerotic glomeruli reveal acellular eosinophilic masses that give a positive staining reaction (PAS-positive masses).
What is concentric arteriolitis?
This is a vascular lesion in malignant hypertension where the arteriolar intima thickens in an "onion-skin" fashion due to concentric proliferation of smooth muscle cells and collagen fibers.
What else to study on this topic
- Clinical forms of chronic glomerulonephritis (latent, hematuric, hypertensive, nephrotic, mixed)
- Morphological types of chronic glomerulonephritis (MPGN and mesangioproliferative)
- Pathogenesis of secondary hyperparathyroidism and renal osteodystrophy in uremia
- Mechanisms of formation of acquired cystic kidney disease during hemodialysis
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