OVERVIEW
Benign small-artery nephrosclerosis is a disease usually associated with chronic hypertension and characterized by involvement of blood vessels, glomeruli, and tubular interstitium. Three factors increase the risk of developing nephrosclerosis: black race, moderate to severe hypertension, and other pre-existing renal disease (e.g., diabetic nephropathy). Treatment of hypertension to a diastolic blood pressure of <90 mm Hg usually prevents exacerbation of renal injury, and ACEI inhibitors may be more protective than other antihypertensive drugs.
Etiology
Nephrosclerosis occurs with age but can be exacerbated by chronic hypertension.The overall incidence of progressive kidney disease is lower in patients with chronic hypertension.Most patients have mild hypertension.However,three factors increase the risk of developing nephrosclerosis: black race,moderate to severe hypertension,and other preexisting renal disease (e.g.,diabetic nephropathy).
Two processes contribute to the development of vascular damage in chronic hypertension: hypertrophy of the middle layer and fibroblastic intimal thickening leading to narrowing of the vessel lumen; and second, deposition of vitreous material (plasma protein components) in the walls of damaged, permeable small arterioles. The most common and specific alterations are severe involvement of the bulbous arterioles with vitreous degeneration, degeneration of the endosteal and basement membranes and fibrinopapillary necrosis throughout the vessel. The internal elastic lamina is often damaged and may be delaminated.
Glomeruli may show focal glomerular and focal segmental sclerosis, with focal glomerular sclerosis due to ischemic injury and loss of renal unit function and focal segmental sclerosis due to glomerular enlargement, which may be a compensatory response to the loss of renal units, and vascular and glomerular involvement associated with ischemic-related, often severe, interstitial nephritis and an active immune process due to altered expression of antigens on the surface of tubular epithelial cells.
Symptoms.
Renal tubules are sensitive to ischemia, so the first clinical manifestations of tubular concentrative dysfunction: nocturia, low specific gravity and hypo-osmolality; when glomerular ischemic lesions occur, urinalysis is abnormal: mild proteinuria, a small number of erythrocytes and tubular pattern; the glomerular function is progressively impaired: a decrease in the endogenous muscle mass clearance rate, followed by an increase in serum creatinine; and gradually progresses to end-stage renal failure. Hypertensive fundopathy and cardiac and cerebral complications often accompany renal damage.
Examination
Patients may exhibit slowly progressive elevations in urea nitrogen and plasma creatinine concentrations, hyperuricemia (not dependent on diuretic therapy), a relatively early finding that may reflect reduced renal blood flow due to vascular disease, urinalysis typically showing a small number of cells or tubular patterns, and protein excretion usually <1 g/day but sometimes within the range of nephropathy; patients with significant proteinuria often have overlapping renal vascular disease.
Diagnosis
1. caused by long-standing poorly controlled benign hypertension, which may show associated pathologic changes if it persists for 5-10 years, and clinical manifestations may appear in l0-15 years.
2. The first manifestation of tubular concentrating dysfunction (nocturia, low relative density and hypo-osmolality), when glomerular ischemia occurs lesions may be mild proteinuria, a small number of red blood cells and tubular and endogenous creatinine rate decreased.
3. The diagnosis is usually made on the basis of clinical manifestations and renal puncture is not performed.
4. A family history of hypertension or evidence of left ventricular hypertrophy supports the diagnosis.
5. Exceptions include a history of nephrotoxic drug exposure, genetic or congenital renal disease, or other systemic diseases that may result in renal damage.
Treatment
Hypertensive treatment of benign small-artery nephrosclerosis to a diastolic blood pressure of <90 mm Hg usually prevents exacerbation of renal injury, and ACEI inhibitors may be more protective than other antihypertensive agents.
Prognosis
Although benign small-artery nephrosclerosis is one of the most common diagnoses in patients with end-stage renal failure (ESRD), in the absence of any risk factors, the rate of progression is generally slow; progressive renal disease can occur in only a few patients with markedly idiopathic primary hypertension; however, such a large number of patients with chronic hypertension, a few of whom are at risk of developing renal failure, comprise a large number of people developing ESRD, and progressive renal insufficiency is directly related to the severity and adequacy of control of hypertension.
Patients with primary glomerular disease have a better survival rate than those with ESRD, and the poor prognosis of patients with ESRD (and also in diabetes mellitus) largely reflects extrarenal vascular disease.