NEPHROSCLEROSIS AND HYPERTENSION
Section snippets
BENIGN NEPHROSCLEROSIS
The term benign nephrosclerosis is often used to describe the kidney of the benign phase of essential hypertension. A patient with benign hypertension may subsequently develop malignant hypertension. Benign essential hypertension is characterized by moderate elevation of blood pressure (diastolic pressure of 90 to 120 mm Hg or occasionally higher than this), cardiac enlargement, congestive heart failure, stroke with hemorrhage and infarction, coronary artery disease, and narrowing of arteries
MALIGNANT NEPHROSCLEROSIS
Accelerated hypertension is a clinical syndrome with severe hypertension, hypertensive encephalopathy, funduscopic findings of hemorrhages and exudates, congestive heart failure, acute and progressive renal failure, and microangiopathic hemolytic anemia.6 The coexistence of papilledema defines malignant hypertension. The difference in the management of these two syndromes may depend on the degree of urgency in treating vital organ involvement rather than on the presence or absence of
HEMODYNAMIC FACTORS
In various rat models of essential hypertension, micropuncture techniques have provided valuable information as to glomerular hemodynamics. Male SHR, the genetic hypertension model bred by Aoki and Okamoto, has significantly increased afferent arteriolar resistance (RA) with mean arterial pressure (MAP) at the 17- to 20-week stage but shows no increase in glomerular hydrostatic pressure (PG), efferent arteriolar resistance (RE), and glomerular plasma flow rate (QA).1 This strain also exhibits
SUMMARY
In patients with benign nephrosclerosis, the histologic changes are characterized by hyaline degeneration of afferent arterioles with reduced kidney size. Although the glomeruli are nearly intact in patients with adult essential hypertension, the greatest numbers of sclerotic glomeruli are seen in nephrosclerosis with the aging process.20 Aging undoubtedly plays a role. In the authors' experience, the kidney of an elderly subject, although with normotensive pressure and normal level of
References (37)
Ultrastructural changes in renal arterioles and juxtaglomerular cells in hypertension
Am Heart J
(1971)The practical management of patients with severe hypertension and hypertensive emergencies
Am Heart J
(1986)- et al.
Mesangiolysis
Kidney Int
(1983) - et al.
Changes of hemodynamics and glomerular ultrafiltration in renal hypertension of rats
Kidney Int
(1979) - et al.
Renal and nephron hemodynamics in spontaneously hypertensive rats
Am J Physiol
(1979) - et al.
Chronic blockade of nitric oxide synthesis in the rat produces systemic hypertension and glomerular damage
J Clin Invest
(1992) - et al.
Renal hyaline arteriolosclerosis: An electron microscopic study
Am J Pathol
(1964) - et al.
Microangiopathic haemolytic anaemia: The possible role of vascular lesions in pathogenesis
Br J Haematol
(1962) The Hypertensive Vascular Crisis: An Experimental Study
(1969)- Campese VM: Clinical aspects and management of essential hypertension. In Massry SG, Glassock RJ (eds): Text of...
Hemodynamic basis for glomerular injury in rats with deoxycorticosterone-salt hypertension
J Clin Invest
Ultrastructural studies in hypertension: I. Comparison of renal vascular and juxtamedullary cell alterations in essential and renal hypertension in man
Lab Invest
Glomerular hypertension (GH) enhances mesangial cell apoptosis: An in vivo study
J Am Soc Nephrol
Benign and malignant nephrosclerosis and renovascular hypertension
Renal insufficiency in nephrosclerosis (benign nephrosclerosis resp. transition from benign to secondary malignant nephrosclerosis): Correlations between morphological and functional parameters
Klin Wochenschr
Malignant hypertension: Improving prognosis in a rare disease
Acta Med Scand
Role of the renin-angiotensin system in renal hypertension: An experimental approach
Curr Top Pathol
Malignant hypertension: A study of fifty-one cases
J Pathol Bacteriol
Cited by (29)
Nonneoplastic Diseases of the Kidney
2020, Urologic Surgical PathologyAerobic exercise training prevents kidney lipid deposition in mice fed a cafeteria diet
2018, Life SciencesCitation Excerpt :These changes can lead to glomerular injury, glomerulosclerosis, irregular tubular atrophy and fibrosis. Usually, hyalilized glomeruli are smaller than the normal due to the loss of cellular elements [24,28]. Although some studies have shown that a hyperlipidic or hypercaloric diet may cause renal morphological alterations [4,10], these results are not well established in the literature.
Transcriptional inhibition of progressive renal disease by gene silencing pyrrole-imidazole polyamide targeting of the transforming growth factor-Β1 promoter
2011, Kidney InternationalCitation Excerpt :The multiple reaction monitoring transition for polyamide 2 was m/z 834>165. After 3-μm paraffin sections were stained with periodic acid-Schiff reagent or Masson's trichrome stain for semiquantitative evaluation, glomerular injury score, and tubulointerstitial injury score were determined as described previously.41,42 Total RNA was extracted from renal cortex by using RNEasy Mini kit (Qiagen, Valencia, CA, USA).
Non-neoplastic diseases of the kidney
2008, Urologic Surgical Pathology: Second EditionNon-neoplastic Diseases of the Kidney
2006, Genitourinary PathologyGreen iguana nephrology: A review of diagnostic techniques
2003, Veterinary Clinics of North America - Exotic Animal Practice
Address reprint requests to, Hidehiko Ono, MD, Division of Hypertension and Cardiorenal Disease, Department of Internal Medicine, Dokkyo University School of Medicine, 880 Kitakobayashi, Mibu-machi, Shimotsuga-gunn, Tochigi 321-02, Japan
- *
Division of Hypertension and Cardiorenal Disease, Department of Internal Medicine (HO), and the Department of Pathology (YO), Dokkyo University School of Medicine, Tochigi, Japan