NEPHROSCLEROSIS AND HYPERTENSION

doi:10.1016/S0025-7125(05)70582-4

Medical Clinics of North America

Volume 81, Issue 6, 1 November 1997, Pages 1273-1288

https://doi.org/10.1016/S0025-7125(05)70582-4 Get rights and content

This article reviews the involvement of the kidney as a target organ of essential hypertension. Essential hypertension has been divided into two forms: benign and malignant. The three major target organs of a patient with essential hypertension are the brain, cardiovascular system, and kidney. End-stage renal disease (ESRD) is a major public health problem, and in 1991, about 190,000 persons in the United States underwent either dialysis or a renal transplant for ESRD.³¹ Benign or malignant nephrosclerosis often is the term used to describe the histologic changes of the kidney associated with the benign or malignant phase of essential hypertension. In this article, gross features, light microscopic and electron microscopic findings, and glomerular hemodynamics of hypertensive experimental models with antihypertensive treatments are demonstrated.

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)

E.R. Fisher
Ultrastructural changes in renal arterioles and juxtaglomerular cells in hypertension
Am Heart J
(1971)
M. Houston
The practical management of patients with severe hypertension and hypertensive emergencies
Am Heart J
(1986)
T. Morita et al.
Mesangiolysis
Kidney Int
(1983)
G. Schwietzer et al.
Changes of hemodynamics and glomerular ultrafiltration in renal hypertension of rats
Kidney Int
(1979)
W.J. Arendshorst et al.
Renal and nephron hemodynamics in spontaneously hypertensive rats
Am J Physiol
(1979)
C. Baylis et al.
Chronic blockade of nitric oxide synthesis in the rat produces systemic hypertension and glomerular damage
J Clin Invest
(1992)
C.G. Biava et al.
Renal hyaline arteriolosclerosis: An electron microscopic study
Am J Pathol
(1964)
M.C. Brain et al.
Microangiopathic haemolytic anaemia: The possible role of vascular lesions in pathogenesis
Br J Haematol
(1962)
F.B. Byrom
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...

L.D. Dworkin et al.

Hemodynamic basis for glomerular injury in rats with deoxycorticosterone-salt hypertension

J Clin Invest

(1984)

E.R. Fisher et al.

Ultrastructural studies in hypertension: I. Comparison of renal vascular and juxtamedullary cell alterations in essential and renal hypertension in man

Lab Invest

(1966)

N. Gibbons et al.

Glomerular hypertension (GH) enhances mesangial cell apoptosis: An in vivo study

J Am Soc Nephrol

(1996)

P.J. Goldblatt et al.

Benign and malignant nephrosclerosis and renovascular hypertension

K.E. Grund et al.

Renal insufficiency in nephrosclerosis (benign nephrosclerosis resp. transition from benign to secondary malignant nephrosclerosis): Correlations between morphological and functional parameters

Klin Wochenschr

(1978)

T. Gudbrandsson et al.

Malignant hypertension: Improving prognosis in a rare disease

Acta Med Scand

(1979)

U. Helmchen et al.

Role of the renin-angiotensin system in renal hypertension: An experimental approach

Curr Top Pathol

(1976)

R.H. Heptinstall

Malignant hypertension: A study of fifty-one cases

J Pathol Bacteriol

(1953)

Cited by (29)

Nonneoplastic Diseases of the Kidney
2020, Urologic Surgical Pathology
In keeping with the spirit of Marcello Malpighi, this chapter also aspires to reveal “the manner of Nature’s operation” as it affects the kidney.¹ However, unlike Malpighi, today’s knowledge draws extensively on the labors, discoveries, and insights of investigators of the past centuries.
Knowledge of the normal structure and function of the kidney has been acquired over centuries of scholarly effort. We have come a long way since Aristotle taught that urine was formed by the bladder and that kidneys were present “not of actual necessity, but as matters of greater finish and perfection.”¹ Reference to the excretory functions of the bladders and kidneys can be found in early Indian Ayurveda, Chinese, or Egyptian literature.2, 3, 4 Some of the earliest scientifically valid experimental methods are described in The Canon of Medicine by the famous Persian Muslim physician Abu Ali Sina, also known as “Avicenna.”5, 6, 7, 8, 9, 10, 11, 12, 13 He meticulously described the layers of the bladder and its two-stage function, the intramural ureter and antireflux mechanisms, and scientifically classified urethral and bladder diseases, notably calculi. The foundation of modern urology was established in the sixteenth century by Leonardo da Vinci and Vesalius, who provided the first accurate and detailed drawings of the female and male genitourinary tracts (Fig. 1.1).14, 15 More than 300 years passed before William Bowman, in 1842, coupled intravascular dye injection with microscopic examination to demonstrate the structural organization of the nephron and its vascular supply (Fig. 1.2).16, 17 Bowman’s observations provided morphologic support for Malpighi’s seventeenth-century speculation of a filtration function for the malpighian body (the glomerulus).1, 18 Sixty years later the embryologic development of the nephron was demonstrated by Huber in a thin-section serial reconstruction study of embryos (Fig. 1.3).¹⁹ Huber’s observations were refined and elegantly illustrated by Brödel in 1907.²⁰
Aerobic exercise training prevents kidney lipid deposition in mice fed a cafeteria diet
2018, Life Sciences
Citation 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.
The objective of this study was to investigate the potential of aerobic exercise training (AET) to prevent kidney lipid accumulation and the contribution of renal metabolism to mediate this response.
Male C57BL/6J mice were assigned into groups CHOW-SED (chow diet, sedentary; n = 13), CHOW-TR (chow diet, trained; n = 13), CAF-SED (cafeteria diet, sedentary; n = 13) and CAF-TR (cafeteria diet, trained; n = 13). AET consisted in running sessions of 60 min at 60% of maximal speed conducted five days per week for eight weeks.
AET prevented weight gain in both trained groups. Food intake was not different among groups, however water intake, urine output, urine potassium and osmolarity were reduced in CAF-SED and CAF-TR groups. Kidney lipid deposition increased in CAF-SED (4.12 ± 0.5%/area) compared with CHOW-SED (1.7 ± 0.54%/area), and the AET prevented this increase in the CAF-TR group (2.1 ± 0.5%/area). The Bowman's capsule area decreased in CAF-SED and CAF-TR groups while the Bowman' space reduced in CAF-SED compared to CHOW-SED group, which was prevented by AET in the CAF-TF group. We observed a 27% increase in the p-AMPK expression in CAF-TR compared to CHOW-SED group without differences in the SIRT-1, PGC1-α, ACC and p-ACC. β-HAD activity increased in CAF-SED (43.9 ± 4.57 nmol·min⁻¹·ug⁻¹) and CAF-TR (44.7 ± 2.6 nmol·min⁻¹·ug⁻¹) groups compared to CHOW-SED (35.1 ± 2.9 nmol·min⁻¹·ug⁻¹) e CHOW-TR (36.6 ± 2.7 nmol·min⁻¹·ug⁻1).
AET prevented kidney lipid accumulation induced by cafeteria diet and this response was not associated with changes in the renal metabolic activity that favors lipid oxidation.
Transcriptional inhibition of progressive renal disease by gene silencing pyrrole-imidazole polyamide targeting of the transforming growth factor-Β1 promoter
2011, Kidney International
Citation 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).
Pyrrole–imidazole (PI) polyamides are small synthetic molecules that recognize and attach to the minor groove of DNA, thereby inhibiting gene transcription by blocking transcription factor binding. These derivatives can act as gene silencers inhibiting target gene expression under stimulatory conditions such as disease. To evaluate PI polyamides as treatments for the progression of renal diseases, we examined morphological effects, pharmacological properties, and the specificity of PI polyamides targeted to the transforming growth factor (TGF)-β1 promoter during salt-induced hypertensive nephrosclerosis in Dahl salt-sensitive rats. The targeted PI polyamide markedly reduced glomerulosclerosis and interstitial fibrosis without side effects. PI polyamide significantly decreased expression of TGF-β1 and extracellular matrix in the renal cortex. Microarray analysis found that only 3% of the transcripts were affected by PI polyamide, but this included decreased expression of extracellular matrix, TGF-β1-related cytokines, angiogenic, and cell stabilizing factors, proteinases, and renal injury-related factors. Thus, targeted PI polyamides are potential gene silencers for diseases not treatable by current remedies.
Non-neoplastic diseases of the kidney
2008, Urologic Surgical Pathology: Second Edition
Non-neoplastic Diseases of the Kidney
2006, Genitourinary Pathology
Green iguana nephrology: A review of diagnostic techniques
2003, Veterinary Clinics of North America - Exotic Animal Practice

View all citing articles on Scopus

: 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

View full text

NEPHROSCLEROSIS AND HYPERTENSION

Section snippets

BENIGN NEPHROSCLEROSIS

MALIGNANT NEPHROSCLEROSIS

HEMODYNAMIC FACTORS

SUMMARY

Am Heart J

Am Heart J

Kidney Int

Kidney Int

Renal and nephron hemodynamics in spontaneously hypertensive rats

Am J Physiol

Chronic blockade of nitric oxide synthesis in the rat produces systemic hypertension and glomerular damage

J Clin Invest

Renal hyaline arteriolosclerosis: An electron microscopic study

Am J Pathol

Microangiopathic haemolytic anaemia: The possible role of vascular lesions in pathogenesis

Br J Haematol

The Hypertensive Vascular Crisis: An Experimental Study

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