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At least 199 records · Page 11Linked to original sources
PubMed2004

Hypertensive nephrosclerosis: update.

UNLABELLED: PURPOSE OF VIEW: A major clinical trial and a meta-analysis completed within the past year addressed the issue of renal disease progression after blood pressure-lowering treatment in patients with hypertension and diminished renal function. Important human and animal studies have addressed mechanistic issues regarding renal disease progression. These advances warrant detailed discussion. RECENT FINDINGS: The African American Study of Kidney Disease and Hypertension Study Group trial found that an angiotensin-converting enzyme inhibitor was superior to a calcium antagonist or beta-blocker in ameliorating renal disease progression in African-Americans. An attempt to show an advantage of lowering blood pressure to less than 130/80 compared with 140/90 mmHg showed no additional benefit. However, a meta-analysis of 2000 non-diabetic hypertensive patients suggested that lower blood pressures are beneficial, particularly in individuals with proteinuria. An autopsy study of hypertensive and normotensive individuals dying in motor vehicle accidents supported the theory that hypertensive individuals have fewer, albeit larger, glomeruli than normotensive individuals. An animal study in sheep showed similar findings in sheep born to dams given dexamethasone compared with placebo. Animal studies involving stress, immunity, and cytokines shed further light on the mechanisms. The transfer of Smad7 ameliorated renal damage in rats with ureteral obstruction and fibrosis. SUMMARY: Guidelines suggest prescribing angiotensin-converting enzyme inhibitor or angiotensin 1 receptor blocker therapy to all patients with decreased renal function and hypertension with or without diabetes. The possibility that essential hypertension involves reduced glomerular numbers received support, as well as the theory of prenatal imprinting. Progress is being made regarding basic mechanisms and novel therapies.

Animals↗
PubMed2002

Prostacyclin-deficient mice develop ischemic renal disorders, including nephrosclerosis and renal infarction.

BACKGROUND: Prostacyclin (PGI2) is a short-lived endogenous inhibitor of platelet aggregation and a potent vasodilator and regulator of the growth of vascular smooth muscle cells. To study the role of PGI2 in the vascular system in vivo, PGI2-deficient (PGID) mice were established by genetic disruption of the PGI2 synthase gene. METHODS AND RESULTS: PGI2 synthase-null mice were generated by replacing the exons of PGI2 synthase gene that encodes for the catalytic site of the enzyme with a neomycin resistance gene. In these mice, PGI2 levels in the plasma, kidneys, and lungs were reduced, whereas thromboxane and prostaglandin E2 levels became elevated. Blood pressure and the amounts of urea nitrogen and creatinine in plasma of the PGID mice were significantly higher than those of wild-type mice (P<0.05). They developed progressive morphological abnormalities in the kidneys, accompanied by atrophy, surface irregularity, fibrosis, cyst, arterial sclerosis, and hypertrophy of vessel walls. Thickening of the thoracic aortic media and adventitia were observed in aged PGID mice. Importantly, these phenotypes have not been reported in PGI2 receptor-deficient mice. CONCLUSIONS: PGI2 deficiency resulted in the development of vascular disorders with the thickening of vascular walls and interstitial fibrosis, especially in mouse kidneys. The findings demonstrated in vivo that PGI2 is important in the homeostasis of blood vessels. Our established PGID mice are useful for studies on the initiation and development of vascular diseases, such as ischemic renal disorders with arterial sclerosis and infarction, and also for studies on the novel signaling pathway of PGI2.

Age Factors↗
PubMed1992

Adverse effect of the calcium channel blocker nitrendipine on nephrosclerosis in rats with renovascular hypertension.

The effect of a 6-week treatment with the calcium channel blocker nitrendipine or the angiotensin converting enzyme inhibitor enalapril on blood pressure, albuminuria, renal hemodynamics, and morphology of the nonclipped kidney was studied in rats with two-kidney, one clip renovascular hypertension. Six weeks after clipping of one renal artery, hypertensive rats (178 +/- 4 mm Hg) were randomly assigned to three groups: untreated hypertensive controls (n = 8), enalapril-treated (n = 8), or nitrendipine-treated (n = 10). Sham-operated rats served as normotensive controls (128 +/- 3 mm Hg, n = 8). After 6 weeks of treatment, renal hemodynamics (glomerular filtration rate and renal plasma flow) were measured in the anesthetized rats. Renal tissue was obtained for determination of glomerular size and sclerosis. Enalapril but not nitrendipine reduced blood pressure significantly. After 6 weeks of therapy, glomerular filtration rate was not different among the studied groups. Renal plasma flow increased, but albumin excretion and glomerulosclerosis did not change after enalapril treatment. In contrast, in the nitrendipine-treated group albuminuria increased from 12.8 +/- 2 progressively to 163 +/- 55 compared with 19.2 +/- 9 mg/24 hr in the hypertensive controls. Furthermore, glomerulosclerosis index was significantly increased in the nitrendipine-treated group compared with the hypertensive controls (0.38 +/- 0.1 versus 0.13 +/- 0.04). In addition, glomerular size was higher in the nitrendipine-treated group (14.9 +/- 0.17 10(-3) mm2) but lower in the enalapril-treated group (11.5 +/- 0.15 10(-3) mm2) compared with the hypertensive controls (12.1 +/- 0.17 10(-3) mm2).(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗
PubMed1994

Renal ablation acutely transforms 'benign' hypertension to 'malignant' nephrosclerosis in hypertensive rats.

The present studies examine the consequences of the hemodynamic changes associated with approximately 5/6 renal ablation in the spontaneously hypertensive rat (SHR), a strain that normally does not exhibit evidence of vascular and/or glomerular injury until late in life despite significant hypertension. Control SHR with intact renal mass demonstrated normal renal autoregulation and an absence of vascular or glomerular injury. Renal mass reduction resulted in an initial expected decrease in renal blood flow to the remnant kidney at 5 days (2.8 +/- 0.3 mL/min) compared with control SHR (8.1 +/- 0.7 mL/min) at a mean arterial pressure of approximately 160 mm Hg (P < .01). By 10 to 14 days after renal ablation, marked renal vasodilation was observed (renal blood flow 8.3 +/- 0.8 mL/min at mean arterial pressure of approximately 160 mm Hg) along with severe impairment of autoregulatory ability. Striking and florid vascular injury to interlobular arteries and afferent arterioles had also developed by 10 to 14 days after approximately 5/6 renal ablation in a pattern similar to that observed in "malignant" hypertension, despite systolic blood pressures that were not significantly different from those in control SHR (168.2 +/- 6.4 versus 165.6 +/- 4.7 mm Hg). An additional group of SHR that were made normotensive with a triple-therapy antihypertensive regimen before and after approximately 5/6 renal ablation also exhibited hemodynamic changes similar to those in the untreated rats at 10 to 14 days but did not develop significant vascular or glomerular injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗