Pathophysiology of Hypertensive Renal Damage

Bidani, A.; Griffin, Karen A.

doi:10.1161/01.hyp.0000145180.38707.84

Cited by 374 publications

(377 citation statements)

References 62 publications

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“…Under these conditions, only modest renovascular impairment is expected. 13 Such a slight change may account for the largely benign outcome in most uninephrectomized individuals, such as those in the present study. Indeed, our donors were, by definition, in excellent health, with even the prospect of a longer life span.…”

Section: Discussionmentioning

confidence: 59%

“…A contributory factor is that, in both animals and humans, kidney size increases significantly, and preglomerular arteriolar resistance decreases in response to unilateral nephrectomy, resulting in greater fractional transmission to the kidney of ambient systemic BP. 12,13 In most cases, arteriolar vasodilatation is not accompanied by substantial impairment of renal autoregulation, severe hypertension, or an age-related loss of kidney function. Under these conditions, only modest renovascular impairment is expected.…”

Section: Discussionmentioning

confidence: 99%

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Aortic Stiffness, Living Donors, and Renal Transplantation

Bahous

Stephan²,

Blacher³

et al. 2006

Hypertension

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Abstract-In subjects with renal disease, reduced renal function and increased arterial stiffness are significantly associated in cross-sectional studies. The relationship is independent of age, blood pressure (BP), and atherosclerosis. Because both variables are independent predictors of cardiovascular risk, time-dependent relationships between them are important to determine. Aortic pulse wave velocity was measured noninvasively by comparison with healthy volunteers in 101 living kidney donors and their 101 corresponding recipients. Healthy volunteers were divided into 2 groups: one was recipient related through familial links and the other was nonrecipient related. Independently of age, gender, and BP, pulse wave velocity was significantly elevated in donors and recipients by comparison with the 2 groups of healthy volunteers. Pulse wave velocity was significantly higher in the recipient-related than in the nonrecipient-related group. Whereas in healthy volunteers, pulse wave velocity was exclusively related to age, gender, and BP, in donors and recipients, it was rather associated with a cluster of cardiovascular risk factors, including smoking habits and plasma glucose. Major factors related to pulse wave velocity were renal: time since nephrectomy (donation date) in donors, in whom pulse pressure was specifically associated with proteinuria, and renal rejection in recipients. Plasma creatinine doubling secondary to chronic allograft nephropathy was significantly associated with renal rejection and donor pulse wave velocity, independent of age.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Aortic Stiffness, Living Donors, and Renal Transplantation

Bahous

Stephan²,

Blacher³

et al. 2006

Hypertension

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“…72 Progressive nephron loss, with diminished capacity for sodium excretion, is the consequence of the loss of these important autoregulatory processes. 73 …”

Section: Impairment In Salt Excretion As a Consequence Of Renal Micromentioning

confidence: 99%

The role of renal microvascular disease and interstitial inflammation in salt-sensitive hypertension

Rodríguez‐Iturbe¹,

Johnson

2010

Hypertens Res

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Primary (essential) hypertension has been shown to be mediated by a relative impairment in sodium excretion by the kidney, but the mechanisms responsible for this defect are still being clarified. Increasing evidence suggests a role for subtle acquired renal injury in mediating this process. Microvascular injury is present in the majority of subjects with hypertension. The development of arteriolosclerosis, primarily of the afferent arteriole, may interfere with glomerular autoregulation, whereas the loss of peritubular capillaries may facilitate local ischemia. These changes favor the localization of T cells and macrophages into the interstitium, which, coupled with local oxidative stress and angiotensin II generation, may contribute to the impaired pressure natriuresis observed with salt-sensitive hypertension. Consistent with this hypothesis, therapies that are aimed at blocking the immune response, including thymectomy, genetic alterations in mice resulting in impaired immune responses, or the use of immunosuppressive agents, can protect against the development of hypertension in experimental models. Preliminary data in humans also suggest that the inhibition of the renal inflammatory response may reduce blood pressure. The present investigations are directed to gain insight in the role of the intrarenal T-cell reactivity and autoimmunity in driving the tubulointerstitial inflammation and its participation in the pathogenesis of salt-sensitive hypertension.

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“…12 Similar results were found in the USA, 20 and provided a good basis for comparison with our study, since further renal damage. 46 An elevation in blood pressure in CKD patients thus increases the rate at which GFR (glomerular filtration rate) and resulting kidney function decline. 44 It is estimated that about 20%-40% of diabetes mellitus type 2 patients encounter a moderate to severe decline in renal function.…”

Section: Discussionmentioning

confidence: 99%