Subtle Acquired Renal Injury as a Mechanism of Salt-Sensitive Hypertension

Johnson, Richard J.; Herrera-Acosta, Jaime; Schreiner, George F.; Rodríguez‐Iturbe, Bernardo

doi:10.1056/nejmra011078

Cited by 402 publications

(265 citation statements)

References 79 publications

Supporting

Mentioning

242

Contrasting

Unclassified

Order By: Relevance

“…ROS-induced vascular remodeling impairs autoregulation and may lead to distal tubulointerstitial ischemia. 33 In genetically hypertensive rats, the number of intrarenal superoxide-positive cells is positively correlated with systolic blood pressure levels. 14,34 Recently, resveratrol was shown to mitigate oxidative stress and normalize angiotensin signaling in the kidney and reduce blood pressure via activation of phase II antioxidant enzymes.…”

Section: Interaction Of Oxidative Stress and Inflammation In The Devementioning

confidence: 99%

Hypertension as an autoimmune and inflammatory disease

et al. 2016

View full text Add to dashboard Cite

Section: Interaction Of Oxidative Stress and Inflammation In The Devementioning

confidence: 99%

Hypertension as an autoimmune and inflammatory disease

et al. 2016

View full text Add to dashboard Cite

“…17 In our study, the association between hsCRP, RRI and RV/RRI in hypertensive patients with normal renal function and without MA, that is, without glomerular damage, is in line with the hypothesis of an early inflammatory involvement of renal interstitium in essential hypertension. In fact, tubules and interstitium, rather than glomerular capillaries, are considered to constitute the initial site of kidney injury, 25 and a common feature of experimental models of salt-sensitive hypertension is the existence of tubulo-interstitial inflammatory infiltration, in addition to intrarenal arteriolopathy. 13 In particular, the experiment by Murphy et al 26 showed 21 (33) 8 (38) 13 (31) 16 (37) Ca-channel blockers (n (%)) 6 (9) 3 (14) 4 (10) 5 (12) Diuretics (n (%))…”

Section: Discussionmentioning

confidence: 99%

Renal resistive index and low-grade inflammation in patients with essential hypertension

et al. 2011

View full text Add to dashboard Cite

In essential hypertension, increased renal resistive index (RRI) is associated to a reduction of renal function and microalbuminuria, and to renal tubulo-interstitial damage. A tubulo-interstitial inflammatory infiltration was found in experimental models of hypertension, and serum high-sensitive C-reactive protein (hsCRP) levels correlated with urinary markers of tubulointerstitial damage in humans. We studied the relationship between RRI and serum hsCRP in hypertensives with preserved renal function, without microalbuminuria. We investigated hypertensive patients without diabetes, renal failure, microalbuminuria or major inflammatory disease. Serum levels of hsCRP were assayed. RRI was calculated by intrarenal Doppler ultrasound and considered pathologic when X0.70 or 495% of upper confidence limit expected for age decade. The renal volume-to-resistive index ratio (RV/RRI) was also calculated. We evaluated 85 patients (57 ± 14 years, 61 males). Patients with pathologic RRI (n ¼ 21) were older and had significantly higher hsCRP levels (4.70 ± 2.30 vs 2.93 ± 2.09 mg l À1 , Po0.01) compared with patients with normal RRI, as well as patients with decreased RV/RRI (n ¼ 43). HsCRP was directly related with RRI (r ¼ 0.41, Po0.001) and inversely with RV/RRI (r ¼ À0.35, Po0.001). HsCRP proved to be a significant predictor of both pathologic RRI and decreased RV/RRI, even after adjustment. In essential hypertension low-grade inflammation is associated with tubulo-interstitial damage evaluated by Doppler ultrasonography.

show abstract

“…Johnson and colleagues have suggested that primary subclinical renal microvascular disease leading to afferent arteriolopathy and tubulointerstitial disease may be responsible for the development of salt-sensitive hypertension. 14 Progressive tubulointerstitial disease will eventually result in microalbuminuria before the development of clinically apparent impairment of glomerular filtration. Concurrent microvascular damage is thought to result in renal vasoconstriction and subsequent local generation of angiotensin II.…”

Section: Volume Expansionmentioning

confidence: 99%

Apparent Treatment-Resistant Hypertension and Chronic Kidney Disease: Another Cardiovascular-Renal Syndrome?

Vemulapalli

Tyson

Svetkey

2014

Advances in Chronic Kidney Disease

View full text Add to dashboard Cite

To identify patients at increased risk of cardiovascular (CV) outcomes, apparent treatment-resistant hypertension (aTRH) is defined as having a blood pressure above goal despite the use of 3 or more antihypertensive therapies of different classes at maximally tolerated doses, ideally including a diuretic. Recent epidemiologic studies in selected populations estimated the prevalence of aTRH as 10% to 15% among patients with hypertension and that aTRH is associated with elevated risk of CV and renal outcomes. Additionally, aTRH and CKD are associated. Although the pathogenesis of aTRH is multifactorial, the kidney is believed to play a significant role. Increased volume expansion, aldosterone concentration, mineralocorticoid receptor activity, arterial stiffness, and sympathetic nervous system activity are central to the pathogenesis of aTRH and are targets of therapies. Although diuretics form the basis of therapy in aTRH, pathophysiologic and clinical data suggest an important role for aldosterone antagonism. Interventional techniques, such as renal denervation and carotid baroreceptor activation, modulate the sympathetic nervous system and are currently in phase III trials for the treatment of aTRH. These technologies are as yet unproven and have not been investigated in relationship to CV outcomes or in patients with CKD.

show abstract

Subtle Acquired Renal Injury as a Mechanism of Salt-Sensitive Hypertension

Cited by 402 publications

References 79 publications

Hypertension as an autoimmune and inflammatory disease

Hypertension as an autoimmune and inflammatory disease

Renal resistive index and low-grade inflammation in patients with essential hypertension

Apparent Treatment-Resistant Hypertension and Chronic Kidney Disease: Another Cardiovascular-Renal Syndrome?

Contact Info

Product

Resources

About