Hypertension-Associated Kidney Disease

Freedman, Barry I.; Sedor, John R.

doi:10.1681/asn.2008060621

Cited by 91 publications

(69 citation statements)

References 43 publications

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“…Furthermore, new mouse models are necessary to investigate the influence of genetic variants conferring an increased susceptibility to hypertensive renal injury associated with hypertension, as demonstrated for the gene that encodes the molecular motor protein nonmuscle myosin 2a (MYH9). 80 …”

Section: Mechanisms Of Experimental Models Of Hypertensionmentioning

confidence: 99%

Immune Mechanisms in Arterial Hypertension

Wenzel¹,

Turner²,

Krebs³

et al. 2016

Journal of the American Society of Nephrology

167

148

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Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive endorgan damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.

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Section: Mechanisms Of Experimental Models Of Hypertensionmentioning

confidence: 99%

Immune Mechanisms in Arterial Hypertension

Wenzel¹,

Turner²,

Krebs³

et al. 2016

Journal of the American Society of Nephrology

167

148

View full text Add to dashboard Cite

show abstract

“…23 Although the term hypertensive nephrosclerosis has been used to denote this form of renal impairment, the usefulness of this term has been questioned as in many cases intrinsic renal disease takes primacy over hypertension. 24,25 One of the functional characteristics of the aging kidney is a disturbed ability to adapt to changes in sodium intake. For instance, after a sudden reduction in dietary salt, older people need more time to attain a new balance during which they lose more sodium than younger individuals.…”

Section: Pathophysiology Of Bp Regulation In the Oldest Oldmentioning

confidence: 99%

Treatment of Hypertension in the Oldest Old

et al. 2014

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A n 88-year-old woman with chronic hypertension was seen in the internal/geriatric medicine outpatient clinic. She had been treated for high blood pressure (BP) for ≈20 years with a low-dose thiazide, to which an angiotensin-converting enzyme-inhibitor had been added 5 years ago. In addition, after a possible transient ischemic attack 10 years ago, aspirin, omeprazole, and simvastatin had been added. She is known with mild cognitive impairment, which is stable with a mini-mental state examination score of 25, and a mild depression for which fluoxetine has been prescribed. In addition, she experienced 2 falls in the past 2 years; calcium/vitamin D and alendronate were started for the management of osteoporosis. On physical examination, she appears vital with a normal fluent gait and no signs of hemiparesis. Her BP is 165/75 mm Hg in the sitting position. Immediately after standing up from her chair, she feels dizzy for ≈10 seconds, but after 1 and 3 minutes, no orthostatic hypotension is found. Estimated glomerular filtration rate is 50 mL/min per 1.73 m 2 . Should antihypertensive treatment be intensified, left unaltered, or reduced?The oldest old, that is, persons aged ≥80 years, will be the fastest growing segment of the population for the next 40 years. By 2050, more than one quarter of all men and women aged ≥65 years in the Western world will be in the oldest old group. 1Despite longer life expectancy, the prevalence of various chronic diseases and functional impairment increases with age. As a result, populations of older individuals are often highly heterogeneous and individuals with same chronological age vary widely in health and functional ability. In other words, there is substantial heterogeneity in their biological age, and those at the higher end of biological age are often referred to as vulnerable or frail.BP rises with age, and ≈80% of people in Western societies aged ≥80 years have hypertension.2 Their hypertension is commonly characterized by elevated systolic BP, with often normal or even low diastolic BP. The widened pulse pressure (PP) is a reflection of increased arterial stiffness. Despite the large body of evidence in middle-aged populations, the predictive value of high BP in this rapidly growing older population is still debated, as is the question of whether hypertension should be treated, and if so, how intensively. Importantly, the current paradigm of lower is better may not apply to (untreated or treated) BP in the oldest old.In this concise narrative review, we summarize evidence from observational studies and randomized clinical trials. We conclude that biological age/frailty is becoming an important criterion for treatment decisions. Finally, we address what we think are the most pressing research questions for the coming years. Pathophysiology of BP Regulation in the Oldest OldAlthough hypertension in the oldest old may reflect a longstanding condition, often it manifests itself as a de novo abnormality. Data from the Framingham Heart Study indicate that the majority of patient...

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“…9,10 The African American Study of Kidney Disease and Hypertension (AASK) demonstrated that APOL1 risk variants were strongly associated with hypertensionattributed CKD in a recessive model with an odds ratio of 2.57; however, only 23% of AASK participants possessed 2 APOL1 risk variants; thus, cases with non-APOL1-mediated arteriolar nephrosclerosis were included in the study. 11 It is unknown whether APOL1-associated CKD has unique histopathology compared with ordinary (non-APOL1-mediated) forms of hypertensive nephrosclerosis.…”

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confidence: 99%

Histopathologic findings associated with APOL1 risk variants in chronic kidney disease

et al. 2015

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The effects of nephropathy risk variants in the apolipoprotein L1 gene (APOL1) on renal histopathology in African Americans with arterionephrosclerosis or putative 'hypertension-associated' nephropathy are unknown. APOL1 genotype-phenotype correlations were performed in a blinded manner from renal biopsies in 196 self-reported African Americans with arterionephrosclerosis on kidney biopsy at a large national nephropathology practice. Subjects had chronic kidney disease without nephrotic syndrome. A discovery analysis compared histopathologic changes in the glomerular and tubulointerstitial compartments in 58 subjects with 2 versus 56 subjects with 0 APOL1 risk variants. Validation was performed in biopsies from 82 additional subjects with 0, 1, and 2 risk variants. Two risk variant versus zero risk variant group genotype associations and subphenotypes were assessed by v 2 analyses. ANOVA compared means of continuous variables. In discovery analyses, significantly less obsolescent glomerulosclerosis, more (solidified and disappearing) glomerulosclerosis, more thyroidization-type tubular atrophy, and more microcystic tubular dilatation were seen in patients with two versus zero APOL1 risk alleles. Greater degrees of arteriosclerosis were present in those with zero risk alleles. Segmental glomerulosclerosis did not differ significantly between groups. Presence of two of the following discriminatory histopathologic findings from discovery, that is, o50% obsolescent glomerulosclerosis, thyroidization-type tubular atrophy, and microcystic tubular dilatation, was specific for the presence of two APOL1 risk alleles in the validation phase. African Americans with arterionephrosclerosis who possess two APOL1 risk variants more often lack obsolescent glomerulosclerosis and have greater degrees of (solidified and disappearing) glomerulosclerosis, thyroidization-type tubular atrophy, and microcystic tubular dilation than patients with fewer than two risk variants. These findings support involvement of multiple cell types in subnephrotic forms of APOL1-associated nephropathy, particularly renal tubule cells with resultant tubulointerstitial disease.

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Hypertension-Associated Kidney Disease

Cited by 91 publications

References 43 publications

Immune Mechanisms in Arterial Hypertension

Immune Mechanisms in Arterial Hypertension

Treatment of Hypertension in the Oldest Old

Histopathologic findings associated with APOL1 risk variants in chronic kidney disease

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