Pathophysiology of Hypertensive Renal Damage

Ritz, Eberhard; Fliser, Danilo; Siebels, M.

doi:10.1093/ajh/6.7.241s

Cited by 23 publications

(11 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mechanisms by which hypertension could cause renal injury are incompletely understood 2,20 and may include glomerular ischemia secondary to vascular narrowing, 21 glomerulosclerosis due to intracapillary hypertension, 22 and interstitial fibrosis. 23 Two recent preliminary reports have stressed the importance of renal inflammatory phenomena, such as leukocyte infiltration, in experimental hypertension.…”

Section: Discussionmentioning

confidence: 99%

Hypertensive Nephrosclerosis as a Relevant Cause of Chronic Renal Failure

et al. 2001

View full text Add to dashboard Cite

Abstract-It is currently unclear whether hypertensive nephrosclerosis (HN), usually diagnosed solely on clinical grounds, is a relevant cause of end-stage renal disease. We biopsied 81 hypertensive outpatients (blood pressure Ն160/ 95 mm Hg) with moderate renal insufficiency, who were referred to our service from 1988 to 1998. Patients with known causes of hypertension, systemic disorders, rheumatic disease, or nephrotic syndrome were excluded. In 65% of patients, HN was the sole histological abnormality associated with renal dysfunction. Benign nephrosclerosis (BN), defined as isolated arteriolar hyalinosis and/or intimal fibrosis, was found in 18 HN patients (22%), whereas malignant nephrosclerosis (MN), denoted mainly by myointimal cell proliferation, appeared in 35 HN patients (43%). Previously undiagnosed primary nephritis (PN) was found in 13 patients (16%), whereas focal and segmental glomerulosclerosis, which might be either primary or secondary to hypertension, appeared in 15 patients (19% Usually, the diagnosis of HN is entirely made on clinical grounds, without renal biopsy or any evidence that hypertension actually preceded renal disease. Thus, HN can be easily mistaken for primary or ischemic nephropathies, which may also exhibit an insidious nature. Only 2 large biopsy-based studies of HN have been reported so far. Zucchelli and Zuccala 8 showed "true" HN in only 48% of 56 white patients clinically diagnosed as such. Fogo et al 9 showed an 85% agreement between clinical and histological diagnoses of HN in African Americans.We performed a 10-year follow-up of 81 hypertensives with impaired renal function and no clinical evidence of primary or ischemic renal disease. We could thus evaluate the frequency of HN among them and whether HN can be safely diagnosed on a clinical basis. Methods PatientsBetween 1988 and 1998, a selected, nonsystematic cohort of 90 hypertensive patients, referred to the Hypertension Clinic of the Renal Division, Department of Clinical Medicine, University of São Paulo, was investigated. Inclusion criteria were arterial hypertension and renal insufficiency. A patient was determined to have arterial hypertension if (1) systolic blood pressure (SBP) was Ն160 mm Hg and/or diastolic blood pressure (DBP) was Ն95 mm Hg, following the then most recent World Health Organization guidelines, 10 or (2) there was a persistent need for antihypertensives. Blood pressure was determined as the average of 2 sphygmomanometric measurements, taken in the seated position after a 5-minute rest. Renal insufficiency was defined by serum creatinine concentration (S creat ) Ͼ133 mol/L (1.5 mg/dL). Exclusion criteria were (1) renal artery stenosis (diagnosed by renal arteriography); (2) other definite causes of hypertension; (3) diabetes mellitus; (4) immune-mediated disease; (5) heart failure (stages III and IV); (6) liver disease; (7) nephrotic syndrome, defined by proteinuria Ͼ3.5 g/d, hypoalbuminemia, edema, and hypercholesterolemia; (8) polycystic nephropathy; (9) urinary obstruction; (10) pregnancy...

show abstract

Section: Discussionmentioning

confidence: 99%

Hypertensive Nephrosclerosis as a Relevant Cause of Chronic Renal Failure

et al. 2001

View full text Add to dashboard Cite

show abstract

“…When the capacity of the kidneys to maintain Na + balance and extracellular fluid volume within the appropriate range is compromised, increases in arterial pressure become necessary to re-establish normal balance [13, 15, 22, 23]. Varying degrees of reduced renal function have been found in hypertensive patients, and subtle disturbances in tubular transport function or microcirculatory dynamics due to either intrarenal defects or inappropriate humoral or neural stimuli are critical factors in the development of hypertension [12, 22, 24, 25]. Multiple renal derangements have been identified including impaired renal hemodynamics, renal autoregulatory capability, and pressure natriuresis, altered microvascular responses to vasoactive stimuli and enhanced Na + reabsorptive activity [26–29].…”

Section: Introductionmentioning

confidence: 99%

Salt-Sensitive Hypertension: Perspectives on Intrarenal Mechanisms

Majid

Prieto²,

Navar³

2015

CHYR

View full text Add to dashboard Cite

Salt sensitive hypertension is characterized by increases in blood pressure in response to increases in dietary salt intake and is associated with an enhanced risk of cardiovascular and renal morbidity. Although researchers have sought for decades to understand how salt sensitivity develops in humans, the mechanisms responsible for the increases in blood pressure in response to high salt intake are complex and only partially understood. Until now, scientists have been unable to explain why some individuals are salt sensitive and others are salt resistant. Although a central role for the kidneys in the development of salt sensitivity and hypertension has been generally accepted, it is also recognized that hypertension is of multifactorial origin and a variety of factors can induce, or prevent, blood pressure responsiveness to the manipulation of salt intake. Excess salt intake in susceptible persons may also induce inappropriate central and sympathetic nervous system responses and increase the production of intrarenal angiotensin II, catecholamines and other factors such as oxidative stress and inflammatory cytokines. One key factor is the concomitant inappropriate or paradoxical activation of the intrarenal renin-angiotensin system, by high salt intake. This is reflected by the increases in urinary angiotensinogen during high salt intake in salt sensitive models. A complex interaction between neuroendocrine factors and the kidney may underlie the propensity for some individuals to retain salt and develop salt-dependent hypertension. In this review, we focus mainly on the renal contributions that provide the mechanistic link between chronic salt intake and the development of hypertension.

show abstract

“…It is also expressed in endothelial cells, which can explain why epithelial injury also involves proteinuria. Ritz et al indicated that renal damage secondary to hypertension may be mediated by injury to endothelial cells [30], and in subsequent studies, endothelial cells were reported to play a vital role in hypertensive renal damage [31]. Deen also demonstrated that proteinuria can occur with endothelial disruption alone [32].…”

Section: Resultsmentioning

confidence: 99%

Alteration of Podocyte Protein Expression and Localization in the Early Stage of Various Hemodynamic Conditions

Wang

Yin

et al. 2013

IJMS

View full text Add to dashboard Cite

Given that podocalyxin (PCX) and nestin play important roles in podocyte morphogenesis and the maintenance of structural integrity, we examined whether the expression and localization of these two podocyte proteins were influenced in the early stage of various hemodynamic conditions. Mice kidney tissues were prepared by in vivo cryotechnique (IVCT). The distribution of glomeruli and podocyte proteins was visualized with DAB staining, confocal laser scanning microscopy and immunoelectron microscopy. The mRNA levels were examined by real-time quantitative PCR. The results showed the following: Under the normal condition, PCX stained intensely along glomerular epithelial cells, whereas nestin was clearly staining in the endothelial cells and appeared only weakly in the podocytes. Under the acute hypertensive and cardiac arrest conditions, PCX and nestin staining was not clear, with a disarranged distribution, but the colocalization of PCX and nestin was apparent under this condition. In addition, under the acute hypertensive and cardiac arrest conditions, the mRNA levels of PCX and nestin were significantly decreased. Collectively, the abnormal redistribution and decreased mRNA expressions of PCX and nestin are important molecular events at the early stage of podocyte injury during hemodynamic disorders. IVCT may have more advantages for morphological analysis when researching renal diseases.

show abstract

Pathophysiology of Hypertensive Renal Damage

Cited by 23 publications

References 0 publications

Hypertensive Nephrosclerosis as a Relevant Cause of Chronic Renal Failure

Hypertensive Nephrosclerosis as a Relevant Cause of Chronic Renal Failure

Salt-Sensitive Hypertension: Perspectives on Intrarenal Mechanisms

Alteration of Podocyte Protein Expression and Localization in the Early Stage of Various Hemodynamic Conditions

Contact Info

Product

Resources

About