Changing Patterns of End-Stage Renal Disease Due to Hypertension

Qualheim, Robert E.; Rostand, Stephen G.; Kirk, Katharine A.; Rutsky, Edwin A.; Luke, Robert G.

doi:10.1016/s0272-6386(12)80092-8

Cited by 51 publications

(17 citation statements)

References 27 publications

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“…We have recently shown a change in the peak incidence by age of hypertensive nephrosclerosis but an overall total increase for all ages between 1978 and 1988 in Jefferson County, Alabama. 80 We interpreted this as a possible delay in the development of ESRD due to primary hypertension because of antihypertensive therapy; however, there is, as yet, no evidence of prevention of development of ESRD.…”

Section: Lack Of Prevention Of End-stage Renal Diseasementioning

confidence: 98%

Essential hypertension: a renal disease? A review and update of the evidence.

Luke

1993

Hypertension

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Section: Lack Of Prevention Of End-stage Renal Diseasementioning

confidence: 98%

Essential hypertension: a renal disease? A review and update of the evidence.

Luke

1993

Hypertension

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“…Since the 1970s, it has been recognized that black Americans are at significantly greater risk of end-stage renal disease than whites. Currently, although they represent less than 13% of the general population, blacks make up almost a third of those with end-stage renal disease (2,3).…”

Section: Introductionmentioning

confidence: 99%

Kidney Transplant in Black Recipients: Are African Europeans Different from African Americans?

Pallet

Thervet

Alberti

et al. 2005

American Journal of Transplantation

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Demographic characteristics were similar for the two cohorts other than cause of end-stage renal failure (more hypertension among AE and more polycystic kidney disease among Cauc) and cold ischemia time (significantly longer for AE). Immunosuppressive treatment was comparable between groups. There were no significant differences between AE and Cauc in the incidence of acute rejection (31% vs. 30%). At 5 years post-transplant, patient survival (93% vs. 92%), graft survival (83% in both groups) and graft function (creatinine clearance 48 mL/min vs. 45 mL/min) were also similar among the AE and Cauc patients.We demonstrate that ethnic origin does not affect outcome after renal transplantation in France. Therefore, differences observed in the United States cannot be only related to immunologic or pharmacologic factors. The results of renal transplantation in patients of African origin could be improved with universal immunosuppressive drug coverage.

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“…The most accepted hypothesis is that the increase in blood pressure causes mechanical damage in the glomerulus. This theory seems to be supported by evidence that antihypertensive agents reduce, or at least postpone, the development of renal failure [9]. However, this hypothesis may not be necessarily true, since not all patients with a similar degree of hypertension progress to develop renal failure.…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress and Renal Dysfunction in Salt-Sensitive Hypertension

Loscalzo³

2001

Kidney Blood Press Res

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Hypertension is a risk factor for the development of end-stage renal disease. The mechanisms underlying hypertensive nephropathy are poorly understood. There is evidence, however, that in hypertension there is an accumulation of partially reduced oxygen and its derivatives, known collectively as reactive oxygen species, which may contribute to progressive renal dysfunction. In the present study, we assess the contribution of oxidative stress in the development of salt-dependent hypertensive nephrosclerosis. Going beyond previous end point studies, which inferred renal function either indirectly or only qualitatively, we have determined oxidative stress concurrently with direct and quantitative measurements of renal function (via inulin and p-aminohippuric acid clearances). Moreover, in this time-dependent study, the measurements have been taken under low- as well as high-salt diets. As was expected from previous studies, in the Dahl salt-sensitive rat, a high-salt diet (8% NaCl) resulted in the development of hypertension, in a decreased glomerular filtration rate, and in a decreased renal plasma flow as compared with the normotensive control, the Dahl salt-resistant rat. In addition, however, we found clear evidence for the accumulation of reactive oxygen species in renal tissue homogenates of Dahl salt-sensitive rats on the high-salt diet. Our time-dependent protocol also indicated that renal oxidative stress follows, in time, the development of hypertension. We also found that after 2 weeks of increased salt loading, Dahl salt-sensitive rats excreted less cyclic guanosine monophosphate and NO_x than Dahl salt-resistant rats on the same diet. It is known that urinary cyclic guanosine monophosphate and NO_x represent the activity and stable derivatives of renal NO·, respectively, and that they closely correlate with renal vascular resistance. Therefore, our results suggest that, in the Dahl salt-sensitive rat, increased oxidative stress is associated with salt-dependent hypertensive nephrosclerosis and that decreased NO· bioavailability may represent a common factor responsible for the vascular and glomerular dysfunction.

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Changing Patterns of End-Stage Renal Disease Due to Hypertension

Cited by 51 publications

References 27 publications

Essential hypertension: a renal disease? A review and update of the evidence.

Essential hypertension: a renal disease? A review and update of the evidence.

Kidney Transplant in Black Recipients: Are African Europeans Different from African Americans?

Oxidative Stress and Renal Dysfunction in Salt-Sensitive Hypertension

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