Hemodynamics of Hypertension in Chronic End-Stage Renal Disease

Abstract

SUMMARYThis study was undertaken to define the hemodynamic changes in hypertension of chronic end-stage renal disease. Mean cardiac index in 75 uremic patients was higher (P < 0.001) than that of 42 normal volunteers while stroke index was not different from normals. The higher cardiac indices of uremic patients were accounted for by increased heart rates. Despite the significantly higher blood pressure in the uremics, their mean total peripheral resistance index was not different from that of normals.The total group of 75 patients included 52 hypertensive and 23 normotensive uremics. Cardiac index, heart rate, and stroke index were the same in 52 hypertensive and 23 normotensive uremics while mean total peripheral resistance index of hypertensive uremics was higher (P < 0.001) than normotensive uremics. Therefore, the hypertension in end-stage renal disease is sustained by a high total peripheral resistance.Bilateral nephrectomy in 12 hypertensive uremics resulted in no changes in cardiac index; a consistent decrease in blood pressure (P <0.001) and a decrease in total peripheral resistance index (P < 0.001) occurred. Bilateral nephrectomy in eight additional uremics with malignant hypertension resulted in an actual increase in cardiac index (P < 0.001) with a consistent reduction in blood pressures (P < 0.001) and an even more dramatic decrease in total peripheral resistance (P < 0.001).These findings imply that a vasopressor substance of renal origin increasing peripheral resistance is the major factor in the pathophysiology of renal hypertension in the late stage

Effect of Blood Pressure on Early Decline in Kidney Function Among Hypertensive Men

“…It is extremely difficult to distinguish cause-and-effect relationships between BP and kidney disease in observational studies. 2,3,7,26 Key advantages to our study are that we examined this relation among hypertensive men who were initially free of chronic kidney disease and we had repeated measures of BP and kidney function over a prolonged period of follow-up. Thus, we can effectively emphasize the importance of interventions aimed at the primary prevention of chronic kidney disease.…”

“…2 Despite the availability and widespread use of antihypertensive medication, elevated BP continues to be a major contributor to chronic kidney disease and the leading cause of ESRD in African-Americans. 2,5,6 It has long been accepted that advanced kidney failure results in hypertension 7 and that untreated severe and malignant hypertension almost always leads to kidney damage. 8 In the general population, however, severe or malignant hypertension is infrequent and appears to account for only a small proportion of all cases of kidney failure.…”

Wave reflections and cardiac hypertrophy in chronic uremia. Influence of body size.

“…In ESRD patients, anemia, arteriovenous fistula, and overhydration induce volume overload with increased cardiac output, 24 cardiac work, and LVH. 13 In the present study, volume load factors (arteriovenous fistula flow, anemia) were similar in the two groups and could not account for the difference in LVM.…”

“…Furthermore, total peripheral resistance was low because of anemia and the arteriovenous fistula, factors that tend to diminish the intensity of AWRs in ESRD patients. 7 Anemia correction or arteriovenous fistula occlusion increases peripheral resistance, 24 favoring an increase of reflections. and AWRs.…”

Proceedings from the Society of Interventional Radiology Foundation Research Consensus Panel on Renal Sympathetic Denervation

“…However, this procedure was also associated with significant morbidity and orthostatic hypotension and was abandoned in the 1960s with the widespread advancements in, and availability of, effective pharmacologic therapy. In the 1970s, operative ligation of the sympathetic fibers in the perirenal space was considered a contributor to the benefits of renal artery surgery for treatment of renovascular HTN or chronic kidney disease (4). More recently, convincing evidence has emerged that chronic elevation of sympathetic nervous system activity is a major contributor to the complex pathophysiology of essential HTN and in particular resistant HTN (5,6).…”