Hypertension in Chronic Kidney Disease: Navigating the Evidence
hypertension with heart disease, ICDCM presumes a cause-and-effect relationship disease with hypertension as hypertensive chronic kidney disease . Keywords: Masked hypertensionRenal arteriolosclerosisGlomerular Therefore, we investigated their relationship in patients with chronic glomerular .. First, we could not establish a cause- effect relationship because of the. Expanded understanding of the role of CKD as both a cause and a target of hypertension vascular calcification and its association with CKD and hypertension. with chronic kidney disease Stage 3/4) that failed to show a beneficial effect of.
Combination Therapy Most patients with CKD require more than one antihypertensive medication for treatment of hypertension.
Choosing agents that have complementary mechanisms of actions or are indicated to address other comorbid conditions is a useful strategy to optimize therapy and minimize side effects. Loop diuretics are often necessary to treat volume overload or hyperkalemia.
Dual blockade with ACE inhibitors and ARBs reduces proteinuria to a greater degree than either class alone, but has not been proven to preserve renal function or improve cardiovascular outcomes [ 71 ]. In this large trial of patients at high risk for vascular disease, the mean serum creatinine was approximately 1. Combining aldosterone antagonists with inhibitors of the RAS, although possessing additional antiproteinuric effects, should be discouraged for the same reasons—lack of proven clinical benefit and increased risk of side effects [ 73 ].
The role and safety of combination blockade of the RAS consisting of a direct renin inhibitor in patients with CKD are not yet fully elucidated. Results of future studies, including that of an ongoing clinical trial of diabetic patients with similar degree of CKD as in AVOID [ 75 ], may answer whether combination blockade of the RAS using direct renin inhibitors results in improvement of hard clinical endpoints. Nonpharmacologic Therapy Although pharmacologic therapy is often necessary to control blood pressure in most patients with CKD, sodium restriction, smoking cessation, moderate alcohol consumption, weight loss, and regular exercise should be part of a comprehensive strategy of effective treatment of hypertension in CKD.
Dietary recommendations need to be modified according to the stage of CKD to optimally regulate protein, phosphorus, and potassium intake [ 47 ]. Since most lesions are asymptomatic, the true prevalence is not known. Studies of insurance claims data and patients undergoing angiography for unrelated indications report wide variations in prevalence ranging from 0.
The natural history of the disease is also controversial, with only a minority of patients developing progressive renal failure or intractable hypertension [ 78 ]. To date, controlled clinical trials have not demonstrated the superiority of percutaneous revascularization over medical therapy [ 79 — 82 ]. These studies, however, spanned a long period of time and employed different interventions, entry criteria, treatment protocols, and endpoints.
Until the results of a large ongoing trial clarify the role of revascularization [ 83 ], medical therapy of hypertension and other atherosclerotic factors remains the mainstay of treatment of atherosclerotic renal artery stenosis. Revascularization may be warranted in patients with recurrent pulmonary edema, solitary or transplanted kidney, or worsening renal failure.
As discussed above, the applicability of this goal to patients who do not have proteinuric native kidney disease has not been established.
Whether specific classes of antihypertensive agents provide additional benefit to transplant recipients beyond what is obtained from control of blood pressure per se is also not known. As long as there are no specific contraindications against or compelling indications for a specific class of agents, any antihypertensive agent could be used in transplant recipients.
Close monitoring is warranted when using nondihydropyridine calcium channel blockers diltiazem, verapamil and inhibitors of the RAS because the former inhibit metabolism of immunosuppressive agents by the cytochrome P system, and the latter could result in hyperkalemia [ 8485 ]. Experimental Approaches Advances in device technology have allowed the resurgence of invasive prepharmacotherapy interventions for resistant hypertension that were abandoned because of technical difficulties or excessive morbidity.
Preliminary results of carotid sinus stimulation and catheter-based renal sympathetic denervation suggest that sustained reduction in blood pressure could be achieved with acceptable risks [ 8687 ]. If these early results could be replicated in diverse clinical settings, including patients with CKD, they would expand the range of options for the treatment of resistant hypertension.
Summary Treatment of hypertension in CKD patients should take into consideration the nature of the underlying kidney disease. Dual or triple blockade of the RAS should generally be avoided.
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Hypertension awareness, treatment, and control in adults with CKD: Low medication adherence and hypertension control among adults with CKD: National health and nutrition examination survey American Journal of Nephrology.
Hypertension awareness, treatment, and control in chronic kidney disease. American Journal of Medicine. Bangash F, Agarwal R. Masked hypertension and white-coat hypertension in chronic kidney disease: Clinical Journal of the American Society of Nephrology. Agarwal R, Lewis RR.
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CKD and Hypertension - Coding Tip - Provident Consulting
Prevalence, treatment, and control of hypertension in chronic hemodialysis patients in the United States. Prevalence of hypertension in patients on peritoneal dialysis: Hypertension after renal transplant. Journal of Clinical Hypertension. Hypertension and survival in hemodialysis patients. In-center hemodialysis six times per week versus three times per week. Hypertension after kidney transplantation. Improved long-term outcomes after renal transplantation associated with blood pressure control.
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Hypertension in Chronic Kidney Disease – Role of Arterial Calcification and Impact on Treatment
Control with an orally active inhibitor of angiotensin-converting enzyme. Most of these abnormalities occur early in the course of CKD and may contribute to the development and progression of vascular calcification and atherosclerosis. The mechanisms regulating the process of vascular calcification and the factors involved are subject to continued investigation. Both calcium and phosphorus directly stimulate vascular smooth muscle cell transformation into osteoblast-like cells and abnormal mineralization In vitro.
The mechanisms whereby smooth muscle cells calcify appears to result from a complex interplay between factors that activate and inhibit tissue calcification. In vitro studies have shown that elevated levels of extracellular calcium and phosphorus can induce mineralization of vascular smooth muscle cells. For example, paricalcitol has been shown to be less pro-calcifying in uraemic rats than calcitriol or doxercalciferol.
However, there are no prospective randomised controlled trials in CKD patients comparing the effect of native vitamin D or active vitamin D derivatives with placebo on vascular calcification. It depends on the arterial wall structure and function but is mainly influenced by age-associated alterations and BP.
Age, mean arterial BP, diabetes and aortic calcification score were all independent determinants of increased PWV. The relationship between measures of arterial stiffness PWV and the extent of calcification in the coronary arteries was also examined by Haydar et al. The next step in validating PWV as a useful tool for the risk assessment of CKD patients was to study the effect of pharmacological intervention. Clinical studies involving essential hypertension and CKD patients have shown that angiotensin-converting enzyme ACE inhibitors and calcium antagonists decreased aortic PWV to a large extent in response to BP lowering.
They showed that the loss of aortic PWV sensitivity to BP was predictive of adverse outcome, indicating that arterial stiffness is not only a risk factor contributing to the development of CV disease but also a marker of more advanced, less reversible arterial damage.
Taken together, these results support the hypothesis that measurement of arterial parameters exploring both structural and functional properties, such as quantification of arterial calcium deposit and determination of PWV, could help in stratifying the risk but also in evaluating the risk reduction strategies by monitoring these arterial parameters under different drug regimens. Significant alterations of the aortic PWV appear at an early stage of the disease; mild-to-moderate renal insufficiency, an elevated stiffness of the central arteries seems to be significantly associated with a reduced creatinine clearance, independent of BP and other standard CV risk factors.
Most of the evidence for reducing BP comes from large randomised controlled trials in the general population. These trials showed that treatment of BP reduces CV outcomes.
In CKD patients with proteinuria, it has been shown that BP reduction is associated with a slower decline of renal function. Numerous randomised controlled trials in diabetic and non-diabetic CKD patients have shown that these agents slow the decline of CKD compared with placebo or with other antihypertensive agent. Aliskiren, the first direct renin inhibitor to receive approval for hypertension treatment, was thought to provide additional renoprotective effects over standard treatment.
This study was terminated prematurely due to higher adverse events occurring in patients receiving aliskiren in addition to the standard care, such as an increased incidence of a non-fatal stroke, renal failure, hyperkalaemia and hypotension. This study, which included 11, high-risk hypertensive patients, showed that events of CKD defined as double serum creatinine or ESRD were lower in the benazepril—amlodipine group compared with the benazepril—hydrochlorothiazide group hazard ratio [HR] 0.
A possible explanation may come from the differential effect of calcium channel blockers compared with thiazides on vascular calcification. In fact, no study has really investigated the effect of treatment on vascular calcifications and BP and the progression of renal diseases.
While the main study failed to show any difference in mortality and morbidity between the two arms, the substudy showed a slower progression of coronary calcification in the nifedipine versus the co-amilozide group.
However, recent evidence from small trials suggest that thiazides may still be useful in advanced CKD.
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- Hypertension in Chronic Kidney Disease: Navigating the Evidence
- CKD and Hypertension – Coding Tip
Indeed, a meta-analysis reported that compared with placebo the risk ratio of all-cause mortality relative risk [RR] 0.