Blood pressure and total peripheral resistance in children with chronic kidney disease

Mitsnefes, Mark; Knilans, Timothy K.; Mays, Wayne A.; Khoury, Philip R.; Daniels, Stephen R.

doi:10.1007/s00467-004-1798-0

Cited by 9 publications

(8 citation statements)

References 9 publications

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“…Consistent with the results obtained in animal models, children with stages 2-4 CKD demonstrate increased total peripheral vascular resistance [12]. Similarly, in hypertensive children without CKD but with an average estimated GFR (eGFR) equivalent to renal insufficiency (70.4± 5.4 mL/min per 1.73 m 2 ), significant elevations of ADMA (230%) and SDMA (116%) are observed, as compared to that of normative controls [13].…”

Section: Introductionsupporting

confidence: 81%

Methylated arginine derivatives in children and adolescents with chronic kidney disease

et al. 2009

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Asymmetric dimethylarginine (ADMA), a methylated L: -arginine (Arg) derivative is associated with endothelial dysfunction, vasoconstriction, and hypertension in animals and humans. We examined the relationship between these derivatives, estimated glomerular filtration rate (eGFR), and awake (AW) and asleep (AS) blood pressure (BP) load in children and adolescents (n = 28) with stage 2-3 chronic kidney disease (CKD) and in matched intra-familial controls (n = 10). Plasma L: -Arg, ADMA, and symmetric dimethylarginine (SDMA) levels were measured by high-performance liquid chromatography-tandem mass spectrometry. Subjects wore a 24-hr ambulatory BP monitor with BP load >95th percentile. ADMA, SDMA/ADMA ratio and SDMA were 38-200% higher in CKD patients while L: -Arg/ADMA and L: -Arg/SDMA ratios and the L: -Arg level were 11-64% lower. The eGFR explained 42-60% of L: -Arg/SDMA, SDMA/ADMA, and SDMA variability (n = 38). Using linear regression, SDMA and SDMA/ADMA separately explained 15-38% of AW and AS systolic (S) BP and diastolic (D) BP load variability (p < 0.001-0.022). Using multivariate stepwise regression with eGFR held constant, SDMA/ADMA was a significant independent variable for AW DBP load (p = 0.03). In conclusion, BP load and a disproportionate elevation of SDMA are seen in children and adolescents with stage 2-3 (mild-moderate) CKD. SDMA is a strong marker for reduced eGFR and serves as a moderate but significant indicator of 24-hr BP load variability.

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Section: Introductionsupporting

confidence: 81%

Methylated arginine derivatives in children and adolescents with chronic kidney disease

et al. 2009

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“…This result is in accordance with Matteucci and collaborators that previously observed an increased peripheral resistance in 11 children after renal transplantation [41]. The mechanisms of elevated vascular resistance in chronic kidney diseases could include either increased vasoconstriction or impaired vasodilation [40]. In this regard, increased activity of sympathetic nervous and the Renin Angiotensin System (RAS), elevated levels of endothelin 1 and thromboxane could mediate vasoconstriction while decreased prostacyclin and nitric oxide activity might be responsible for an abnormally reduced vasodilation.…”

Section: Clinical Studiessupporting

confidence: 90%

“…More recently, in an observational study, Mitsnefes and coworkers [40] evaluated the relative role of total peripheral resistance and cardiac output at rest and during peak exercise in the development of hypertension in children at different stages of chronic kidney disease. These authors concluded that increased total peripheral resistance is a major contributor to elevated blood pressure [40]. This result is in accordance with Matteucci and collaborators that previously observed an increased peripheral resistance in 11 children after renal transplantation [41].…”

Section: Clinical Studiesmentioning

confidence: 99%

Pathophysiology of Arterial Hypertension: Insights from Pediatric Studies

Silva¹

2006

CPR

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Blood pressure is the direct product of cardiac output and total peripheral resistance. Cardiac output is regulated by preload, myocardium contractility and heart rate, while total peripheral resistance depends on afterload and vessel elasticity. The maintenance of blood pressure within normal limits is influenced by neural, humoral and local control mechanisms, which have extensive and complex interactions, making difficult an individual analysis. Thus, isolated or combined disarrangements in these mechanisms can lead to the development of hypertension. Neural blood pressure regulation mainly depends on lower brain stem centers of cardiovascular control and the autonomous nervous system, integrating the cardiovascular reflexes. In regard to humoral mechanisms, several substances/ systems contribute for increasing blood pressure (Angiotensin II, circulating cathecolamines), while others can play a counterregulatory role [Angiotensin-(1-7), kallikrein-kinin system and natriuretic peptides]. Moreover, local factors, such as nitric oxide and endothelins, act as determinants of vascular resistance and as systemic or local modifiers of neural and humoral mechanisms. Recently, research has begun to disclose the mechanisms related to blood pressure regulation at cellular and molecular level. In this review, we discussed experimental and clinical evidence relating to regulatory mechanisms probably involved in the pathophysiology of arterial hypertension with insights from pediatric studies.

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“…A study of children with CKD stages 2-4 demonstrated that elevated BP was associated with an increase in vascular resistance [20]. They found that children on ACEI or ARB therapy had lower total peripheral resistance suggesting an important role for the renin-angiotensin system.…”

Section: Discussionmentioning

confidence: 99%