Regulation of Plasma Arginine Vasopressin in Patients with Chronic Renal Failure Maintained on Hemodialysis

Mh, Jawadi; Ls, Ho; DiPette, Donald J.; Dl, Ross

doi:10.1159/000167108

Cited by 19 publications

(14 citation statements)

References 11 publications

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“…Other stimuli for the release of AVP during HD include nausea and pain related to puncture of the fistula. The effect of conventional HD on plasma osmolality is not well delineated, with some studies reporting no change [29,34] and others reporting a decrease in plasma osmolality [15,35,36,37,38,39,40,41,42,43,44]. Table 1 summarizes the theoretical effects of HD on AVP release.…”

Section: Stimuli For Avp Release During Hdmentioning

confidence: 99%

“…Plasma AVP levels in patients varied widely, with some studies reporting pre-HD plasma AVP levels above the concentration regarded as the upper level of normal of 4 pg/ml [2,16,24,25,35,37,38,39,40,41,45,46,47,48,49,50,51,52,53,54], while others found pretreatment plasma AVP levels around or below 4 pg/ml [32,33,34,43,44,55,56,57] (fig. 3a).The variation in pretreatment plasma AVP levels might be due to analytical variation resulting from the use of different assays.…”

Section: Plasma Vasopressin Levels In Dialysis Patients and Healthy Imentioning

confidence: 99%

“…Twenty-six of these studies, comprising 496 patients, were eligible for the meta-analysis since these studies reported the mean and standard deviation of plasma AVP levels before and after standard HD. Several studies observed a significant increase in plasma AVP levels during HD [15,16,29,38,52,53,57], whereas the other studies did not [32,33,34,35,36,37,39,40,41,42,43,44,46,49,50,51,54,55,56,58]. Overall, plasma AVP levels showed little or no increase during standard HD (7.0 ± 4.9 and 8.8 ± 9.3 pg/ml for pre- and post-HD, respectively; p = 0.433) .…”

Section: Effect Of Dialysis On Plasma Avp Levelsmentioning

confidence: 99%

“…Other studies did not specify whether their patient populations were hypotension-prone or not, but also found no change, or even a decrease, in plasma AVP levels during HD, irrespective of whether blood pressure remained stable [41,43,50,51,58] or decreased during HD [33,35,36,39,40,46]. …”

Section: Effect Of Dialysis On Plasma Avp Levelsmentioning

confidence: 99%

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Dialysis Hypotension: A Role for Inadequate Increase in Arginine Vasopressin Levels? A Systematic Literature Review and Meta-Analysis

Ettema¹,

Zittema²,

Kuipers

et al. 2014

Am J Nephrol

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Background: Intradialytic hypotension is a common complication of hemodialysis (HD). Some studies have suggested that inadequate arginine vasopressin (AVP) increase could play a role in the pathogenesis of intradialytic hypotension. However, AVP levels during HD and its relation to hypotension has never been systematically studied. Summary: PubMed and Embase were searched (1970-2013, search terms ‘vasopressin' and ‘hemodialysis') for studies reporting on AVP levels during standard HD or other dialysis techniques. Observational studies reporting on AVP levels pre- and postdialysis were additionally included in a meta-analysis. Thirty-seven studies were included in the systematic literature review, of which 26 studies were eligible for meta-analysis. The main findings were that pretreatment AVP levels were higher in dialysis patients compared with healthy controls (6.4 ± 3.5 vs. 2.5 ± 1.3 pg/ml, p = 0.003) and that plasma AVP levels showed little or no increase during HD (from 7.0 ± 4.9 to 8.8 ± 9.3, p = 0.433). Significant heterogeneity was found between studies. Meta-regression analysis revealed no significant associations between AVP and patient or study characteristics. Studies on other dialysis techniques showed mixed results regarding the AVP course. The eight studies that addressed the relation between intradialytic hypotension and AVP also showed inconsistent results. Key Messages: Plasma AVP levels are higher in dialysis patients compared with healthy controls, but show little or no increase during HD. The lack of a rise in AVP levels during HD may be pathophysiologically involved in the onset of intradialytic hypotension, but firm conclusions are not possible from our review of the literature.

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Section: Stimuli For Avp Release During Hdmentioning

confidence: 99%

Section: Plasma Vasopressin Levels In Dialysis Patients and Healthy Imentioning

confidence: 99%

Section: Effect Of Dialysis On Plasma Avp Levelsmentioning

confidence: 99%

Section: Effect Of Dialysis On Plasma Avp Levelsmentioning

confidence: 99%

See 2 more Smart Citations

Dialysis Hypotension: A Role for Inadequate Increase in Arginine Vasopressin Levels? A Systematic Literature Review and Meta-Analysis

Ettema¹,

Zittema²,

Kuipers

et al. 2014

Am J Nephrol

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“…The 1. Abbreviations used in this paper: AC, adenylyl cyclase; AVP, arginine vasopressin; CCT, cortical medullary collecting tubule; CRF, chronic renal failure; CT, cholera toxin; IMCD, inner medullary collecting duct; IMCT, inner medullary collecting tubule; PKC, protein kinase C; PM, plasma membrane; PT, pertussis toxin; RT, reverse transcription; V2R, V2 receptor. urinary concentrating defect in uremia is not due to deficient arginine vasopressin (AVP) secretion from the pituitary gland as both the neurophysin for AVP (3) and AVP itself (4) are found in increased quantity in the sera of patients with CRF. Furthermore, Tannen et al have demonstrated persistent excretion of hypotonic urine by patients with CRF despite the administration of exogenous AVP (5) suggesting that the concentrating defect is at least in part due to impaired AVP responsiveness of the collecting duct.…”

Section: Introductionmentioning

confidence: 99%

Vasopressin resistance in chronic renal failure. Evidence for the role of decreased V2 receptor mRNA.

Teitelbaum¹,

McGuinness²

1995

J. Clin. Invest.

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Studies were performed to determine the mechanism underlying deficient arginine vasopressin (AVP) -stimulated adenylyl cyclase activity in chronic renal failure (CRF). As compared to control, principal cells cultured from the inner medullary collecting tubule of rats previously made uremic by 5/6 nephrectomy fail to accumulate cAMP when stimulated with AVP. CRF cells do respond normally to forskolin or cholera toxin and the defect in AVP responsiveness is not prevented by treatment with pertussis toxin, by cyclooxygenase inhibition, or by inhibition or down-regulation of protein kinase C. In contrast to their lack of responsiveness to AVP, CRF cells respond normally to other agonists of adenylyl cyclase such as isoproterenol or prostaglandin E2. Plasma membranes prepared from the inner medullae of CRF rats exhibit a marked decrease in apparent AVP receptor number but no change in the apparent number of beta adrenergic receptors. Reverse transcriptase PCR of total RNA from the inner medullae of CRF animals reveals virtual absence of V 2 receptor mRNA; mRNA for a, is present in normal abundance. These studies indicate that AVP resistance in CRF is due, at least in part, to selective downregulation of the V 2 receptor as a consequence of decreased V 2 receptor mRNA. (J. Clin. Invest. 1995.96:378-385.)

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Blood Pressure Control in Chronic Hemodialysis Patients

London¹,

Marchais²,

Guérin³

Replacement of Renal Function by Dialysis

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Regulation of Plasma Arginine Vasopressin in Patients with Chronic Renal Failure Maintained on Hemodialysis

Cited by 19 publications

References 11 publications

Dialysis Hypotension: A Role for Inadequate Increase in Arginine Vasopressin Levels? A Systematic Literature Review and Meta-Analysis

Dialysis Hypotension: A Role for Inadequate Increase in Arginine Vasopressin Levels? A Systematic Literature Review and Meta-Analysis

Vasopressin resistance in chronic renal failure. Evidence for the role of decreased V2 receptor mRNA.

Blood Pressure Control in Chronic Hemodialysis Patients

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