Posttransplant Hypertension: Multipathogenic Disease Process

Barbari, A

doi:10.6002/ect.2012.0311

Cited by 12 publications

(10 citation statements)

References 97 publications

(186 reference statements)

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“…71 The causes of posttransplant hypertension are diverse and may be related to both recipient and donor factors, transplant factors, renal dysfunction, and immunotherapy. 72,73 Blood pressure during the first year after transplantation has been associated with allograft survival independent of graft function. 74 There are, however, no randomized trials to date which have evaluated optimal levels of blood pressure control in transplant recipients.…”

Section: Blood Pressure Controlmentioning

confidence: 99%

Evaluation and Management of Proteinuria After Kidney Transplantation

Tsampalieros

Knoll

2015

Transplantation

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Proteinuria occurs commonly after kidney transplantation. Because there are no specific guidelines for defining and detecting proteinuria in transplant recipients, its prevalence can vary depending on the methods used. Most often, the same cutoffs for defining proteinuria in the nontransplant population are applied. There are several risk factors for proteinuria, including some transplant-specific diagnoses and immunosuppressive medications. Posttransplantation proteinuria is associated with reduced graft survival as well as an increased risk of cardiovascular events and death. Treatments to decrease proteinuria have been based on blocking the renin-angiotensin-aldosterone system with the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. This review describes the measurement, prevalence, etiology, prognostic significance, and management of proteinuria in both adult and pediatric transplant recipients.

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Section: Blood Pressure Controlmentioning

confidence: 99%

Evaluation and Management of Proteinuria After Kidney Transplantation

Tsampalieros

Knoll

2015

Transplantation

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“…38, [41][42][43] The absence of proteinuria may be explained by the introduction of the angiotensin receptor blocker telmisartan during the early posttransplant period for treatment of hypertension and the gradual tapering of everolimus levels. 7,8,11,44,45 The third graft biopsy was prompted by a sudden rise in serum creatinine levels in the absence of proteinuria after nearly 1 year of stable renal function and reduced maintenance immunosuppressive therapy. Histologic findings in the third biopsy included a partial regression in TIV ( Figure 5B) that was associated with doubling in IFTA to 30% ( Figure 5C), with electron microscopy showing mild glomerular and peritubular capillaries and endothelial cell damage with focal effacement of the foot processes ( Figure 6) but no presence of microinflammation or lamellation.…”

Section: Case Discussion and Review Of The Literaturementioning

confidence: 99%

Untitled

2015

Exp Clin Transplant

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Mammalian target of rapamycin inhibitors, such as rapamycin and more recently everolimus, have substituted calcineurin inhibitors in many minimization strategies. Despite their acclaimed renal safety profile, several lines of evidence are emerging on their potential nephrotoxic effect. Predisposing conditions for nephrotoxicity involve a complex interplay between several environmental and genetic factors in the donor-recipient pair. Renal injury may be enhanced by pharmacodynamic interactions when combined with other drugs such as calcineurin inhibitors or nutrients that are predominantly related to an increase in local tissue exposure. These toxic interactions may occur within adequate doses and therapeutic blood levels. This explains the occurrence of nephrotoxicity in some but not all cases. Here, we postulated that activity of a low permeability glycoprotein efflux pump related to low protein expression and/or inhibition enhanced immunosuppressive drug entry in different cells. A rise in intracellular drug concentration increases bioactivity, leading to greater immunosuppression and more immune-related, nonrenal adverse events in the recipient and increased nephrotoxicity in the kidney graft. Under specific isolated or combined environmental and/or genetic conditions in both the recipient and donor affecting the glycoprotein efflux pump and/or the mammalian target of rapamycin pathway, these renal injuries may be aggravated by heightened drug tissue concentrations despite adherence to therapeutic drug and blood levels. Mammalian target of rapamycin inhibitors may induce predominantly a dose-dependent renal epithelial cell injury affecting either the glomerular or the renal tubular epithelial cells, leading to cell death and apoptosis. Epithelial mesenchymal transitionmediated interstitial fibrosis and tubular atrophy observed with these drugs may be the result of a cumulative toxic renal tubular injury induced by the direct insult of the drug itself and/or podocytopathy-associated proteinuria. The resulting glomerular tubular damage will ultimately lead to graft failure and loss, if exposure persists.

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“…Nonetheless, 24 hr monitoring should be performed routinely [18,19] in this category of patients, due to involvement of immunosuppressant drugs and pro-inflammatory status in the development of arterial hypertension [20,21,22].…”

Section: Discussionmentioning

confidence: 99%

Office Assessed Blood Pressure and Ambulatory Blood Pressure Monitoring in Chronic Kidney Disease Patients Versus Kidney Transplant Recipients

Tarta

Denise

Tarta

et al. 2015

Acta Medica Marisiensis

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How reliable is office assessed blood pressure (BP) in chronic kidney disease (CKD) patients and kidney transplant (KTx) recipients is yet to be determined, although the diagnosis of arterial hypertension has been based on these measurements. The aim of this study was to investigate the potential differences between office assessed BP and ambulatory blood pressure monitoring (ABPM) in CKD patients and KTx recipients. We conducted a prospective study which enrolled 45 patients. Morning and evening seated office BPs were assessed using a sphygmomanometer at 5 consecutive outpatient visits. A mean systolic BP (SBP) and diastolic BP (DBP) was calculated. Ambulatory blood pressure was measured over 24 hours using a Meditech ABPM-05 device. Office SBP was statistically significant higher in CKD patients than KTx recipients both in the morning and evening (p=0.0433 and p=0.0066 respectively). ABPM showed higher night-time SBPs (p=0.0445) and higher overall, day-time and night-time DBPs in KTX recipients (p=0.0001, p=0.0006, p<0.0001 respectively). In CKD patients, office SBPs and DBPs are significantly higher than overall SBPs and DBPs as assessed by 24hr ABPM. Office BP monitoring as assessed by clinician is acceptable but tends to overestimate BP in both CKD and KTx study groups.

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Posttransplant Hypertension: Multipathogenic Disease Process

Cited by 12 publications

References 97 publications

Evaluation and Management of Proteinuria After Kidney Transplantation

Evaluation and Management of Proteinuria After Kidney Transplantation

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Office Assessed Blood Pressure and Ambulatory Blood Pressure Monitoring in Chronic Kidney Disease Patients Versus Kidney Transplant Recipients

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