Severe and malignant hypertension are common in primary atypical hemolytic uremic syndrome

Cavero, Teresa; Arjona, Emilia; Soto, Karina; Caravaca-Fontán, Fernando; Rabasco, Cristina; Bravo, Luis Eduardo; Cerda, Francisco de la; Martín, Nàdia; Blasco, Miquel; Ávila, Ana; Huerta, Ana; Cabello, Virginia; Jarque, Ana; Alcázar, Concepción; Fulladosa, Xavier; Carbayo, Javier; Anaya, S; Cobelo, Carmen; Ramos, Natália; Iglesias, Elena; Baltar, José; Martínez-Gallardo, Rocío; Pérez, L. Figuero; Morales, Enrique; González, Roberto; Macía, Manuel; Draibe, Juliana; Pallardó, Luís; Quintana, Luís F.; Espinosa, Mario; Barros, Xoana; Pereira, Fernando; Cao, Mercedes; Moreno, Juan Antonio; Córdoba, Santiago Rodrı́guez de; Praga, Manuel

doi:10.1016/j.kint.2019.05.014

Cited by 56 publications

(51 citation statements)

References 32 publications

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“…A considerable percentage of patients with MHT or hypertension‐MOD had MAHA. These patients may have atypical uremic hemolytic syndrome and complement abnormalities 37,38 . In patients with MHT, those who presented MAHA had worse renal function but better renal recovery, consistent with the finding that MAHA predicts renal insufficiency and recovery in MHT 39 .…”

Section: Discussionsupporting

confidence: 79%

Clinical value of multiorgan damage in hypertensive crises: A prospective follow‐up study

Jiang

Zhuo

et al. 2020

J of Clinical Hypertension

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Hypertensive crises are associated with high rates of target organ complications and poor outcomes. A recent shift from the definition of malignant hypertension to hypertension‐multiorgan damage (MOD) contributes to the diagnosis and management of hypertensive crises. Here, we prospectively included 166 adult (≥18 years old) patients with hypertensive crises (blood pressure >180/120 mm Hg). Target organs and causes of hypertension were assessed. Patients who were diagnosed with malignant hypertensive retinopathy, the absence of malignant hypertensive retinopathy but the presence of damage to at least 3 organs, and the absence of both retinopathy and MOD were classified as the malignant hypertension (n = 48), hypertension‐MOD (n = 42), and hypertension without MOD (n = 76) groups, respectively. Patients were followed to evaluate renal and cardiovascular prognoses. At baseline, patients with malignant hypertension had worse renal function, higher level of albuminuria, and more severe microvascular damage than those with hypertension‐MOD. Both had similar proportions of malignant arteriolar nephrosclerosis (83% vs 64%), left ventricular hypertrophy (90% vs 88%), abnormal repolarization (71% vs 60%), and left ventricular dysfunction (12% vs 21%). At the twenty months of follow‐up, both the malignant hypertension and hypertension‐MOD groups had similar blood pressure control rates and proteinuria. Both groups had worse renal outcomes than the hypertension without MOD group (P = .002). Patients with hypertension‐MOD (HR = 0.67, [95% CI: 0.30‐1.46], P = .31) had similar renal event‐free survival than patients with MHT after adjustments of age, sex, blood pressure, and proteinuria control. These results suggest that in hypertensive crises, both malignant hypertension and hypertension‐MOD have impact on adverse renal outcomes.

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Section: Discussionsupporting

confidence: 79%

Clinical value of multiorgan damage in hypertensive crises: A prospective follow‐up study

Jiang

Zhuo

et al. 2020

J of Clinical Hypertension

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“…Indeed, increased levels of complement degradation products, low levels of intact C3, and complement depositions in kidneys were reported in patients and animal models with secondary TMA. 2,3 Moreover, the membrane surface alterations in endothelial cell injury may lead to increased binding of C3b and decreased binding of complement factor H, thus changing the balance between activating and inhibitory complement components. However, there are many other causes of endothelial cell injury (toxins, heme, cytokines, thrombin, lipopolysaccharide, iron, and increased shear stress), which lead to increased expression or production of adhesion molecules, tissue factor, von Willebrand factor, and endothelin-1; recruitment of inflammatory cells; decreased expression of thrombomodulin and nitric oxide; and altered sensitivity to angiotensin II.…”

Section: Endothelial Damage: It Is Not All Complementmentioning

confidence: 99%

“…Although this issue is controversial, pregnancy-associated aHUS and hypertension-induced TMA are not included in the list because recent studies suggest that most patients with these entities could have primary, complement-mediated aHUS. 1,2 Complement activation in secondary HUS…”

mentioning

confidence: 99%

Complement inhibitors are useful in secondary hemolytic uremic syndromes

Caravaca-Fontán

Praga

2019

Kidney International

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“…Given the severity of renal disease presenting with TMA in the setting of malignant hypertension, early detection of complement involvement may help identify a subset of patients that would benefit from complement inhibition especially when blood pressure lowering does not improve TMA (48). Eculizumab (Soliris, Alexion Pharma.)…”

Section: In Another Cohort Of Patients With Ahus Hellp (Hemolysis Ementioning

confidence: 99%

Complement in Secondary Thrombotic Microangiopathy

Palma

Sridharan

Sethi

2021

Kidney International Reports

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Severe and malignant hypertension are common in primary atypical hemolytic uremic syndrome

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Cited by 56 publications

References 32 publications

Clinical value of multiorgan damage in hypertensive crises: A prospective follow‐up study

Clinical value of multiorgan damage in hypertensive crises: A prospective follow‐up study

Complement inhibitors are useful in secondary hemolytic uremic syndromes

Complement in Secondary Thrombotic Microangiopathy

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