Renal Thrombotic Microangiopathies Induced by Severe Hypertension

Zhang, Bo; Xing, Changying; Yu, Xiangbao; Sun, Bin; Zhao, Xia; Qian, Jun

doi:10.1291/hypres.31.479

Cited by 54 publications

(43 citation statements)

References 16 publications

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“…Disruption of the vascular endothelium causes plasma constituents (including fibrinoid material) to enter the vascular wall and obliterate the vascular lumen [Strandgaard and Paulson, 1989]. In most patients with renal failure related to malignant hypertension, renal biopsy demonstrates an obliterative vasculopathy with fibrinoid necrosis as well as fibrin and platelet clots [Zhang et al 2008]. This luminal narrowing is believed to fragment erythrocytes and consume platelets leading to TMA [Akimoto et al 2011].…”

Section: Introductionmentioning

confidence: 99%

Differentiating malignant hypertension-induced thrombotic microangiopathy from thrombotic thrombocytopenic purpura

Khanal

Dahal

Upadhyay

et al. 2015

Therapeutic Advances in Hematology

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Objectives: Malignant hypertension can cause thrombotic microangiopathy (TMA) and the overall presentation may mimic thrombotic thrombocytopenic purpura (TTP). This presents a dilemma of whether or not to initiate plasma exchange. The objective of the study was to determine the clinical and laboratory manifestations of malignant hypertension-induced TMA, and its outcomes. Methods: Using several search terms, we reviewed English language articles on malignant hypertension-induced TMA, indexed in MEDLINE by 31 December 2013. We also report a new case. All these cases were analyzed using descriptive statistics. Results: A total of 19 patients, with 10 males, had a median age of 38 years at diagnosis; 58% had a history of hypertension. Mean arterial pressure at presentation was 159 mmHg (range 123-190 mmHg). All had prominent renal dysfunction (mean creatinine of 5.2 mg/dl, range 1.7-13 mg/dl) but relatively modest thrombocytopenia (mean platelet count of 60 × 103/µl, range 12-131 × 10 3 /µl). Reported cases (n = 9) mostly had preserved ADAMTS-13 activity (mean 64%, range 18-96%). Following blood pressure control, the majority had improvement in presenting symptoms (100%) and platelet counts (84%); however, only 58% had significant improvement in creatinine. More than half (53%) needed hemodialysis. One patient died of cardiac arrest during pacemaker insertion. Conclusion: Prior history of hypertension, high mean arterial pressure, significant renal impairment but relatively modest thrombocytopenia and lack of severe ADAMTS-13 deficiency (activity <10%) at diagnosis are clues to diagnose malignant hypertension-induced TMA. Patients with malignant hypertension respond well to antihypertensive agents and have favorable nonrenal outcomes.

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Section: Introductionmentioning

confidence: 99%

Differentiating malignant hypertension-induced thrombotic microangiopathy from thrombotic thrombocytopenic purpura

Khanal

Dahal

Upadhyay

et al. 2015

Therapeutic Advances in Hematology

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“…These abnormalities include increased mean platelet volume, 6 platelet activation, 7 increased platelet norepinephrine level 8 and efflux, 9 and increased renal platelet consumption/destruction (ie, thrombotic microangiopathy). 10 These data suggest platelet norepinephrine overload in hypertension. Given that (1) platelet phenol sulfotransferase activity is positively correlated with the level of its metabolite norepinephrine sulfate in plasma 11 and (2) hypertension occurs rapidly (within several weeks) after an increase in mean platelet volume, 12,13 increased mean platelet volume may reflect saturation of platelet norepinephrine-degrading enzymes or, in other words, functional platelet failure.…”

Section: To the Editormentioning

confidence: 89%

Renal Sympathetic Hyperactivity in Hypertension: True or False?

Zhou

2016

Circulation Research

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Increased renal norepinephrine spillover, observed by using isotope-dilution method, is thought to indicate renal sympathetic hyperactivity and to play a crucial role in hypertension. However, SYMPLICITY HTN-3 (Renal Denervation in Patients With Uncontrolled Hypertension), the first randomized shamcontrolled trial, failed to show a benefit of renal denervation for resistant hypertension.1 This raises the issue of whether the sympathetic hyperactivity hypothesis is true.In a recent issue of Circulation Research, Grassi et al 2 have emphasized the presence and importance of sympathetic hyperactivity in hypertension, primarily based on the results of isotopedilution studies. However, the isotope-dilution method cannot exclude the involvement of intraorgan platelet release of norepinephrine. We would argue that platelet norepinephrine release, rather than sympathetic nervous system alterations, may be the cause of increased norepinephrine spillover in hypertension for the following reasons.First, the platelets may serve as a reservoir for regional norepinephrine spillover. The platelets, the carriers of norepinephrine in the blood, link the upstream (the sympathetic nervous system) and downstream (the detoxifying and excretory organs) of the norepinephrine removal system. Namely, platelets take up and store norepinephrine released from the sympathetic nervous system 3 and carry it to the detoxifying and excretory organs for removal through an intraorgan platelet destruction mechanism. Moreover, platelet phenol sulfotransferase and monoamine oxidase can degrade norepinephrine, 3 which can explain the slower and smaller change in platelet norepinephrine level in response to stress than that of plasma norepinephrine level. The platelets contain a much higher norepinephrine concentration, with a platelet:plasma ratio of 1855:1. 4 The high intraplatelet norepinephrine concentration, together with a daily destruction of ≈10% of total platelets (platelet lifespan ≈10 days), constitutes an important source of regional norepinephrine spillover.Second, platelet norepinephrine release may contribute to regional differences in norepinephrine spillover. Kopin et al 5 found that although the mean renal norepinephrine release rate is only 2× that of the heart, the mean norepinephrine spillover from the kidneys is 10-fold greater than from the heart. 5 The high level of renal norepinephrine spillover cannot be explained by sympathetic activity but may be related to platelet norepinephrine release because intraorgan platelet destruction differs from organ to organ.Third, hypertension is associated with platelet abnormalities. These abnormalities include increased mean platelet volume, 6 platelet activation, 7 increased platelet norepinephrine level 8 and efflux, 9 and increased renal platelet consumption/destruction (ie, thrombotic microangiopathy).10 These data suggest platelet norepinephrine overload in hypertension. Given that (1) platelet phenol sulfotransferase activity is positively correlated with the level of its metabolite ...

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“…The study findings of the association between ADAMTS13 and renal dysfunction didn't prove causality in the study and ADAMTS13 represented a marker for the degree of endothelial damage rather than being causally related to the TMA and renal insufficiency of malignant hypertension [4]. Recent studies have investigated the utility of in-house ADAMTS assays [5], however to avoid the unnecessary use of plasmapharesis some institutions have used clinical prediction score method based on (platelet count, ddimer, creatinine, reticulocyte count, indirect bilirubin) [6], results of this score were validated in a recent cohort [7][8][9][10].…”

Section: Discussionmentioning

confidence: 99%

Thrombotic Microangiopathy and Low ADAMTS 13: Case Report and Review of the Literature

Almuwaqqat¹,

Ali²

2015

J Cytol Histol

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Background: Thrombotic Microangiopathy (TMA) is a multi-organ dysfunction syndrome characterized by microvascular thrombosis, thrombocytopenia and hemolytic anemia with diverse etiologies ranging from primary Thrombotic thrombocytopenic purura (TTP) and Hemolytic uremic syndrome (HUS) to secondary phenomena to medications, severe uncontrolled hypertension and autoimmune disorders i.e Scleroderma renal crises, catastrophic antiphospholipid syndrome and pre-eclampsia, prompt diagnosis, identification of potential etiologies and treatment are essential steps for reducing morbidity and mortality.

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Renal Thrombotic Microangiopathies Induced by Severe Hypertension

Cited by 54 publications

References 16 publications

Differentiating malignant hypertension-induced thrombotic microangiopathy from thrombotic thrombocytopenic purpura

Differentiating malignant hypertension-induced thrombotic microangiopathy from thrombotic thrombocytopenic purpura

Renal Sympathetic Hyperactivity in Hypertension: True or False?

Thrombotic Microangiopathy and Low ADAMTS 13: Case Report and Review of the Literature

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