Malignant hypertension with thrombotic microangiopathy and persistent acute kidney injury (AKI)

Nzerue, Chike; Oluwole, Kemi; Adejorin, David; Paueksakon, Paisit; Fremont, Richard D.; Akatue, Richmond A.; Faulkner, Marquetta

doi:10.1093/ckj/sfu116

Cited by 18 publications

(6 citation statements)

References 12 publications

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“…Salt-loaded stroke-prone spontaneously hypertensive rats are included as a model of malignant hypertension, which is a common cause of AKI in pregnancy, especially in areas with less maternal care, where preeclampsia and eclampsia are more common and less well managed (109). However, malignant hypertension of unknown (131) and stimulant-related causes (55) cause AKI in other settings as well.…”

Section: Causes Of Akimentioning

confidence: 99%

Comparison of acute kidney injury of different etiology reveals in-common mechanisms of tissue damage

Hultström

Becirovic‐Agic

Jönsson

2018

Physiological Genomics

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Acute kidney injury (AKI) is a syndrome of reduced glomerular filtration rate and urine production caused by a number of different diseases. It is associated with renal tissue damage. This tissue damage can cause tubular atrophy and interstitial fibrosis that leads to nephron loss and progression of chronic kidney disease (CKD). This review describes the in-common mechanisms behind tissue damage in AKI caused by different underlying diseases. Comparing six high-quality microarray studies of renal gene expression after AKI in disease models (gram-negative sepsis, gram-positive sepsis, ischemia-reperfusion, malignant hypertension, rhabdomyolysis, and cisplatin toxicity) identified 5,254 differentially expressed genes in at least one of the AKI models; 66% of genes were found only in one model, showing that there are unique features to AKI depending on the underlying disease. There were in-common features in the form of four genes that were differentially expressed in all six models, 49 in at least five, and 215 were found in common between at least four models. Gene ontology enrichment analysis could be broadly categorized into the injurious processes hypoxia, oxidative stress, and inflammation, as well as the cellular outcomes of cell death and tissue remodeling in the form of epithelial-to-mesenchymal transition. Pathway analysis showed that MYC is a central connection in the network of activated genes in-common to AKI, which suggests that it may be a central regulator of renal gene expression in tissue injury during AKI. The outlining of this molecular network may be useful for understanding progression from AKI to CKD.

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Section: Causes Of Akimentioning

confidence: 99%

Comparison of acute kidney injury of different etiology reveals in-common mechanisms of tissue damage

Hultström

Becirovic‐Agic

Jönsson

2018

Physiological Genomics

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“…Less common clinical presentations may include fibrinoid necrosis within abdominal arteries producing major gastrointestinal tract infarction with an acute abdomen, necrotizing vasculitis as a feature of lupus, polyarteritis nodosa, or Takayasu arteritis. [29][30][31][32][33] Urine may contain protein and red cells. In a few patients, acute oliguric renal failure may be the presenting manifestation, and various features of renal dysfunction (including proteinuria) may be present.…”

Section: The Immune System In Malignant Hypertensionmentioning

confidence: 99%

Malignant hypertension: new aspects of an old clinical entity

Januszewicz¹,

Guzik²,

Prejbisz³

et al. 2015

Polish Archives of Internal Medicine

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Malignant hypertension (MHT), also known as accelerated-malignant hypertension or malignant-phase hypertension, is the most severe form of arterial hypertension. It is defined clinically as high blood pressure (BP) levels associated with lesions of the retinal fundus (flame-shaped hemorrhages, exudates, or cotton wool spots, with or without papilledema). Despite the availability of a vast range of antihypertensive agents, MHT continues to be a significant clinical challenge. Although its prevalence is very low, the absolute number of new cases has not changed over the past decades. While the role of the activation of the renin-angiotensin-aldosterone system and endothelial dysfunction in the pathogenesis of MHT has been well described, recent studies have indicated that the immune system may also play an important role in the development of this condition. Patients with MHT are characterized by pronounced target organ damage, including structural and functional cardiac abnormalities. MHT is frequently complicated by renal insufficiency and end-stage renal disease. The survival rates for patients with MHT have improved considerably with increased availability of antihypertensive treatment. However, renal insufficiency and end-stage renal disease still remain a significant cause of morbidity and mortality in this patient group. In conclusion, MHT is not a "vanishing disease" because there is a relatively stable number of new cases per year. Nonetheless, prognosis and survival rates in these patients have improved significantly owing to earlier detection, stricter BP control, lower BP targets, better choice of antihypertensive drugs, and availability of hemodialysis and renal transplantation.

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“…MHTN is characterized by severe hypertension and acute multi-organ ischemic complications including thrombotic microangiopathy (TMA). Renal TMA accompanying MHTN is due to thrombosis of small vessels, intravascular hemolysis with red cell fragments (Schistocytes), and platelet consumption 3 .…”

mentioning

confidence: 99%

CD4+CD25+ T Cells in primary malignant hypertension related kidney injury

Huang

Luo

Liang

et al. 2016

Sci Rep

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CD4+CD25+ T cells are critical for maintenance of immunologic self-tolerance. We measured the number of CD4+CD25+ cells in the patients with primary malignant hypertension related kidney injury, to explore the molecular pathogenesis of this disease. We selected 30 patients with primary malignant hypertension related kidney injury and 30 healthy volunteers. Information on clinical characteristics and laboratory tests was obtained from each subject. The number of CD4+CD25+ cells and glomerular injury were assessed by flow cytometry and histopathology, respectively. Both serum IL-2, IL-4, and IL-6 and endothelial cell markers were analyzed by ELISA. ADAMTS13 antibody was detected by Western blotting. CD4+CD25+ cells were significantly reduced in patients with primary malignant hypertension related kidney injury compared to controls (P < 0.05). The number of CD4+CD25+ cells was negatively related to blood urea nitrogen, serum uric acid, proteinuria, and supernatant IL-4; whereas positively associated with estimated glomerular filtration rate in patients. Gradually decreasing CD4+CD25+ cells were also found as increasing renal injury. Additionally, patients exhibited increasing supernatant IL-4, serum IL-2 and IL-6, endothelial cell markers, and anti-ADAMTS13 antibody compared with controls (all P < 0.05). CD4+CD25+ cells may play a key role in the pathogenesis of primary malignant hypertension related kidney injury.

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Malignant hypertension with thrombotic microangiopathy and persistent acute kidney injury (AKI)

Cited by 18 publications

References 12 publications

Comparison of acute kidney injury of different etiology reveals in-common mechanisms of tissue damage

Comparison of acute kidney injury of different etiology reveals in-common mechanisms of tissue damage

Malignant hypertension: new aspects of an old clinical entity

CD4+CD25+ T Cells in primary malignant hypertension related kidney injury

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