Medullary Microvascular Thrombosis and Injury in Sickle Hemoglobin C Disease

Bissonnette, Mei Lin Z.; Henriksen, Kammi J.; Delaney, Kristie; Stankus, Nicole; Chang, Anthony

doi:10.1681/asn.2015040399

Cited by 5 publications

(2 citation statements)

References 27 publications

(41 reference statements)

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“…These factors ultimately result in impaired blood flow, microinfarctions, and ischemia. Over time, this leads to remodeling of the medullary vasa recta peritubular capillaries with multilayering of the basement membranes, peritubular capillary loss, interstitial fibrosis and tubular atrophy, and papillary necrosis when severe [6][7][8]. The clinical manifestations of renal medullary injury include hyposthenuria, polyuria, metabolic acidosis, and hyperkalemia.…”

Section: Sickle Cell Nephropathymentioning

confidence: 99%

Acute kidney injury in children with sickle cell disease—compounding a chronic problem

2017

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In an article recently published in Pediatric Nephrology, Baddam and colleagues discuss the relatively underreported clinical problem of repeated episodes of acute kidney injury (AKI) in children with sickle cell disease (SCD). Their report is a cautionary note about the importance of repeated kidney injury on the background of underlying chronic kidney injury and its potential implications on long-term kidney outcome. In children and adults with SCD, this includes the effects of repeated vaso-occlusive crises and the management of these painful episodes with non-steroidal anti-inflammatory drugs. Here we review the scope of kidney involvement in SCD in children and discuss the potential short-and long-term consequences of AKI in children with SCD.

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Section: Sickle Cell Nephropathymentioning

confidence: 99%

Acute kidney injury in children with sickle cell disease—compounding a chronic problem

2017

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“…Endothelial interaction with multiple blood components, including sickled red blood cells, leukocytes and platelets, injure the endothelium and obstruct the vasculature impacting internal organs [69]. Renal pathology in sickle cell nephropathy includes extensive peritubular microvascular congestions and chronic thrombotic microangiopathy that can lead to CKD by peritubular microvascular rarefaction, interstitial fibrosis and tubular atrophy [70][71][72].…”

Section: Renal Endothelium and Pathogenesis Of Chronic Kidney Disease...mentioning

confidence: 99%

Kidney Injuries in Sickle Cell Disease

Ghosh¹

2022

Sickle Cell Disease

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Sickle cell disease (SCD), characterized by the presence of unstable sickle hemoglobin in the homozygous state (HbSS), results in progressive organ damage and early mortality with the median age of death in the 40s. The kidney is one of the most severely affected organs in SCD. Kidney diseases gradually develop in individuals with SCD. Microalbuminuria is evident in childhood, progressing to apparent proteinuria, deteriorating glomerular filtration rate (GFR) in early adulthood. While CKD becomes prevalent in adults. Moreover, among SCD patients, exacerbation of anemia is an independent risk factor for acute kidney injury (AKI) which is a predisposing factor for CKD and End Stage Renal Diseases (ESRD), altogether contributing to 16–18% mortality among this patients’ population. The pathogenesis of renal diseases in SCD is not completely understood. While epidemiological studies have shown a strong association between rate of hemolysis, severity of anemia and CKD, intrinsic inflammatory, oxidative and hypercoagulative stress that contribute to the characteristic endothelial dysfunction also promotes development of renal diseases in SCD. This chapter will elaborately discuss current research on the pathogenesis of AKI, AKI-to-CKD transition and future research perspectives for development of novel therapeutic strategies.

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Current pathological perspectives on chronic rejection in renal allografts

Hara

2016

Clin Exp Nephrol

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Chronic rejection in renal transplantation clinically manifests as slow deterioration in allograft function and is a major contributor of late renal graft loss. Most cases of chronic rejection involve chronic antibody-mediated rejection (ABMR) triggered by the interaction of donor-specific alloantibodies with endothelial cells of the microcirculation. The evolution of the Banff classification involved a major revision of the ABMR criteria during the 2000s and led to the inclusion of detailed pathological characteristics of chronic ABMR in the 2013 Banff scheme, including microcirculation damage observed as newly formed basement membranes and arterial fibrous intimal proliferation. Inflammation of microvasculature including glomeruli and/or peritubular capillaries is also seen in substantial cases of chronic ABMR, defined as chronic active ABMR. Chronic active T cell-mediated rejection (TCMR) results from chronic T cell-mediated injury involving renal arteries but is less characterized under the current Banff classification, mainly due to the expanding histological criteria of chronic active ABMR. Characteristics shared by these two chronic rejection types can potentially cause diagnostic confusion. Hence, the diagnostic criteria or categories of chronic renal rejection require amendment of the current Banff classification. Assessment of rejection cases with molecular phenotyping advanced the mechanistic understanding of various dysfunctions in renal allograft, including ABMR and TCMR. Identification of disease-specific changes in gene expression by immunohistological studies, especially in chronic ABMR, has already been validated by several studies, warranting potential application to the pathological diagnostic process. This review provides an overview of current pathological perspectives on chronic rejection of renal allografts and future directions.

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Medullary Microvascular Thrombosis and Injury in Sickle Hemoglobin C Disease

Cited by 5 publications

References 27 publications

Acute kidney injury in children with sickle cell disease—compounding a chronic problem

Acute kidney injury in children with sickle cell disease—compounding a chronic problem

Kidney Injuries in Sickle Cell Disease

Current pathological perspectives on chronic rejection in renal allografts

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