Update on Innate Immunity in Acute Kidney Injury—Lessons Taken from COVID-19

Musiał, Kinga

doi:10.3390/ijms232012514

Cited by 3 publications

(3 citation statements)

References 79 publications

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“…This virus swiftly propagated, culminating in a global respiratory outbreak named coronavirus disease 2019 (COVID- 19), officially declared a pandemic by the World Health Organization on March 11, 2020 [2], resulting in a total count of over 6 million deaths [2,3]. SARS-CoV-2 harbors structural proteins, including nucleocapsid protein (N) and membrane glycoprotein (M), integral to stabilizing viral genetic material and facilitating the viral replication cycle [4,5]. Another critical component is the spike (S) glycoprotein, responsible for initiating host cell entry by binding to the angiotensin-converting enzyme 2 (ACE2) receptor [4,5].…”

Section: Introductionmentioning

confidence: 99%

“…SARS-CoV-2 harbors structural proteins, including nucleocapsid protein (N) and membrane glycoprotein (M), integral to stabilizing viral genetic material and facilitating the viral replication cycle [4,5]. Another critical component is the spike (S) glycoprotein, responsible for initiating host cell entry by binding to the angiotensin-converting enzyme 2 (ACE2) receptor [4,5].…”

Section: Introductionmentioning

confidence: 99%

“…Research indicates an upregulation of ACE2 expression in renal cells [3,5,7]. Pathological mechanisms, both direct (viral tropism in the kidney) and indirect (inflammatory system activation, hypercoagulability, microangiopathy, and hypovolemia), contribute to the diverse and multifactorial pathophysiology of kidney injury in COVID-19 [1,2,7].…”

Section: Introductionmentioning

confidence: 99%

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Renal Histopathological Lesions Associated with SARS-CoV-2 Infection in Patients with no History of Kidney Disease: A Systematic Review

Santos,

Souza,

Sá

et al. 2024

JAMMR

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Background and Aims: Structural and functional lung damage is the most documented impairment in SARS-CoV-2. Nevertheless, the virus's impact extends beyond pulmonary manifestations, affecting various organs and tissues, including the kidneys, known for their expression of ACE2, the virus's cell entry receptor. The objective of this review is to provide a comprehensive summary of studies investigating kidney injuries in individuals lacking prior renal conditions following SARS-CoV-2 infection. Methodology: A literature search encompassed studies published between December 2019 and September 2022, adhering to the PRISMA protocol. Electronic search strategies were developed to identify relevant studies across several bibliographic databases, including Pubmed, Scopus, Web of Knowledge, Embase, Scielo, Lilacs, Bireme, and Cochrane databases. A comprehensive analysis was undertaken, encompassing 43 studies involving 128 patients selected based on stringent inclusion criteria: a confirmed diagnosis of SARS-COV-2 infection, observable renal alterations through microscopy, and/or viral presence detected in the kidneys. Results: The included patients, primarily male (60.1%) with an average age of 53, exhibited prevalent comorbidities such as hypertension, diabetes, and obesity. The predominant outcome was death (43.7%), and various renal lesions were identified, with sclerosis, hyalinosis, tubular necrosis, and vascular injuries being the most common. Tubular lesions combined with glomerular lesions were frequently observed, regardless of comorbidity status. A greater predominance of renal involvement in patients with associated comorbidities, mainly arterial hypertension. The limited detection of the virus in renal tissue suggests a multifactorial origin of renal lesions, not solely attributed to the virus itself. The risk of bias assessment revealed mostly high-quality studies, with 24 assessed as low risk, 15 as moderate, and four as high risk. Conclusion: Ours results provides a comprehensive analysis of kidney injuries in COVID-19 patients, emphasizing the significant role of comorbidities such as hypertension, diabetes, and obesity in contributing to the severity and occurrence of renal complications. Notably, hypertension emerges as a prominent risk factor. The findings suggest a multifaceted manifestation of kidney injury induced by SARS-CoV-2, involving both direct viral impact on kidney tissue and a systemic response to the infection. The study underscores the importance of understanding the renal implications of COVID-19 for guiding targeted interventions and future research in this critical area.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Renal Histopathological Lesions Associated with SARS-CoV-2 Infection in Patients with no History of Kidney Disease: A Systematic Review

Santos,

Souza,

Sá

et al. 2024

JAMMR

View full text Add to dashboard Cite

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New insights into kidney disease after COVID-19 infection and vaccination: histopathological and clinical findings

Gong

2023

QJM: An International Journal of Medicine

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In addition to its pulmonary effects, COVID-19 has also been found to cause acute kidney injury (AKI), which has been linked to high mortality rates. In this review, we collected data from 20 clinical studies on post-COVID-19-related AKI and 97 cases of AKI associated with COVID-19 vaccination. Acute tubular injury was by far the most common finding in the kidneys of patients with COVID-19-related AKI. Among patients hospitalized for COVID-19, 34.0% developed AKI, of which 59.0%, 19.1%, and 21.9% were stage 1, 2, and 3, respectively. Though kidney disease and other adverse effects after COVID-19 vaccination overall appear rare, case reports have accumulated suggesting that COVID-19 vaccination may be associated with a risk of subsequent kidney disease. Among the patients with post-vaccination AKI, the most common pathologic findings include crescentic glomerulonephritis (29.9%), acute tubular injury (23.7%), IgA nephropathy (18.6%), ANCA-associated vasculitis (17.5%), minimal change disease (17.5%), and thrombotic microangiopathy (10.3%). It is important to note that crescentic glomerulonephritis appears to be more prevalent in patients who have newly diagnosed renal involvement. The proportions of patients with AKI stages 1, 2, and 3 after COVID-19 vaccination in case reports were 30.9%, 22.7%, and 46.4%, respectively. In general, clinical cases of new-onset and recurrent nephropathy with AKI after COVID-19 vaccination have a positive prognosis. In this article, we also explore the underlying pathophysiological mechanisms of AKI associated with COVID-19 infection and its vaccination by describing key renal morphological and clinical features and prognostic findings.

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Formononetin Alleviates Ischemic Acute Kidney Injury by Regulating Macrophage Polarization through KLF6/STAT3 Pathway

Zhang,

Guan,

et al. 2024

Am. J. Chin. Med.

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Recent research has indicated that formononetin demonstrates a potent anti-inflammatory effect in various diseases. However, its impact on sterile inflammation kidney injury, specifically acute kidney injury (AKI), remains unclear. In this study, we utilized an ischemia/reperfusion-induced AKI (IRI-AKI) mouse model and bone marrow-derived macrophages (BMDMs) to investigate the effects of formononetin on sterile inflammation of AKI and to explore the underlying mechanism. The administration of formononetin significantly preserved kidney function from injury, as evidenced by lower serum creatinine and blood urea nitrogen levels compared to IRI-AKI mice without treatment. This was further confirmed by less pathological changes in renal tubules and low expression of tubular injury markers such as KIM-1 and NGAL in the formononetin-treated IRI-AKI group. Furthermore, formononetin effectively suppressed the expression of pro-inflammatory cytokines (MCP-1, TNF-[Formula: see text], and IL-1[Formula: see text]) and macrophage infiltration into the kidneys of AKI mice. In vitro studies showed that formononetin led to less macrophage polarization towards a pro-inflammatory phenotype in BMDMs stimulated by LPS and IFN-[Formula: see text]. The mechanism involved the KLF6 and p-STAT3 pathway, as overexpression of KLF6 restored pro-inflammatory cytokine levels and pro-inflammatory polarization. Our findings demonstrate that formononetin can significantly improve renal function and reduce inflammation in IRI-AKI, which may be attributed to the inhibition of KLF6/STAT3-mediated macrophage pro-inflammatory polarization. This discovery presents a new promising therapeutic option for the treatment of IRI-AKI.

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Update on Innate Immunity in Acute Kidney Injury—Lessons Taken from COVID-19

Cited by 3 publications

References 79 publications

Renal Histopathological Lesions Associated with SARS-CoV-2 Infection in Patients with no History of Kidney Disease: A Systematic Review

Renal Histopathological Lesions Associated with SARS-CoV-2 Infection in Patients with no History of Kidney Disease: A Systematic Review

New insights into kidney disease after COVID-19 infection and vaccination: histopathological and clinical findings

Formononetin Alleviates Ischemic Acute Kidney Injury by Regulating Macrophage Polarization through KLF6/STAT3 Pathway

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