Urine sediment findings were milder in patients with COVID-19-associated renal injuries than in those with non-COVID-19-associated renal injuries

Morita, Yoshifumi; Kurano, Makoto; Jubishi, Daisuke; Ikeda, Mahoko; Okamoto, Koh; Tanaka, Masami; Harada, Sohei; Okugawa, Shu; Moriya, Kyoji; Yatomi, Yutaka

doi:10.1016/j.ijid.2022.02.024

Cited by 7 publications

(13 citation statements)

References 35 publications

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“…Martínez et al 8 , analyzed the urinalyses and urine electrolytes of patients with community-acquired and hospital-acquired C19-AKI, and they reported a high prevalence of FeNa < 0.5% (71 vs. 71%), a similar proportion of cases with proteinuria > 2 + (34 vs. 41%), but a higher proportion of hematuria in patients with hospital-acquired C19-AKI (59 vs. 28%). These findings are in line with a study reported by Morita et al 63 , in which the urinary sediment findings in subjects with COVID-19 were more severe as renal function declined. These two cohorts suggest that glomerular hypoperfusion might be largely involved in the pathogenesis of C19-AKI and at least partially conserved tubular sodium absorption, without a full-blown classic acute tubular injury presentation 8,63 .…”

Section: C19-aki: Recognitionsupporting

confidence: 93%

“…These findings are in line with a study reported by Morita et al 63 , in which the urinary sediment findings in subjects with COVID-19 were more severe as renal function declined. These two cohorts suggest that glomerular hypoperfusion might be largely involved in the pathogenesis of C19-AKI and at least partially conserved tubular sodium absorption, without a full-blown classic acute tubular injury presentation 8,63 . Thus, the use of these markers in C19-AKI appears to be even more limited since C19-AKI has a complex pathophysiology that affects more functions other than tubular reabsorption.…”

Section: C19-aki: Recognitionsupporting

confidence: 93%

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What did we learn about coronavirus disease-19-associated acute kidney injury during the pandemic?

Toro-Cisneros¹,

Caballero-Islas²,

Ramirez‐Sandoval³

et al. 2022

RIC

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Initial reports suggested that kidney involvement after coronavirus disease 19 (COVID-19) infection was uncommon, but this premise appears to be incorrect. Acute kidney injury can occur through various mechanisms and complicate the course of up to 25% of patients with COVID-19 hospitalized in our Institution, and of over 50% of those on invasive mechanical ventilation.Mechanisms of injury include direct kidney injury and predominantly tubular, although glomerular injury has been reported, and resulting from severe hypoxic respiratory failure, secondary infection, and exposure to nephrotoxic drugs. The mainstay of treatment remains the prevention of progressive kidney damage and, in some cases, the use of renal replacement therapy.Although the use of blood purification techniques has been proposed as a potential treatment, results to date have not been conclusive. In this manuscript, the mechanisms of kidney injury by COVID-19, risk factors, and the mainstays of treatment are reviewed. (REV INVEST CLIN. [AHEAD OF PRINT]

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Section: C19-aki: Recognitionsupporting

confidence: 93%

Section: C19-aki: Recognitionsupporting

confidence: 93%

What did we learn about coronavirus disease-19-associated acute kidney injury during the pandemic?

Toro-Cisneros¹,

Caballero-Islas²,

Ramirez‐Sandoval³

et al. 2022

RIC

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“…The majority (76%) of patients in our literature review (19 out of 25) had active urine sediments with haematuria and proteinuria while AKI was present in 44% compared with 19% in the COVID-19-only cohort [ 14 ]. Interestingly Morita et al found that, while the activity of urine sediments increased with the severity of COVID-19 disease, this activity was lower than in patients with non-COVID-19-related AKI, matched for level of renal dysfunction [ 15 ]. This suggests that the presence of very active urinary sediment in patients with COVID-19 should prompt clinicians to consider other causes of kidney injury and have a low threshold for further investigation such as ANCA testing.…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 Infection: A Forerunner or Precursor in Anti-neutrophil Cytoplasmic Antibody-Associated Vasculitis With Kidney Injury

Aung¹,

Oluyombo²,

Karim³

et al. 2022

Cureus

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COVID-19 disease and anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis are both multisystemic conditions. It is postulated there is a causal relationship between both conditions and this is supported by some case reports. The symptoms of COVID-19 can mimic those of vasculitis especially when the respiratory system is affected. Early diagnosis and treatment of ANCA-vasculitis cannot be overemphasized as this reduces the risk of severe organ damage. We report a 64-year-old lady with SARS-CoV-2 infection who developed ANCA-vasculitis with acute kidney injury and we reviewed the literature on this plausible association.We performed an electronic search of the MEDLINE, EMBASE, CINAHL, and EMCARE databases for research studies and case series and reports published in the English language between April 2020 and February 2022. Our review suggests that patients with COVID-19 infection who had proteinase 3-ANCA positive vasculitis with diffuse alveolar haemorrhage had fatal outcomes. We also noticed an increased incidence of active urine sediments. We emphasize the importance of a high index of suspicion for diagnosis and early treatment of vasculitis to ensure an improved outcome.

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“…To measure the urinary clinical markers, we used the reagents as described previously [35]. Renal tubular epithelial cells (RTE) were counted per high-power field of view (/HPF); urinary casts were classified into hyaline casts (HyaC), granular casts (GraC), epithelial casts (RTEC), and waxy casts (WaxC), and their numbers were counted per whole field (/WF).…”

Section: Urinalysismentioning

confidence: 99%

“…Urine samples rapidly and accurately reflect renal conditions. Actually, recent studies have revealed that urinary chemical biomarkers (urinary total protein [TP], N-acetyl-β-d-glucosaminidase [NAG], α1-microglobulin [α1-MG], neutrophil gelatinase-associated lipocalin [NGAL], and liver type fatty acid-binding protein [L-FABP]) and urine sediment findings are correlated with both the severity of COVID-19 and COVID-19-associated kidney injuries [16,19,35]. Therefore, in the present study, we investigated urinary biomarkers for COVID-19-associated kidney injuries.…”

Section: Introductionmentioning

confidence: 99%

Dynamic modulations of urinary sphingolipid and glycerophospholipid levels in COVID-19 and correlations with COVID-19-associated kidney injuries

et al. 2022

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Background Among various complications of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), renal complications, namely COVID-19-associated kidney injuries, are related to the mortality of COVID-19. Methods In this retrospective cross-sectional study, we measured the sphingolipids and glycerophospholipids, which have been shown to possess potent biological properties, using liquid chromatography-mass spectrometry in 272 urine samples collected longitudinally from 91 COVID-19 subjects and 95 control subjects without infectious diseases, to elucidate the pathogenesis of COVID-19-associated kidney injuries. Results The urinary levels of C18:0, C18:1, C22:0, and C24:0 ceramides, sphingosine, dihydrosphingosine, phosphatidylcholine, lysophosphatidylcholine, lysophosphatidic acid, and phosphatidylglycerol decreased, while those of phosphatidylserine, lysophosphatidylserine, phosphatidylethanolamine, and lysophosphatidylethanolamine increased in patients with mild COVID-19, especially during the early phase (day 1–3), suggesting that these modulations might reflect the direct effects of infection with SARS-CoV-2. Generally, the urinary levels of sphingomyelin, ceramides, sphingosine, dihydrosphingosine, dihydrosphingosine l-phosphate, phosphatidylcholine, lysophosphatidic acid, phosphatidylserine, lysophosphatidylserine, phosphatidylethanolamine, lysophosphatidylethanolamine, phosphatidylglycerol, lysophosphatidylglycerol, phosphatidylinositol, and lysophosphatidylinositol increased, especially in patients with severe COVID-19 during the later phase, suggesting that their modulations might result from kidney injuries accompanying severe COVID-19. Conclusions Considering the biological properties of sphingolipids and glycerophospholipids, an understanding of their urinary modulations in COVID-19 will help us to understand the mechanisms causing COVID-19-associated kidney injuries as well as general acute kidney injuries and may prompt researchers to develop laboratory tests for predicting maximum severity and/or novel reagents to suppress the renal complications of COVID-19.

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Urine sediment findings were milder in patients with COVID-19-associated renal injuries than in those with non-COVID-19-associated renal injuries

Cited by 7 publications

References 35 publications

What did we learn about coronavirus disease-19-associated acute kidney injury during the pandemic?

What did we learn about coronavirus disease-19-associated acute kidney injury during the pandemic?

SARS-CoV-2 Infection: A Forerunner or Precursor in Anti-neutrophil Cytoplasmic Antibody-Associated Vasculitis With Kidney Injury

Dynamic modulations of urinary sphingolipid and glycerophospholipid levels in COVID-19 and correlations with COVID-19-associated kidney injuries

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