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1.
PLoS One ; 16(4): e0250581, 2021.
Article in English | MEDLINE | ID: covidwho-1199979

ABSTRACT

BACKGROUNDS: Data on how lifestyle changes due to the coronavirus disease 2019 (COVID-19) pandemic have influenced the clinical features of kidney disease patients remain scarce. METHODS: This study retrospectively analyzed clinical variables in patients with stage G1-G4 chronic kidney disease (CKD) with complete or incomplete remission of proteinuria, who were managed in a nephrology outpatient clinic of a university hospital in Tokyo. The clinical variables during the COVID-19 pandemic (term 1, June-July 2020) were compared to those one year before the pandemic (term 0, June-July 2019). The urinary protein excretion (UPE) was used as the primary outcome measure. RESULTS: This study included 325 patients with stage G1-G4 CKD (mean age 58.5 years old, 37.5% female, 80.6% on renin-angiotensin aldosterone system inhibitors [RAASis], 12.0% on maintenance dose immunosuppression therapy) evaluated at term 0. The UPE at terms 0 and 1 was 247 (92-624) and 203 (84-508) mg/day [median (25th-75th percentile)], respectively; the value in term 1 was 18% lower than that in term 0 (p<0.001), with no marked difference in body weight, blood pressure, protein intake or urinary salt excretion. In multivariable analyses, incomplete remission of proteinuria in term 0 (odds ratio [OR] = 2.70, p = <0.001), RAASi use (OR = 2.09, p = 0.02) and decreased urinary salt excretion in term 1 vs. term 0 (OR = 1.94, p = 0.002) were identified as independent variables associated with reduced UPE in term 1 vs. term 0. No significant interactions between the variables were observed. CONCLUSION: In kidney disease patients receiving standard medical care from nephrologists, the UPE after the emergency declaration in relation to the COVID-19 pandemic was lower than before the declaration. The UPE reduction may be associated with reduced dietary salt intake during the pandemic in patients treated with RAASi for insufficient control of proteinuria. Our results support the current proposal to continue therapeutic approaches to these patients, which involve RAASi therapy along with optimizing dietary habits, even while dealing with the COVID-19 pandemic.


Subject(s)
Proteinuria/pathology , Renal Insufficiency, Chronic/pathology , Adult , Aged , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , COVID-19/epidemiology , COVID-19/pathology , COVID-19/virology , Female , Humans , Japan/epidemiology , Logistic Models , Male , Middle Aged , Odds Ratio , Proteinuria/complications , Remission Induction , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/drug therapy , Retrospective Studies , SARS-CoV-2/isolation & purification , Severity of Illness Index
2.
Am J Kidney Dis ; 77(1): 82-93.e1, 2021 01.
Article in English | MEDLINE | ID: covidwho-851328

ABSTRACT

RATIONALE & OBJECTIVE: Kidney biopsy data inform us about pathologic processes associated with infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We conducted a multicenter evaluation of kidney biopsy findings in living patients to identify various kidney disease pathology findings in patients with coronavirus disease 2019 (COVID-19) and their association with SARS-CoV-2 infection. STUDY DESIGN: Case series. SETTING & PARTICIPANTS: We identified 14 native and 3 transplant kidney biopsies performed for cause in patients with documented recent or concurrent SARS-CoV-2 infection treated at 7 large hospital systems in the United States. OBSERVATIONS: Men and women were equally represented in this case series, with a higher proportion of Black (n=8) and Hispanic (n=5) patients. All 17 patients had SARS-CoV-2 infection confirmed by reverse transcriptase-polymerase chain reaction, but only 3 presented with severe COVID-19 symptoms. Acute kidney injury (n=15) and proteinuria (n=11) were the most common indications for biopsy and these symptoms developed concurrently or within 1 week of COVID-19 symptoms in all patients. Acute tubular injury (n=14), collapsing glomerulopathy (n=7), and endothelial injury/thrombotic microangiopathy (n=6) were the most common histologic findings. 2 of the 3 transplant recipients developed active antibody-mediated rejection weeks after COVID-19. 8 patients required dialysis, but others improved with conservative management. LIMITATIONS: Small study size and short clinical follow-up. CONCLUSIONS: Cases of even symptomatically mild COVID-19 were accompanied by acute kidney injury and/or heavy proteinuria that prompted a diagnostic kidney biopsy. Although acute tubular injury was seen among most of them, uncommon pathology such as collapsing glomerulopathy and acute endothelial injury were detected, and most of these patients progressed to irreversible kidney injury and dialysis.


Subject(s)
Acute Kidney Injury/etiology , Acute Kidney Injury/pathology , COVID-19/complications , COVID-19/pathology , Proteinuria/etiology , Proteinuria/pathology , Adult , Aged , Diagnosis, Differential , Female , Follow-Up Studies , Humans , Kidney/pathology , Male , Middle Aged
3.
Rev Med Virol ; 31(3): e2176, 2021 05.
Article in English | MEDLINE | ID: covidwho-815924

ABSTRACT

The novel coronavirus (SARS-CoV-2) has turned into a life-threatening pandemic disease (Covid-19). About 5% of patients with Covid-19 have severe symptoms including septic shock, acute respiratory distress syndrome, and the failure of several organs, while most of them have mild symptoms. Frequently, the kidneys are involved through direct or indirect mechanisms. Kidney involvement mainly manifests itself as proteinuria and acute kidney injury (AKI). The SARS-CoV-2-induced kidney damage is expected to be multifactorial; directly it can infect the kidney podocytes and proximal tubular cells and based on an angiotensin-converting enzyme 2 (ACE2) pathway it can lead to acute tubular necrosis, protein leakage in Bowman's capsule, collapsing glomerulopathy and mitochondrial impairment. The SARS-CoV-2-driven dysregulation of the immune responses including cytokine storm, macrophage activation syndrome, and lymphopenia can be other causes of the AKI. Organ interactions, endothelial dysfunction, hypercoagulability, rhabdomyolysis, and sepsis are other potential mechanisms of AKI. Moreover, lower oxygen delivery to kidney may cause an ischaemic injury. Understanding the fundamental molecular pathways and pathophysiology of kidney injury and AKI in Covid-19 is necessary to develop management strategies and design effective therapies.


Subject(s)
Acute Kidney Injury/pathology , COVID-19/physiopathology , Cytokine Release Syndrome/pathology , Disseminated Intravascular Coagulation/pathology , Lymphopenia/pathology , Necrosis/pathology , Proteinuria/pathology , Sepsis/pathology , Acute Kidney Injury/immunology , Acute Kidney Injury/virology , Angiotensin-Converting Enzyme 2/genetics , Angiotensin-Converting Enzyme 2/immunology , COVID-19/immunology , COVID-19/virology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/virology , Cytokines/genetics , Cytokines/immunology , Disseminated Intravascular Coagulation/immunology , Disseminated Intravascular Coagulation/virology , Host-Pathogen Interactions/genetics , Host-Pathogen Interactions/immunology , Humans , Kidney Tubules, Proximal/immunology , Kidney Tubules, Proximal/physiopathology , Lymphopenia/immunology , Lymphopenia/virology , Necrosis/immunology , Necrosis/virology , Podocytes/immunology , Podocytes/pathology , Proteinuria/immunology , Proteinuria/virology , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity , Sepsis/immunology , Sepsis/virology , Serine Endopeptidases/genetics , Serine Endopeptidases/immunology , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/immunology
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