Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 199
Filter
1.
Arch Med Res ; 53(3): 323-328, 2022 04.
Article in English | MEDLINE | ID: covidwho-1859320

ABSTRACT

BACKGROUND: Different interventions have been implemented worldwide for the house-hold monitoring of patients with mild COVID-19 to reduce the burden of healthcare systems and guarantee quality of care. Telephone follow up and treatment kits have not been evaluated in the context of a national-wide primary care program. AIM OF THE STUDY: To compare the risk of hospitalization and death for COVID-19 between ambulatory patients who received and those who did not receive a treatment kit and telephone follow-up in a developing country METHODS: A two-group comparative analysis was conducted using data from the medical information systems of the Mexican Institute of Social Security. We included a total of 28,048 laboratory-confirmed SARS-CoV-2 patients: 7,898 (28.2%) received a medical kit and 20,150 (71.8%) did not. The incidence rates of hospitalization and death combined were calculated. To identify significant associations between hospitalization or death and treatment medical kits, we calculated the risk ratios using a multivariate logistic model. RESULTS: The incidence of hospitalization was 6.14% in patients who received a kit and 11.71% in those who did not. Male sex, age, and a medical history of obesity, hypertension, diabetes, immunosuppression, or kidney disease were associated with increased risk of hospitalization or death. The risk rates were reduced in patients who received a medical kit or telephone follow-up. In the multivariate model, receiving a medical kit was associated with a lower risk of hospitalization or death from COVID-19: adjusted risk ratio 0.41 (95% confidence interval 0.36-0.47). CONCLUSION: Use of a multimodal strategy may reduce the risk of hospitalization and death in adult outpatients with mild COVID-19.


Subject(s)
COVID-19 , Kidney Diseases , Adult , COVID-19/epidemiology , COVID-19/therapy , Female , Hospitalization , Humans , Incidence , Male , SARS-CoV-2
2.
Circ Res ; 130(10): 1618-1641, 2022 May 13.
Article in English | MEDLINE | ID: covidwho-1846593

ABSTRACT

Viruses are ubiquitous in the environment and continue to have a profound impact on human health and disease. The COVID-19 pandemic has highlighted this with impressive morbidity and mortality affecting the world's population. Importantly, the link between viruses and hypertension, cardiovascular disease, and kidney disease has resulted in a renewed focus and attention on this potential relationship. The virus responsible for COVID-19, SARS-CoV-2, has a direct link to one of the major enzymatic regulatory systems connected to blood pressure control and hypertension pathogenesis, the renin-angiotensin system. This is because the entry point for SARS-CoV-2 is the ACE2 (angiotensin-converting enzyme 2) protein. ACE2 is one of the main enzymes responsible for dampening the primary effector peptide Ang II (angiotensin II), metabolizing it to Ang-(1-7). A myriad of clinical questions has since emerged and are covered in this review. Several other viruses have been linked to hypertension, cardiovascular disease, and kidney health. Importantly, patients with high-risk apolipoprotein L1 (APOL1) alleles are at risk for developing the kidney lesion of collapsing glomerulopathy after viral infection. This review will highlight several emerging viruses and their potential unique tropisms for the kidney and cardiovascular system. We focus on SARS-CoV-2 as this body of literature in regards to cardiovascular disease has advanced significantly since the COVID-19 pandemic.


Subject(s)
COVID-19 , Cardiovascular Diseases , Hypertension , Kidney Diseases , Angiotensin-Converting Enzyme 2 , Apolipoprotein L1/metabolism , Cardiovascular Diseases/epidemiology , Female , Humans , Hypertension/epidemiology , Kidney Diseases/epidemiology , Male , Pandemics , Peptidyl-Dipeptidase A/metabolism , Renin-Angiotensin System/physiology , SARS-CoV-2
3.
J Investig Med High Impact Case Rep ; 10: 23247096221093888, 2022.
Article in English | MEDLINE | ID: covidwho-1808264

ABSTRACT

We report a case of dialysis dependence in a patient with COVID-19-associated nephropathy (COVAN) who had minimal respiratory manifestations. A 25-year-old man with a history of multiple sclerosis in remission presented with mild dyspnea due to COVID-19 pneumonia and was found to have rapidly worsening kidney function. He only required nasal cannula and was able to be weaned off within a few days. Despite having only mild respiratory disease, his kidney function worsened and urgent hemodialysis was started for hyperkalemia and uremic encephalopathy. Kidney biopsy demonstrated collapsing glomerulopathy due to COVID-19 with moderate interstitial fibrosis and tubular atrophy. His kidney function did not recover, and he unfortunately now has been dependent on hemodialysis for over 3 months. Multiple case reports have described COVAN causing dialysis dependence, but to our knowledge this is the first reported case of COVAN causing dialysis dependence in a patient with such mild respiratory disease. Currently the indications for intensive COVID-19 therapies are based on oxygen requirements. This case demonstrates that the oxygen requirement may not fully reflect the severity of COVID-19 and raises the question of whether these therapies should be considered in patients with COVAN.


Subject(s)
COVID-19 , Kidney Diseases , Adult , COVID-19/complications , Female , Humans , Kidney Diseases/pathology , Male , Oxygen , Renal Dialysis
4.
JCI Insight ; 7(11)2022 Jun 08.
Article in English | MEDLINE | ID: covidwho-1807764

ABSTRACT

COVID-19 infection causes collapse of glomerular capillaries and loss of podocytes, culminating in a severe kidney disease called COVID-19-associated nephropathy (COVAN). The underlying mechanism of COVAN is unknown. We hypothesized that cytokines induced by COVID-19 trigger expression of pathogenic APOL1 via JAK/STAT signaling, resulting in podocyte loss and COVAN phenotype. Here, based on 9 biopsy-proven COVAN cases, we demonstrated for the first time, to the best of our knowledge, that APOL1 protein was abundantly expressed in podocytes and glomerular endothelial cells (GECs) of COVAN kidneys but not in controls. Moreover, a majority of patients with COVAN carried 2 APOL1 risk alleles. We show that recombinant cytokines induced by SARS-CoV-2 acted synergistically to drive APOL1 expression through the JAK/STAT pathway in primary human podocytes, GECs, and kidney micro-organoids derived from a carrier of 2 APOL1 risk alleles, but expression was blocked by a JAK1/2 inhibitor, baricitinib. We demonstrate that cytokine-induced JAK/STAT/APOL1 signaling reduced the viability of kidney organoid podocytes but was rescued by baricitinib. Together, our results support the conclusion that COVID-19-induced cytokines are sufficient to drive COVAN-associated podocytopathy via JAK/STAT/APOL1 signaling and that JAK inhibitors could block this pathogenic process. These findings suggest JAK inhibitors may have therapeutic benefits for managing cytokine-induced, APOL1-mediated podocytopathy.


Subject(s)
COVID-19 , Cytokines , Janus Kinase Inhibitors , Kidney Diseases , Apolipoprotein L1/genetics , Azetidines/pharmacology , COVID-19/drug therapy , COVID-19/metabolism , Cytokines/metabolism , Endothelial Cells/metabolism , Humans , Janus Kinase Inhibitors/pharmacology , Janus Kinases/metabolism , Kidney Diseases/drug therapy , Kidney Diseases/metabolism , Kidney Diseases/virology , Organoids/metabolism , Purines/pharmacology , Pyrazoles/pharmacology , SARS-CoV-2/isolation & purification , STAT Transcription Factors/metabolism , Signal Transduction/drug effects , Sulfonamides/pharmacology
5.
Kidney Int ; 101(5): 880-882, 2022 05.
Article in English | MEDLINE | ID: covidwho-1796378

ABSTRACT

Collapsing glomerulopathy frequently shows focal lesions on biopsy, creating challenges with transcriptomic investigations because of inadequate tissue sample. This challenge is overcome with spatial transcriptomics, technology linking transcriptomic data to histology. Applying this technology to investigate patients with collapsing glomerulopathy related to HIV infection or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Smith et al. provide provocative evidence that collapsing glomerulopathy may have different molecular signatures despite the similar morphologic appearance.


Subject(s)
COVID-19 , Glomerulosclerosis, Focal Segmental , HIV Infections , Kidney Diseases , Biopsy/adverse effects , COVID-19/complications , Female , Glomerulosclerosis, Focal Segmental/pathology , HIV Infections/complications , Humans , Kidney Diseases/complications , Male , SARS-CoV-2
8.
PLoS One ; 17(3): e0265073, 2022.
Article in English | MEDLINE | ID: covidwho-1742018

ABSTRACT

BACKGROUND: Telenephrology has become an important health care delivery modality during the COVID-19 pandemic. However, little is known about patient perspectives on the quality of care provided via telenephrology compared to face-to-face visits. We aimed to use objective data to study patients' perspectives on outpatient nephrology care received via telenephrology (phone and video) versus face-to-face visits. METHODS: We retrospectively studied adults who received care in the outpatient Nephrology & Hypertension division at Mayo Clinic, Rochester, from March to July 2020. We used a standardized survey methodology to evaluate patient satisfaction. The primary outcome was the percent of patients who responded with a score of good (4) or very good (5) on a 5-point Likert scale on survey questions that asked their perspectives on access to their nephrologist, relationship with care provider, their opinions on the telenephrology technology, and their overall assessment of the care received. Wilcoxon rank sum tests and chi-square tests were used as appropriate to compare telenephrology versus face-to-face visits. RESULTS: 3,486 of the patient encounters were face-to-face, 808 phone and 317 video visits. 443 patients responded to satisfaction surveys, and 21% of these had telenephrology encounters. Established patients made up 79.6% of telenephrology visits and 60.9% of face-to-face visits. There was no significant difference in patient perceived access to health care, satisfaction with their care provider, or overall quality of care between patients cared for via telenephrology versus face-to-face. Patient satisfaction was also equally high. CONCLUSIONS: Patient satisfaction was equally high amongst those patients seen face-to-face or via telenephrology.


Subject(s)
Ambulatory Care , COVID-19 , Kidney Diseases/therapy , Outpatients , Patient Satisfaction , SARS-CoV-2 , Telemedicine , Aged , Female , Humans , Male , Middle Aged , Retrospective Studies
9.
Med Sci Monit ; 28: e935300, 2022 Mar 15.
Article in English | MEDLINE | ID: covidwho-1732485

ABSTRACT

BACKGROUND The recurrence of COVID-19 and the continuous escalation of prevention and control policies can lead to an increase in mental health problems. This study aimed to investigate the perceived stress, coping style, resilience, and social support among patients on maintenance hemodialysis (MHD) during the COVID-19 epidemic lockdown in China. MATERIAL AND METHODS This cross-sectional observational study enrolled 197 patients on MHD from the Guangdong Province Traditional Chinese Medical Hospital and the Hedong Hospital of Guangzhou Liwan District People's Hospital during July 2021. AMOS 24.0 and PROCESS Macro 3.1 model 6 were used for analyses of moderating mediating effects. RESULTS Perceived stress was negatively correlated with positive coping style (r=-0.305, P<0.001) and resilience (r=-0.258, P<0.001), whereas resilience (r=0.631, P<0.001) and social support (r=0.300, P<0.001) were positively correlated with positive coping style among patients on MHD. In the moderated mediating model, perceived stress had significant direct predictive effects on positive coping style (95% CI -0.33, -0.07), and perceived stress had significant indirect predictive effects on positive coping styles through resilience (95% CI -0.26, -0.06) or social support (95% CI 0.01, 0.06). Perceived stress had significant indirect predictive effects on positive coping style through both resilience and social support (95% CI -0.04, -0.01). CONCLUSIONS Perceived stress not only predicted coping style directly, but also indirectly predicted coping style through resilience and social support. Coping style was affected by internal and external factors during the COVID-19 pandemic lockdown period.


Subject(s)
Adaptation, Psychological/physiology , COVID-19/psychology , Kidney Diseases/psychology , Adult , COVID-19/complications , China/epidemiology , Communicable Disease Control , Cross-Sectional Studies , Female , Humans , Kidney Diseases/complications , Kidney Diseases/virology , Male , Middle Aged , Pandemics , Renal Dialysis , Resilience, Psychological/physiology , SARS-CoV-2/pathogenicity , Social Support , Stress, Psychological/psychology , Surveys and Questionnaires
10.
Nat Rev Nephrol ; 18(3): 133-134, 2022 03.
Article in English | MEDLINE | ID: covidwho-1708723
12.
Kidney Int ; 101(5): 1017-1026, 2022 05.
Article in English | MEDLINE | ID: covidwho-1700922

ABSTRACT

Collapsing glomerulopathy is a histologically distinct variant of focal and segmental glomerulosclerosis that presents with heavy proteinuria and portends a poor prognosis. Collapsing glomerulopathy can be triggered by viral infections such as HIV or SARS-CoV-2. Transcriptional profiling of collapsing glomerulopathy lesions is difficult since only a few glomeruli may exhibit this histology within a kidney biopsy and the mechanisms driving this heterogeneity are unknown. Therefore, we used recently developed digital spatial profiling (DSP) technology which permits quantification of mRNA at the level of individual glomeruli. Using DSP, we profiled 1,852 transcripts in glomeruli isolated from formalin fixed paraffin embedded sections from HIV or SARS-CoV-2-infected patients with biopsy-confirmed collapsing glomerulopathy and used normal biopsy sections as controls. Even though glomeruli with collapsing features appeared histologically similar across both groups of patients by light microscopy, the increased resolution of DSP uncovered intra- and inter-patient heterogeneity in glomerular transcriptional profiles that were missed in early laser capture microdissection studies of pooled glomeruli. Focused validation using immunohistochemistry and RNA in situ hybridization showed good concordance with DSP results. Thus, DSP represents a powerful method to dissect transcriptional programs of pathologically discernible kidney lesions.


Subject(s)
COVID-19 , Glomerulosclerosis, Focal Segmental , HIV Infections , Kidney Diseases , Female , Glomerulosclerosis, Focal Segmental/pathology , Humans , Kidney Diseases/genetics , Kidney Diseases/pathology , Kidney Glomerulus/pathology , Male , SARS-CoV-2
14.
J Am Soc Nephrol ; 32(11): 2851-2862, 2021 11.
Article in English | MEDLINE | ID: covidwho-1690622

ABSTRACT

BACKGROUND: COVID-19 is associated with increased risk of post-acute sequelae involving pulmonary and extrapulmonary organ systems-referred to as long COVID. However, a detailed assessment of kidney outcomes in long COVID is not yet available. METHODS: We built a cohort of 1,726,683 US Veterans identified from March 1, 2020 to March 15, 2021, including 89,216 patients who were 30-day survivors of COVID-19 and 1,637,467 non-infected controls. We examined risks of AKI, eGFR decline, ESKD, and major adverse kidney events (MAKE). MAKE was defined as eGFR decline ≥50%, ESKD, or all-cause mortality. We used inverse probability-weighted survival regression, adjusting for predefined demographic and health characteristics, and algorithmically selected high-dimensional covariates, including diagnoses, medications, and laboratory tests. Linear mixed models characterized intra-individual eGFR trajectory. RESULTS: Beyond the acute illness, 30-day survivors of COVID-19 exhibited a higher risk of AKI (aHR, 1.94; 95% CI, 1.86 to 2.04), eGFR decline ≥30% (aHR, 1.25; 95% CI, 1.14 to 1.37), eGFR decline ≥40% (aHR, 1.44; 95% CI, 1.37 to 1.51), eGFR decline ≥50% (aHR, 1.62; 95% CI, 1.51 to 1.74), ESKD (aHR, 2.96; 95% CI, 2.49 to 3.51), and MAKE (aHR, 1.66; 95% CI, 1.58 to 1.74). Increase in risks of post-acute kidney outcomes was graded according to the severity of the acute infection (whether patients were non-hospitalized, hospitalized, or admitted to intensive care). Compared with non-infected controls, 30-day survivors of COVID-19 exhibited excess eGFR decline (95% CI) of -3.26 (-3.58 to -2.94), -5.20 (-6.24 to -4.16), and -7.69 (-8.27 to -7.12) ml/min per 1.73 m2 per year, respectively, in non-hospitalized, hospitalized, and those admitted to intensive care during the acute phase of COVID-19 infection. CONCLUSIONS: Patients who survived COVID-19 exhibited increased risk of kidney outcomes in the post-acute phase of the disease. Post-acute COVID-19 care should include attention to kidney disease.


Subject(s)
COVID-19/complications , Kidney Diseases/epidemiology , Kidney Diseases/virology , Veterans/statistics & numerical data , Aged , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/therapy , Case-Control Studies , Cohort Studies , Critical Care , Female , Glomerular Filtration Rate , Hospitalization , Humans , Kidney Diseases/diagnosis , Male , Middle Aged , United States
15.
Biomolecules ; 12(2)2022 02 12.
Article in English | MEDLINE | ID: covidwho-1686604

ABSTRACT

The onset of coronavirus disease (COVID-19) as a pandemic infection, has led to increasing insights on its pathophysiology and clinical features being revealed, such as a noticeable kidney involvement. In this study, we describe the histopathological, immunofluorescence, and ultrastructural features of biopsy-proven kidney injury observed in a series of SARS-CoV-2 positive cases in our institution from April 2020 to November 2021. We retrieved and retrospectively reviewed nine cases (two pediatric and seven adults) that experienced nephrotic syndrome (six cases), acute kidney injury (two cases), and a clinically silent microhematuria and leukocyturia. Kidney biopsies were investigated by means of light microscopy, direct immunofluorescence, and electron microscopy. The primary diagnoses were minimal change disease (four cases), acute tubular necrosis (two cases), collapsing glomerulopathy (two cases), and C3 glomerulopathy (one case). None of the cases showed viral or viral-like particles on ultrastructural analysis. Novel and specific histologic features on kidney biopsy related to SARS-CoV-2 infection have been gradually disclosed and reported, harboring relevant clinical and therapeutic implications. Recognizing and properly diagnosing renal involvement in patients experiencing COVID-19 could be challenging (due to the lack of direct proof of viral infection, e.g., viral particles) and requires a proper integration of clinical and pathological data.


Subject(s)
COVID-19/complications , Kidney Diseases/complications , Kidney Diseases/virology , Kidney/injuries , Kidney/virology , Adolescent , Aged , Aged, 80 and over , Biopsy , COVID-19/pathology , COVID-19/virology , Female , Humans , Italy , Kidney/pathology , Kidney/ultrastructure , Kidney Diseases/pathology , Male , Middle Aged , Retrospective Studies
16.
BMC Nephrol ; 23(1): 57, 2022 02 05.
Article in English | MEDLINE | ID: covidwho-1666636

ABSTRACT

BACKGROUND: Publicly available genomics datasets have grown drastically during the past decades. Although most of these datasets were initially generated to answer a pre-defined scientific question, their repurposing can be useful when new challenges such as COVID-19 arise. While the establishment and use of experimental models of COVID-19 are in progress, the potential hypotheses for mechanisms of onset and progression of COVID-19 can be generated by using in silico analysis of known molecular changes during COVID-19 and targets for SARS-CoV-2 invasion. METHODS: Selecting condition: COVID-19 infection leads to pneumonia and mechanical ventilation (PMV) and associated with acute kidney injury (AKI). There is increasing data demonstrating mechanistic links between AKI and lung injury caused by mechanical ventilation. Selecting targets: SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) for cell entry. We hypothesized that expression of ACE2 and TMPRSS2 would be affected in models of AKI and PMV. We therefore evaluated expression of ACE2 and TMPRSS2 as well as other novel molecular players of AKI and AKI-lung cross-talk in the publicly available microarray datasets GSE6730 and GSE60088, which represent gene expression of lungs and kidneys in mouse models of AKI and PMV, respectively. RESULTS: Expression of COVID-19 related genes ACE2 and TMPRSS2 was downregulated in lungs after 6 h of distant AKI effects. The expression of ACE2 decreased further after 36 h, while expression of TMPRSS2 recovered. In kidneys, both genes were downregulated by AKI, but not by distant lung injury. We also identified 53 kidney genes upregulated by PMV; and 254 lung genes upregulated by AKI, 9 genes of which were common to both organs. 3 of 9 genes were previously linked to kidney-lung cross-talk: Lcn2 (Fold Change (FC)Lung (L) = 18.6, FCKidney (K) = 6.32), Socs3 (FCL = 10.5, FCK = 10.4), Inhbb (FCL = 6.20, FCK = 6.17). This finding validates the current approach and reveals 6 new candidates, including Maff (FCL = 7.21, FCK = 5.98). CONCLUSIONS: Using our in silico approach, we identified changes in COVID-19 related genes ACE2 and TMPRSS2 in traditional mouse models of AKI and kidney-lung cross-talk. We also found changes in new candidate genes, which could be involved in the combined kidney-lung injury during COVID-19.


Subject(s)
COVID-19/complications , Computer Simulation , Kidney Diseases/etiology , Lung Diseases/etiology , SARS-CoV-2/genetics , Animals , Disease Models, Animal , Male , Mice , Mice, Inbred C57BL
17.
J Mycol Med ; 32(2): 101252, 2022 May.
Article in English | MEDLINE | ID: covidwho-1665312

ABSTRACT

BACKGROUND AND AIMS: Published studies on coronavirus disease 19 (COVID-19) associated rhino-orbito-cerebral mucormycosis (CAROCM) were primarily descriptive. Therefore, we aimed to identify features of COVID-19 that could predispose to CAROCM and explore the pathogenic pathways. PATIENTS AND METHODS: This retrospective hospital-based study was done during the first (March 2020 - January 2021) and the second (February 2021 - June 2021) waves of the COVID-19 pandemic. Subjects were grouped into four categories: first-wave CAROCM (n-4); second-wave CAROCM (n-27); first-wave non-mucor COVID (n-75), and second-wave non-mucor COVID (n-50). Data elements included age, gender, comorbidities, COVID-19 severity, steroid therapy, peak values of interleukin-6 (IL-6), serum ferritin and D-dimer, nadir values of absolute lymphocyte count (ALC), absolute neutrophil count (ANC) and platelet count (Pl. C). RESULTS: Thirty-one patients of CAROCM were included. The mean (SD) age was 51.26 (11.48) years. 27 (87.1%) were aged ≥ 40 years and males. Severe COVID-19 was seen more often in the second wave than the first wave (P-0.001). CAROCM group was significantly younger (P-0.008) and showed a higher incidence of uncontrolled diabetes (P-0.001) and renal dysfunction (P-0.004) than non-mucor COVID. While IL-6, ferritin and D-dimer were significantly elevated in CAROCM than non-mucor COVID, clinical severity, ANC, ALC and Pl. C showed no significant difference. CONCLUSION: CAROCM is seen often in middle-aged diabetic males with uncontrolled hyperglycaemia, diabetic ketoacidosis, renal dysfunction and those infected by more transmissible delta variants and treated with steroids. IL-6, D-dimer, serum ferritin are more often elevated in CAROCM and might play a pathogenic role.


Subject(s)
COVID-19 , Diabetic Ketoacidosis , Kidney Diseases , Mucormycosis , COVID-19/complications , Ferritins/therapeutic use , Humans , Interleukin-6/therapeutic use , Kidney Diseases/epidemiology , Male , Middle Aged , Mucormycosis/drug therapy , Pandemics , Retrospective Studies , SARS-CoV-2 , Virulence Factors
18.
Kidney Int ; 101(6): 1216-1231, 2022 Jun.
Article in English | MEDLINE | ID: covidwho-1665244

ABSTRACT

Risk variants of the apolipoprotein-L1 (APOL1) gene are associated with severe kidney disease, putting homozygous carriers at risk. Since APOL1 lacks orthologs in all major model organisms, a wide range of mechanisms frequently in conflict have been described for APOL1-associated nephropathies. The genetic toolkit in Drosophila allows unique in vivo insights into disrupted cellular homeostasis. To perform a mechanistic analysis, we expressed human APOL1 control and gain-of-function kidney risk variants in the podocyte-like garland cells of Drosophila nephrocytes and a wing precursor tissue. Expression of APOL1 risk variants was found to elevate endocytic function of garland cell nephrocytes that simultaneously showed early signs of cell death. Wild-type APOL1 had a significantly milder effect, while a control transgene with deletion of the short BH3 domain showed no overt phenotype. Nephrocyte endo-lysosomal function and slit diaphragm architecture remained unaffected by APOL1 risk variants, but endoplasmic reticulum (ER) swelling, chaperone induction, and expression of the reporter Xbp1-EGFP suggested an ER stress response. Pharmacological inhibition of ER stress diminished APOL1-mediated cell death and direct ER stress induction enhanced nephrocyte endocytic function similar to expression of APOL1 risk variants. We confirmed APOL1-dependent ER stress in the Drosophila wing precursor where silencing the IRE1-dependent branch of ER stress signaling by inhibition with Xbp1-RNAi abrogated cell death, representing the first rescue of APOL1-associated cytotoxicity in vivo. Thus, we uncovered ER stress as an essential consequence of APOL1 risk variant expression in vivo in Drosophila, suggesting a central role of this pathway in the pathogenesis of APOL1-associated nephropathies.


Subject(s)
Kidney Diseases , Podocytes , Animals , Apolipoprotein L1/genetics , Drosophila/genetics , Endoplasmic Reticulum Stress/genetics , Humans , Kidney Diseases/pathology , Podocytes/pathology
19.
Infection ; 50(3): 719-724, 2022 Jun.
Article in English | MEDLINE | ID: covidwho-1664540

ABSTRACT

BACKGROUND: Proteinuria (both tubular and glomerular in origin) and its implications are well-known features of adult patients with COVID19. However currently studies addressing proteinuria and its role in the outcome of kidney and patients of pediatric COVID 19 is scarce. We aimed to evaluate the presence of microalbuminuria in order to detect early renal involvement in pediatric COVID 19 patients. METHODS: We prospectively evaluated 100 pediatric patients hospitalized with COVID 19 between April and July 2020. Clinical presentations, laboratory findings and outcomes were investigated. Microalbuminuria was compared with the age, gender, disease severity, and hemoglobin, platelet, leukocyte count and serum CRP levels of the patients. RESULTS: Twenty seven out of 100 patients had microalbuminuria. Fourteen patients had mild and fourteen had moderate disease. There was not any significant relation according to age and gender. Microalbuminuria was not related to the severity of the disease. Also the mean microalbuminuria level did not differ according to the disease course. Hemoglobin, platelet, leukocyte counts and serum CRP levels were also were not correlated with microalbuminuria levels. CONCLUSION: Although there was no difference between the groups with different disease course; microalbuminuria is detected in an important ratio of pediatric patients with COVID 19 in this study. In the highlight of our findings we suggest that urinary findings of pediatric COVID patients should be carefully evaluated.


Subject(s)
COVID-19 , Kidney Diseases , Adult , Albuminuria , Child , Humans , Kidney , Proteinuria
20.
Mol Biol Rep ; 49(3): 2321-2324, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1664478

ABSTRACT

Numerous studies demonstrate parallels between CVD, type 2 diabetes mellitus (T2DM) and COVID-19 pathology, which accentuate pre-existing complications in patients infected with COVID-19 and potentially exacerbate the infection course. Antidiabetic drugs such as sodium-glucose transporter-2 (SGLT-2) inhibitors have garnered substantial attention recently due to their efficacy in reducing the severity of cardiorenal disease. The effect of SGLT-2 inhibitors in patients with COVID-19 remains unclear particularly since SGLT-2 inhibitors contribute to altering the RAAS cascade activity, which includes ACE-2, the major cell entry receptor for SARS-CoV2. A study, DARE-19, was carried out to unveil the effects of SGLT-2 inhibitor treatment on comorbid disease complications and concomitant COVID-19 outcomes and demonstrated no statistical significance. However, the need for further studies is essential to provide conclusive clinical findings.


Subject(s)
Benzhydryl Compounds/therapeutic use , COVID-19/complications , Glucosides/therapeutic use , Renin-Angiotensin System/drug effects , Respiratory Insufficiency/drug therapy , SARS-CoV-2 , Sodium-Glucose Transporter 2 Inhibitors/therapeutic use , Angiotensin-Converting Enzyme 2/physiology , Clinical Trials, Phase III as Topic , Double-Blind Method , Drug Repositioning , Heart Diseases/prevention & control , Humans , Kidney Diseases/prevention & control , Mitochondria/drug effects , Multicenter Studies as Topic , Oxidative Stress/drug effects , Randomized Controlled Trials as Topic , Receptors, Virus/physiology , Respiratory Insufficiency/etiology , Sodium-Glucose Transporter 2/physiology , Sodium-Glucose Transporter 2 Inhibitors/pharmacology
SELECTION OF CITATIONS
SEARCH DETAIL