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1.
Nat Rev Nephrol ; 17(11): 725-739, 2021 11.
Article in English | MEDLINE | ID: covidwho-1821594

ABSTRACT

Obesity, diabetes mellitus, hypertension and cardiovascular disease are risk factors for chronic kidney disease (CKD) and kidney failure. Chronic, low-grade inflammation is recognized as a major pathogenic mechanism that underlies the association between CKD and obesity, impaired glucose tolerance, insulin resistance and diabetes, through interaction between resident and/or circulating immune cells with parenchymal cells. Thus, considerable interest exists in approaches that target inflammation as a strategy to manage CKD. The initial phase of the inflammatory response to injury or metabolic dysfunction reflects the release of pro-inflammatory mediators including peptides, lipids and cytokines, and the recruitment of leukocytes. In self-limiting inflammation, the evolving inflammatory response is coupled to distinct processes that promote the resolution of inflammation and restore homeostasis. The discovery of endogenously generated lipid mediators - specialized pro-resolving lipid mediators and branched fatty acid esters of hydroxy fatty acids - which promote the resolution of inflammation and attenuate the microvascular and macrovascular complications of obesity and diabetes mellitus highlights novel opportunities for potential therapeutic intervention through the targeting of pro-resolution, rather than anti-inflammatory pathways.


Subject(s)
Diabetic Nephropathies/metabolism , Inflammation Mediators/metabolism , Inflammation/metabolism , Kidney/metabolism , Lipid Metabolism , Lipids , Renal Insufficiency, Chronic/metabolism , Diabetes Mellitus/metabolism , Diabetic Angiopathies/metabolism , Humans , Obesity/metabolism
3.
Int J Mol Sci ; 23(7)2022 Mar 30.
Article in English | MEDLINE | ID: covidwho-1785735

ABSTRACT

Acute kidney injury (AKI) is a sudden decline of renal function and represents a global clinical problem due to an elevated morbidity and mortality. Despite many efforts, currently there are no treatments to halt this devastating condition. Extracellular vesicles (EVs) are nanoparticles secreted by various cell types in both physiological and pathological conditions. EVs can arise from distinct parts of the kidney and can mediate intercellular communication between various cell types along the nephron. Besides their potential as diagnostic tools, EVs have been proposed as powerful new tools for regenerative medicine and have been broadly studied as therapeutic mediators in different models of experimental AKI. In this review, we present an overview of the basic features and biological relevance of EVs, with an emphasis on their functional role in cell-to-cell communication in the kidney. We explore versatile roles of EVs in crucial pathophysiological mechanisms contributing to AKI and give a detailed description of the renoprotective effects of EVs from different origins in AKI. Finally, we explain known mechanisms of action of EVs in AKI and provide an outlook on the potential clinical translation of EVs in the setting of AKI.


Subject(s)
Acute Kidney Injury , Extracellular Vesicles , Mesenchymal Stem Cells , Acute Kidney Injury/pathology , Extracellular Vesicles/metabolism , Humans , Kidney/metabolism , Mesenchymal Stem Cells/metabolism
4.
Exp Clin Transplant ; 20(Suppl 1): 156-160, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1780229

ABSTRACT

OBJECTIVES: The new coronavirus SARS-CoV-2 (COVID-19) first appeared in Turkey in March 2020, spread rapidly, and caused many deaths. Although COVID-19 is mostly a respiratory disease, it can cause kidney and multiorgan failure in some cases. We believe that by sharing information about the course and effects of COVID-19 infection in kidney transplant recipients receiving long-term immunosuppressive therapy our understanding will improve. MATERIALS AND METHODS: Between March 2020 and October 2021, COVID-19 was researched in kidney transplant recipients under the age of 20 years who were followed at the Baskent University Transplantation Center. We documented the clinical characteristics and prognosis of pediatric kidney transplant recipients with COVID-19 disease. RESULTS: Our study group included 23 patients with COVID-19 infection from 215 pediatric kidney transplant recipients. The mean age of the patients was 14.6 ± 4.7 years; there were 9 female patients. The mean follow-up time posttransplant was 62.3 ± 43.2 months. In 13 patients (56.5%), fever was the most frequent symptom. Most patients (n = 18, 78%) had minor symptoms and recovered completely after receiving supportive treatment. Four patients (17%) required hospitalization. One was diagnosed with COVID-19 infection 1 week after being treated with rituximab for acute antibody-mediated rejection. That patient died because of significant lung disease and multiorgan failure. CONCLUSIONS: Despite the fact that most of our pediatric transplant recipients had mild symptoms of COVID-19, we believe that particular caution should be observed in patients who have recently received intensive immunosuppressive medications. As a result of potential new vaccines, national immunization programs, and the emergence of novel virus strains, the clinical picture may change in the future. We believe that, as information sharing increases, we will learn more about COVID-19 in renal transplant recipients.


Subject(s)
COVID-19 , Kidney Transplantation , Adolescent , Adult , Child , Female , Humans , Kidney , Kidney Transplantation/adverse effects , SARS-CoV-2 , Transplant Recipients , Treatment Outcome , Young Adult
6.
Kidney360 ; 2(1): 141-153, 2021 Jan 28.
Article in English | MEDLINE | ID: covidwho-1776882

ABSTRACT

The COVID-19 outbreak has had substantial effects on the incidence and management of kidney diseases, including AKI, ESKD, GN, and kidney transplantation. Initial reports from China suggested a lower AKI incidence in patients with COVID-19, but more recent studies from North America reveal a much higher incidence, likely due to the higher prevalence of comorbid conditions, such as hypertension, diabetes, and CKD. AKI in this setting is associated with worse outcomes, including the requirement for vasopressors or mechanical ventilation and death. Performing RRT in those with AKI poses challenges, such as limiting exposure of staff, preserving PPE, coagulopathy, and hypoxemia due to acute respiratory distress syndrome. Continuous RRT is the preferred modality, with sustained low-efficiency dialysis also an option, both managed without 1:1 hemodialysis nursing support. Regional citrate is the preferred anticoagulation, but systemic unfractionated heparin may be used in patients with coagulopathy. The ultrafiltration rate has to be set carefully, taking into consideration hypotension, hypoxemia, and responsiveness to presser and ventilatory support. The chance of transmission puts in-center chronic hemodialysis and other immunosuppressed patients at particularly increased risk. Limited data show that patients with CKD are also at increased risk for more severe disease, if infected. Little is known about the virus's effects on immunocompromised patients with glomerular diseases and kidney transplants, which introduces challenges for management of immunosuppressant regimens. Although there are no standardized guidelines regarding the management of immunosuppression, several groups recommend stopping the antimetabolite in hospitalized transplant patients and continuing a reduced dose of calcineurin inhibitors. This comprehensive review critically appraises the best available evidence regarding the effect of COVID-19 on the incidence and management of kidney diseases. Where evidence is lacking, current expert opinion and clinical guidelines are reviewed, and knowledge gaps worth investigation are identified.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/epidemiology , COVID-19/epidemiology , Heparin , Humans , Incidence , Kidney , Risk Factors
7.
Kidney360 ; 3(2): 269-278, 2022 Feb 24.
Article in English | MEDLINE | ID: covidwho-1776878

ABSTRACT

Background: Remdesivir is not currently approved for patients with eGFR <30 ml/min per 1.73 m2. We aimed to determine the safety of remdesivir in patients with kidney failure. Methods: This study was a retrospective cohort study of patients with COVID-19 hospitalized between May 2020 and January 2021 with eGFR <30 ml/min per 1.73 m2 who received remdesivir and historical controls with COVID-19 hospitalized between March 1, 2020 and April 30, 2020 prior to the emergency use authorization of remdesivir within a large health care system. Patients were 1:1 matched by propensity scores accounting for factors associated with treatment assignment. Adverse events and hospital outcomes were recorded by manual chart review. Results: The overall cohort included 34 hospitalized patients who initiated remdesivir within 72 hours of hospital admission with eGFR<30 ml/min per 1.73 m2 and 217 COVID-19 controls with eGFR <30 ml/min per 1.73 m2. The propensity score-matched cohort included 31 remdesivir-treated patients and 31 nonremdesivir-treated controls. The mean age was 74.0 (SD=13.8) years, 57% were women, and 68% were white participants. A total of 26% had ESKD. Among patients who were not on dialysis prior to initiating remdesivir, one developed worsening kidney function (defined as ≥50% increase in creatinine or initiation of KRT) compared with three in the historical control group. There was no increased risk of cardiac arrythmia, cardiac arrest, altered mental status, or clinically significant anemia or liver function test abnormalities. There was a significantly increased risk of hyperglycemia, which may be partly explained by the increased use of dexamethasone in the remdesivir-treated population. Conclusions: In this propensity score-matched study, remdesivir was well tolerated in patients with eGFR <30 ml/min per 1.73 m2.


Subject(s)
COVID-19 , Renal Insufficiency , Adenosine Monophosphate/analogs & derivatives , Aged , Alanine/analogs & derivatives , Antiviral Agents/adverse effects , COVID-19/drug therapy , Female , Humans , Kidney , Propensity Score , Renal Dialysis , Renal Insufficiency/drug therapy , Retrospective Studies , SARS-CoV-2
8.
Kidney360 ; 3(1): 28-36, 2022 Jan 27.
Article in English | MEDLINE | ID: covidwho-1776874

ABSTRACT

Background: AKI is a common sequela of infection with SARS-CoV-2 and contributes to the severity and mortality from COVID-19. Here, we tested the hypothesis that kidney alterations induced by COVID-19-associated AKI could be detected in cells collected from urine. Methods: We performed single-cell RNA sequencing (scRNAseq) on cells recovered from the urine of eight hospitalized patients with COVID-19 with (n=5) or without AKI (n=3) as well as four patients with non-COVID-19 AKI (n=4) to assess differences in cellular composition and gene expression during AKI. Results: Analysis of 30,076 cells revealed a diverse array of cell types, most of which were kidney, urothelial, and immune cells. Pathway analysis of tubular cells from patients with AKI showed enrichment of transcripts associated with damage-related pathways compared with those without AKI. ACE2 and TMPRSS2 expression was highest in urothelial cells among cell types recovered. Notably, in one patient, we detected SARS-CoV-2 viral RNA in urothelial cells. These same cells were enriched for transcripts associated with antiviral and anti-inflammatory pathways. Conclusions: We successfully performed scRNAseq on urinary sediment from hospitalized patients with COVID-19 to noninvasively study cellular alterations associated with AKI and established a dataset that includes both injured and uninjured kidney cells. Additionally, we provide preliminary evidence of direct infection of urinary bladder cells by SARS-CoV-2. The urinary sediment contains a wealth of information and is a useful resource for studying the pathophysiology and cellular alterations that occur in kidney diseases.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/etiology , COVID-19/complications , Humans , Kidney , SARS-CoV-2 , Sequence Analysis, RNA
9.
Kidney360 ; 2(7): 1095-1106, 2021 Jul 29.
Article in English | MEDLINE | ID: covidwho-1776832

ABSTRACT

Background: The actions of angiotensin-converting enzyme 2 (ACE2) oppose those of the renin-angiotensin-aldosterone system. ACE2 may be a cytoprotectant in some tissues. This study examined ACE2 expression in models of AKI. Methods: ACE2 mRNA and protein expression and ACE2 activity were assessed in murine ischemic AKI. Renal ACE2 mRNA expression was evaluated in LPS-induced AKI in wild-type (C57BL/6J) mice, in heme oxygenase-1+/+ and heme oxygenase-1-/- mice, and after unilateral ureteral obstruction (UUO) in wild-type mice. The effect of sex and age on renal ACE2 protein expression was also assessed. Results: In ischemic AKI, ACE2 mRNA and protein expression and ACE2 activity were reduced as compared with such indices in the intact kidney. In ischemic AKI, ACE2, which, in health, is prominently expressed in the tubular epithelium, especially proximal tubules, is decreased in expression in these segments. Decreased ACE2 expression in AKI did not reflect reduced GFR, because ACE2 mRNA expression was unaltered after UUO. LPS induced renal ACE2 mRNA expression in wild-type mice, but this effect did not occur in heme oxygenase-1-deficient mice. In ischemic and LPS-induced AKI, renal expression of the Mas receptor was increased. In the intact kidney, renal ACE2 protein expression decreased in female mice as compared with male mice, but was unaltered with age. Conclusion: We conclude that renal ACE2 expression is decreased in ischemic AKI, characterized by decreased GFR and abundant cell death, but is upregulated in LPS-induced AKI, an effect requiring heme oxygenase-1. Determining the significance of ACE2 expression in experimental AKI merits further study. We suggest that understanding the mechanism underlying ACE2 downregulation in AKI may offer insights relevant to COVID-19: ACE2 expression is downregulated after ACE2 mediates SARS-CoV-2 cellular entry; such downregulation is proinflammatory; and AKI commonly occurs and determines outcomes in COVID-19.


Subject(s)
Acute Kidney Injury , Angiotensin-Converting Enzyme 2 , Acute Kidney Injury/genetics , Angiotensin-Converting Enzyme 2/genetics , Animals , Female , Kidney , Male , Mice , Mice, Inbred C57BL , Mice, Knockout
10.
Eur Rev Med Pharmacol Sci ; 26(6): 2188-2195, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1776798

ABSTRACT

OBJECTIVE: COVID-19 disease can cause damage to various organs, especially the kidneys, so the main purpose of this study was to investigate the effect of different aspects of kidney damages caused by COVID-19 in a narrative review study. MATERIALS AND METHODS: To conduct this study, all studies related to the topic under discussion during 2020-2021 were reviewed by systematic search in internationally available databases including Web of Science, Science Direct, Scopus, PubMed, and Google Scholar. Finally, 42 completely related studies were selected to extract the results. RESULTS: The prevalence of acute kidney injury (AKI) varies in different parts of the world and has reached almost 70%. The results showed that, in general, a high percentage of COVID-19 patients had symptoms of renal dysfunction at the time of hospitalization, and the most important of these symptoms were proteinuria, hematuria, and increased serum creatinine. Based on the results, it can be said that AKI most likely occurs early in the disease and in parallel with lung damage. So far, various drugs have been used to control or treat COVID-19 and reduce inflammation in patients. Regardless of their usefulness, some of these drugs may adversely affect kidney function and damage the kidneys. The study results show that chronic kidney disease (CKD) in COVID-19 patients plays a minor role in renal replacement therapy (RRT), and the highest impact on the need for RRT is COVID-19. CONCLUSIONS: This study showed that one of the major negative effects of COVID-19 on the human body is kidney damage, among which acute kidney injury (AKI) is the most important one. In addition, the prevalence of AKI due to COVID-19 varies widely around the world. Although any medication may damage the kidneys, COVID-19 or anti-inflammatory drugs are not an exception to this rule, but more research is needed to gain more information.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/diagnosis , Acute Kidney Injury/epidemiology , Acute Kidney Injury/therapy , Humans , Kidney , Proteinuria , Renal Replacement Therapy/adverse effects
11.
J Vet Sci ; 23(2): e27, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1776501

ABSTRACT

BACKGROUND: The role of Toll-like receptors (TLRs) in a feline infectious peritonitis virus (FIPV) infection is not completely understood. OBJECTIVES: This study examined the expression of TLR3, TLR7, TLR9, tumor necrosis factor-alpha (TNF-α), interferon (IFN)-ß, and interleukin (IL)-10 upon an FIPV infection in Crandell-Reese feline kidney (CRFK) cells and feline monocytes. METHODS: CRFK cells and monocytes from feline coronavirus (FCoV)-seronegative cats and FCoV-seropositive cats were infected with type II FIPV-79-1146. At four, 12, and 24 hours post-infection (hpi), the expression of TLR3, TLR7, TLR9, TNF-α, IFN-ß, and IL-10, and the viral load were measured using reverse transcription quantitative polymerase chain reaction. Viral protein production was confirmed using immunofluorescence. RESULTS: FIPV-infected CRFK showed the upregulation of TLR9, TNF-α, and IFN-ß expression between 4 and 24 hpi. Uninfected monocytes from FCoV-seropositive cats showed lower TLR3 and TLR9 expression but higher TLR7 expression compared to uninfected monocytes from FCoV-seronegative cats. FIPV-infected monocytes from FCoV-seropositive cats downregulated TLR7 and TNF-α expression between 4 and 24 hpi, and 4 and 12 hpi, respectively. IFN-ß was upregulated early in FIPV-infected monocytes from FCoV-seropositive cats, with a significant difference observed at 12 hpi compared to FCoV-seronegative cats. The viral load in the CRFK and FIPV-infected monocytes in both cohorts of cats was similar over time. CONCLUSION: TLR7 may be the key TLR involved in evading the innate response against inhibiting TNF-α production. Distinct TLR expression profiles between FCoV-seronegative and FCoV-seropositive cats were observed. The associated TLR that plays a role in the induction of IFN-ß needs to be explored further.


Subject(s)
Cat Diseases , Coronavirus, Feline , Feline Infectious Peritonitis , Animals , Cats , Coronavirus, Feline/genetics , Coronavirus, Feline/metabolism , Cytokines/genetics , Cytokines/metabolism , Kidney/metabolism , Monocytes/metabolism , Toll-Like Receptor 3
12.
BMC Nephrol ; 23(1): 117, 2022 03 24.
Article in English | MEDLINE | ID: covidwho-1770497

ABSTRACT

BACKGROUND: Host factors such as angiotensin-converting enzyme 2 (ACE2) and the transmembrane protease, serine-subtype-2 (TMPRSS2) are important factors for SARS-CoV-2 infection. Clinical and pre-clinical studies demonstrated that RAAS-blocking agents can be safely used during a SARS-CoV-2 infection but it is unknown if DPP-4 inhibitors or SGLT2-blockers may promote COVID-19 by increasing the host viral entry enzymes ACE2 and TMPRSS2. METHODS: We investigated telmisartan, linagliptin and empagliflozin induced effects on renal and cardiac expression of ACE2, TMPRSS2 and key enzymes involved in RAAS (REN, AGTR2, AGT) under high-salt conditions in a non-diabetic experimental 5/6 nephrectomy (5/6 Nx) model. In the present study, the gene expression of Ace2, Tmprss2, Ren, Agtr2 and Agt was assessed with qRT-PCR and the protein expression of ACE2 and TMPRSS2 with immunohistochemistry in the following experimental groups: Sham + normal diet (ND) + placebo (PBO); 5/6Nx + ND + PBO; 5/6Nx + high salt-diet (HSD) + PBO; 5/6Nx + HSD + telmisartan; 5/6Nx + HSD + linagliptin; 5/6Nx + HSD + empagliflozin. RESULTS: In the kidney, the expression of Ace2 was not altered on mRNA level under disease and treatment conditions. The renal TMPRSS2 levels (mRNA and protein) were not affected, whereas the cardiac level was significantly increased in 5/6Nx rats. Intriguingly, the elevated TMPRSS2 protein expression in the heart was significantly normalized after treatment with telmisartan, linagliptin and empagliflozin. CONCLUSIONS: Our study indicated that there is no upregulation regarding host factors potentially promoting SARS-CoV-2 virus entry into host cells when the SGLT2-blocker empagliflozin, telmisartan and the DPP4-inhibitor blocker linagliptin are used. The results obtained in a preclinical, experimental non-diabetic kidney failure model need confirmation in ongoing interventional clinical trials.


Subject(s)
COVID-19 , Dipeptidyl-Peptidase IV Inhibitors , Angiotensin Receptor Antagonists , Angiotensin-Converting Enzyme Inhibitors , Animals , COVID-19/drug therapy , Dipeptidyl-Peptidase IV Inhibitors/pharmacology , Dipeptidyl-Peptidase IV Inhibitors/therapeutic use , Humans , Kidney/metabolism , Nephrectomy , Rats , SARS-CoV-2 , Sodium-Glucose Transporter 2 , Spike Glycoprotein, Coronavirus/genetics , Spike Glycoprotein, Coronavirus/metabolism
13.
Medicine (Baltimore) ; 101(11)2022 Mar 18.
Article in English | MEDLINE | ID: covidwho-1769455

ABSTRACT

ABSTRACT: This study aimed to characterize survivors of Coronavirus disease 2019 (COVID-19) infection and acute kidney injury (AKI) that recover their renal function or progress to acute kidney disease (AKD) on discharge; and determine factors associated with progression to AKD during hospital stay.One thousand seventy four patients with COVID-19 infection were followed up until discharge/death. The incidence of AKI was 59.7%. Two hundred and sixty-six patients were discharged alive and included in the analysis, 71.8% had renal recovery (RR) while 28.2% were discharged with AKD. The AKD subset has higher rate of chronic kidney disease (CKD) ≥3 (33.4% vs 14.1%, P = .001), congestive heart failure (18.7% vs 5.8%, P = .001), use of non-invasive mechanical ventilation (10.7% vs 3.7%, P = .026) and vasopressors (25.3% vs 12.0%, P = .007). Of 19 patients in the AKI survivor cohort who received renal replacement therapy, 1 had RR while 18 progressed to AKD on discharge. Predictors to progression to AKD were CKD ≥3 (Odds Ratio [OR]: 3.23, 95% confidence interval [CI] 1.59-6.56, P = .001), congestive heart failure (OR: 4.59, 95% CI 1.76-11.78, P = .002), AKI on admission (OR: 2.71, 95% CI, 1.14-6.46, P = .025), and ongoing diarrhea (OR: 3.19, 95% CI, 1.02-9.96, P = .025).This study demonstrates a higher proportion of RR among survivors of COVID-19 infection in our minority predominant cohort. Early identification and appropriate management of patients at-risk to progress to AKD could improve outcomes, reduce long term sequalae of CKD/end stage renal disease, and have a major impact on health outcome and financial strain on healthcare system.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , Acute Kidney Injury/therapy , COVID-19/complications , COVID-19/epidemiology , COVID-19/therapy , Cohort Studies , Humans , Kidney/physiology , Retrospective Studies , Risk Factors
14.
Matrix Biol ; 105: 31-52, 2022 01.
Article in English | MEDLINE | ID: covidwho-1757644

ABSTRACT

The basement membrane (BM) is a specialized layer of extracellular matrix components that plays a central role in maintaining lung and kidney functions. Although the composition of the BM is usually tissue specific, the lung and the kidney preferentially use similar BM components. Unsurprisingly, diseases with BM defects often have severe pulmonary or renal manifestations, sometimes both. Excessive remodeling of the BM, which is a hallmark of both inflammatory and fibrosing diseases in the lung and the kidney, can lead to the release of BM-derived matrikines, proteolytic fragments with distinct biological functions. These matrikines can then influence disease activity at the site of liberation. However, they are also released to the circulation, where they can directly affect the vascular endothelium or target other organs, leading to extrapulmonary or extrarenal manifestations. In this review, we will summarize the current knowledge of the composition and function of the BM and its matrikines in health and disease, both in the lung and in the kidney. By comparison, we will highlight, why the BM and its matrikines may be central in establishing a renal-pulmonary interaction axis.


Subject(s)
Kidney , Lung , Basement Membrane , Endothelium, Vascular
15.
Medicine (Baltimore) ; 101(7): e28754, 2022 Feb 18.
Article in English | MEDLINE | ID: covidwho-1746192

ABSTRACT

RATIONALE: Kidney involvement with COVID-19 infection is a well-known complication, and the majority of kidney involvement is related to ischemic injury/acute tubular injury. However, there are some cases of glomerulonephritis, the etiology of which is not yet known, but an immune process is likely to be the trigger. PATIENT CONCERNS: A 27-year-old man presented to our hospital with facial puffiness and lower-limb swelling. DIAGNOSIS: Laboratory assessment revealed features of impaired kidney function with proteinuria and hematuria; COVID-19 polymerase chain reaction was positive, which was consistent with pauci-immune crescentic focal segmental glomerulonephritis. INTERVENTION: After renal biopsy, the patient was started on methylprednisolone and rituximab. Due to worsening kidney parameters, he underwent intermittent hemodialysis as needed. OUTCOME: Kidney function tests partially improved; he was discharged on oral steroids with follow-up in the nephrology clinic to observe for the need for further hemodialysis. LESSONS: We conducted a literature review of cases of glomerulonephritis associated with COVID-19 and described numerous types of glomerulonephritis. This report highlights the importance of recognizing emerging glomerulonephritis with COVID-19, the different pathological patterns of renal biopsies, and management interventions and responses.


Subject(s)
COVID-19 , Glomerulonephritis, Membranoproliferative , Glomerulonephritis , Acute Disease , Adult , COVID-19/complications , Glomerulonephritis/complications , Glomerulonephritis, Membranoproliferative/pathology , Humans , Kidney/pathology , Male
16.
Am J Transplant ; 22 Suppl 2: 21-136, 2022 03.
Article in English | MEDLINE | ID: covidwho-1735851

ABSTRACT

The year 2020 presented significant challenges to the field of kidney transplantation. After increasing each year since 2015 and reaching the highest annual count to date in 2019, the total number of kidney trans- plants decreased slightly, to 23642, in 2020. The decrease in total kidney transplants was due to a decrease in living donor transplants; the number of deceased donor transplants rose in 2020. The number of patients waiting for a kidney transplant in the United States declined slightly in 2020, driven by a slight drop in the number of new candidates added in 2020 and an increase in patients removed from the waiting list owing to death-important patterns that correlated with the COVID-19 pandemic. The complexities of the pandemic were accompanied by other ongoing challenges. Nationwide, only about a quarter of waitlisted patients receive a deceased donor kidney transplant within 5 years, a proportion that varies dramatically by donation service area, from 14.8% to 73.0%. The nonutilization (discard) rate of recovered organs rose to its highest value, at 21.3%, despite a dramatic decline in the discard of organs from hepatitis C-positive donors. Nonutilization rates remain particularly high for Kidney Donor Profile Index ≥85% kidneys and kidneys from which a biopsy specimen was obtained. Due to pandemic-related disruption of living donation in spring 2020, the number of living donor transplants in 2020 declined below annual counts over the last decade. In this context, only a small proportion of the waiting list receives living donor transplants each year, and racial disparities in living donor transplant access persist. As both graft and patient survival continue to improve incrementally, the total number of living kidney transplant recipients with a functioning graft exceeded 250,000 in 2020. Pediatric transplant numbers seem to have been impacted by the COVID-19 pandemic. The total number of pediatric kidney transplants performed decreased to 715 in 2020, from a peak of 872 in 2009. Despite numerous efforts, living donor kidney transplant remains low among pediatric recipients, with continued racial disparities among recipients. Of concern, the rate of deceased donor transplant among pediatric waitlisted candidates continued to decrease, reaching its lowest point in 2020. While this may be partly explained by the COVID-19 pandemic, close attention to this trend is critically important. Congenital anomalies of the kidney and urinary tract remain the leading cause of kidney disease in the pediatric population. While most pediatric de- ceased donor recipients receive a kidney from a donor with KDPI less than 35%, most pediatric deceased donor recipients had four or more HLA mis- matches. Graft survival continues to improve, with superior survival for living donor recipients versus deceased donor recipients.


Subject(s)
COVID-19 , Tissue and Organ Procurement , COVID-19/epidemiology , Child , Graft Survival , Humans , Kidney , Living Donors , Pandemics , Registries , SARS-CoV-2 , Tissue Donors , United States/epidemiology , Waiting Lists
17.
J Crit Care ; 68: 38-41, 2022 04.
Article in English | MEDLINE | ID: covidwho-1729887

ABSTRACT

PURPOSE: To describe the kidney histopathology of patients with S-AKI and correlate the histological findings with AKI severity, presence of septic shock, and the degree of multiple organic dysfunction (MOD) using the SOFA score. MATERIALS AND METHODS: This was a prospective, observational, and analytical study of a cohort of critically ill patients with S-AKI who died from sepsis at the "Hospital Español" intensive care unit (ICU). Kidney necropsies were performed within 2 h after death. RESULTS: We considered twenty (20) patients, with all of them exhibiting S-AKI stage 3 at the same time. In renal histopathology analysis, nonspecific tubulointerstitial (TI) lesions were found in almost all patients (95%). The more frequently found nonspecific TI lesions involved leukocyte infiltration (85%). Necrotic TI lesions were found in 6 patients (30%), and necrotic tubular cell casts were the most frequent lesions (50% of patients). It was not possible to demonstrate an association between the presence of necrotic TI lesions and factors such as the APACHE II score, the global SOFA score, ICU stays, AKI length and renal replacement therapy (RRT). CONCLUSIONS: The main histopathological findings in kidney necropsies in patients with S-AKI KDIGO 3, showed nonspecific TI lesions, and TI necrosis was only observed in 30% of the cases; therefore, S-AKI cannot be considered to be synonymous with acute tubular necrosis (ATN).


Subject(s)
Acute Kidney Injury , Critical Illness , APACHE , Acute Kidney Injury/therapy , Female , Humans , Intensive Care Units , Kidney , Male , Necrosis , Prospective Studies
18.
Saudi J Kidney Dis Transpl ; 32(4): 1034-1042, 2021.
Article in English | MEDLINE | ID: covidwho-1715893

ABSTRACT

We aimed to study the effect of remdesivir therapy on renal and hepatic function in coronavirus disease-2019 (COVID-19) patients with renal dysfunction at baseline or after starting therapy and identify the factors, if any, related to the efficacy of remdesivir therapy on patient outcome. Patients included in the study were those who met all the following criteria irrespective of baseline glomerular filtration rate [including those already on maintenance hemodialysis (HD)] or baseline deranged liver function test. (1) Age >18 years, (2) COVID-19 reverse transcriptase-polymerase chain reaction positive, (3) Meeting criteria for administration of remdesivir - [any one of the following: (a) COVID-19 pneumonia with respiratory rate >30/min or SPO2<94% on room air, (b) Acute respiratory distress syndrome (ARDS)]. (4) Renal dysfunction at baseline, during or within 48 h of completion of therapy. Thirty-four patients had renal dysfunction at baseline or developed it after remdesivir therapy - 16 were acute kidney injury (AKI), 10 chronic kidney diseases (CKD), four CKD stage 5D, and four were postrenal transplant. The overall mortality was 18/34 (52.9%). Eight out of 30 (26.66%) needed HD during or after therapy and of these, 15 died and among 15 survivors, 14 returned to their baseline renal function after cessation of therapy, one patient is still dialysis dependent. In the dialysis-dependent CKD (n = 4) subgroup, three died and one was discharged. In the postrenal transplant (n = 4) group, all developed AKI during or after the completion of therapy. None required HD, two returned to their baseline renal function, and two died. Only five had alanine aminotransferase elevation (×1 upper limit of normal) during or within 48 h of completion of therapy - three died and two returned to baseline. Lower PaO2/FiO2 (severe ARDS) (P = 0.0001), higher C-reactive protein (P = 0.022), higher serum lactate dehydrogenase (P = 0.038), and duration of symptoms before starting therapy (P = 0.05) were statistically significant variables at baseline associated with higher mortality. Remdesivir can be tried in moderate-to-severe COVID-19 cases with renal dysfunction as a complete recovery of renal function was noted in survivors. However, larger and well-controlled studies evaluating its safety and efficacy in patients with AKI and CKD are needed.


Subject(s)
Acute Kidney Injury , COVID-19 , Acute Kidney Injury/chemically induced , Acute Kidney Injury/epidemiology , Acute Kidney Injury/therapy , Adenosine Monophosphate/analogs & derivatives , Adolescent , Alanine/analogs & derivatives , COVID-19/drug therapy , Humans , Kidney/physiology , SARS-CoV-2
19.
J Am Coll Surg ; 234(2): 115-120, 2022 Feb 01.
Article in English | MEDLINE | ID: covidwho-1713820

ABSTRACT

BACKGROUND: Living donor liver transplantation (LDLT) continues to be the primary modality of liver transplantation in Asia, but it accounts for about 5% of all liver transplantations in the US. ABO incompatibility is the primary reason motivated donors are declined. Although kidney paired exchanges are common, liver paired exchange (LPE) is still evolving in the US. STUDY DESIGN: This is a retrospective review (between January 1, 2019, and July 31, 2021) of our initial experience with LPE. RESULTS: A total of 10 LPEs (20 LDLTs) were performed during the study period. Seven LPEs were initiated by a nondirected O donor. The other 3 pair sets involved 1 ABO compatible and 1 ABO incompatible pair. Transplantations in a pair set were completed within a mean of 4.8 (range 1-14) days of each other. All 20 donors are doing well with no major complications at 12.7 (range 1-20) months. Seventeen of 20 recipients are alive and have good allograft function. One recipient died in the early postoperative period. Two late deaths of patients with functioning allografts were due to COVID-19 (at 8 months) and peritoneal carcinomatosis and gram-negative sepsis (at 9 months). CONCLUSIONS: LPE is feasible in a high-volume LDLT center and is a useful option to increase LDLT by overcoming ABO incompatibility. Nondirected donors can be utilized to initiate an LPE.


Subject(s)
Liver Transplantation/statistics & numerical data , Living Donors/statistics & numerical data , Tissue and Organ Procurement/methods , ABO Blood-Group System , Adolescent , Adult , Aged , Blood Group Incompatibility , COVID-19/mortality , Cause of Death , Female , Humans , Kidney , Living Donors/supply & distribution , Male , Middle Aged , Postoperative Complications/etiology , Retrospective Studies , Tissue and Organ Procurement/statistics & numerical data , Transplant Recipients/statistics & numerical data , Young Adult
20.
Cell Metab ; 34(3): 352-354, 2022 03 01.
Article in English | MEDLINE | ID: covidwho-1712532

ABSTRACT

SARS-CoV-2 can cause diverse severe and lasting damage to the kidneys. In the latest issue of Cell Stem Cell, Jansen et al. utilized data gleaned from human kidney autopsies and human induced pluripotent stem cell-derived kidney organoids to investigate the direct effects of SARS-CoV-2 infection on kidney cells. They found that such infections resulted in renal scarring (notably, tubulointerstitial fibrosis).


Subject(s)
COVID-19 , Induced Pluripotent Stem Cells , Cicatrix , Humans , Kidney , SARS-CoV-2
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