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Junjiong Zheng, Hao Yu, JesuR Batur, Zhenfeng Shi, Aierken Tuerxun, Abudukeyoumu Abulajiang, Sihong Lu, Jianqiu Kong, Lifang Huang, Shaoxu Wu, et al.
Kidney International; doi:10.1016/j.kint.2021.05.031

The publisher has not yet granted permission to display this abstract.
, Nassim Kamar, Francois Vergez, Stanislas Faguer, Olivier Marion, Audrey Beq, Yasmine Lathrache, Florence Abravanel, Jacques Izopet, Emmanuel Treiner
Kidney International; doi:10.1016/j.kint.2021.05.032

The publisher has not yet granted permission to display this abstract.
Chao Zhou, Quan He, Hua Gan, Tingting Zeng, Qiao Liu, John F. Moorhead, Zac Varghese, ,
Published: 1 June 2021
Kidney International, Volume 99, pp 1342-1353; doi:10.1016/j.kint.2021.01.016

The publisher has not yet granted permission to display this abstract.
, Sarit Freiman, Ma'anit Shapira, Samar Wishahi, Munir Hamze, Mohamad Elhaj, Maha Zaher, Zaher Armaly
Published: 1 June 2021
Kidney International, Volume 99, pp 1496-1498; doi:10.1016/j.kint.2021.04.006

The publisher has not yet granted permission to display this abstract.
, P. Toby Coates, Brad H. Rovin, Pierre Ronco
Published: 1 June 2021
Kidney International, Volume 99, pp 1275-1279; doi:10.1016/j.kint.2021.04.007

Abstract:
In this issue of Kidney International, the initial experience regarding the immunogenicity of prior coronavirus disease 2019 (COVID-19) infection and the response to the COVID-19 vaccines among patients on maintenance dialysis and kidney transplant recipients is summarized. Preliminary data suggest that there is durability of immune response after COVID-19 infection. Although immune response to the first dose of vaccine is less in infection-naïve patients than healthy individuals in both groups, after the second vaccine dose a significant portion of patients receiving maintenance dialysis develop robust antibody titers, whereas kidney transplant recipients show a less-strong immune response.
Roseanne E. Billany, Haresh Selvaskandan, Sherna F. Adenwalla, Katherine L. Hull, Daniel S. March, James O. Burton, Nicolette C. Bishop, Edward J. Carr, Rupert Beale, Julian W. Tang, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1492-1494; doi:10.1016/j.kint.2021.04.008

The publisher has not yet granted permission to display this abstract.
, Maria Prendecki, Amrita Dhutia, Jaslyn Gan, Claire Edwards, Virginia Prout, Liz Lightstone, Eleanor Parker, Federica Marchesin, Megan Griffith, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1470-1477; doi:10.1016/j.kint.2021.03.009

Abstract:
Patients with end stage kidney disease receiving in-center hemodialysis (ICHD) have had high rates of SARS-CoV-2 infection. Following infection, patients receiving ICHD frequently develop circulating antibodies to SARS-CoV-2, even with asymptomatic infection. Here, we investigated the durability and functionality of the immune responses to SARS-CoV-2 infection in patients receiving ICHD. Three hundred and fifty-six such patients were longitudinally screened for SARS-CoV-2 antibodies and underwent routine PCR-testing for symptomatic and asymptomatic infection. Patients were regularly screened for nucleocapsid protein (anti-NP) and receptor binding domain (anti-RBD) antibodies, and those who became seronegative at six months were screened for SARS-CoV-2 specific T-cell responses. One hundred and twenty-nine (36.2%) patients had detectable antibody to anti-NP at time zero, of whom 127 also had detectable anti-RBD. Significantly, at six months, 71/111 (64.0%) and 99/116 (85.3%) remained anti-NP and anti-RBD seropositive, respectively. For patients who retained antibody, both anti-NP and anti-RBD levels were reduced significantly after six months. Eleven patients who were anti-NP seropositive at time zero, had no detectable antibody at six months; of whom eight were found to have SARS-CoV-2 antigen specific T cell responses. Independent of antibody status at six months, patients with baseline positive SARS-CoV-2 serology were significantly less likely to have PCR confirmed infection over the following six months. Thus, patients receiving ICHD mount durable immune responses six months post SARS-CoV-2 infection, with fewer than 3% of patients showing no evidence of humoral or cellular immunity.
Jennifer Arroyo, Diana Escobar-Zarate, Harrison H. Wells, Megan M. Constans, Ka Thao, Jessica M. Smith, Cynthia J. Sieben, Madeline R. Martell, Timothy L. Kline, Maria V. Irazabal, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1392-1407; doi:10.1016/j.kint.2021.01.028

The publisher has not yet granted permission to display this abstract.
, Rosanna Coppo, Lee Er, Maria Luisa Russo, , Jie Ding, Ritsuko Katafuchi, Norishige Yoshikawa, Hong Xu, Shoji Kagami, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1439-1450; doi:10.1016/j.kint.2020.10.033

The publisher has not yet granted permission to display this abstract.
, Gülşah Kaya Aksoy, Elif Çomak, , Sema Akman
Published: 1 June 2021
Kidney International, Volume 99, pp 1500-1501; doi:10.1016/j.kint.2021.02.032

Published: 1 June 2021
Kidney International, Volume 99, pp 1252-1254; doi:10.1016/j.kint.2021.04.004

Published: 1 June 2021
Kidney International, Volume 99; doi:10.1016/s0085-2538(21)00400-2

Published: 1 June 2021
Kidney International, Volume 99; doi:10.1016/s0085-2538(21)00402-6

, Agnes B. Fogo
Published: 1 June 2021
Kidney International, Volume 99, pp 1262-1264; doi:10.1016/j.kint.2021.01.021

The publisher has not yet granted permission to display this abstract.
Published: 1 June 2021
Kidney International, Volume 99; doi:10.1016/j.kint.2021.04.003

Peter Sohn, Yoko Narasaki,
Published: 1 June 2021
Kidney International, Volume 99, pp 1269-1272; doi:10.1016/j.kint.2021.03.012

Abstract:
Intradialytic hypotension (IDH) is a major complication of hemodialysis, leading to myocardial stunning, cerebral hypoperfusion, gut ischemia, loss of residual kidney function, high symptom burden, and death. This study by Keane et al. provides new data on the incidence of IDH over well-defined time intervals during the hemodialysis treatment session, clinical parameters associated with the timing of IDH onset, and whether timing of IDH impacts survival in a nationally representative hemodialysis cohort.
, Michael Liu, Charalampos Saganas, Matteo Montani, Bruno Vogt, Uyen Huynh-Do, Daniel G. Fuster
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.05.016

The publisher has not yet granted permission to display this abstract.
Rui Fu,
Published: 1 June 2021
Kidney International, Volume 99, pp 1303-1308; doi:10.1016/j.kint.2021.03.018

The publisher has not yet granted permission to display this abstract.
Published: 1 June 2021
Kidney International, Volume 99, pp 1296-1302; doi:10.1016/j.kint.2021.03.013

The publisher has not yet granted permission to display this abstract.
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.04.043

Abstract:
Patients with chronic kidney disease (CKD) experience an increased fracture risk due to impaired bone quality and quantity. Low bone mineral density (BMD) predicts fracture risk in all CKD stages, including advanced CKD (CKD G4-5D). Pharmacological therapy improves BMD and reduces fracture risk in moderate CKD. Its efficacy in advanced CKD remains to be determined, although pilot studies suggest a positive effect on BMD. Currently, antiresorptive agents are the most commonly prescribed drugs for prevention and therapy of osteoporosis. Their use in advanced CKD has been limited by lack of large clinical trials and fear of causing kidney dysfunction and adynamic bone disease (ABD). In recent decades, ABD has evolved as the most predominant form of renal osteodystrophy, commonly associated with poor outcomes, including premature mortality and progression of vascular calcification. Evolving evidence indicates that reduction of bone turnover by parathyroidectomy or pharmacological therapies, such as calcimimetics and antiresorptive agents, are not associated with premature mortality or accelerated vascular calcification in CKD. In contrast, chronic inflammation, oxidative stress, malnutrition, and diabetes can induce low bone turnover and associate with poor prognosis. Thus, the conditions causing suppression of bone turnover rather than the low bone turnover per se may account for the perceived association with outcomes. Anabolic treatment, in contrast, has been suggested to improve turnover and bone mass in patients with advanced CKD and low bone turnover, however, uncertainty about safety even exceeds that of antiresorptive agents. Here, we critically review the pathophysiologic concept of ABD and discuss the impact of low bone turnover on safety and efficacy of anti-osteoporosis pharmacotherapy in advanced CKD.
Lavinia Negrea,
Published: 1 June 2021
Kidney International, Volume 99, pp 1487-1487; doi:10.1016/j.kint.2021.03.002

The publisher has not yet granted permission to display this abstract.
Matthew P.M. Graham-Brown, Daniel S. March, Robin Young, Patrick J. Highton, Hannah M.L. Young, Darren R. Churchward, Maurice Dungey, David J. Stensel, Nicolette C. Bishop, Nigel J. Brunskill, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1478-1486; doi:10.1016/j.kint.2021.02.027

Abstract:
Cardiovascular disease is the leading cause of death for patients receiving hemodialysis. Since exercise mitigates many risk factors which drive cardiovascular disease for these patients, we assessed effects of a program of intra-dialytic cycling on left ventricular mass and other prognostically relevant measures of cardiovascular disease as evaluated by cardiac MRI (the CYCLE-HD trial). This was a prospective, open-label, single-blinded cluster-randomized controlled trial powered to detect a 15g difference in left ventricular mass measured between patients undergoing a six-month program of intra-dialytic cycling (exercise group) and patients continuing usual care (control group). Pre-specified secondary outcomes included measures of myocardial fibrosis, aortic stiffness, physical functioning, quality of life and ventricular arrhythmias. Outcomes were analyzed as intention-to-treat according to a pre-specified statistical analysis plan. Initially, 130 individuals were recruited and completed baseline assessments (65 each group). Ultimately, 101 patients completed the trial protocol (50 control group and 51 exercise group). The six-month program of intra-dialytic cycling resulted in a significant reduction in left ventricular mass between groups (-11.1g; 95% confidence interval -15.79, -6.43), which remained significant on sensitivity analysis (missing data imputed) (-9.92g; 14.68, -5.16). There were significant reductions in both native T1 mapping and aortic pulse wave velocity between groups favoring the intervention. There was no increase in either ventricular ectopic beats or complex ventricular arrhythmias as a result of exercise with no significant effect on physical function or quality of life. Thus, a six-month program of intradialytic cycling reduces left ventricular mass and is safe, deliverable and well tolerated.
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.06.004

The publisher has not yet granted permission to display this abstract.
, , Hanjie Zhang, Joanna Willetts, Stephan Thijssen, Peter Kotanko
Published: 1 June 2021
Kidney International, Volume 99, pp 1408-1417; doi:10.1016/j.kint.2021.01.018

Abstract:
Intradialytic hypotension (IDH) is a common complication of hemodialysis, but there is no data about the time of onset during treatment. Here we describe the incidence of IDH throughout hemodialysis and associations of time of hypotension with clinical parameters and survival by analyzing data from 21 dialysis clinics in the United States to include 785682 treatments from 4348 patients. IDH was defined as a systolic blood pressure of 90 mmHg or under while IDH incidence was calculated in 30-minute intervals throughout the hemodialysis session. Associations of time of IDH with clinical and treatment parameters were explored using logistic regression and with survival using Cox-regression. Sensitivity analysis considered further IDH definitions. IDH occurred in 12% of sessions at a median time interval of 120-149 minutes. There was no notable change in IDH incidence across hemodialysis intervals (range: 2.6-3.2 episodes per 100 session-intervals). Relative blood volume and ultrafiltration volume did not notably associate with IDH in the first 90 minutes but did thereafter. Associations between central venous but not arterial oxygen saturation and IDH were present throughout hemodialysis. Patients prone to IDH early as compared to late in a session had worse survival. Sensitivity analyses suggested IDH definition affects time of onset but other analyses were comparable. Thus, our study highlights the incidence of IDH during the early part of hemodialysis which, when compared to later episodes, associates with clinical parameters and mortality.
Amaury Dujardin, Mélanie Chesneau, Florian Dubois, Richard Danger, Linh Bui, Clarisse Kerleau, Pierrick Guérif, , Jacques Dantal
Published: 1 June 2021
Kidney International, Volume 99, pp 1418-1429; doi:10.1016/j.kint.2020.09.036

Abstract:
Operationally tolerant kidney transplant recipients harbor an immunological signature, associated with low rejection risk, and focused on B lymphocytes. Here, we investigated whether patients with long-term transplantation and still on immunosuppressive therapy would present such a signature of low immunological rejection risk, compared to more recently transplanted patients. Of 114 kidney transplant recipients enrolled, 38 with more than 25 years of graft survival and stable graft function under calcineurin inhibitors, were matched with two different groups of transplanted patients (10-15 and 5-7 years after transplantation). Three phenotypes associated with low immunological rejection risk (Tfh, B and regulatory T cells), initially found in operationally tolerant kidney transplant recipients, and the composite score of tolerance (combination of six transcriptomic markers, age at transplantation and age at sampling) were analyzed. We found that very long-term patients were characterized by a significantly lower percentage of total B cells, a significantly higher proportion of CD24HiCD38Lo memory B cells, significantly fewer CD24LoCD38Lo naive B cells, and a significantly lower proportion of PD1HiCCR7Lo Tfh lymphocytes than more recently transplanted patients. This phenotype is associated with a positive composite score of tolerance in patients transplanted for more than 25 years. Thus, our study suggests a dual phenotype in very long-term kidney transplanted patients with an immunological profile associated with low rejection risk.
, Olga Bielska, Patrycja Daca-Roszak, Maciej Jankowski, Maria Szczepańska, Dagmara Roszkowska-Bjanid, Elżbieta Kuźma-Mroczkowska, Małgorzata Pańczyk-Tomaszewska, Anna Moczulska, Dorota Drożdż, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1451-1458; doi:10.1016/j.kint.2020.10.040

Abstract:
A study of 269 children enrolled into a National Registry for children with persistent glomerular hematuria identified 131 individuals with genetically confirmed X-linked Alport Syndrome. A single variant c.1871G>A p.Gly624Asp (G624D) in COL4A5 was predominant and accounted for 39% of X-linked Alport Syndrome in unrelated Polish families (44 of 113). To evaluate its origins, the genetic variation in a 2.79 Mb segment encompassing the COL4A5 locus on chromosome X was assessed. All G624D alleles were found on the same rare haplotype background, indicating a founder effect dating back to the 12-13th century. The phenotypic data of 131 children with X-linked Alport Syndrome and their 195 affected adult relatives revealed that the G624D variant was associated with a significantly milder clinical course in comparison to other pathogenic COL4A5 variants. Furthermore the clinical course of this genetically uniform cohort was milder than that observed in individuals with other COL4A5 missense mutations. In spite of the benign clinical manifestation throughout childhood and early adulthood, the G624D variant confers significant risk for both kidney failure and deafness in males, albeit 20-30 years later than that observed in individuals with other COL4A5 pathogenic variants (50% cumulative risk of starting dialysis at 54 years (95% confidence interval: 50-62) v. 26 years (95% confidence interval: 22-30)). Thus, males with G624D are candidates for existing and emerging therapies for Alport Syndrome.
, Mostafa El Moumni, Eelaha Wali, Martin B.A. Heemskerk, Robert A. Pol, Meindert J. Crop, Nichon E. Jansen, Andries Hoitsma, Friedo W. Dekker, M. van Diepen, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1459-1469; doi:10.1016/j.kint.2020.11.016

Abstract:
With a rising demand for kidney transplantation, reliable pre-transplant assessment of organ quality becomes top priority. In clinical practice, physicians are regularly in doubt whether suboptimal kidney offers from older donors should be accepted. Here, we externally validate existing prediction models in a European population of older deceased donors, and subsequently developed and externally validated an adverse outcome prediction tool. Recipients of kidney grafts from deceased donors 50 years of age and older were included from the Netherlands Organ Transplant Registry (NOTR) and United States organ transplant registry from 2006-2018. The predicted adverse outcome was a composite of graft failure, death or chronic kidney disease stage 4 plus within one year after transplantation, modelled using logistic regression. Discrimination and calibration were assessed in internal, temporal and external validation. Seven existing models were validated with the same cohorts. The NOTR development cohort contained 2510 patients and 823 events. The temporal validation within NOTR had 837 patients and the external validation used 31987 patients in the United States organ transplant registry. Discrimination of our full adverse outcome model was moderate in external validation (C-statistic 0.63), though somewhat better than discrimination of the seven existing prediction models (average C-statistic 0.57). The model's calibration was highly accurate. Thus, since existing adverse outcome kidney graft survival models performed poorly in a population of older deceased donors, novel models were developed and externally validated, with maximum achievable performance in a population of older deceased kidney donors. These models could assist transplant clinicians in deciding whether to accept a kidney from an older donor.
, Michele F. Eisenga, Volker H. Haase, Abhijit V. Kshirsagar, Adeera Levin, Francesco Locatelli, Jolanta Małyszko, Dorine W. Swinkels, Der-Cherng Tarng, Michael Cheung, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1280-1295; doi:10.1016/j.kint.2021.03.020

Abstract:
In chronic kidney disease, anemia and disordered iron homeostasis are prevalent and associated with significant adverse consequences. In 2012, Kidney Disease: Improving Global Outcomes (KDIGO) issued an anemia guideline for managing the diagnosis, evaluation, and treatment of anemia in chronic kidney disease. Since then, new data have accrued from basic research, epidemiological studies, and randomized trials that warrant a re-examination of previous recommendations. Therefore, in 2019, KDIGO decided to convene 2 Controversies Conferences to review the latest evidence, explore new and ongoing controversies, assess change implications for the current KDIGO anemia guideline, and propose a research agenda. The first conference, described here, focused mainly on iron-related issues, including the contribution of disordered iron homeostasis to the anemia of chronic kidney disease, diagnostic challenges, available and emerging iron therapies, treatment targets, and patient outcomes. The second conference will discuss issues more specifically related to erythropoiesis-stimulating agents, including epoetins, and hypoxia-inducible factor-prolyl hydroxylase inhibitors. Here we provide a concise overview of the consensus points and controversies resulting from the first conference and prioritize key questions that need to be answered by future research.
Published: 1 June 2021
Kidney International, Volume 99, pp 1259-1261; doi:10.1016/j.kint.2021.02.016

, Gabriela Gautier-Vargas, Noëlle Cognard, Jérôme Olagne, Françoise Heibel, Laura Braun-Parvez, Jonas Martzloff, Peggy Perrin, Bruno Moulin, Samira Fafi-Kremer, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1498-1500; doi:10.1016/j.kint.2021.04.005

The publisher has not yet granted permission to display this abstract.
Philippe Attias, Hamza Sakhi, Philippe Rieu, Arvish Soorkia, David Assayag, Sabrina Bouhroum, Patrice Nizard,
Published: 1 June 2021
Kidney International, Volume 99, pp 1490-1492; doi:10.1016/j.kint.2021.04.009

The publisher has not yet granted permission to display this abstract.
Janina Paula T. Sy-Go, Prince Singh,
Published: 1 June 2021
Kidney International, Volume 99; doi:10.1016/j.kint.2020.09.012

Hong Sang Choi, Chang Seong Kim, Seong Kwon Ma, Soo Wan Kim,
Published: 1 June 2021
Kidney International, Volume 99, pp 1505-1506; doi:10.1016/j.kint.2020.12.026

Published: 1 June 2021
Kidney International, Volume 99, pp 1264-1267; doi:10.1016/j.kint.2021.02.022

The publisher has not yet granted permission to display this abstract.
, Xavier Bassand, Ilies Benotmane, Nicolas Bouvier
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.05.022

The publisher has not yet granted permission to display this abstract.
, Thibaut Objois, Michel Brazier, Youssef Bennis, Cédric Boudot, Gaëlle Lenglet, Julien Paccou, Jean-Marc Bugnicourt, Gabriel Choukroun, Tilman B. Drueke, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1382-1391; doi:10.1016/j.kint.2021.01.026

Abstract:
In chronic kidney disease (CKD), calcium-sensing receptor (CaSR) expression and function have been extensively studied in parathyroid tissue and vascular tissues. To examine whether similar changes occurred in other tissues, we measured total and surface CaSR expression in monocytes of patients with various stages of CKD and healthy volunteers respectively in cross-sectional studies. We further explored in vitro the impact of uremic serum on CaSR expression in monocytes (U937 and THP-1 cell lines), and whether human peripheral blood mononuclear cells or U937 and THP-1 monocytes might modify vascular calcium deposition in rat carotid arteries in vitro. CKD was associated with a decrease in peripheral blood mononuclear cell CaSR expression both in total and at the monocyte surface alone (43% and 34%, respectively in CKD stages 4-5). This decrease was associated with a reduction in the ability of monocytes to inhibit vascular calcification in vitro. Pretreatment with the calcimimetic NPSR568 of peripheral blood mononuclear cells isolated from patients with CKD significantly improved monocyte capacity to reduce carotid calcification in vitro. The fewer peripheral blood mononuclear cells expressing cell surface CaSR, the more calcimimetic treatment enhanced the decrease of carotid calcium content. Thus, we demonstrate that monocyte CaSR expression is decreased in patients with CKD and provide in vitro evidence for a potential role of this decrease in the promotion of vascular calcification. Hence, targeting this alteration or following monocyte CaSR expression as an accessible marker might represent a promising therapeutic strategy in CKD-associated arterial calcification.
, Delphine Kervella, Christine Kandel-Aznar, Aurélie Fantou, Gilles Blancho, Mohamed Hamidou
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.06.002

The publisher has not yet granted permission to display this abstract.
Bethany C. Birkelo, Sharidan K. Parr, Amy M. Perkins, Robert A. Greevy, Adriana M. Hung, Shailja C. Shah, Juan Pablo Arroyo, Jason Denton, Andrew J. Vincz, , et al.
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.05.029

The publisher has not yet granted permission to display this abstract.
, Carlijn C.E. Jordans, Anne P.J. de Pagter, Dorine Bresters, Cornelia M. Jol-Van der Zijde, Joell E. Bense, Roos W.G. van Rooij-Kouwenhoven, Ram N. Sukhai, Marloes Louwerens, Eiske M. Dorresteijn, et al.
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.05.030

Abstract:
Chronic kidney disease (CKD) is an important sequela of hematopoietic stem cell transplantation (HSCT), but data regarding CKD after pediatric HSCT are limited. In this single center cohort study, we evaluated the estimated glomerular filtration rate (eGFR) dynamics, proteinuria and hypertension in the first decade after HSCT and assessed risk factors for CKD in 216 pediatric HSCT survivors, transplanted 2002-2012. The eGFR decreased from a median of 148 to 116 ml/min/1.73m2 between pre-HSCT to ten years post-HSCT. CKD, (KDIGO stages G2 or A2 or more; eGFR under 90ml/min/1.73m2 and/or albuminuria) occurred in 17% of patients. In multivariate analysis, severe prolonged stage 2 or more acute kidney injury (AKI), with an eGFR under 60ml/min/1.73m2 and duration of 28 days or more, was the main risk factor for CKD (hazard ratio 9.5, 95% confidence interval 3.4-27). Stage 2 or more AKI with an eGFR of 60ml/min/1.73m2 or more and KDIGO stage 2 or more AKI with eGFR under 60ml/min/1.73m2 but recovery within 28 days were not associated with CKD. Furthermore, hematological malignancy as HSCT indication was an independent risk factor for CKD. One third of patients had both CKD criteria, one third had isolated eGFR reduction and one third only had albuminuria. Hypertension occurred in 27% of patients with CKD compared to 4.4% of patients without. Tubular proteinuria was present in 7% of a subgroup of 71 patients with available β2-microglobulinuria. Thus, a significant proportion of pediatric HSCT recipients developed CKD within ten years. Our data stress the importance of structural long term monitoring of eGFR, urine and blood pressure after HSCT to identify patients with incipient CKD who can benefit from nephroprotective interventions.
Allan Sacker, Vanderlene Kung,
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.06.006

The publisher has not yet granted permission to display this abstract.
Christopher D. Blosser, Gregory Haber,
Published: 1 June 2021
Kidney International, Volume 99, pp 1430-1438; doi:10.1016/j.kint.2020.10.018

Abstract:
Recipients of kidney transplants have elevated cancer risk compared with the general population. Improvements over time in transplant care and cancer treatment may have affected incidence and outcomes of cancer among recipients of kidney transplant. To evaluate this, we used linked United States transplant and cancer registry data to study 101,014 adult recipients of kidney transplants over three decades (1987-1996, 1997-2006, 2007-2016). Poisson regression was used to assess trends in incidence for cancer overall and seven common cancers. Associations of cancer with risk of death-censored graft failure (DCGF) and death with functioning graft (DWFG) were evaluated with Cox regression. We also estimated absolute risks of DCGF and graft failure following cancer for recipients transplanted in 2007-2016. There was no significant change in the incidence of cancer overall or for six common cancers in recipients across the 1987-2016 period. Only the incidence of prostate cancer significantly decreased across this period after multivariate adjustment. Among recipients of kidney transplants with non-Hodgkin lymphoma, there were significant declines over time in elevated risks for DCGF and DWFG but no significant changes for other combined cancers. For recipients transplanted in the most recent period (2007-2016), risks following cancer diagnosis remained high, with 38% experiencing DWFG and 14% graft failure within four years of diagnosis. Absolute risk of DWFG was especially high following lung cancer (78%), non-Hodgkin lymphoma (38%), melanoma (35%), and colorectal cancer (49%). Thus, across a 30-year period in the United States, there was no overall change in cancer incidence among recipients of kidney transplants. Despite improvements for non-Hodgkin lymphoma, cancer remains a major cause of morbidity and mortality.
, Sophie Blanchi, Antioco Fois, Hafedh Fessi, Giorgina Barbara Piccoli
Published: 1 June 2021
Kidney International, Volume 99, pp 1494-1496; doi:10.1016/j.kint.2021.04.010

The publisher has not yet granted permission to display this abstract.
Moritz Anft, Arturo Blazquez-Navarro, Krystallenia Paniskaki, Sarah Skrzypczyk, Heiner Appel, Thiemo Pfab, Andrea Uhle, Michael Frahnert, Michael Barenbrock, Eckhart Büssemaker, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1489-1490; doi:10.1016/j.kint.2021.03.032

Abstract:
The outcome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in patients receiving hemodialysis (HD) is significantly worse compared with the general population.1Seidel M. Holzer B. Appel H. et al.Impact of renal disease and comorbidities on mortality in hemodialysis patients with COVID-19: a multicenter experience from Germany.J Nephrol. 2020; 33: 871-874Crossref PubMed Scopus (3) Google Scholar, 2Jager K.J. Kramer A. Chesnaye N.C. et al.Results from the ERA-EDTA Registry indicate a high mortality due to COVID-19 in dialysis patients and kidney transplant recipients across Europe.Kidney Int. 2020; 98: 1540-1548Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar, 3Ng J.H. Hirsch J.S. Wanchoo R. et al.Outcomes of patients with end-stage kidney disease hospitalized with COVID-19.Kidney Int. 2020; 98: 1530-1539Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar Whether the SARS-CoV-2–specific immunity in patients with coronavirus disease 2019 (COVID-19) receiving dialysis is impaired as a possible cause for the inferior outcome is not known so far.
, Murray Epstein
Published: 1 June 2021
Kidney International, Volume 99, pp 1321-1330; doi:10.1016/j.kint.2021.02.037

The publisher has not yet granted permission to display this abstract.
Szu-Yu Pan, Pei-Zhen Tsai, Yu-Hsiang Chou, Yu-Ting Chang, Fan-Chi Chang, Yen-Ling Chiu, Wen-Chih Chiang, Tien Hsu, Yung-Ming Chen, Tzong-Shinn Chu, et al.
Published: 1 June 2021
Kidney International, Volume 99, pp 1354-1368; doi:10.1016/j.kint.2021.01.017

Abstract:
Prolyl hydroxylase domain enzyme (PHD) inhibitors are effective in the treatment of chronic kidney disease (CKD)-associated anemia by stabilizing hypoxia inducible factor (HIF), thereby increasing erythropoietin and consequently erythropoiesis. However, concern for CKD progression needs to be addressed in clinical trials. Although pre-clinical studies showed an anti-inflammatory effect in kidney disease models, the effect of PHD inhibitors on kidney fibrosis was inconsistent probably because the effects of HIF are cell type and context dependent. The major kidney erythropoietin-producing cells are pericytes that produce erythropoietin through HIF-2α-dependent gene transcription. The concern for the impact of HIF in pericytes on kidney fibrosis arises from the fact that pericytes are the major precursor cells of myofibroblasts in CKD. Since cells expressing Gli1 fulfill the morphologic and anatomic criteria for pericytes, we induced Gli1+ cell-specific HIF stabilization or knockout to study the impact of HIF in pericytes on kidney pathology of mice with or without fibrotic injury induced by unilateral ureteral obstruction. Compared with the littermate controls, mice with pericyte-specific HIF stabilization due to von Hippel-Lindau protein or PHD2 knockout showed increased serum erythropoietin and polycythemia rather than a discernible difference in kidney fibrosis. Compared with Gli1+ pericytes sorted from littermate controls, Gli1+ pericytes sorted from PHD2 knockout mice showed increased erythropoietin gene expression rather than discernible changes in Col1a1 or Acta2 expression. Furthermore, pericyte-specific knockout of HIF-1α or HIF-2α did not affect kidney fibrosis. Thus, our study supports the absence of negative effects of PHD inhibitors on kidney fibrosis of mice despite HIF stabilization in pericytes.
Yuankai Huo, Ruining Deng, Quan Liu, Agnes B. Fogo,
Published: 1 June 2021
Kidney International, Volume 99, pp 1309-1320; doi:10.1016/j.kint.2021.01.015

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Pragyi Shrestha, Saleh Yazdani, Romain R. Vivès, Rana El Masri, Wendy Dam, Bart van de Sluis,
Published: 1 June 2021
Kidney International, Volume 99, pp 1369-1381; doi:10.1016/j.kint.2021.01.023

Abstract:
Hepatic uptake of triglyceride-rich remnant lipoproteins is mediated by the low-density lipoprotein receptor, a low-density lipoprotein receptor related protein and the heparan sulfate proteoglycan, syndecan-1. Heparan sulfate proteoglycan also mediates low-density lipoprotein receptor degradation by a regulator of cholesterol homeostasis, proprotein convertase subtilisin kexin type 9 (PCSK9), thereby hampering triglyceride-rich remnant lipoproteins uptake. In this study, we investigated the effects of proteinuria on PCSK9, hepatic heparan sulfate proteoglycan and plasma triglyceride-rich remnant lipoproteins. Adriamycin-injected rats developed proteinuria, elevated triglycerides and total cholesterol (all significantly increased). Proteinuria associated with triglycerides and total cholesterol and serum PCSK9 (all significant associations) without loss of the low-density lipoprotein receptor as evidenced by immunofluorescence staining and western blotting. In proteinuric rats, PCSK9 accumulated in sinusoids, whereas in control rats PCSK9 was localized in the cytoplasm of hepatocytes. Molecular profiling revealed that the heparan sulfate side chains of heparan sulfate proteoglycan to be hypersulfated in proteinuric rats. Competition assays revealed sulfation to be a major determinant for PCSK9 binding. PCSK9 partly colocalized with hypersulfated heparan sulfate in proteinuric rats, but not in control rats. Hence, proteinuria induces hypersulfated hepatic heparan sulfate proteoglycans, increasing their affinity to PCSK9. This might impair hepatic triglyceride-rich remnant lipoproteins uptake, causing proteinuria-associated dyslipidemia. Thus, our study reveals PCSK9/heparan sulfate may be a novel target to control dyslipidemia.
Victor G. Puelles, Alexander N. Combes,
Published: 1 June 2021
Kidney International; doi:10.1016/j.kint.2021.04.042

Abstract:
For decades, measurements of kidney microanatomy using two-dimensional (2D) sections has provided us with a detailed knowledge of kidney morphology under physiological and pathological conditions. However, the rapid development of tissue clearing methods in recent years, in combination with the development of novel three-dimensional (3D) imaging modalities have provided new insights into kidney structure and function. This review article describes a range of novel insights into kidney development and disease obtained recently using these new methodological approaches. For example, in the developing kidney these approaches have provided new understandings of ureteric branching morphogenesis, nephron progenitor cell proliferation and commitment, interactions between ureteric tip cells and nephron progenitor cells, and the establishment of nephron segmentation. In whole adult mouse kidneys, tissue clearing combined with light sheet microscopy can image and quantify the total number of glomeruli, a major breakthrough in the field. Similar approaches have provided new insights into the structure of the renal vasculature and innervation, tubulo-interstitial remodelling, podocyte loss and hypertrophy, cyst formation, the evolution of cellular crescents and the structure of the glomerular filtration barrier. We can expect many more advances in our understanding of kidney biology and pathology as additional clearing and imaging techniques are developed and adopted by more investigators.
Savannah Herbek, Daniel L. Edmonston,
Published: 1 June 2021
Kidney International, Volume 99, pp 1267-1269; doi:10.1016/j.kint.2021.02.014

Abstract:
While excitement has grown for the use of hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitors for treating renal anemia, multiple preclinical studies have shown the complex and cell-type–dependent roles of HIFs in kidney disease pathogenesis, including renal fibrosis. Pan et al. now clearly show that activating the HIF signaling in the Gli1-lineage myofibroblasts restores erythropoietin production while not adversely affecting matrix production, mitigating the concerns of exacerbated fibrosis by HIF prolyl hydroxylase inhibitors.
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