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1.
Kidney function monitoring in inflammatory bowel disease: The MONITORED consensus.
Guillo, L, Delanaye, P, Flamant, M, Figueres, L, Karam, S, Lemoine, S, Benezech, A, Pelletier, AL, Amiot, A, Caron, B, et al
Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. 2022;(3):309-315
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Abstract
BACKGROUND AND AIMS Patients with inflammatory bowel diseases (IBD) are exposed to drug-related nephrotoxicity and kidney-related extra-intestinal manifestations (EIMs). Patients should be monitored but guidance is lacking in current international recommendations. The objective of the Kidney Function Monitoring in Inflammatory Bowel Disease (MONITORED) initiative was to achieve an expert consensus about monitoring kidney function in IBD. METHODS A literature review was first conducted. Then, an expert consensus meeting, involving 28 attendees representing French-speaking gastroenterologists and nephrologists, was held as part of an academic initiative on May 28, 2021. An anonymous Delphi process was used to discuss and vote on statements. Agreement was defined as at least 75% of participants voting for any one statement. RESULTS Experts reached consensus on 11 criteria for referral to the nephrologist. Concerning kidney function monitoring, participants unanimously validated the use of serum creatinine with estimation of the glomerular filtration rate via the MDRD or CKD-EPI equations. A blood ionogram and a urine sample with measurement of a protein-to-creatinine ratio were also broadly agreed validated. Experts recommended performing this monitoring at IBD diagnosis, prior introducing a new treatment, and annually for EIMs screening and evaluation of treatment tolerance. An evaluation 3 months after starting mesalamine and then every 6 months was felt necessary, while for biologics an annually monitoring was deemed sufficient. CONCLUSION The MONITORED consensus proposed guidelines on how to monitor kidney function in IBD. These recommendations should be considered in clinical practice to preserve kidney function and ensure the best approach to our patients.
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Febuxostat combined with hydration for the prevention of contrast-induced nephropathy in hyperuricemia patients undergoing percutaneous coronary intervention: A CONSORT-compliant randomized controlled trial.
Ma, G, Li, M, Teng, W, He, Z, Zhai, X, Xia, Z
Medicine. 2022;(4):e28683
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Abstract
BACKGROUND To assess the efficacy of febuxostat combined with hydration on contrast-induced nephropathy (CIN) in coronary heart disease patients with hyperuricemia undergoing percutaneous coronary intervention (PCI). METHODS Patients with hyperuricemia who underwent PCI were randomly assigned to 2 groups. The control group was given hydration only, and the febuxostat group received febuxostat 40 mg daily before administration of contrast agent and hydration. The primary endpoint of the study was the incidence of CIN, defined as an increase in baseline serum creatinine concentration by 25% at 2 days after contrast media administration, and variations in the serum levels of creatinine, neutrophil gelatinase-associated lipocalin, uric acid, and estimated glomerular filtration rate were compared. RESULTS A total of 202 patients with hyperuricemia were randomly assigned to either the febuxostat group (n = 100) or the control group (n = 102). The baseline characteristics of the 2 groups were similar. The incidence of CIN was 6.0% (6/100) in the febuxostat group and 14.71% (15/102) in the control group.The levels of neutrophil gelatinase-associated lipocalin at 6-hour and serum creatinine and uric acid at 48-hour in the febuxostat combined hydration group were lower than those in the control group after surgery, and the level of estimated glomerular filtration rate was higher than that in the control group (all P < .05). Multivariate logistic regression analysis revealed that febuxostat was an independent predictor of CIN. CONCLUSION Our study demonstrated that prophylactic treatment with febuxostat combined with hydration can reduce the incidence of CIN in patients with coronary heart disease and hyperuricemia after PCI.
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Renoprotection with sodium-glucose cotransporter-2 inhibitors in children: Knowns and unknowns.
Jiang, B, Cheng, Z, Liu, F, Li, Q, Fu, H, Mao, J
Nephrology (Carlton, Vic.). 2022;(2):126-132
Abstract
Sodium-glucose cotransporter-2 (SGLT2) inhibitors represent novel hypoglycemic drugs for the treatment of adult diabetes that have shown considerable potential for cardioprotection and renoprotection. This new drug can inhibit SGLT2 at the proximal tubule, increase glucosuria and natriuresis, and thus decreases the serum glucose level and blood pressure. Furthermore, the tubuloglomerular feedback activated by the natriuresis can decrease glomerular hyperfiltration, acknowledged as the main foundation of renoprotection. Several studies have confirmed the protective effects of SGLT2 inhibitors on the kidneys of adult diabetic patients and those with non-diabetic nephropathy; however, limited researches are seen in paediatric patients. In this review, we have summarized the mechanisms of action of SGLT2 inhibitors, the current experiences in adults, results of exploratory studies in children, and adverse events & obstacles of paediatric use. We further explore the potential and possible future research direction of SGLT2 inhibitors in paediatric diseases.
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The Continuum of Acid Stress.
Wesson, DE
Clinical journal of the American Society of Nephrology : CJASN. 2021;(8):1292-1299
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Abstract
Acid-related injury from chronic metabolic acidosis is recognized through growing evidence of its deleterious effects, including kidney and other organ injury. Progressive acid accumulation precedes the signature manifestation of chronic metabolic acidosis, decreased plasma bicarbonate concentration. Acid accumulation that is not enough to manifest as metabolic acidosis, known as eubicarbonatemic acidosis, also appears to cause kidney injury, with exacerbated progression of CKD. Chronic engagement of mechanisms to mitigate the acid challenge from Western-type diets also appears to cause kidney injury. Rather than considering chronic metabolic acidosis as the only acid-related condition requiring intervention to reduce kidney injury, this review supports consideration of acid-related injury as a continuum. This "acid stress" continuum has chronic metabolic acidosis at its most extreme end, and high-acid-producing diets at its less extreme, yet detrimental, end.
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Kidney injury and disease in patients with haematological malignancies.
Bridoux, F, Cockwell, P, Glezerman, I, Gutgarts, V, Hogan, JJ, Jhaveri, KD, Joly, F, Nasr, SH, Sawinski, D, Leung, N
Nature reviews. Nephrology. 2021;(6):386-401
Abstract
Acute kidney injury (AKI) is common in patients with cancer, especially in those with haematological malignancies. Kidney injury might be a direct consequence of the underlying haematological condition. For example, in the case of lymphoma infiltration or extramedullary haematopoiesis, it might be caused by a tumour product; in the case of cast nephropathy it might be due to the presence of monoclonal immunoglobulin; or it might result from tumour complications, such as hypercalcaemia. Kidney injury might also be caused by cancer treatment, as many chemotherapeutic agents are nephrotoxic. High-intensity treatments, such as high-dose chemotherapy followed by haematopoietic stem cell transplantation, not only increase the risk of infection but can also cause AKI through various mechanisms, including viral nephropathies, engraftment syndrome and sinusoidal obstruction syndrome. Some conditions, such as thrombotic microangiopathy, might also result directly from the haematological condition or the treatment. Novel immunotherapies, such as immune checkpoint inhibitors and chimeric antigen receptor T cell therapy, can also be nephrotoxic. As new therapies for haematological malignancies with increased anti-tumour efficacy and reduced toxicity are developed, the number of patients receiving these treatments will increase. Clinicians must gain a good understanding of the different mechanisms of kidney injury associated with cancer to better care for these patients.
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Potential Therapeutic Effects of Natural Plant Compounds in Kidney Disease.
Avila-Carrasco, L, García-Mayorga, EA, Díaz-Avila, DL, Garza-Veloz, I, Martinez-Fierro, ML, González-Mateo, GT
Molecules (Basel, Switzerland). 2021;(20)
Abstract
BACKGROUND The blockade of the progression or onset of pathological events is essential for the homeostasis of an organism. Some common pathological mechanisms involving a wide range of diseases are the uncontrolled inflammatory reactions that promote fibrosis, oxidative reactions, and other alterations. Natural plant compounds (NPCs) are bioactive elements obtained from natural sources that can regulate physiological processes. Inflammation is recognized as an important factor in the development and evolution of chronic renal damage. Consequently, any compound able to modulate inflammation or inflammation-related processes can be thought of as a renal protective agent and/or a potential treatment tool for controlling renal damage. The objective of this research was to review the beneficial effects of bioactive natural compounds on kidney damage to reveal their efficacy as demonstrated in clinical studies. METHODS This systematic review is based on relevant studies focused on the impact of NPCs with therapeutic potential for kidney disease treatment in humans. RESULTS Clinical studies have evaluated NPCs as a different way to treat or prevent renal damage and appear to show some benefits in improving OS, inflammation, and antioxidant capacity, therefore making them promising therapeutic tools to reduce or prevent the onset and progression of KD pathogenesis. CONCLUSIONS This review shows the promising clinical properties of NPC in KD therapy. However, more robust clinical trials are needed to establish their safety and therapeutic effects in the area of renal damage.
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Bisphenol a Exposure and Kidney Diseases: Systematic Review, Meta-Analysis, and NHANES 03-16 Study.
Moreno-Gómez-Toledano, R, Arenas, MI, Vélez-Vélez, E, Coll, E, Quiroga, B, Bover, J, Bosch, RJ
Biomolecules. 2021;(7)
Abstract
Bisphenol A (BPA) is a compound that is especially widespread in most commonly used objects due to its multiple uses in the plastic industry. However, several data support the need to restrict its use. In recent years, new implications of BPA on the renal system have been discovered, which denotes the need to expand studies in patients. To this end, a systematic review and a meta-analysis was performed to explore existing literature that examines the BPA-kidney disease paradigm and to determine what and how future studies will need to be carried out. Our systematic review revealed that only few relevant publications have focused on the problem. However, the subsequent meta-analysis revealed that high blood concentrations of BPA could be a factor in developing kidney disease, at least in people with previous pathologies such as diabetes or hypertension. Furthermore, BPA could also represent a risk factor in healthy people whose urinary excretion is higher. Finally, the data analyzed from the NHANES 03-16 cohort provided new evidence on the possible involvement of BPA in kidney disease. Therefore, our results underline the need to carry out a thorough and methodologically homogeneous study, delving into the relationship between urinary and blood BPA, glomerular filtration rate, and urine albumin-to-creatinine ratio, preferably in population groups at risk, and subsequently in the general population, to solve this relevant conundrum with critical potential implications in Public Health.
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Empagliflozin and Major Renal Outcomes in Heart Failure.
Packer, M, Butler, J, Zannad, F, Pocock, SJ, Filippatos, G, Ferreira, JP, Brueckmann, M, Jamal, W, Zeller, C, Wanner, C, et al
The New England journal of medicine. 2021;(16):1531-1533
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Targeting immune cell metabolism in kidney diseases.
Basso, PJ, Andrade-Oliveira, V, Câmara, NOS
Nature reviews. Nephrology. 2021;(7):465-480
Abstract
Insights into the relationship between immunometabolism and inflammation have enabled the targeting of several immunity-mediated inflammatory processes that underlie infectious diseases and cancer or drive transplant rejection, but this field remains largely unexplored in kidney diseases. The kidneys comprise heterogeneous cell populations, contain distinct microenvironments such as areas of hypoxia and hypersalinity, and are responsible for a functional triad of filtration, reabsorption and secretion. These distinctive features create myriad potential metabolic therapeutic targets in the kidney. Immune cells have crucial roles in the maintenance of kidney homeostasis and in the response to kidney injury, and their function is intricately connected to their metabolic properties. Changes in nutrient availability and biomolecules, such as cytokines, growth factors and hormones, initiate cellular signalling events that involve energy-sensing molecules and other metabolism-related proteins to coordinate immune cell differentiation, activation and function. Disruption of homeostasis promptly triggers the metabolic reorganization of kidney immune and non-immune cells, which can promote inflammation and tissue damage. The metabolic differences between kidney and immune cells offer an opportunity to specifically target immunometabolism in the kidney.
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ESPEN guideline on clinical nutrition in hospitalized patients with acute or chronic kidney disease.
Fiaccadori, E, Sabatino, A, Barazzoni, R, Carrero, JJ, Cupisti, A, De Waele, E, Jonckheer, J, Singer, P, Cuerda, C
Clinical nutrition (Edinburgh, Scotland). 2021;(4):1644-1668
Abstract
Acute kidney disease (AKD) - which includes acute kidney injury (AKI) - and chronic kidney disease (CKD) are highly prevalent among hospitalized patients, including those in nephrology and medicine wards, surgical wards, and intensive care units (ICU), and they have important metabolic and nutritional consequences. Moreover, in case kidney replacement therapy (KRT) is started, whatever is the modality used, the possible impact on nutritional profiles, substrate balance, and nutritional treatment processes cannot be neglected. The present guideline is aimed at providing evidence-based recommendations for clinical nutrition in hospitalized patients with AKD and CKD. Due to the significant heterogeneity of this patient population as well as the paucity of high-quality evidence data, the present guideline is to be intended as a basic framework of both evidence and - in most cases - expert opinions, aggregated in a structured consensus process, in order to update the two previous ESPEN Guidelines on Enteral (2006) and Parenteral (2009) Nutrition in Adult Renal Failure. Nutritional care for patients with stable CKD (i.e., controlled protein content diets/low protein diets with or without amino acid/ketoanalogue integration in outpatients up to CKD stages four and five), nutrition in kidney transplantation, and pediatric kidney disease will not be addressed in the present guideline.