The Experts below are selected from a list of 321249 Experts worldwide ranked by ideXlab platform
Susan J. Allison - One of the best experts on this subject based on the ideXlab platform.
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Chronic Kidney Disease: Actin cytoskeleton alterations in podocytes: a therapeutic target for chronic Kidney Disease
Nature Reviews Nephrology, 2015Co-Authors: Susan J. AllisonAbstract:Chronic Kidney Disease: Actin cytoskeleton alterations in podocytes: a therapeutic target for chronic Kidney Disease
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Polycystic Kidney Disease: Trial of a long-acting somatostatin analogue for autosomal dominant polycystic Kidney Disease
Nature reviews. Nephrology, 2013Co-Authors: Susan J. AllisonAbstract:Polycystic Kidney Disease: Trial of a long-acting somatostatin analogue for autosomal dominant polycystic Kidney Disease
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Chronic Kidney Disease: Association of chronic Kidney Disease with adverse outcomes in the absence of hypertension and diabetes.
Nature Reviews Nephrology, 2012Co-Authors: Susan J. AllisonAbstract:Chronic Kidney Disease: Association of chronic Kidney Disease with adverse outcomes in the absence of hypertension and diabetes
Carel Le W Roux - One of the best experts on this subject based on the ideXlab platform.
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metabolic surgery to treat obesity in diabetic Kidney Disease chronic Kidney Disease and end stage Kidney Disease what are the unanswered questions
Frontiers in Endocrinology, 2020Co-Authors: William P Martin, James White, Francisco J Lopezhernandez, Neil G Docherty, Carel Le W RouxAbstract:Obesity is a major factor in contemporary clinical practice in nephrology. Obesity accelerates the progression of both diabetic and non-diabetic chronic Kidney Disease and in renal transplantation both recipient and donor obesity increases the risk of allograft complications. Obesity is thus a major driver of renal Disease progression and a barrier to deceased and living donor Kidney transplantation. Large observational studies have highlighted that metabolic surgery reduces the incidence of albuminuria, slows chronic Kidney Disease progression, and reduces the incidence of end-stage Kidney Disease over extended follow-up in people with and without type 2 diabetes. The surgical treatment of obesity and its metabolic sequelae has therefore the potential to improve management of diabetic and non-diabetic chronic Kidney Disease and aid in the slowing of renal decline towards end-stage Kidney Disease. In the context of patients with end-stage Kidney Disease, although complications of metabolic surgery are higher, absolute event rates are low and it remains a safe intervention in this population. Pre-transplant metabolic surgery increases access to Kidney transplantation in people with obesity and end-stage Kidney Disease. Metabolic surgery also improves management of metabolic complications post-Kidney transplantation, including new-onset diabetes. Procedure selection may be critical to mitigate the risks of oxalate nephropathy and disruption to immunosuppressant pharmacokinetics. Metabolic surgery may also have a role in the treatment of donor obesity, which could increase the living Kidney donor pool with potential downstream impact on Kidney paired exchange programmes. The present paper provides a comprehensive coverage of the literature concerning renal outcomes in clinical studies of metabolic surgery and integrates findings from relevant mechanistic pre-clinical studies. In so doing the key unanswered questions for the field are brought to the fore for discussion.
Vicente E. Torres - One of the best experts on this subject based on the ideXlab platform.
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Polycystic Kidney Disease.
Nature reviews. Disease primers, 2018Co-Authors: Carsten Bergmann, Lisa M Guay-woodford, Peter C Harris, Shigeo Horie, Dorien J M Peters, Vicente E. TorresAbstract:Cystic Kidneys are common causes of end-stage renal Disease, both in children and in adults. Autosomal dominant polycystic Kidney Disease (ADPKD) and autosomal recessive polycystic Kidney Disease (ARPKD) are cilia-related disorders and the two main forms of monogenic cystic Kidney Diseases. ADPKD is a common Disease that mostly presents in adults, whereas ARPKD is a rarer and often more severe form of polycystic Kidney Disease (PKD) that usually presents perinatally or in early childhood. Cell biological and clinical research approaches have expanded our knowledge of the pathogenesis of ADPKD and ARPKD and revealed some mechanistic overlap between them. A reduced 'dosage' of PKD proteins is thought to disturb cell homeostasis and converging signalling pathways, such as Ca2+, cAMP, mechanistic target of rapamycin, WNT, vascular endothelial growth factor and Hippo signalling, and could explain the more severe clinical course in some patients with PKD. Genetic diagnosis might benefit families and improve the clinical management of patients, which might be enhanced even further with emerging therapeutic options. However, many important questions about the pathogenesis of PKD remain. In this Primer, we provide an overview of the current knowledge of PKD and its treatment.
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Vasopressin Antagonists in Polycystic Kidney Disease
Seminars in nephrology, 2008Co-Authors: Vicente E. TorresAbstract:Increased cell proliferation and fluid secretion, probably driven by alterations in intracellular calcium homeostasis and cyclic adenosine 3,5-phosphate, play an important role in the development and progression of polycystic Kidney Disease. Hormone receptors that affect cyclic adenosine monophosphate and are preferentially expressed in affected tissues are logical treatment targets. There is a sound rationale for considering the arginine vasopressin V2 receptor as a target. The arginine vasopressin V2 receptor antagonists OPC-31260 and tolvaptan inhibit the development of polycystic Kidney Disease in cpk mice and in three animal orthologs to human autosomal recessive polycystic Kidney Disease (PCK rat), autosomal dominant polycystic Kidney Disease (Pkd2/WS25 mice), and nephronophthisis (pcy mouse). PCK rats that are homozygous for an arginine vasopressin mutation and lack circulating vasopressin are markedly protected. Administration of V2 receptor agonist 1-deamino-8-D-arginine vasopressin to these animals completely recovers the cystic phenotype. Administration of 1-deamino-8-D-arginine vasopressin to PCK rats with normal arginine vasopressin aggravates the Disease. Suppression of arginine vasopressin release by high water intake is protective. V2 receptor antagonists may have additional beneficial effects on hypertension and chronic Kidney Disease progression. A number of clinical studies in polycystic Kidney Disease have been performed or are currently active. The results of phase 2 and phase 2-3 clinical trials suggest that tolvaptan is safe and well tolerated in autosomal dominant polycystic Kidney Disease. A phase 3, placebo-controlled, double-blind study in 18- to 50-yr-old patients with autosomal dominant polycystic Kidney Disease and preserved renal function but relatively rapid progression, as indicated by a total Kidney volume >750 ml, has been initiated and will determine whether tolvaptan is effective in slowing down the progression of this Disease.
Rebecca Ireland - One of the best experts on this subject based on the ideXlab platform.
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Chronic Kidney Disease: Use of urine albumin and cystatin C levels improves risk stratification in chronic Kidney Disease
Nature Reviews Nephrology, 2011Co-Authors: Rebecca IrelandAbstract:Chronic Kidney Disease: Use of urine albumin and cystatin C levels improves risk stratification in chronic Kidney Disease
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Polycystic Kidney Disease: Promising new potential therapies for patients with autosomal dominant polycystic Kidney Disease.
Nature reviews. Nephrology, 2010Co-Authors: Rebecca IrelandAbstract:Polycystic Kidney Disease: Promising new potential therapies for patients with autosomal dominant polycystic Kidney Disease
Manisha Jhamb - One of the best experts on this subject based on the ideXlab platform.
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Pain management in patients with chronic Kidney Disease and end-stage Kidney Disease.
Current opinion in nephrology and hypertension, 2020Co-Authors: Payel Jhoom Roy, Melanie Weltman, Laura M. Dember, Jane M. Liebschutz, Manisha JhambAbstract:Purpose of review This review evaluates current recommendations for pain management in chronic Kidney Disease (CKD) and end-stage Kidney Disease (ESKD) with a specific focus on evidence for opioid analgesia, including the partial agonist, buprenorphine. Recent findings Recent evidence supports the use of physical activity and other nonpharmacologic therapies, either alone or with pharmacological therapies, for pain management. Nonopioid analgesics, including acetaminophen, topical analgesics, gabapentinoids, serotonin-norepinephrine reuptake inhibitors, and TCA may be considered based on pain cause and type, with careful dose considerations in Kidney Disease. NSAIDs may be used in CKD and ESKD for short durations with careful monitoring. Opioid use should be minimized and reserved for patients who have failed other therapies. Opioids have been associated with increased adverse events in this population, and thus should be used cautiously after risk/benefit discussion with the patient. Opioids that are safer to use in Kidney Disease include oxycodone, hydromorphone, fentanyl, methadone, and buprenorphine. Buprenorphine appears to be a promising and safer option due to its partial agonism at the mu opioid receptor. Summary Pain is poorly managed in patients with Kidney Disease. Nonpharmacological and nonopioid analgesics should be first-line approaches for pain management. Opioid use should be minimized with careful monitoring and dose adjustment.
