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https://www.readbyqxmd.com/read/29198849/oxalate-degrading-enzyme-recombined-lactic-acid-bacteria-strains-reduce-hyperoxaluria
#1
Chenming Zhao, Huan Yang, Xiaojing Zhu, Yang Li, Ning Wang, Shanfu Han, Hua Xu, Zhiqiang Chen, Zhangqun Ye
OBJECTIVE: To develop recombinant lactic acid bacteria (LAB) strains that express oxalate-degrading enzymes through biotechnology-based approach for the treatment of hyperoxaluria by oral administration. MATERIAL AND METHODS: The coding gene of oxalate decarboxylase (ODC) and oxalate oxidase (OxO) was transformed into Lactococcus lactis MG1363. The oxalate degradation ability in vitro was evaluated in media with high concentration of oxalate. Hyperoxaluria rat models through high oxalate diet were given recombinant LAB through oral administration...
November 30, 2017: Urology
https://www.readbyqxmd.com/read/29144803/endocrine-manifestations-of-primary-hyperoxaluria
#2
Shatha Murad, Yuval Eisenberg
OBJECTIVE: Primary hyperoxaluria type 1 (PH1) is a rare metabolic disorder of oxalate overproduction. It is associated with urolithiasis and nephrocalcinosis which progress to ESRD and systemic oxalosis. As oxalate deposits in tissues, non-parathyroid hormone (nonPTH) mediated hypercalcemia, oxalate osteopathy, primary hypothyroidism and primary hypogonadism develop. In this review, we will present a case of PH1 and provide an overview of this clinical entity and its endocrine manifestations...
November 16, 2017: Endocrine Practice
https://www.readbyqxmd.com/read/29102553/type-1-primary-hyperoxaluria-a-case-report-and-focus-on-bone-impairment-of-systemic-oxalosis
#3
L Pijnenburg, S Caillard, G Boivin, S Rizzo, R M Javier
Primary hyperoxaluria is a rare genetic disorder characterized by oxalate overproduction, leading to kidney failure due to nephrocalcinosis, and is eventually responsible for systemic oxalosis. Bone impairment, secondary to oxalate deposits, is one of the many complications that may occur. Skeletal involvement can be difficult to diagnose because of lack of clinical symptoms and therefore needs to be confirmed by invasive testing, such as transiliac bone biopsy. If confirmed, bone oxalosis is the proof of disease severity and that combined liver-kidney transplantation should be performed...
November 1, 2017: Morphologie: Bulletin de L'Association des Anatomistes
https://www.readbyqxmd.com/read/28859746/oxalosis-in-a-patient-with-livedo-reticularis
#4
Meriam Triki, Meriem Ksentini, Rim Kallel, Emna Bahloul, Faiçal Jarraya, Abderrahmen Masmoudi, Tahya Boudawara
A 27-year-old man with terminal renal failure requiring peritoneal dialysis for the past 2 years was referred to the dermatologist for evaluation of red violaceous macular skin lesions consistent with livedo reticularis. These lesions had appeared suddenly on his legs (Figure 1). He had first experienced recurrent nephrolithiasis at the age of 14. Results from urine analysis and abdominal ultrasound revealed chronic kidney failure. Because the patient had a sister with similar findings, primary hyperoxaluria (PH) was suspected and genetic testing was performed in all members of his family...
2017: Skinmed
https://www.readbyqxmd.com/read/28718073/a-randomised-phase-ii-iii-study-to-evaluate-the-efficacy-and-safety-of-orally-administered-oxalobacter-formigenes-to-treat-primary-hyperoxaluria
#5
Dawn Milliner, Bernd Hoppe, Jaap Groothoff
Primary hyperoxaluria (PH) patients overproduce oxalate because of rare genetic errors in glyoxylate metabolism. Recurrent urolithiasis and/or progressive nephrocalcinosis are PH hallmarks and can lead to kidney damage, systemic oxalosis and death. Based on previous studies, we hypothesised that treatment with the oxalate-metabolizing bacterium Oxalobacter formigenes would mediate active elimination of oxalate from the plasma to the intestine of PH patients, thereby reducing urinary oxalate excretion (Uox)...
July 17, 2017: Urolithiasis
https://www.readbyqxmd.com/read/28653384/in-this-issue-july-2017-rhdv-vaccine-protects-against-both-strains-of-virus-%C3%A2-%C3%A2-%C3%A2-olfactory-neuroblastoma-in-a-malamute-%C3%A2-%C3%A2-%C3%A2-coincidental-conditions-affecting-dysphagia-in-a-miniature-poodle-%C3%A2-%C3%A2-%C3%A2-support-for-storing-high-quality-bovine-colostrum-%C3%A2-%C3%A2-%C3%A2-sarcoptic
#6
EDITORIAL
https://www.readbyqxmd.com/read/28653383/hyperoxaluria-hyperglycoluria-and-renal-oxalosis-in-gilbert-s-potoroos-potorous-gilbertii
#7
D Forshaw, A M Horwitz, K Ellard, J A Friend, L Greed, M Metz
CASE REPORT: Six Gilbert's potoroos (Potorous gilbertii) in a captive colony, five of which were closely related, died or were euthanased with severe renal disease. Clinical signs were mostly non-specific. Renal calculi were seen on ultrasound of two affected potoroos and oxalate crystalluria was seen in two of three affected potoroos that had urine samples examined. Necropsies revealed extensive severe renal oxalosis in all affected potoroos. These findings and markedly increased concentrations of glycolate in the urine of the four affected potoroos for which it was measured, confirmed a disorder of oxalate metabolism and suggested a condition similar to primary hyperoxaluria type 1 in humans...
July 2017: Australian Veterinary Journal
https://www.readbyqxmd.com/read/28364032/sodium-glucose-transporter-2-inhibition-has-no-renoprotective-effects-on-non-diabetic-chronic-kidney-disease
#8
Qiuyue Ma, Stefanie Steiger, Hans-Joachim Anders
Sodium glucose transporter (SGLT)-2 inhibition has renoprotective effects in diabetic kidney disease. Whether similar effects can be achieved also in non-diabetic kidney disease is speculative. Chronic kidney disease was induced in C57BL/6N mice by feeding an oxalate-rich diet for 14 days, known to induce nephrocalcinosis-related tubular atrophy and interstitial fibrosis without directly affecting the glomerular compartment. Empagliflozin treatment started from day 0 of oxalate feeding had no effect on the decline of glomerular filtration rate, crystal deposition, blood urea nitrogen or serum creatinine levels on day 7 and 14...
April 2017: Physiological Reports
https://www.readbyqxmd.com/read/28346094/drug-library-screening-for-the-identification-of-ionophores-that-correct-the-mistrafficking-disorder-associated-with-oxalosis-kidney-disease
#9
Shurong Hou, Franck Madoux, Louis Scampavia, Jo Ann Janovick, P Michael Conn, Timothy P Spicer
Primary hyperoxaluria is the underlying cause of oxalosis and is a life-threatening autosomal recessive disease, for which treatment may require dialysis or dual liver-kidney transplantation. The most common primary hyperoxaluria type 1 (PH1) is caused by genetic mutations of a liver-specific enzyme alanine:glyoxylate aminotransferase (AGT), which results in the misrouting of AGT from the peroxisomes to the mitochondria. Pharmacoperones are small molecules with the ability to modify misfolded proteins and route them correctly within the cells, which may present an effective strategy to treat AGT misrouting in PH1 disorders...
August 2017: SLAS Discovery
https://www.readbyqxmd.com/read/28260452/unusual-indications-for-a-liver-transplant-a-single-center-experience
#10
Aydincan Akdur, Mahir Kirnap, Ebru H Ayvazoglu Soy, Figen Ozcay, Gokhan Moray, Gulnaz Arslan, Mehmet Haberal
OBJECTIVES: This study sought to evaluate the efficacy of liver transplant for unusual liver diseases. MATERIALS AND METHODS: The results of 476 patients who underwent liver transplant from 1988 to January 2015 were retrospectively analyzed. Two hundred forty-five of them were adult patients and 231 of them were pediatric. Thirty-one patients had unusual liver disease. RESULTS: Of the 31 patients with unusual liver disease, 9 (29%) were adult and 22 (71%) were pediatric patients...
February 2017: Experimental and Clinical Transplantation
https://www.readbyqxmd.com/read/28236885/ajkd-atlas-of-renal-pathology-oxalosis
#11
Agnes B Fogo, Mark A Lusco, Behzad Najafian, Charles E Alpers
No abstract text is available yet for this article.
March 2017: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
https://www.readbyqxmd.com/read/27924398/a-randomised-phase-i-ii-trial-to-evaluate-the-efficacy-and-safety-of-orally-administered-oxalobacter-formigenes-to-treat-primary-hyperoxaluria
#12
Bernd Hoppe, Patrick Niaudet, Rémi Salomon, Jérôme Harambat, Sally-Anne Hulton, William Van't Hoff, Shabbir H Moochhala, Georges Deschênes, Elisabeth Lindner, Anna Sjögren, Pierre Cochat
BACKGROUND: Primary hyperoxaluria (PH) is a rare, genetic disorder which involves the overproduction of endogenous oxalate, leading to hyperoxaluria, recurrent urolithiasis and/or progressive nephrocalcinosis and eventually resulting in kidney failure and systemic oxalosis. The aim of this trial was to investigate whether treatment involving an oxalate-metabolising bacterium (Oxalobacter formigenes) could reduce urinary oxalate excretion in PH patients. METHODS: The efficacy and safety of O...
May 2017: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
https://www.readbyqxmd.com/read/27844104/primary-hyperoxaluria-spectrum-of-clinical-and-imaging-findings
#13
REVIEW
Sara B Strauss, Temima Waltuch, William Bivin, Frederick Kaskel, Terry L Levin
Primary hyperoxaluria is a rare autosomal recessive inborn error of metabolism with three known subtypes. In primary hyperoxaluria type 1, the most common of the subtypes, a deficiency in the hepatic enzymes responsible for the metabolism of glycoxylate to glycine, leads to excessive levels of glyoxylate, which is converted to oxalate. The resultant elevation in serum and urinary oxalate that characterizes primary hyperoxaluria leads to calcium oxalate crystal deposition in multiple organ systems (oxalosis)...
January 2017: Pediatric Radiology
https://www.readbyqxmd.com/read/27815516/systemic-oxalosis-in-hyperoxaluria-type-1
#14
Marília Rodrigues, José Carlos Cardoso, José A P da Silva
No abstract text is available yet for this article.
November 3, 2016: Rheumatology
https://www.readbyqxmd.com/read/27805528/splenic-peliosis-resulting-in-spontaneous-splenic-rupture-in-a-concomitant-hepatic-and-renal-allograft-recipient
#15
Pelin Börcek, B Handan Özdemir, Eda Yılmaz Akçay, Mehmet Haberal
Splenic peliosis is an exceedingly rare complication following liver and kidney transplant, with few previously reported cases. A 24-year-old man with chronic renal and hepatic failure due to primary oxalosis underwent concomitant renal and hepatic transplant. On the eighth day of successful transplant, he showed signs and symptoms of hypovolemia with suspicion of intra-abdominal bleeding. Diagnostic laparotomy was performed, yielding splenic rupture, and a splenectomy was performed. Macroscopically, the spleen was ruptured, and the cut surface displayed multiple parenchymal blood-filled cysts...
November 2016: Experimental and Clinical Transplantation
https://www.readbyqxmd.com/read/27568336/identification-of-a-novel-agxt-gene-mutation-in-primary-hyperoxaluria-after-kidney-transplantation-failure
#16
Saoussen M'dimegh, Asma Omezzine, Mériam Ben Hamida-Rebai, Cécile Aquaviva-Bourdain, Ibtihel M'barek, Wissal Sahtout, Dorsaf Zellama, Geneviéve Souche, Abdellatif Achour, Saoussen Abroug, Ali Bouslama
Primary hyperoxaluria is a genetic disorder in glyoxylate metabolism that leads to systemic overproduction of oxalate. Functional deficiency of alanine-glyoxylate aminotransferase in this disease leads to recurrent nephrolithiasis, nephrocalcinosis, systemic oxalosis, and kidney failure. The aim of this study was to determine the molecular etiology of kidney transplant loss in a young Tunisian individual. We present a young man with end-stage renal disease who received a kidney allograft and experienced early graft failure...
November 2016: Transplant Immunology
https://www.readbyqxmd.com/read/27432743/an-investigational-rnai-therapeutic-targeting-glycolate-oxidase-reduces-oxalate-production-in-models-of-primary-hyperoxaluria
#17
Abigail Liebow, Xingsheng Li, Timothy Racie, Julia Hettinger, Brian R Bettencourt, Nader Najafian, Patrick Haslett, Kevin Fitzgerald, Ross P Holmes, David Erbe, William Querbes, John Knight
Primary hyperoxaluria type 1 (PH1), an inherited rare disease of glyoxylate metabolism, arises from mutations in the enzyme alanine-glyoxylate aminotransferase. The resulting deficiency in this enzyme leads to abnormally high oxalate production resulting in calcium oxalate crystal formation and deposition in the kidney and many other tissues, with systemic oxalosis and ESRD being a common outcome. Although a small subset of patients manages the disease with vitamin B6 treatments, the only effective treatment for most is a combined liver-kidney transplant, which requires life-long immune suppression and carries significant mortality risk...
February 2017: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27372182/-primary-hyperoxaluria-a-review
#18
Hassan Bouzidi, Ali Majdoub, Michel Daudon, Mohamed Fadhel Najjar
Primary hyperoxalurias (PH) are inborn errors in the metabolism of glyoxalate and oxalate with recessive autosomal transmission. As a result, an increased endogenous production of oxalate leads to exessive urinary oxalate excretion. PH type 1, the most common form, is due to a deficiency of the peroxisomal enzyme alanine: Glyoxylate aminotransferase (AGT) in the liver. PH type 2 is due to the deficiency of the glyoxylate reductase/hydroxypyruvate réductase, present in the cytosol of hepatocytes and leucocytes...
November 2016: Néphrologie & Thérapeutique
https://www.readbyqxmd.com/read/27265723/plasma-oxalate-levels-in-prevalent-hemodialysis-patients-and-potential-implications-for-ascorbic-acid-supplementation
#19
Yuguan Liu, Lawrence S Weisberg, Craig B Langman, Amanda Logan, Krystal Hunter, Deepali Prasad, Jose Avila, Thaliga Venkatchalam, Jeffrey S Berns, Garry J Handelman, William D Sirover
OBJECTIVES: Ascorbic acid (AA) supplementation may increase hemoglobin levels and decrease erythropoiesis-stimulating agent dose requirement in patients with end stage renal disease (ESRD). While plasma AA levels >100μM may be supratherapeutic, levels of at least 30μM may be needed to improve wound healing and levels may need to reach 70μM to optimize erythropoiesis. Of concern, oxalate (Ox), an AA metabolite, can accumulate in ESRD. Historically, if plasma Ox levels remain ≥30μM, oxalosis was of concern...
October 2016: Clinical Biochemistry
https://www.readbyqxmd.com/read/27061278/an-institutional-experience-of-pre-emptive-liver-transplantation-for-pediatric-primary-hyperoxaluria-type-1
#20
Shirin Elizabeth Khorsandi, Marianne Samyn, Akhila Hassan, Hector Vilca-Melendez, Simon Waller, Rukshana Shroff, Geoff Koffman, William Van't Hoff, Alastair Baker, Anil Dhawan, Nigel Heaton
Primary hyperoxaluria type 1 (PH1) is an inherited metabolic disease that culminates in ESRF. Pre-emptive liver transplantation (pLTx) treats the metabolic defect and avoids the need for kidney transplantation (KTx). An institutional experience of pediatric PH1 LTx is reported and compared to the literature. Between 2004 and 2015, eight children underwent pLTx for PH1. Three underwent pLTx with a median GFR of 40 (30-46) mL/min/1.73 m(2) and five underwent sequential combined liver-kidney transplantation (cLKTx); all were on RRT at the time of cLKTx...
June 2016: Pediatric Transplantation
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