Excretion of an excessive amount of OXALATES in the urine.
| Excerpt | Reference |
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| "Hyperoxaluria is an important risk factor in patients who form calcium oxalate stones within the urinary tract." | ( Smith, LH, 1991) |
| "Primary oxalosis is a rare disorder of oxalate metabolism, characterized by nephrocalcinosis, nephrolithiasis, and extrarenal deposition of calcium oxalate in several tissues, including the heart." | ( Andreoli, A; Di Pasquale, G; Pinelli, G; Ribani, M; Zampa, GA, 1989) |
| "Oxalosis is a rare disorder, in which there are widely and evenly spread deposits of oxalate crystals in the kidneys with progressive renal failure." | ( Bocchini, R; Carnazza, G; Cavallotti, GP; Genovese, MG; Marangella, MM, 1989) |
| "Primary oxalosis is a rare congenital disorder." | ( Benhamou, CL; Chavassieux, P; Edouard, C; Geslin, N; Maitre, F; Meunier, PJ; Pierre, D; Viala, JF, 1987) |
| "Mild idiopathic hyperoxaluria is reported in 8-50% of idiopathic calcium oxalate stoneformers." | ( Sutton, RA; Walker, VR, 1994) |
| "Systemic oxalosis is a constant feature in patients with primary hyperoxaluria type 1 (PH1) and chronic renal failure (CRF) and is not prevented by regular dialysis (RDT), because removal cannot keep up with retention and overproduction of oxalate." | ( Cosseddu, D; Linari, F; Marangella, M; Petrarulo, M; Vitale, C, 1993) |
| "We conclude: (1) hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets; (2) prolonged phosphate treatment alone does not induce nephrocalcinosis in HHRH patients, and (3) we believe that in XLH patients, nephrocalcinosis is essentially due to vitamin D overdosage at some stage, or noncompliance in phosphate intake, leading to repeated undetected hypercalciuric periods." | ( Blonder, J; Gabizon, D; Manor, H; Maor, J; Sela, BA; Shaked, U; Strauss, S; Tieder, M, 1993) |
| "Oxalosis is an unusual metabolic disease that results either from an inherited hepatic enzyme deficiency or as the result of poor oxalate clearance during chronic hemodialysis." | ( Fish, DN; Freiberg, AA; Louis, DS, 1993) |
| "Oxalosis is an unusual pathological condition with calcium oxalate deposits in soft tissue and bone, recognized as osteosclerosis on radiography." | ( Elmståhl, B; Rausing, A, 1997) |
| "Oxalosis is a rare condition but it should be considered in patients with radiological skeletal changes and chronic renal failure and should not be misinterpreted as renal osteodystrophy." | ( Elmståhl, B; Rausing, A, 1997) |
| "Hyperoxaluria is a recognized cause of tubulointerstitial lesions, and this could contribute to development of hypertension and chronic renal failure." | ( Angerosa, M; de Cavanagh, E; Ferder, L; Inserra, F; Stella, I; Toblli, JE, 1999) |
| "The primary hyperoxalurias are autosomal recessive disorders resulting from deficiency of hepatic alanine:glyoxylate aminotransferase (PHI) or D-glycerate dehydrogenase/glyoxylate reductase (PHII)." | ( Milliner, DS; Smith, LH; Wilson, DM, 2001) |
| "Hyperoxaluria is a recognized cause of tubulointerstitial lesions and it may contribute to chronic renal failure." | ( Angerosa, M; Ferder, L; Inserra, F; Stella, I; Toblli, JE, 2001) |
| "Enteric hyperoxaluria is a commonly seen adverse event after the jejunoileal bypass procedure." | ( Hassan, I; Juncos, LA; Milliner, DS; Sarmiento, JM; Sarr, MG, 2001) |
| "Hyperoxaluria is a major risk factor for renal stones, and in most cases, it appears to be sustained by increased dietary load or increased intestinal absorption." | ( Bertuzzi, V; Campieri, C; Campieri, M; Centi, C; De Simone, C; Famularo, G; Matteuzzi, D; Pirovano, F; Stefoni, S; Swennen, E; Ulisse, S, 2001) |
| "Hyperoxaluria is a recognized cause of tubulointerstitial lesions and this circumstance could contribute to cause chronic renal disease." | ( Angerosa, M; De Cavanaugh, EM; Ferder, L; Inserra, F; Stella, I; Toblli, JE, 2002) |
| "Hyperoxaluria is a major predisposing factor in calcium oxalate urolithiasis." | ( Ebert, D; Hesse, A; Nicolay, C; Siener, R, 2003) |
| "Secondary hyperoxaluria is due either to increased intestinal oxalate absorption or to excessive dietary oxalate intake." | ( Hesse, A; Hoppe, B; Laube, N; Leumann, E; von Unruh, G, 2003) |
| "Hyperoxaluria is defined as urinary oxalate excretion exceeding 0." | ( Bilińska, W; Nowicki, M; Rogowska-Kalisz, A; Tkaczyk, M, 2003) |
| "Hyperoxaluria is a major risk factor of calcium oxalate stone disease and renal injury is thought to be a significant initiating event." | ( Freel, RW; Green, ML; Hatch, M, 2005) |
| "Hyperoxaluria is the most significant abnormality of urine chemistry studies in patients with kidney stones who have undergone bariatric surgery." | ( Asplin, JR; Coe, FL, 2007) |
| "We conclude that hyperoxaluria is a potential complicating factor of RYGB surgery manifested as a risk for calcium oxalate stones." | ( Collazo-Clavell, ML; Kumar, R; Lieske, JC; Milliner, DS; Nelson, W; Rule, A; Sarr, MG; Sinha, MK, 2007) |
| "Hyperoxaluria is a condition where excessive oxalate is present in the urine." | ( Aggarwal, K; Bijarnia, RK; Kaur, T; Singla, SK; Tandon, C, 2008) |
| "Hyperoxaluria is a major risk factor for recurrent urolithiasis and nephrocalcinosis." | ( Grujic, D; Jung, CW; Langman, CB; Mandapati, S; Margolin, AL; McGrath, ME; Patel, RJ; Rashid, A; Salido, EC; Shenoy, BC, 2009) |
| "Hyperoxaluria is one of the crucial risk factors for calcium stone formation." | ( Bieniaś, B; Sikora, P; Wawrzyszuk, M; Zajaczkowska, M, 2008) |
| "Hyperoxaluria is a major risk factor for the formation of calcium oxalate stones, but dietary restriction of oxalate intake might not be a reliable approach to prevent recurrence of stones." | ( Barrack, ER; Bhandari, M; Menon, M; Reddy, GP; Siva, S; Thamilselvan, S; Thamilselvan, V, 2009) |
| "Hyperoxaluria is a major problem causing nephrolithiasis." | ( Burckhardt, BC; Burckhardt, G; Schnedler, N, 2011) |
| "Enteric hyperoxaluria is often present in patients after the operations of RYGB and BPD-DS that utilize an element of intestinal malabsorption as a mechanism for weight loss." | ( Bergstralh, EJ; Collazo-Clavell, ML; Kumar, R; Li, X; Lieske, JC; Olson, ER; Sarr, MG; Vrtiska, TJ, 2011) |
| "Primary hyperoxalurias are rare recessive inherited inborn errors of glyoxylate metabolism." | ( Bacchetta, J; Bertholet-Thomas, A; Cochat, P; Fargue, S; Harambat, J; Sabot, JF, 2011) |
| "As the etiology of hyperoxaluria is diverse, a good understanding of how oxalate is absorbed and transported throughout the body, together with a better insight in the regulatory mechanisms, is crucial in the setting of future treatment strategies of this disorder." | ( D'Haese, PC; Hoppe, B; Robijn, S; Verhulst, A; Vervaet, BA, 2011) |
| "Hyperoxaluria is a rare metabolic disorder characterized by calcium oxalate deposition in different tissues." | ( Augusto, JF; Beloncle, F; Besson, V; Croue, A; Duveau, A; Sayegh, J; Subra, JF, 2013) |
| "Enteric hyperoxalosis is a recognized complication of bariatric surgery, with consequent oxalate nephropathy leading to chronic kidney disease and occasionally end-stage renal failure." | ( Batiuk, TD; Bennett, WM; Hawkey, M; Houghton, DC; Troxell, ML, 2013) |
| "Hyperoxaluria is one of etiologic factors of calcium oxalate kidney stone disease." | ( Fong-Ngern, K; Kanlaya, R; Thongboonkerd, V, 2013) |
| "Primary hyperoxaluria is a rare autosomal recessive disorder." | ( Mollamehmetoğlu, H; Ok, ES; Özkök, G; Soyer, N; Taşlı, F; Vardar, E, 2013) |
| "When oxalosis is diagnosed, intensifying hemodialysis (HD) to eliminate calcium oxalate can help in the recovery of renal function in some cases." | ( Boudawara, T; Chaabouni, Y; Charfeddine, K; Hachicha, J; Kammoun, K; Kharrat, M; Makni, S; Yaich, S; Zaghdane, S, 2014) |
| "Hyperoxaluria is a major risk factor in the formation of kidney stones, and oxalate is derived from both the diet and the liver metabolism of glyoxylate." | ( Hatch, M, 2014) |
| "The primary hyperoxalurias are a group of recessive kidney diseases, characterised by extensive accumulation of calcium oxalate that progressively coalesces into kidney stones." | ( Bargal, R; Belostotsky, R; Frishberg, Y; Lyakhovetsky, R; Zeharia, A, 2014) |
| "New causes of hyperoxaluria are arising recently, in particular after gastric bypass surgery, which requires regular and preemptive monitoring." | ( Bonny, O; Lu, Y, 2015) |
| "Enteric hyperoxaluria is a common occurrence in the setting of fat malabsorption, usually due to intestinal resection or intestinal bypass surgery." | ( Asplin, JR, 2016) |
| "If hyperoxaluria is indeed caused by fat malabsorption, magnitudes of hyperoxaluria and steatorrhea should correlate." | ( Asplin, JR; Cole, JA; Fordtran, JS; Holmes, RP; Kuhn, JA; Martinez, JG; Moreland, AM; Odstrcil, EA; Santa Ana, CA; Van Dinter, TG, 2017) |
| "Hyperoxaluria is a stress that leads to calcium oxalate crystal deposition which further causes inflammation and renal cell necroptosis." | ( Bhardwaj, A; Bhardwaj, R; Bijarnia, RK; Dhawan, DK; Kaur, T; Tandon, C, 2017) |
| "Hyperoxaluria is one such pathological condition where NADPH oxidase is involved in eliciting renal injury." | ( Bhardwaj, R; Bijarnia, RK; Kaur, T; Parmar, A; Sharma, S, 2018) |
| "Hyperoxaluria is characterized by an increased excretion of urinary oxalate which is caused by inherited disorders or high oxalate intake leading to renal stone ailment." | ( Bhardwaj, R; Kaur, T; Randhawa, R, 2019) |
| "Hyperoxaluria is also observed in individuals with diabetes mellitus and obesity, which are in turn risk factors for chronic kidney disease (CKD)." | ( Efe, O; Verma, A; Waikar, SS, 2019) |
| "Enteric hyperoxaluria is commonly observed in malabsorptive conditions including Roux en Y gastric bypass (RYGB) and inflammatory bowel diseases (IBD)." | ( Liu, M; Nazzal, L, 2019) |
| "Oxalosis is a metabolic disorder characterized by the accumulation of calcium oxalate deposits in various organ systems." | ( Chee, CG; Choi, EJ; Chung, HW; Kim, W; Song, JS, 2020) |
| "Primary hyperoxaluria is a rare monogenic disorder characterized by excessive hepatic production of oxalate leading to recurrent nephrolithiasis, nephrocalcinosis, and progressive kidney damage." | ( Enders, FT; Lieske, JC; Mehta, RA; Milliner, DS; Sas, DJ; Seide, BM; Tang, X; Zhao, F, 2020) |
| "Hyperoxaluria is well known to cause renal injury and end-stage kidney disease." | ( Duan, X; He, Z; Lan, Y; Li, S; Liu, Y; Lu, S; Luo, L; Mai, X; Wu, C; Xiao, C; Yang, Z; Zeng, G; Zhang, X; Zhong, W; Zhu, W, 2020) |
| "Hyperoxaluria is a rare cause of hereditary crystalline retinopathy." | ( Ferguson, A; Khanna, RK; Le Lez, ML; Pisella, PJ, 2022) |
| "Hyperoxaluria is a feature of genetic diseases, known as primary hyperoxaluria, leading to chronic kidney disease." | ( Daudon, M; Letavernier, E, 2021) |
| "Hyperoxaluria is a major cause of kidney stone disease." | ( Mawatari, K; Shimohata, T; Suyama, M; Takahashi, A; Uebanso, T, 2021) |
| "Hyperoxaluria is a major risk factor for NL." | ( Aronson, PS; Badreddine, A; Bonnefond, A; Brinkmann, L; Burlein, S; Chambrey, R; Cornière, N; Dechaume, A; Derhourhi, M; Durand, E; Dynia, DW; Eladari, D; Froguel, P; Karp, S; Thauvin, S; Thomson, RB; Vaillant, E; Villoutreix, BO, 2022) |
| "Hyperoxaluria is a severe challenge in nephrology and has led to the novel gut eubiosis as current therapy." | ( Hiremath, S; Viswanathan, P, 2022) |
| "Hyperoxaluria is major risk factor for calcium oxalate kidney stones, which constitute two-thirds of all kidney stones." | ( Chu, T; Cil, O; Haggie, PM; Lee, S; Verkman, AS, 2022) |
| "Systemic oxalosis is a condition in which calcium oxalate crystals deposit into various bodily tissues." | ( Bering, JL; DiBaise, JK; Sproat, L; Wiedmeier-Nutor, JE, 2023) |
| "Secondary hyperoxaluria is associated with poor kidney allograft outcomes after the kidney transplant." | ( Aziz, F; Garg, N; Jorgenson, M, 2023) |
| "Hyperoxaluria is well known to cause renal injury and end-stage kidney disease." | ( Ai, G; Huang, Z; Liu, Y; Luo, L; Wu, C; Zeng, G; Zhang, G; Zhao, Z; Zhong, W; Zhou, Z; Zhu, W, 2023) |
| "Hyperoxaluria is defined by an increase of urinary oxalate, leading to kidney stones, nephrocalcinosis and/or chronic kidney disease." | ( Abid, N; Acquaviva-Bourdain, C; Bacchetta, J; Chambrier, C; Derain Dubourg, L; Grocholski, C; Guebre-Egziabher, F; Lemoine, S, 2023) |
| "Primary hyperoxaluria is an autosomal recessive disease that usually develops in childhood, whereas secondary hyperoxaluria is observed following excessive oxalate intake or reduced excretion, with no difference in age of onset." | ( Cao, L; Wang, L; Wang, X; Zhang, R; Zhang, X; Zhang, Y, 2023) |
| "Hyperoxaluria is a clinically relevant metabolic entity that portends a high morbidity burden." | ( Mutugi, A; Owino, C; Tang, J, 2023) |
| Excerpt | Reference |
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| "Hyperuraturia and hyperoxaluria occurred in the treatment with immunosuppressants, diuretics and correlated with the impairment of other tubular functions of the kidneys." | ( Kutafina, EK; Sergeeva, TV; Sil'vestrova, LA, 1991) |
| "Conventional treatment of enteric hyperoxaluria (EHO) consists of dietary restriction of oxalate and fat and correction of its underlying cause whenever possible." | ( D'Cruz, DP; Gertner, DJ; Kasidas, GP; Rampton, DS; Rose, GA; Samuell, CT, 1989) |
| "A 16-year-old girl with primary oxalosis type I presented with progressive claudication soon after being treated with chronic intermittent hemodialysis." | ( Alexandre, G; Proesmans, W; Serrus, M; van Damme-Lombaerts, R; van Dyck, M; Wilms, G, 1988) |
| "Treatment of patients with primary hyperoxaluria with orthophosphate and pyridoxine decreases urinary calcium oxalate crystallization and appears to preserve renal function." | ( Bergstralh, EJ; Eickholt, JT; Milliner, DS; Smith, LH; Wilson, DM, 1994) |
| "We conclude: (1) hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets; (2) prolonged phosphate treatment alone does not induce nephrocalcinosis in HHRH patients, and (3) we believe that in XLH patients, nephrocalcinosis is essentially due to vitamin D overdosage at some stage, or noncompliance in phosphate intake, leading to repeated undetected hypercalciuric periods." | ( Blonder, J; Gabizon, D; Manor, H; Maor, J; Sela, BA; Shaked, U; Strauss, S; Tieder, M, 1993) |
| "We present two cases of oxalosis and describe the hand manifestations of this condition and their treatment." | ( Fish, DN; Freiberg, AA; Louis, DS, 1993) |
| "In this study, a case of renal oxalosis probably secondary to excessive parenteral vitamin C administration in a patient with acute post-traumatic oliguric renal failure is reported." | ( Alkhunaizi, AM; Chan, L, 1996) |
| "The classification of oxalosis as primary or secondary is important for further treatment." | ( Elmståhl, B; Rausing, A, 1997) |
| "formigenes in regulating hyperoxaluria, laboratory rats known to be noncolonized were colonized with live bacteria or treated with a preparation of oxalate-degrading enzymes derived from O." | ( Cornelius, JG; Hesse, A; Khan, SR; Peck, AB; Schmidt, ME; Sidhu, H; Thamilselvan, S, 1999) |
| "LKT is effective therapy for primary oxalosis with ESRF but has a high morbidity and mortality rate in children who present in infancy with nephrocalcinosis and systemic oxalosis." | ( de Ville de Goyet , J; Ellis, SR; Hulton, SA; Kelly, DA; McKiernan, PJ, 2001) |
| "Hyperoxaluria was induced in male Sprague-Dawley rats by administering 0." | ( Glenton, PA; Khan, SR; Moriyama, MT, 2001) |
| "Hyperoxaluria in groups 2 and 3 rats was induced by administering 1% ethylene glycol, a precursor for oxalates, in the tap water continuously throughout the whole study." | ( Angerosa, M; Ferder, L; Inserra, F; Stella, I; Toblli, JE, 2001) |
| "Subclinical evidence of enteric hyperoxaluria should be looked for and appropriate therapy instituted as early as possible." | ( Cosyns, JP; Cuvelier, C; de Strihou, Cv; Goffin, E; Wauthier, M, 2002) |
| "Hyperoxaluria was induced in two of these groups by intraperitoneal infusion of sodium oxalate (70 mg/kg) and a pretreatment of phycocyanin (100 mg/kg) as a single oral dosage was given, 1h prior to sodium oxalate infusion." | ( Asokan, D; Farooq, SM; Kalaiselvi, P; Sakthivel, R; Varalakshmi, P, 2004) |
| "Hyperoxaluria was induced in two of these groups by intraperitoneal infusion of sodium oxalate (70 mg/kg), and a pretreatment of phycocyanin (100 mg/kg) as a single oral dosage was given to one of these groups by 1 h prior to sodium oxalate infusion challenges." | ( Asokan, D; Farooq, SM; Kalaiselvi, P; Sakthivel, R; Varalakshmi, P, 2004) |
| "Hyperoxaluria was induced in two groups by administration of 0." | ( Josephine, A; Preetha, SP; Sundarapandiyan, R; Varalakshmi, P; Veena, CK, 2006) |
| "To determine whether evaluation and treatment of hyperoxaluria in vulvar vestibulitis syndrome (VVS) is justified." | ( Abramov, L; Chen, J; Greenstein, A; Lessing, JB; Matzkin, H; Militscher, I, 2006) |
| "Women with hyperoxaluria (urine oxalate >50 mg/24 h) were placed on a low-oxalate diet and oral calcium citrate as single therapy and reevaluated 3 months later." | ( Abramov, L; Chen, J; Greenstein, A; Lessing, JB; Matzkin, H; Militscher, I, 2006) |
| "Hyperoxaluria was induced in two groups by the administration of 0." | ( Josephine, A; Preetha, SP; Varalakshmi, P; Veena, CK, 2007) |
| "After 3 months of therapy, the mean oxaluria level had decreased from 50." | ( Allegri, F; Borghi, L; Fiaccadori, E; Guerra, A; Maggiore, U; Meschi, T; Nouvenne, A; Prati, B, 2009) |
| "These effects of hyperoxaluria were reversed by concurrent PGG treatment along with decreased urinary oxalate levels and CaOx supersaturation." | ( Bae, H; Jeong, SJ; Kim, SH; Lee, EO; Lee, HJ; Lieske, JC, 2011) |
| "We induced hyperoxaluria in 8-week-old male Otsuka Long-Evans Tokushima fatty (OLETF) rats, and a control strain, Long-Evans Tokushima Otsuka (LETO) rats, by administering 1." | ( Hara, I; Iba, A; Kohjimoto, Y; Okamoto, M; Saji, F; Shigematsu, T, 2010) |
| "Administration of EG induced hyperoxaluria to the same degree in both strains." | ( Hara, I; Iba, A; Kohjimoto, Y; Okamoto, M; Saji, F; Shigematsu, T, 2010) |
| "Hyperoxaluria was induced by continuous administration of ethylene glycol (0." | ( Aydin, M; Ekici, ID; Miroglu, C; Sarıca, K; Tanriverdi, O; Telci, D, 2012) |
| "Hyperoxaluria was induced in 6-week-old male Sprague-Dawley rats by administering 1." | ( De Velasco, MA; Khan, SR; Nozawa, M; Shimizu, N; Tsuji, H; Uemura, H; Umekawa, T; Yoshimura, K, 2014) |
| "Hyperoxaluria was induced in male SD rats by administering ethylene glycol." | ( Khan, SR; Peck, AB; Shimizu, N; Sunil, J; Tsuji, H; Uemura, H; Wang, W; Yoshimura, K, 2016) |
| "HS did not affect the hyperoxaluria, hypocalciuria or supersaturation caused by HP; however, it increased calcium oxalate crystal deposition soon after 7 days of co-treatment." | ( Huang, HS; Ma, MC, 2015) |
| "Enteric hyperoxaluria was attributed to the orlistat treatment." | ( Aydin, S; Buysschaert, B; Demoulin, N; Hermans, MP; Jadoul, M; Morelle, J, 2016) |
| "Hyperoxaluria was induced in male Wistar rats by administering 0." | ( Kaur, T; Sharma, M; Singla, SK, 2016) |
| "Hyperoxaluria was induced in Group 1 by continuous administration of ethylene glycol (EG)." | ( Eryildirim, B; Hamarat, B; Kafkasli, A; Narter, F; Ozturk, O; Sahin, C; Sarica, K; Yazici, O, 2016) |
| "In the hyperoxaluria group, urinary oxalate levels were higher than the control group; yet, lower in the treatment group compared to hyperoxaluria group (p < 0." | ( Aydın Candan, I; Calapoğlu, M; Ergün, O; Oksay, T; Onaran, İ; Özorak, A; Yunusoğlu, S, 2017) |
| "Experimental induction of hyperoxaluria by ethylene glycol (EG) administration is disapproved as it causes metabolic acidosis while the oral administration of chemically synthesized potassium oxalate (KOx) diet does not mimic our natural system." | ( Albert, A; Ganesan, D; Govindan Sadasivam, S; Mariaraj Sivakumar, S; Paul, E; Ponnusamy, S; Prabhakaran, R; Tiwari, V, 2018) |
| "Hyperoxaluria rat models through high oxalate diet were given recombinant LAB through oral administration." | ( Chen, Z; Han, S; Li, Y; Wang, N; Xu, H; Yang, H; Ye, Z; Zhao, C; Zhu, X, 2018) |
| "Hyperoxaluria associated with CaOx crystal deposition will require administration of angiotensin II receptor blockers, and NADPH oxidase or NLRP3 inflammasome inhibitors." | ( Joshi, S; Khan, SR, 2019) |
| "Hyperoxaluria-induced calcium oxalate (CaOx) deposition is the key factor in kidney stone formation, for which adipose-derived stromal cells (ADSCs) have been used as a therapeutic treatment." | ( Duan, J; Gong, H; Pang, Y; Shi, J; Wang, L; Yan, Y, 2019) |
| "Hyperoxaluria is a severe challenge in nephrology and has led to the novel gut eubiosis as current therapy." | ( Hiremath, S; Viswanathan, P, 2022) |