Serum Oxalate Research Articles

32-year-old diabetic patient with progressive vision loss and crystalline retinopathy.

To report the case of severe bilateral retinal vascular occlusion in a patient with hyperoxalosis and chronic renal failure. Observational case report. Medical and imaging records were retrospectively reviewed. The patient was imaged with ultra-widefield (UWF) fundus photography and fluorescein angiography (UWF-FA), cross sectional and en face spectral-domain optical coherence tomography (SD-OCT), and OCT angiography. A 32-year-old diabetic patient receiving peritoneal dialysis was referred because of severe vision loss. UWF color fundus photography showed diffuse sclerotic retinal vessels and diffuse intraretinal crystals in both eyes. UWF-FA illustrated near-complete retinal vascular occlusion and capillary wipe out in both eyes. SD-OCT demonstrated diffuse inner and middle retina thinning in both eyes and multiple intraretinal hyperreflective foci consistent with crystalline deposits in all retina layers of both eyes. OCT angiography revealed severe capillary and large vessel non-perfusion in the superficial and deep retinal capillary plexus of each eye. The serum oxalate levels were increased at 28 µmol/L (reference range < 2 µmol/L) and genetic testing was positive for a heterozygous mutation of the AGXT (Alanine-Glyoxylate Amino Transferase) gene that causes type 1 autosomal recessive primary hyperoxaluria. A diagnosis of hyperoxalosis causing severe retinal vascular occlusion was rendered. Hyperoxalosis was the result of multiple factors including heterozygous AGXT mutation, chronic renal failure insufficiently treated with peritoneal dialysis, and a diet high in oxalate. This case highlights the importance of ruling out retinal oxalosis in patients on peritoneal dialysis in order to initiate prompt hemodialysis and prevent severe retinal vascular occlusion.

Serum oxalate concentration is associated with coronary artery calcification and cardiovascular events in Japanese dialysis patients

Coronary artery calcification (CAC) is associated with cardiovascular disease (CVD). CAC might contain calcium oxalate, and a high serum oxalate (SOx) concentration is associated with cardiovascular mortality in dialysis patients. We assessed the associations between SOx and CAC or CVD events in Japanese hemodialysis patients. This cross-sectional and retrospective cohort study was done in 2011. Seventy-seven hemodialysis patients’ Agatston CAC score was measured, and serum samples were collected. SOx concentrations were measured in 2021 by using frozen samples. Also, new-onset CVD events in 2011–2021 were retrospectively recorded. The association between SOx concentration and CAC score ≥ 1000, and new-onset CVD events were examined. Median SOx concentration and CAC score were 266.9 (229.5–318.5) µmol/L and 912.5 (123.7–2944), respectively. CAC score ≥ 1000 was associated with SOx [adjusted odds ratio (OR) 1.01, 95% confidence interval (CI), 1.00–1.02]. The number of new-onset CVD events was significantly higher in patients with SOx ≥ median value [hazard ratio (HR) 2.71, 95% CI 1.26–6.16]. By Cox proportional hazard models, new-onset CVD events was associated with SOx ≥ median value (adjusted HR 2.10, 95% CI 0.90–4.91). SOx was associated with CAC score ≥ 1000 and new-onset CVD events in Japanese hemodialysis patients.

The preventive effects of Ulva lactuca aqueous extract, ulvan polysaccharides and atorvastatin on ethylene glycol-induced hyperoxaluria.

Kidney stones are a common complication of hyperoxaluria. The aim of this study is to investigate the protective and preventive effects of Ulva lactuca aqueous extract, ulvan polysaccharides and atorvastatin on ethylene glycol-induced hyperoxaluria. Male Wistar rats between 110 and 145 g in weight were used in the study, Ulva lactuca aqueous extract and polysaccharides were prepared. The male albino rats were supplemented with 0.75 percent ethylene glycol (v/v) in their drinking water for six weeks to induce hyperoxaluria. Ulvan infusions (100 mg/kg body weight), ulvan polysaccharides (100 mg/kg body weight), and atorvastatin (two milligrams/kg body weight) to treat hyperoxaluric rats for four weeks (every other day) were used. Weight loss, serum creatinine, serum urea, serum uric acid, serum oxalate, kidney oxalate, kidney lipid peroxidation, and kidney DNA fragmentation and kidney histopathological studies were done. Weight loss, rise of serum creatinine, serum urea, serum uric acid, serum oxalate, kidney oxalate, kidney lipid peroxidation, and kidney DNA fragmentation were all shown to be prevented by the addition of atorvastatin, polysaccharides, or aqueous extract, respectively. Catalase (CAT) activity, glutathione peroxidase (GPX) activity, glutathione-S-transferase (GST) activity, and histopathological perturbations were all significantly reduced by the medicines that were studied. Hyperoxaluria caused by ethylene glycol may be prevented by a combination of Ulva lactuca aqueous extract, ulvan polysaccharides, and atorvastatin. A reduction in renal oxidative stress and an improvement of the antioxidant defense system may be responsible for these protective benefits. However, Ulva lactuca infusion and ulvan polysaccharides need to be studied further in humans, in order to determine their efficacy and safety.

Primary hyperoxaluria I, II, III types in children (review of literature)

This review presents the latest data on the classification, pathogenesis, clinical and genetic features, and therapy of primary hyperoxaluria types I, II, and III in children with autosomal recessive inheritance. ORPHA portal of orphan diseases presents genes responsible for primary hyperoxaluria type I AGXT (93598); type II and type II GRHPR (93599), type III HOGA1 (93600). Worldwide genetic studies have established the pathogenesis, clinical phenotype and genotype features of primary hyperoxaluria. The pathogenesis of primary hyperoxaluria in children is based on impaired hepatic glyoxylate metabolism. The enzyme AGT catalyzes the conversion of L-alanine and glyoxylate to pyruvate and glycine, with vitamin B6 (pyridoxine) serving as a coenzyme for this reaction. Increased production of endogenous oxalate leads to increased blood oxalate concentrations and urinary oxalate excretion with the formation of renal calcium oxalate crystals and radiopaque concrements (calcium oxalate monohydrate – vevelite, calcium oxalate dihydrate – vedellite). High risk of progression to chronic kidney disease in primary hyperoxaluria in children of types I and II. Systemic oxalosis develops with increasing serum oxalate levels and the formation of calcium oxalate crystals with deposition in many organs and tissues. Therapy for primary hyperoxaluria in children includes: hydration (3l/m2/day) and citrates 100–150 mg/kg/day (potassium citrate 0.3–0.5 mmol/kg/day), pyridoxine at a dose of 5 to 20 mg/kg/day for vitamin B6 sensitive type I primary hyperoxaluria. Administration of oxalobacter formigenes and diet is effective. Combined liver and then kidney transplantation or simultaneous liver and kidney transplantation in patients with type I PH in B6-insensitive and isolated liver transplantation in B6-sensitive variants are performed. Timely molecular genetic testing in children with nephrocalcinosis makes it possible to establish a clinical and genetic diagnosis of type I, II, III PH, to carry out a personalised approach to treatment and to predict future health status.

LIMITED TREATMENT OPTIONS FOR PRIMARY HYPEROXALURIA WITH RENAL INSUFFICIENCY

Primary hyperoxaluria (PH) is a rare autosomal recessive metabolic disorder in which the serum levels of oxalate increase because of overproduction.The renal tubule is the primary target of the oxalate deposit, which damages the kidney and leads to cause ESRD. Here, we present a 54-year-old man with a terminal kidney disease; which is dependent on hemodialysis and is likely due to type 2 or 3 PH. Renal insufciency is uncommon to be found in PH patients. With exceedingly high levels of serum oxalate (70 ฀mol/L), this patient had few treatment options available for his rare condition.This report details a unique introduction to a rare condition where renal biopsy was instrumental to reach the diagnosis.

MO734: High Serum Oxalate Concentration Associated with Coronary Artery Calcification and Lanthanum Carbonate in Hemodialysis Patients

Abstract BACKGROUND AND AIMS Oxalate is an organic acid found in abundance in plants and can also be synthesized as a terminal metabolite by the organic acid metabolism systems in humans. As a major excretion pathway of oxalate is urine, serum oxalate (SOx) concentration elevates in end-stage renal disease (ESRD) patients and causes calcium oxalate deposition to tissues. We previously reported that calcium oxalate might be one of the major components of coronary artery calcification (CAC) in ESRD patients; however, the association between SOx and CAC is unknown. This study aimed to demonstrate the relationship between SOx and CAC in haemodialysis patients. METHOD A total of 77 patients undergoing maintenance haemodialysis at a single facility who underwent an atherosclerosis check-up from 2011 to 2012 were enrolled and measured SOx retrospectively in 2021. Of those, 17 extremely outlying SOx patients were excluded, and 60 patients including 42 males were analysed. The median age was 64 (35–85) years, and median dialysis duration was 87.5 (17.1–410) months. Gender, Agastston's CAC score, major artery calcification volume, laboratory data and medications around the atherosclerosis check-up date and new-onset cardiovascular disease (CVD) events and deaths during the 10-year observation period were recorded. A CVD event is defined as an admission due to non-fatal myocardial infarction, coronary artery disease or heart failure. SOx level was measured by the commercial colorimetric oxalate assay kit, and the normal SOx level was 181 µmol/L. RESULTS The median SOx was 267 (221–563) µmol/L and new-onset CVD events, all-cause deaths occurred in 28 (47%) and 22 (37%) patients, respectively. In univariate analysis, SOx was associated with males (r = 0.27, P = 0.03), serum albumin (r = –0.25, P = 0.05), uric acid (r = 0.29, P = 0.02), phosphate (r = 0.26, P = 0.04), alkaline phosphatase (r = –0.28, P = 0.03), lanthanum carbonate (r = 0.32, P = 0.01), major artery calcification volume (r = 0.28, P = 0.03) and CAC score (r = 0.29, P = 0.02). In multivariate regression analysis, SOx was associated with lanthanum carbonate (F = 5.96, P = 0.02) and CAC score (F = 4.47, P = 0.03, Table 1). Receiver operating characteristic curve showed SOx = 269.5 µmol/L was the best cut-off for predicting CVD events. We divided subjects into two groups by this cut-off SOx value and revealed SOx was associated with new-onset CVD events (N = 60, P = 0.01) even after adjusted by age under 75 years (N = 52, P = 0.03) or both age under 75 years and CAC score under 1000 (N = 28, P = 0.04) by the Kaplan–Meier method (Fig. 1). CONCLUSION SOx was associated with CAC score, lanthanum carbonate and CVD events in ESRD patients undergoing haemodialysis.

OP31 Dietary and Multi-Omic characterization of new onset treatment naive Crohn Disease identifies factors that may contribute to disease pathogenesis

Abstract Background Crohn Disease (CD) prevalence is rising worldwide. As altered genetics are improbable, this phenomenon likely relates to environmental-dietary changes linked with gut microbiome. We aimed to define host and microbial factors at CD diagnosis. Methods Multiomics analyses of SOURCE cohort including clinical, biomarkers (CRP, fecal calprotectin), food frequency questionnaire (FFQ), serum metabolomics, mucosal terminal ileum (TI) transcriptomics, and fecal and mucosal biopsy samples for 16S microbial amplicon sequencing. Results 25 newly-diagnosed CD and 33 controls (median age 28 years, 50% males). Gender, age, and BMI did not differ between groups, but CRP (p=0.001) and calprotectin (p=E-10) were significantly higher in CD. FFQ results showed that compared to controls, pre-diagnosis CD patients consumed significantly more added sugar (g/day), starch (g/day) nitrite (mg/day), and significantly less vitamin K, D, vegetables, and olive oil (Fig 1). Microbial analyses highlighted significant differences (FDR&amp;lt;0.1) in amplicon sequence variants (ASVs) abundance between stool and biopsies samples (73 ASVs) and between CD and Controls samples (82 ASVs). Biopsy vs. stool samples were enriched for Veillonella, Fusobacterium, Neisseria, and Ruminococcus gnavus. CD showed higher abundance of Enterobacteriaceae and Ruminococcus gnavus with reduction of several Ruminococcaceae and Lachnospiraceae taxa (Fig. 1). Ileal transcriptomics differential expression (FC&amp;gt;1.5, FDR&amp;lt;0.05) replicated previous results with significant induction in CD of DUOX2, CXCL9, and DEFB4A and pathways linked to innate and adaptive immunity, and to extracellular matrix. CD down regulated genes included GUCA2B, SLC10A2, and GSTA1, and pathways linked with epithelial transporters. Serum metabolomics highlighted significant variations (FDR&amp;lt;0.25) in Linoleic acid, aKG, Tryptophan, nicotinamide, Docosahexaenoic acid, oxalate, and GABA between CD and controls. We next tested for significant association (FDR&amp;lt;0.25) between diet and multi-OMICs (Fig. 2). Associations between gut microbiome and TI transcriptomics, and serum metabolomics showed that Erysipelotrichacea taxa positivity correlated with serum oxalate, and TI expression of CEACAM6 and DUOX2. Associations between diet and TI transcriptomics and serum metabolomics indicated that B12, tryptophan and riboflavin consumptions were negatively associated with the bile acid transporter SLC10A2 in the TI, and vegetables consumption was positively associated with oxalate degrading Oxalobacter. Conclusion Conclusions: FFQ identifies difference in diet at the onset of CD that may contribute to pathogenesis. Integration between dietary and OMICs layers disclosed novel correlations warranting further exploration.

High Oxalate Concentrations Correlate with Increased Risk for Sudden Cardiac Death in Dialysis Patients.

The clinical significance of accumulating toxic terminal metabolites such as oxalate in patients with kidney failure is not well understood. To evaluate serum oxalate concentrations and risk of all-cause mortality and cardiovascular events in a cohort of patients with kidney failure requiring chronic dialysis, we performed a post-hoc analysis of the randomized German Diabetes Dialysis (4D) Study; this study included 1255 European patients on hemodialysis with diabetes followed-up for a median of 4 years. The results obtained via Cox proportional hazards models were confirmed by competing risk regression and restricted cubic spline modeling in the 4D Study cohort and validated in a separate cohort of 104 US patients on dialysis after a median follow-up of 2.5 years. A total of 1108 patients had baseline oxalate measurements, with a median oxalate concentration of 42.4 µM. During follow-up, 548 patients died, including 139 (25.4%) from sudden cardiac death. A total of 413 patients reached the primary composite cardiovascular end point (cardiac death, nonfatal myocardial infarction, and fatal or nonfatal stroke). Patients in the highest oxalate quartile (≥59.7 µM) had a 40% increased risk for cardiovascular events (adjusted hazard ratio [aHR], 1.40; 95% confidence interval [95% CI], 1.08 to 1.81) and a 62% increased risk of sudden cardiac death (aHR, 1.62; 95% CI, 1.03 to 2.56), compared with those in the lowest quartile (≤29.6 µM). The associations remained when accounting for competing risks and with oxalate as a continuous variable. Elevated serum oxalate is a novel risk factor for cardiovascular events and sudden cardiac death in patients on dialysis. Further studies are warranted to test whether oxalate-lowering strategies improve cardiovascular mortality in patients on dialysis.

Hyperoxalemia Leads to Oxidative Stress in Endothelial Cells and Mice with Chronic Kidney Disease

Introduction: Cardiovascular disease is the most common cause of morbidity and mortality in patients with ESRD. In addition to phosphate overload, oxalate, a common uremic toxin, is also involved in vascular calcification in patients with ESRD. The present study investigated the role and mechanism of hyperoxalemia in vascular calcification in mice with uremia. Methods: A uremic atherosclerosis (UA) model was established by left renal excision and right renal electrocoagulation in apoE^−/− mice to investigate the relationship between oxalate loading and vascular calcification. After 12 weeks, serum and vascular levels of oxalate, vascular calcification, inflammatory factors (TNF-α and IL-6), oxidative stress markers (malondialdehyde [MDA], and advanced oxidation protein products [AOPP]) were assessed in UA mice. The oral oxalate-degrading microbe Oxalobacter formigenes (O. formigenes) was used to evaluate the effect of a reduction in oxalate levels on vascular calcification. The mechanism underlying the effect of oxalate loading on vascular calcification was assessed in cultured human aortic endothelial cells (HAECs) and human aortic smooth muscle cells (HASMCs). Results: Serum oxalate levels were significantly increased in UA mice. Compared to the control mice, UA mice developed more areas of aortic calcification and showed significant increases in aortic oxalate levels and serum levels of oxidative stress markers and inflammatory factors. The correlation analysis showed that serum oxalate levels were positively correlated with the vascular oxalate levels and serum MDA, AOPP, and TNF-α levels, and negatively correlated with superoxide dismutase activity. The O. formigenes intervention decreased serum and vascular oxalate levels, while did not improve vascular calcification significantly. In addition, systemic inflammation and oxidative stress were also improved in the O. formigenes group. In vitro, high concentrations of oxalate dose-dependently increased oxidative stress and inflammatory factor expression in HAECs, but not in HASMCs. Conclusions: Our results indicated that hyperoxalemia led to the systemic inflammation and the activation of oxidative stress. The reduction in oxalate levels by O. formigenes might be a promising treatment for the prevention of oxalate deposition in calcified areas of patients with ESRD.

Unusual presentation of oxalate nephropathy causing acute kidney injury: A case report

Oxalate nephropathy due to Hyperoxaluria and elevated serum oxalate level is a well-known cause for interstitial fibrosis, and ESRD. Conditions associated with high serum Oxalate, should be considered as a possible contributing factor for a patient’s tubular injury. Well known cause for Hyperoxaluria including enteric Hyperoxaluria (due to gastric bypass, chronic pancreatitis, small Bowel resection, or malabsorption, as well as depletion of enteric oxalate-degrading bacteria [e.g., Oxalobacter). Other known causes of oxalate nephropathy include primary Hyperoxaluria, ethylene glycol intoxication, vitamin B6 deficiency, excessive ingestion of vitamin C or dietary substances rich in oxalic acid, aspergillosis, prolonged renal failure and various drugs (e.g., Known medications to cause Oxalate Nephropathy are: Orlistat, Praxilene, COX-2 inhibitors). Unusual presentation with Acute Kidney Injury with incidental finding of high serum Oxalate in a patient with a known CKD stage III, recently started on Polyethelene Glycol to treat his constipation.

Vitamin C deficiency and impact of vitamin C administration among pediatric patients with advanced chronic kidney disease.

Vitamin C deficiency is common in chronic kidney disease (CKD) due to losses through dialysis and dietary intake below requirement. We investigated prevalence of vitamin C deficiency and impact of vitamin C treatment in deficient/insufficient patients. A prospective cohort study in patients aged 1-18years with CKD stages 4 and 5D collected demographic data including underlying disease, treatment, and anthropometric assessment. Vitamin C intake was assessed using 24-h dietary recall. Hemoglobin, iron status, serum vitamin C, and serum oxalate were measured at baseline and after treatment. Vitamin C (250mg/day) was given orally for 3months to deficient/insufficient patients. Nineteen patients (mean age 12.00 ± 4.1years) showed prevalence of 10.6% vitamin C insufficiency and 78.9% deficiency. There were no associations between vitamin C level and daily vitamin C intake (p = 0.64) or nutritional status (p = 0.87). Median serum vitamin C was 1.51 (0.30-1.90) mg/L. In 16 patients receiving treatment, median serum vitamin C increased from 1.30 (0.23-1.78) to 3.22 (1.77-5.96) mg/L (p = 0.008) without increasing serum oxalate (79.92 (56.6-106.84) vs. 80.47 (56.88-102.95) μmol/L, p = 0.82). However, 62.5% failed to achieve normal vitamin C levels. Ordinal regression analysis revealed patients with non-oligoanuric CKD were less likely to achieve normal vitamin C levels (β = - 3.41, p = 0.03). We describe high prevalence of vitamin C insufficiency/deficiency among pediatric CKD patients. Vitamin C levels could not be solely predicted by nutritional status or daily intake. The treatment regimen raised serum vitamin C without increasing serum oxalate; however, it was largely insufficient to normalize levels, particularly in non-oligoanuric CKD. Graphical abstract .

Effect of dimethyl fumarate on the renal calcium oxalate stone formation in rats and possible mechanism

Objective To observe the effect of dimethyl fumarate (DMF) on the renal calcium oxalate crystals formation in SD rats induced by glyoxylic acid monohydrate, and explore the possible mechanism. Methods Thirty male Sprague-Dawley rats were randomly divided into 3 groups: control group, model group and DMF group (n=10 each). The control group was free to drink purified water. Model group was induced by intraperitoneal injection of glyoxylic acid monohydrate to establish a kidney calcium oxalate stone model, and DMF group was treat with DMF by gastric administration on the basis of modeling. After 10 days of continuous treatment, the 24 h urine, serum and kidney of rats in each group were collected. Serum creatinine (SCr) value, calcium and oxalate (Ox) contents in urine were measured. Von Kossa staining method was used to detect the deposition of calcium oxalate crystals in kidney tissue. Western blotting was used to detect the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1 protein in renal tissue. The frozen section DHE staining was used to detect the ROS level in the kidney, thiobarbituric acid method was used to test malondialdehyde (MDA) content, and the xanthine oxidase method was used to detect superoxide dismutase (SOD) activity. Results There was no visible calcium crystal in the kidney of the control group. Compared to the model group, the amounts of renal calcium crystal were significantly reduced in the DMF group (76.07±4.87) /HP vs. (37.94±4.63) /HP (t=17.940, P 0.05). There was no significant difference in 24-hour urinary calcium ion content between the three groups (F=1.670, P>0.05). Compared with the control group, renal ROS levels (t=20.920, P<0.01), Nrf2 (t=17.290, P<0.01) and HO-1 protein (t=38.030, P<0.01) expression levels were significantly increased in the model group. Compared with the model group, renal ROS levels were significantly reduced in the DMF group (t=16.000, P<0.01), while the expression levels of Nrf2 (t=25.580, P<0.01) and HO-1 protein (t=79.290, P<0.01) were significantly increased. Conclusion The formation of calcium oxalate kidney stones is related to oxalate-mediated oxidative stress. DMF may interfere with the pathogenesis of calcium oxalate kidney stones by activating Nrf2 to induce HO-1 to inhibit oxidative stress. Key words: Calcium oxalate stones; Oxidative stress; Nuclear factor erythroid 2-related factor 2; Dimethyl fumarate

Bilateral native nephrectomy to reduce oxalate stores in children at the time of combined liver-kidney transplantation for primary hyperoxaluria type 1.

Primary hyperoxaluria type-1 (PH-1) is a rare genetic disorder in which normal hepatic metabolism of glyoxylate is disrupted resulting in diffuse oxalate deposition and end-stage renal disease (ESRD). While most centers agree that combined liver-kidney transplant (CLKT) is the appropriate treatment for PH-1, perioperative strategies for minimizing recurrent oxalate-related injury to the transplanted kidney remain unclear. We present our management of children with PH-1 and ESRD on hemodialysis (HD) who underwent CLKT at our institution from 2005 to 2015. On chart review, three patients (2 girls, 1 boy) met study criteria. Two patients received deceased-donor split-liver grafts, while one patient received a whole liver graft. All patients underwent bilateral native nephrectomy at transplant to minimize the total body oxalate load. Median preoperative serum oxalate was 72μmol/L (range 17.8-100). All patients received HD postoperatively until predialysis serum oxalate levels fell <20μmol/L. All patients, at a median of 7.5years of follow-up (range 6.5-8.9), demonstrated stable liver and kidney function. While CLKT remains the definitive treatment for PH-1, bilateral native nephrectomy at the time of transplant reduces postoperative oxalate stores and may mitigate damage to the renal allograft.

In female rats, ethylene glycol treatment elevates protein expression of hepatic and renal oxalate transporter sat-1 (Slc26a1) without inducing hyperoxaluria.

AimTo investigate whether the sex-dependent expression of hepatic and renal oxalate transporter sat-1 (Slc26a1) changes in a rat model of ethylene glycol (EG)-induced hyperoxaluria.MethodsRats were given tap water (12 males and 12 females; controls) or EG (12 males and 12 females; 0.75% v/v in tap water) for one month. Oxaluric state was confirmed by biochemical parameters in blood plasma, urine, and tissues. Expression of sat-1 and rate-limiting enzymes of oxalate synthesis, alcohol dehydrogenase 1 (Adh1) and hydroxy-acid oxidase 1 (Hao1), was determined by immunocytochemistry (protein) and/or real time reverse transcription polymerase chain reaction (mRNA).ResultsEG-treated males had significantly higher (in μmol/L; mean ± standard deviation) plasma (59.7 ± 27.2 vs 12.9 ± 4.1, P < 0.001) and urine (3716 ± 1726 vs 241 ± 204, P < 0.001) oxalate levels, and more abundant oxalate crystaluria than controls, while the liver and kidney sat-1 protein and mRNA expression did not differ significantly between these groups. EG-treated females, in comparison with controls had significantly higher (in μmol/L) serum oxalate levels (18.8 ± 2.9 vs 11.6 ± 4.9, P < 0.001), unchanged urine oxalate levels, low oxalate crystaluria, and significantly higher expression (in relative fluorescence units) of the liver (1.59 ± 0.61 vs 0.56 ± 0.39, P = 0.006) and kidney (1.77 ± 0.42 vs 0.69 ± 0.27, P < 0.001) sat-1 protein, but not mRNA. The mRNA expression of Adh1 was female-dominant and that of Hao1 male-dominant, but both were unaffected by EG treatment.ConclusionsAn increased expression of hepatic and renal oxalate transporting protein sat-1 in EG-treated female rats could protect from hyperoxaluria and oxalate urolithiasis.

Chronic metabolic acidosis reduces urinary oxalate excretion and promotes intestinal oxalate secretion in the rat.

Urinary oxalate excretion is reduced in rats during a chronic metabolic acidosis, but how this is achieved is not clear. In this report, we re-examine our prior work on the effects of a metabolic acidosis on urinary oxalate handling [Green et al., Am J Physiol Ren Physiol 289(3):F536-F543, 2005], offering a more detailed analysis and interpretation of the data, together with new, previously unpublished observations revealing a marked impact on intestinal oxalate transport. Sprague-Dawley rats were provided with 0.28 M ammonium chloride in their drinking water for either 4 or 14 days followed by 24 h urine collections, blood-gas and serum ion analysis, and measurements of (14)C-oxalate fluxes across isolated segments of the distal colon. Urinary oxalate excretion was significantly reduced by 75% after just 4 days compared to control rats, and this was similarly sustained at 14 days. Oxalate:creatinine clearance ratios indicated enhanced net re-absorption of oxalate by the kidney during a metabolic acidosis, but this was not associated with any substantive changes to serum oxalate levels. In the distal colon, oxalate transport was dramatically altered from net absorption in controls (6.20 ± 0.63 pmol cm(-2) h(-1)), to net secretion in rats with a metabolic acidosis (-5.19 ± 1.18 and -2.07 ± 1.05 pmol cm(-2) h(-1) at 4 and 14 days, respectively). Although we cannot rule out modifications to bi-directional oxalate movements along the proximal tubule, these findings support a gut-kidney axis in the management of oxalate homeostasis, where this shift in renal handling during a metabolic acidosis is associated with compensatory adaptations by the intestine.

The Association between Vitamin C Prescription and Serum Oxalate Among Hemodialysis Patients

Background and Objective: Vitamin C consumption is necessary to compensate for its deficiency in hemodialysis patients, but excessive use raises concerns about increased levels of serum oxalate and oxalosis. This study was performed to compare the influence of intravenous and oral Vitamin C consumption on serum oxalate among hemodialysis patients in the 5 th Azar Hospital in Golestan (north of Iran). Materials and Methods: In the randomized controlled trial, 75 hemodialysis patients were selected via convenience methods. They were randomly allocated into controls ( n = 25), oral Vitamin C (OAA) ( n = 25) and intravenous Vitamin C (IAA) groups ( n = 25). After the dialysis session (three times weekly), patients took 300 mg intravenous Vitamin C in the IAA group and orally 500 mg Vitamin C in the OAA group for 8 weeks. Serum oxalate was examined before and after therapy. SPSS 16.0 software was used for the statistical analysis. Chi-square and ANOVA were used for comparing groups. A P -value less than 0.05 was considered to be statistically significant. Results: There was no significant difference among the three groups based on mean of serum oxalate before and after intervention. After intervention, the mean value of serum oxalate was not significantly increased in the IAA and OAA groups compared with the control group. A mean difference of serum oxalate before and after IAA was not statistically significant. The mean of serum oxalate before and after intervention significantly increased in the two intervention groups ( P Conclusion: In the hemodialysis patients, the procedure of Vitamin C supplementation was associated with the serum oxalate level. Serum oxalate level unchanged in the injected method but it is significantly increased in daily oral Vitamin C supplementation.

Quiz Page August 2013: Kidney Failure in a Transplant From an Identical Twin

Quiz Page August 2013: Kidney Failure in a Transplant From an Identical Twin

Nocturnal Home Hemodialysis for a Patient With Type 1 Hyperoxaluria

Type 1 primary hyperoxaluria is a genetic disorder caused by deficiency of the liver-specific peroxisomal enzyme alanine-glyoxylate aminotransferase. This enzyme deficiency leads to excess oxalate production and deposition of calcium oxalate salts, resulting in kidney failure and systemic oxalosis. Aside from combined liver/kidney transplantation, no curative treatment exists. Various strategies for optimizing dialysis treatment have been evaluated, but neither conventional hemodialysis nor peritoneal dialysis can keep pace with oxalate production in this patient population. In this report, we describe a patient with end-stage renal disease from type 1 primary hyperoxaluria managed with nocturnal home hemodialysis. Performing hemodialysis 8-10 hours each night with blood flow of 350 mL/min and total dialysate volume of 60 L, she has maintained pre- and postdialysis serum oxalate levels at or below the level of supersaturation. We also review published literature regarding oxalate removal in various modalities of dialysis in patients with type 1 primary hyperoxaluria. In our patient, nocturnal hemodialysis has controlled serum oxalate levels better than conventional hemodialysis therapies. Home nocturnal hemodialysis should be considered an option for management of patients with end-stage renal disease from type 1 hyperoxaluria who are awaiting transplantation.

Stroke in Primary Hyperoxaluria Type I

We report the case of a 27-year-old man with a history of previously undiagnosed renal disease that presented with multiple cerebrovascular infarctions. Workup for traditional causes of cerebrovascular infarction including cardiac telemetry, multiple echocardiograms, and hypercoagulative workup was negative. However, a transcranial Doppler detected circulating microemboli at the rate of 14 per hour. A serum oxalate level greater than the supersaturation point of calcium oxalate was detected, providing a potential source of the microemboli. Furthermore, serial imaging recorded rapid mineralization of the infarcted territories. In the absence of any proximal vessel irregularities, atherosclerosis, valvular abnormalities, arrhythmias, or systemic shunt as potential stroke etiology in this patient, we propose that circulating oxalate precipitate may be a potential mechanism for stroke in patients with primary oxalosis.

1557 DEVELOPMENT OF A NOVEL METHOD FOR MEASURING SERUM OXALATE BY USING A TRIS(2,2`-BIPYRIDYL) RUTHENIUM(II) CHEMILUMINESCENCE ANALYSIS SYSTEM, AND ITS IMPORTANCE FOR UROLITHIASIS PATIENTS

You have accessJournal of UrologyStone Disease: New Technology1 Apr 20131557 DEVELOPMENT OF A NOVEL METHOD FOR MEASURING SERUM OXALATE BY USING A TRIS(2,2`-BIPYRIDYL) RUTHENIUM(II) CHEMILUMINESCENCE ANALYSIS SYSTEM, AND ITS IMPORTANCE FOR UROLITHIASIS PATIENTS Yasuhiko Ito, Takahiro Yasui, Atsushi Okada, Zuo Li, Takahiro Kobayashi, Masahito Hirose, Shuzo Hamamoto, Yasunori Itoh, Shoichi Sasaki, and Kenjiro Kohri Yasuhiko ItoYasuhiko Ito Nagoya, Japan More articles by this author , Takahiro YasuiTakahiro Yasui Nagoya, Japan More articles by this author , Atsushi OkadaAtsushi Okada Nagoya, Japan More articles by this author , Zuo LiZuo Li Nagoya, Japan More articles by this author , Takahiro KobayashiTakahiro Kobayashi Nagoya, Japan More articles by this author , Masahito HiroseMasahito Hirose Nagoya, Japan More articles by this author , Shuzo HamamotoShuzo Hamamoto Nagoya, Japan More articles by this author , Yasunori ItohYasunori Itoh Nagoya, Japan More articles by this author , Shoichi SasakiShoichi Sasaki Nagoya, Japan More articles by this author , and Kenjiro KohriKenjiro Kohri Nagoya, Japan More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.3067AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Urinary and serum oxalate measurements are important for evaluating the pathogenesis and diagnosis of urolithiasis. Measuring serum oxalate is difficult because its density is much lower than that of urinary oxalate; many procedures have been reported for urinary oxalate measurement. We report the development of a method for measuring serum oxalate by using a tris(2,2`-bipyridyl) ruthenium(II) chemiluminescence analysis system. METHODS Measurement method: Blood specimens were centrifuged (2,000 × g, for 10 min) after standing at room temperature to separate serum. An equal amount of deproteinization liquid was added to each sample; the mixture was centrifuged (5,000 × g, 15 min) and the supernatant was collected. The samples were mixed with the tris(2,2`-bipyridyl) ruthenium(II) complex and light emission was measured using a light detector (FOM-110A, Hokuto Denko, Yokohama, Japan). The detectable oxalate range was 0.2-10 μmol/L. A fixed-quantity straight line was plotted by measuring the control oxalate solution and the samples were diluted 2, 4, and 8 times. This line was used to calculate the oxalate density of each specimen. Specimens: Blood samples were obtained from 50 patients with calcium oxalate urolithiasis (38 men, 12 women), 30 healthy men, and 2 patients with primary hyperoxaluria. RESULTS Sample preparation and measurement were rapid (20 minutes). The serum oxalate density was approximately constant at each dilution. The serum oxalate densities were 14.8 ± 6.1 μmol/L and 13.5 ± 5.7 μmol/L, respectively, for men and women with urolithiasis. The level in men with urolithiasis was significantly higher than that in men without urolithiasis (5.1 ± 1.5 μmol/L, p < 0.05). The serum oxalate density for the primary hyperoxaluria patients was 80-110 μmol/L, but fell to approximately 40 μmol/L at 2 months after liver and renal transplantation. CONCLUSIONS A novel serum oxalate measurement method was developed. The analytical characteristics of this chemiluminescence method indicated that it has high sensitivity, a wide range, few contamination problems, and a low background level. Serum oxalate levels were higher in urolithiasis patients than in healthy men. Serum oxalate measurement is useful not only as an index for primary hyperoxaluria treatment but also for the screening of and evaluating the disease pathogenesis of calcium oxalate urolithiasis. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e639 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Yasuhiko Ito Nagoya, Japan More articles by this author Takahiro Yasui Nagoya, Japan More articles by this author Atsushi Okada Nagoya, Japan More articles by this author Zuo Li Nagoya, Japan More articles by this author Takahiro Kobayashi Nagoya, Japan More articles by this author Masahito Hirose Nagoya, Japan More articles by this author Shuzo Hamamoto Nagoya, Japan More articles by this author Yasunori Itoh Nagoya, Japan More articles by this author Shoichi Sasaki Nagoya, Japan More articles by this author Kenjiro Kohri Nagoya, Japan More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...