oxalates and Inflammation

Hyperoxaluria can cause kidney disease through multiple mechanisms, including tubular obstruction from calcium oxalate crystals, sterile inflammation, and tubular epithelial cell injury. Hyperoxaluria is also observed in individuals with diabetes mellitus and obesity, which are in turn risk factors for chronic kidney disease (CKD). Whether hyperoxaluria is a potential mediator of increased risk of CKD in diabetes mellitus and obesity is unknown.. Individuals with diabetes have increased levels of plasma glyoxal (a protein glycation product) and glyoxylate, both of which are precursors for oxalate. Increased gut absorption of oxalate in obesity may be because of obesity-associated inflammation. A recent study in individuals with CKD found that higher 24 h urinary oxalate excretion was independently associated with increased risk of kidney disease progression, especially in individuals with diabetes and obesity.. Both diabetes mellitus and obesity are associated with higher urinary oxalate excretion through distinct mechanisms. Hyperoxaluria could be a mechanism by which kidney disease develops in individuals with diabetes mellitus or obesity and could also contribute to progressive loss of renal function. Future research on pharmacologic or dietary measures to limit oxalate absorption or generation are required to test whether lowering urinary oxalate excretion is beneficial in preventing kidney disease development and progression in diabetes mellitus and obesity.

Topics: Diabetic Nephropathies; Humans; Hyperoxaluria; Inflammation; Obesity; Oxalates; Renal Insufficiency, Chronic

Historical studies have demonstrated that the prevalence of symptomatic nephrolithiasis is higher in patients with inflammatory bowel disease (IBD), compared to general population. The aim of the review was to analyze literature data in order to identify the main risk conditions described in literature and the proposed treatment.. A research on the databases PubMed, Medline, Embase and Google Scholar was performed by using the keywords "renal calculi/lithiasis/stones" and "inflammatory bowel diseases". A research on textbooks of reference for Pediatric Nephrology was also performed, with focus on secondary forms of nephrolithiasis.. Historical studies have demonstrated that the prevalence of symptomatic nephrolithiasis is higher in patients with inflammatory bowel disease (IBD), compared to general population, typically in patients who underwent extensive small bowel resection or in those with persistent severe small bowel inflammation. In IBD, kidney stones may arise from chronic inflammation, changes in intestinal absorption due to inflammation, surgery or intestinal malabsorption. Kidney stones are more closely associated with Crohn's Disease (CD) than Ulcerative Colitis (UC) in adult patients for multiple reasons: mainly for malabsorption, but in UC intestinal resection may be an additional risk. Nephrolithiasis is often under-diagnosed and might be a rare but noticeable extra-intestinal presentation of pediatric IBD. Secondary enteric hyperoxaluria the main risk factor of UL in IBD, this has been mainly studied in CD, whether in UC has not been completely explained. In the long course of CD recurrent urolithiasis and calcium-oxalate deposition may cause severe chronic interstitial nephritis and, as a consequence, chronic kidney disease. ESRD and systemic oxalosis often develop early, especially in those patients with multiple bowel resections. Even if we consider that many additional factors are present in IBD as hypomagnesuria, acidosis, hypocitraturia, and others, the secondary hyperoxaluria seems to finally have a central role. Some medications as parenteral vitamin D, long-term and high dose steroid treatment, sulfasalazine are reported as additional risk factors. Hydration status may also play an important role in this process. Intestinal surgery is a widely described independent risk factor. Patients with ileostomy post bowel resection may have relative dehydration from liquid stool, which, added to the acidic pH from bicarbonate loss, is responsible for this process. In this acidic pH, the urinary citrate level excretion reduces. The stones most commonly seen in these patients contain uric acid or are mixed. In addition, the risk of calcium containing stones also increases with ileostomy. The treatment of UL in IBD involves correction of the basic gastrointestinal tract inflammation, restricted dietary oxalate intake, and, at times, increased calcium intake. Citrate therapy that increases both urine pH and urinary citrate could also provide an additional therapeutic benefit. Finally, patients with IBD in a pediatric study had less urologic intervention for their calculosi

Topics: Bicarbonates; Child; Citrates; Dehydration; Disease Susceptibility; Humans; Inflammation; Inflammatory Bowel Diseases; Malabsorption Syndromes; Oxalates; Risk; Urolithiasis

Oxalate is an end product of metabolism excreted via the kidney. Excess urinary oxalate, whether from primary or enteric hyperoxaluria, can lead to oxalate deposition in the kidney. Oxalate crystals are associated with renal inflammation, fibrosis, and progressive renal failure. It has long been known that as the glomerular filtration rate becomes reduced in chronic kidney disease (CKD), there is striking elevation of plasma oxalate. Taken together, these findings raise the possibility that elevation of plasma oxalate in CKD may promote renal inflammation and more rapid progression of CKD independent of primary cause.. The inflammasome has recently been identified to play a critical role in oxalate-induced renal inflammation. Oxalate crystals have been shown to activate the NOD-like receptor family, pyrin domain containing 3 inflammasome (also known as NALP3, NLRP3, or cryopyrin), resulting in release of IL-1β and macrophage infiltration. Deletion of inflammasome proteins in mice protects from oxalate-induced renal inflammation and progressive renal failure.. The findings reviewed in this article expand our understanding of the relevance of elevated plasma oxalate levels leading to inflammasome activation. We propose that inhibiting oxalate-induced inflammasome activation, or lowering plasma oxalate, may prevent or mitigate progressive renal damage in CKD, and warrants clinical trials.

Topics: Animals; Disease Progression; Fibrosis; Humans; Inflammasomes; Inflammation; Interleukin-1beta; Kidney; Macrophages; Mice; NLR Family, Pyrin Domain-Containing 3 Protein; Oxalates; Renal Insufficiency, Chronic

Topics: Calcium Pyrophosphate; Crystallization; Gout; Humans; Inflammation; Lipid Metabolism; Oxalates; Oxalic Acid; Rheumatic Diseases; Synovial Fluid

Topics: Animals; Ferroptosis; Glycogen Synthase Kinase 3 beta; Inflammation; Nephrolithiasis; NF-E2-Related Factor 2; Oxalates; Rats; Rats, Sprague-Dawley

Ovarian cancer G protein-coupled receptor 1 (OGR1) (Gpr68) and G protein-coupled receptor 4 (GPR4) (Gpr4) are proton-activated G protein-coupled receptors that are stimulated upon increased extracellular acidity. These receptors have various physiological and pathophysiological roles in renal acid-base physiology, tissue inflammation, and fibrosis among others. Their function in injured renal tissue, however, remains mostly unclear. To address this, we investigated their role in crystalline nephropathy by increasing the oxalate intake of GPR4 KO and OGR1 KO mice. After 10 days of high-oxalate intake and 4 days of recovery, renal crystal content, histopathology, filtration function, and inflammation were assessed. While GPR4 deficiency did not show major alterations in disease progression, OGR1 KO mice had higher urinary calcium levels and exacerbated crystal accumulation accompanied by decreased creatinine clearance and urea excretion and a decreased presence of regulatory T (Treg) cells in kidney tissue. When lowering the severity of the kidney injury, OGR1 KO mice were more prone to develop crystalline nephropathy. In this setting, OGR1 KO mice displayed an increased activation of the immune system and a higher production of proinflammatory cytokines by T cells and macrophages. Taken together, in the acute setting of oxalate-induced nephropathy, the lack of the proton-activated G protein-coupled receptor (GPCR) GPR4 does not influence disease. OGR1 deficiency, however, increases crystal deposition leading to impaired kidney function. Thus, OGR1 may be important to limit kidney crystal deposition, which might subsequently be relevant for the pathophysiology of oxalate kidney stones or other crystallopathies.

Topics: Animals; Female; Humans; Inflammation; Kidney; Mice; Ovarian Neoplasms; Oxalates; Protons; Receptors, G-Protein-Coupled

Oxalate exposure to human renal epithelial cells triggers a vicious cycle of oxidative stress leading to cellular injury and deposition of calcium oxalate crystals on the injured cells. This results in further oxidative damage causing inflammation and loss of cell-cell adhesion factors, ultimately leading to irreparable kidney damage. However, these events can be attenuated or prevented by plants rich in antioxidants used in the traditional system of medicine for treatment of kidney stones. To delineate the mechanism by which Bergenia ligulata extract exerts its cytoprotective role in oxalate-induced injury we designed this study. Our results revealed that oxalate-injured HK2 cells cotreated with ethanolic extract of Bergenia ligulata displayed increased viability, reduced oxidative stress due to lowered production of intracellular reactive oxygen species (ROS) and decreased apoptosis. We also observed lowered markers of inflammation, along with increased expression of epithelial marker E-cadherin and decreased expression of mesenchymal markers Vimentin, F-actin, Transforming growth factor beta 1 (TGF-β1) and EMT-related proteins in renal tubular epithelial cells through immunocytochemistry, real-time PCR and western blotting. Our findings collectively suggest that by reducing oxidative stress, modulating crystal structure and preventing crystal-cell adhesion, B. ligulata inhibits the EMT pathway by downregulating the various mediators and thereby exerts its cytoprotective effect.

Topics: Epithelial Cells; Epithelial-Mesenchymal Transition; Female; Humans; Inflammation; Kidney Calculi; Male; Oxalates; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Plant Extracts; Transforming Growth Factor beta1

Meals rich in oxalate are associated with calcium oxalate (CaOx) kidney stone disease. Hydroxy-L-proline (HLP) is an oxalate precursor found in milk and collagen-containing foods. HLP has been shown to induce CaOx crystal formation in rodents. The purpose of this study was to evaluate the effect of HLP induced oxalate levels on inflammation and renal leukocytes during crystal formation. Male Sprague-Dawley rats (6-8 weeks old) were fed a control diet containing no oxalate for 3 days before being randomized to continue the control diet or 5% HLP for up to 28 days. Blood, 24 h urine, and kidneys were collected on Days 0, 7, 14, or 28. Urinary oxalate levels, crystal deposition, and renal macrophage markers were evaluated using ion chromatography-mass spectrometry, immunohistochemistry, and qRT-PCR. Renal leukocytes were assessed using flow cytometry and RNA-sequencing. HLP feeding increased urinary oxalate levels and renal crystal formation in animals within 7 days. HLP also increased renal macrophage populations on Days 14 and 28. Transcriptome analysis revealed that renal macrophages from animals fed HLP for 7 days were involved in inflammatory response and disease, stress response to LPS, oxidative stress, and immune cell trafficking. Renal macrophages isolated on Day 14 were involved in cell-mediated immunological pathways, ion homeostasis, and inflammatory response. Collectively, these findings suggest that HLP-mediated oxalate levels induce markers of inflammation, leukocyte populations, and reprograms signaling pathways in macrophages in a time-dependent manner. Additional studies investigating the significance of oxalate on renal macrophages could aid in our understanding of kidney stone formation.

Topics: Animals; Calcium Oxalate; Hydroxyproline; Inflammation; Kidney Calculi; Macrophages; Male; Nephrolithiasis; Oxalates; Rats; Rats, Sprague-Dawley

Inflammation worsens oxalate nephropathy by exacerbating tubular damage. The transient receptor potential vanilloid 1 (TRPV1) channel is present in kidney and has a polymodal sensing ability. Here, we tested whether TRPV1 plays a role in hyperoxaluria-induced renal inflammation. In TRPV1-expressed proximal tubular cells LLC-PK

Topics: Acute Kidney Injury; Animals; Hyperoxaluria; Inflammation; Male; Nephritis; Oxalates; Oxidative Stress; Rats; Rats, Wistar; TRPV Cation Channels

Chemiluminescence (CL) sensing without external excitation by light and autofluorescence interference has been applied to high-contrast in vitro immunoassays and in vivo inflammation and tumor microenvironment detection. However, conventional CL sensing usually operates in the range of 400-850 nm, which limits the performance of in vivo imaging due to serious light scattering effects and signal attenuation in tissue. To address this challenge, a new type of CL sensor is presented that functions in the second near-infrared window (NIR-II CLS) with a deep penetration depth (≈8 mm). Successive CL resonance energy transfer (CRET) and Förster resonance energy transfer (FRET) from the activated CL substrate to two rationally designed donor-acceptor-donor fluorophores BTD540 and BBTD700 occurs. NIR-II CLS can be selectively activated by hydrogen peroxide over other reactive oxygen species (ROSs). Moreover, NIR-II CLS is capable of detecting local inflammation in mice with a 4.5-fold higher signal-to-noise ratio (SNR) than that under the NIR-II fluorescence modality.

Topics: Animals; Disease Models, Animal; Fluorescence Resonance Energy Transfer; Fluorescent Dyes; Hydrogen Peroxide; Inflammation; Infrared Rays; Luminescent Measurements; Lymph Nodes; Mice; Optical Imaging; Oxalates; Oxidation-Reduction; Signal-To-Noise Ratio

This study investigated the repair effects of three Astragalus polysaccharides (APSs) with different molecular weights (Mws) on injured human renal proximal tubular epithelial (HK-2) cells to reveal the effect of Mw of polysaccharide on cell repair. A damage model was established by injuring HK-2 cells with 2.6 mM oxalate, and APS0, APS1, and APS2 with Mw of 11.03, 4.72, and 2.61 KDa were used to repair the damaged cells. After repair by APSs, the morphology of damaged HK-2 cells gradually returned to normal, the destruction of intercellular junctions recovered, intracellular reactive oxygen species production amount decreased, and their mitochondrial membrane potential increased. In addition, the cell cycle progression gradually normalized, lysosome integrity increased, and cell apoptotic rates obviously declined in the repaired cells. All three APSs could promote the expression of Keap1, Nrf2, SOD1, and CAT. In addition, the expression levels of inflammation markers containing MCP-1 and IL-6 decreased after APS repair. We deduced that APSs exert their repair function by activating the Nrf2-Keap1 signaling pathway and inhibiting inflammation. Among the APSs, APS1 with a moderate Mw provided the strongest repair effect. APSs may have a preventive effect on kidney stones.

Topics: Antioxidants; Apoptosis; Astragalus Plant; Biomarkers; Cell Cycle; Cell Line; Epithelial Cells; Humans; Inflammation; Kidney Tubules, Proximal; Lysosomes; Membrane Potential, Mitochondrial; Molecular Weight; Oxalates; Oxidation-Reduction; Polysaccharides; Reactive Oxygen Species; Signal Transduction

H2O2-specific peroxalate chemiluminescence is recognized as a potential signal for sensitive in vivo imaging of inflammation but the effect of underlying peroxalate-emitter energetics on its efficiency has rarely been understood. Here we report a simple nanophotonic way of boosting near-infrared chemiluminescence with no need of complicated structural design and synthesis of an energetically favored emitter. The signal enhancement was attained from the construction of a nanoparticle imaging probe (∼26 nm in size) by dense nanointegration of multiple molecules possessing unique photonic features, i.e., i) a peroxalate as a chemical fuel generating electronic excitation energy in response to inflammatory H2O2, ii) a low-bandgap conjugated polymer as a bright near-infrared emitter showing aggregation-induced emission (AIE), and iii) an energy gap-bridging photonic molecule that relays the chemically generated excitation energy to the emitter for its efficient excitation. From static and kinetic spectroscopic studies, a green-emissive BODIPY dye has proven to be an efficient relay molecule to bridge the energy gap between the AIE polymer and the chemically generated excited intermediate of H2O2-reacted peroxalates. The energy-relayed nanointegration of AIE polymer and peroxalate in water showed a 50-times boosted sensing signal compared to their dissolved mixture in THF. Besides the high H2O2 detectability down to 10(-9) M, the boosted chemiluminescence presented a fairly high tissue penetration depth (>12 mm) in an ex vivo condition, which enabled deep imaging of inflammatory H2O2 in a hair-covered mouse model of peritonitis.

Topics: Animals; Inflammation; Luminescent Measurements; Mice, Inbred BALB C; Mice, Inbred C57BL; Nanoparticles; Oxalates; Polymers; Spectroscopy, Near-Infrared

To obtain an additional pharmacological agent for the diagnosis of inflammation, we investigated the medical use of (89)Zr-oxalate as a positron emission tomography (PET) probe for the in vivo imaging of inflammation and compared its efficacy to that of 2-deoxy-2-[(18)F]fluoro-d-glucose ([(18)F]FDG) and sodium [(18)F]fluoride. (89)Zr-oxalate exhibited observable higher uptake in a macrophage cell line than in tumor cells. The inflammatory lesions and tumors were clearly visualized by PET imaging and autoradiography using (89)Zr-oxalate. Compared to [(18)F]FDG and sodium [(18)F]fluoride, (89)Zr-oxalate demonstrated a high selectivity index to the tumor at an early time point after injection and to inflammation at a delayed time point after injection (24 h). Through histological examination, large numbers of macrophages and neutrophils were observed in the tumor lesions with the highest (89)Zr-oxalate uptake. In a rheumatoid arthritis (RA) mouse model, (89)Zr-oxalate demonstrated a high level of accumulation in inflammatory lesions. (89)Zr-oxalate is a new strategic tool for tumor imaging and inflammatory processes.

Topics: Animals; Arthritis, Rheumatoid; Cell Line, Tumor; Fluorodeoxyglucose F18; Humans; Inflammation; Male; Mice; Oxalates; Positron-Emission Tomography; RAW 264.7 Cells

Intrarenal crystal formation activates the Nlrp3 inflammasome in myeloid cells and triggers a profound inflammatory response. Here, we studied whether a specific inhibitor of the Nlrp3 inflammasome, CP-456,773, can prevent kidney fibrosis in a murine model of crystal nephropathy induced by diets rich in oxalate or adenine. Inflammasome activation in renal dendritic cells and the resulting interleukin (IL)-1β and IL-18 production were markedly reduced by CP-456,773 treatment both ex vivo and in vivo. We directly visualized intrarenal inflammasome activation and its inhibition by CP-456,773 in vivo by adoptive transfer of bone marrow cells transduced with interleukin-1β-Gaussia luciferase, a proteolytic luciferase-based reporter for inflammasome activation, into irradiated mice. CP-456,773 treatment strongly attenuated kidney fibrosis when given early in the genesis of crystal nephropathy, but was unable to reverse established crystal-induced fibrosis. The urinary IL-18 concentration appeared to be a useful noninvasive biomarker for renal inflammasome activation. Finally, NLRP3 inhibition did not compromise adaptive immune responses as previously reported for the global inhibition of IL-1 signaling. Thus, early NLRP3 inhibition by CP-456,773 may be an effective treatment for crystal nephropathy. Use of iGLuc transfected cells introduces a novel imaging technique for inflammasome activation in mice.

Topics: Adenine; Adoptive Transfer; Animals; Cells, Cultured; Dendritic Cells; Disease Models, Animal; Fibrosis; Furans; Heterocyclic Compounds, 4 or More Rings; Humans; Immunohistochemistry; Indenes; Inflammasomes; Inflammation; Interleukin-18; Interleukin-1beta; Kidney; Mice; Mice, Inbred C57BL; Mice, Knockout; Nephritis; NLR Family, Pyrin Domain-Containing 3 Protein; Oxalates; Primary Cell Culture; Signal Transduction; Sulfonamides; Sulfones

Oxalate (Ox) is a very common component of the human diet, capable to collect in the renal tissue and bind calcium to form calcium oxalate (CaOx) crystals. A supersaturation of CaOx crystal may cause nephrocalcinosis and nephrolithiasis. The inflammation derived from the CaOx crystal accumulation, together with innate or secondary renal alterations, could strongly affect the renal function. In this case a consumption of probiotics with either oxalate-degrading activity at intestinal level and systemic anti-inflammatory activity could be an alternative approach to treat the subjects with excess of urinary oxalate excretion. 11 strains of lactic acid bacteria (Lactobacilli and Bifidobacteria), already included in the list of bacteria safe for the human use, were investigated for their capability to degrade oxalate by mean of RP-HPLC-UV method and modulate inflammation in an in vitro model system based on peripheral blood mononuclear cells. Four promising bacterial strains (Lactobacillus plantarum PBS067, Lactobacillus acidophilus LA-14, Bifidobacterium breve PBS077, Bifidobacterium longum PBS078) were identified as innovative biological tools for the prevention and the therapeutic treatment of hyperoxaluria and the inflammatory events associated to the Ox accumulation.. The oxalate-degrading activity of some probiotics and their capability to modulate the release of inflammation mediators could be exploited as a new nutraceutical and therapeutic approach for the treatment of oxalate accumulation and the related inflammatory state.

Topics: Anti-Inflammatory Agents; Bifidobacterium; Calcium, Dietary; Diet; Humans; Hyperoxaluria; In Vitro Techniques; Inflammation; Lactobacillus; Lactobacillus acidophilus; Leukocytes, Mononuclear; Oxalates; Probiotics

Acute inflammatory diseases are one of major causes of death in the world and there is great need for developing drug delivery systems that can target drugs to macrophages and enhance their therapeutic efficacy. Poly(amino oxalate) (PAOX) is a new family of fully biodegradable polymer that possesses tertiary amine groups in its backbone and has rapid hydrolytic degradation. In this study, we developed PAOX particles as drug delivery systems for treating acute liver failure (ALF) by taking the advantages of the natural propensity of particulate drug delivery systems to localize to the mononuclear phagocyte system, particularly to liver macrophages. PAOX particles showed a fast drug release kinetics and excellent biocompatibility in vitro and in vivo. A majority of PAOX particles were accumulated in liver, providing a rational strategy for effective treatment of ALF. A mouse model of acetaminophen (APAP)-induced ALF was used to evaluate the potential of PAOX particles using pentoxifylline (PTX) as a model drug. Treatment of PTX-loaded PAOX particles significantly reduced the activity of alanine transaminase (ALT) and inhibited hepatic cell damages in APAP-intoxicated mice. The high therapeutic efficacy of PTX-loaded PAOX particles for ALF treatment may be attributed to the unique properties of PAOX particles, which can target passively liver, stimulate cellular uptake and trigger a colloid osmotic disruption of the phagosome to release encapsulated PTX into the cytosol. Taken together, we believe that PAOX particles are a promising drug delivery candidate for the treatment of acute inflammatory diseases.

Topics: Acetaminophen; Acute Disease; Animals; Cell Line; Chemical and Drug Induced Liver Injury; Cytosol; Disease Models, Animal; Drug Carriers; Drug Delivery Systems; Inflammation; Liver; Macrophages; Mice; Mice, Inbred BALB C; Mononuclear Phagocyte System; Oxalates; Pentoxifylline; Tissue Distribution

Polyoxalate and copolyoxalate were developed in the 1970s and have been used for biomedical applications such as suture coating purposes, owing to their biocompatibility and biodegradability. They are known to degrade into diols and oxalic acid, which are considered biocompatible. One of the advantages of oxalate-based polymer is the ease of control of physicochemical properties, such as biodegradability, crystallinity and mechanical strength. The composition and hydrophobicity of diols greatly influenced their hydrolytic stability and mechanical properties. Oxalate-based polymers have faster hydrolytic-degradation kinetics than the commercial biodegradable polymers, poly(lactide-co-glycolide) and poly(caprolactone). Recently, our group has developed fully biodegradable polymer drug carriers based on oxalate-based polymers that are composed of various diols. The hydrophobicity of the oxalate-based polymers allowed them to be formulated into nano- or micro-particles, which are suitable for targeting macrophages in inflammatory diseases. The nano- or micro-particles exhibited excellent cytotoxicity profiles and fast drug-release kinetics, suggesting great potential as drug-delivery systems for the treatment of acute inflammatory diseases. In this article, we discuss the synthesis and physicochemical properties of oxalate-based polymers which can be used as a drug-delivery vehicle for the treatment of inflammatory diseases.

Topics: Animals; Crystallization; Drug Delivery Systems; Humans; Hydrophobic and Hydrophilic Interactions; Inflammation; Macrophages; Microspheres; Nanoparticles; Oxalates; Particle Size; Polyesters; Polyglactin 910; Polymers

Wild yams make a significant contribution to diets of tribal people in Nepal. However, these wild tubers are unpalatable, taste bitter, produce inflammation and show occasional toxicity. Four wild yam species, which are eaten after primary treatment by Nepali aborigines, were analyzed for bitter and toxic principles. Bitter components were identified as furanoid norditerpenes (diosbulbins A and B). Diosbulbins A and B were found in the range of 0.023-0.046 and 0.151-0.442 g kg(-1), respectively. Results demonstrated that diosbulbin B, with an average value of 0.314 g kg(-1), was the principal bitter compound as compared to diosbulbin A (0.037 g kg(-1)). The toxic alkaloid, dioscorine and histamine (an allergen) were not detected in these tubers, whereas cyanogens (as HCN equivalent) content were found ranging from 3.2 to 6.0 ppm. Our results revealed that Nepali wild yam tubers are not toxic varieties, as they do not contain either toxic dioscorine or histamine and cyanogens contents were satisfactorily below the safety limits. The inflammation and occasional toxicity observed could possibly be due to the presence of high level of oxalate in these tubers. Domestic cooking methods were found to be very efficient in removing bitterness, thus making the bitter yams palatable.

Topics: Consumer Product Safety; Dioscorea; Diterpenes; Food Analysis; Humans; Inflammation; Nepal; Nitriles; Nutritive Value; Oxalates; Species Specificity; Taste

Kidney stones in patients with inflammatory bowel disease are usually composed of calcium oxalate. Two factors are important in the increased absorption of dietary oxalate which is responsible for those stones: 1) increased absorption of oxalate in the presence of steatorrhea, and 2) increased permeability of the colon to oxalate. Fortunately, some of the physiologic abnormalities can be corrected. A therapeutic approach is detailed.

Topics: Calcium Oxalate; Calcium, Dietary; Colon; Humans; Inflammation; Intestinal Absorption; Intestinal Diseases; Kidney Calculi; Oxalates; Oxalic Acid

Topics: Animals; Calcium; Child; Conjunctivitis; Cornea; Fluoresceins; Humans; Inflammation; Keratoconjunctivitis; Male; Oxalates; Plant Extracts; Plants; Rabbits; Syndrome; Time Factors

Topics: Adrenocorticotropic Hormone; Adult; Calcium; Colitis, Ulcerative; Crohn Disease; Female; Humans; Ileitis; Inflammation; Intestinal Diseases; Kidney Calculi; Male; Oxalates; Proctoscopy; Uric Acid; Urologic Diseases