oxalates and Uremia

Topics: Arthritis; Chondrocalcinosis; Durapatite; Humans; Hydroxyapatites; Oxalates; Renal Dialysis; Uremia; Uric Acid

In the late stages of chronic renal damage the functional mass of the kidney is reduced and there is progression to renal insufficiency, usually called uremia, in which all aspects of renal function are affected. The complexity of the biochemical aspects of the syndrome of uremia is a manifestation of the wide variety and nature of the individual disorders that contribute to the pathogenesis of the final clinical syndrome. One major feature is the retention of metabolic end products and their effects, as toxins, on intermediary metabolism. The retained end products, working singly or in combination, probably affect metabolic pathways by some modification of enzymic reactions. They act at the cell membrane level. Although "middle molecules" have been incriminated as uremic toxins, recent attention has also focused on trace elements--especially aluminum, which has been implicated in the pathogenesis of two major disorders, osteomalacic dialysis osteodystrophy and dialysis encephalopathy.

Topics: Aluminum; Animals; Creatinine; Dimethylamines; Enzyme Inhibitors; Guanidines; Humans; Inositol; Metabolic Clearance Rate; Neural Conduction; Oxalates; Oxalic Acid; Parathyroid Hormone; Toxins, Biological; Urea; Uremia; Uric Acid

Topics: alpha 1-Antitrypsin Deficiency; Amyloidosis; Bone Marrow Transplantation; Fabry Disease; Gaucher Disease; Genetic Diseases, Inborn; Gout; Granulomatous Disease, Chronic; Hemoglobinopathies; Hemophilia A; Hepatolenticular Degeneration; Humans; Immunologic Deficiency Syndromes; Kidney Transplantation; Leukodystrophy, Metachromatic; Liver Transplantation; Lymphocytes; Metabolism, Inborn Errors; Mucopolysaccharidoses; Nephritis, Hereditary; Niemann-Pick Diseases; Osteopetrosis; Oxalates; Oxalic Acid; Transplantation; Tyrosine; Uremia

Topics: Alkalosis; Animals; Animals, Domestic; Calcium; Cattle; Digestive System; Horse Diseases; Horses; Hydrogen-Ion Concentration; Hypocalcemia; Oxalates; Plant Poisoning; Poisoning; Rumen; Sheep; Sheep Diseases; Swine; Swine Diseases; Uremia; Water

Topics: Adolescent; Ascorbic Acid; Biochemical Phenomena; Biochemistry; Child; Classification; Diet; Genetics, Medical; Glycine; Glycolates; Humans; Hyperoxaluria, Primary; Infant; Kidney Calculi; Metabolic Diseases; Metabolism; Nephrocalcinosis; Oxalates; Pathology; Terminology as Topic; Uremia; Urine; Vitamin B 6 Deficiency

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.. 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).. 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.. 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.

Topics: Animals; Atherosclerosis; Cell Line; Disease Models, Animal; Endothelial Cells; Humans; Male; Mice; Oxalates; Oxidative Stress; Renal Insufficiency, Chronic; Uremia; Vascular Calcification

To determine the clinical, biological, and radiological futures of primary hyper-oxaluria type 1 in Tunisian children, we retrospectively studied 44 children with primary hyper-oxaluria type 1 who were treated in our center from 1995 to 2009. The diagnosis was established by quantitative urinary oxalate excretion. In patients with renal impairment, the diagnosis was made by infrared spectroscopy of stones or kidney biopsies. The male-to-female ratio was 1:2. The median age at diagnosis was 5.75 years. About 43% of the patients were diagnosed before the age of five years with initial symptoms dominated by uremia. Four patients were asymptomatic and diagnosed by sibling screenings of known patients. Nephrocalcinosis was present in all the patients; it was cortical in 34%, medullary in 32%, and global in 34%. At diagnosis, 12 (27%) children were in end-stage renal disease. Pyridoxine response, which is defined by a reduction in urine oxalate excretion of 60% or more, was obtained in 27% of the cases. In the majority of patients, the clinical expression of primary hyperoxaluria type 1 was characterized by nephrocalcinosis, urolithiasis, and renal failure; pyridoxine sensitivity was associated with better outcome.

Topics: Child, Preschool; Female; Humans; Hyperoxaluria, Primary; Kidney Failure, Chronic; Male; Nephrocalcinosis; Oxalates; Retrospective Studies; Tunisia; Ultrasonography; Uremia; Urolithiasis

The methylation of carrier-free 74As-arsenite by liver cytosol of Flemish Giant rabbits is highly susceptible to additions of trace elements. In vitro supplementation of essential trace elements like zinc (Zn2+), vanadium (V5+), iron (Fe2+), copper (Cu2+) and selenate was shown to increase the methylation efficiency. Trivalent metal ions (e.g. Al3+, Cr3+ and Fe3+), Hg2+, Tl+ and SeO3(2-) had a deleterious effect. The inhibitory effect of EDTA, oxime and many divalent cations (Ca2+, Mg2+, Sr2+, ...) suggest a co-factor role for a specific divalent metal ion, possibly Zn2+. Chelating agents used in clinical treatment of acute and chronic inorganic arsenic poisoning lower the methylation capacity of cytosol by rendering the trivalent arsenic unavailable for the methyltransferase enzymes. S-adenosylhomocysteine and periodate-oxidized adenosine, inhibitors of s-adenosylmethionine dependent methylation pathways, inhibit the methylation of arsenite. Pyrogallol, a catechol-O-methyltransferase inhibitor, blocks the action of arsenite- and monomethylarsonic methyltransferase enzymes, suggesting a close structural relationship between the active sites of the different enzymes. Some uraemic toxins, namely oxalate, p-cresol, hypoxanthine, homocysteine and myo-inositol, inhibit arsenic methylation.

Topics: Animals; Arsenites; Cresols; Cytosol; Edetic Acid; Enzyme Inhibitors; Homocysteine; Hypoxanthine; In Vitro Techniques; Inositol; Liver; Male; Metals, Heavy; Methylation; Oxalates; Pyrogallol; Rabbits; Radioisotopes; S-Adenosylhomocysteine; Substrate Specificity; Uremia

Whether pyridoxine (B6) supplements decrease plasma oxalate concentrations in patients on maintenance dialysis is unresolved. The effect of two dose levels of B6, 0.59 mmol/day (100 mg/day) over 6 months and 4.43 mmol (750 mg) after each dialysis treatment for 4 wk, on plasma oxalate and oxalate removal rate (dialysis plus urinary excretion) was studied in patients on maintenance hemodialysis. In both studies, a control group unsupplemented with B6, who remained on their regular diet, was also studied. The vitamin B6 status of the patients was assessed by the erythrocyte glutamate pyruvate transaminase activity and index before and during supplementation. No decrease in plasma oxalate or oxalate removal rate was found in either study. The plasma oxalate and oxalate removal rates of the unsupplemented hemodialysis patients were not different from those receiving B6 either before or after supplementation. These studies demonstrate that high-dose B6 supplementation does not decrease plasma oxalate concentration in a population of hemodialysis patients.

Topics: Alanine Transaminase; Creatinine; Humans; Hyperoxaluria; Kidney Calculi; Kidney Failure, Chronic; Oxalates; Pyridoxine; Renal Dialysis; Uremia; Vitamin B 6 Deficiency

In preliminary studies, rats with chronic renal failure (CRF) demonstrated worsening renal function, as measured by urea clearance, when fed vitamin B-6-deficient diets. However, urea clearance is not a precise measure of glomerular filtration rate (GFR) and these studies did not indicate the mechanism for the reduced GFR. To measure renal function more precisely and to assess whether B-6 deficiency augments renal injury, we examined [14C]inulin clearance, urine oxalate excretion, and renal histopathology in rats with CRF pair fed to receive a pyridoxine-replete or -deficient diet for 3 or 6 wk. After 3 or 6 wk, pyridoxine-deficient rats had significantly lower [14C]inulin clearances and increased urine oxalate excretion. Histological evaluation indicated increased renal damage in kidneys from pyridoxine-deficient rats as compared with tissue from pyridoxine-replete rats. These findings suggest that in rats with CRF, vitamin B-6 deficiency reduces the GFR and increases renal scarring.

Topics: Animals; Aspartate Aminotransferases; Erythrocytes; Glomerular Filtration Rate; Inulin; Kidney; Male; Oxalates; Oxalic Acid; Proteinuria; Rats; Rats, Inbred Strains; Uremia; Vitamin B 6 Deficiency

To examine the possible effects of hyperoxalaemia on anaerobic metabolism and erythrocyte pyruvate kinase activity, we induced a rise in plasma oxalate in 11 dialysis patients by the oral administration of ascorbic acid, 500 mg day-1 for 3 weeks. Blood samples were taken from the same antecubital vein before and after the supplementation period, without venous stasis, after an overnight fast. This protocol allowed patients to be used as their own controls. Five healthy subjects underwent an identical protocol to exclude any effect of ascorbate per se. Mean (SEM) plasma oxalate (mumol l-1) rose from 30.3 (3.5) to 48.4 (6.1) in patients and from 1.4 (0.2) to 6.8 (0.9) in healthy subjects. Whole blood ascorbate (mg l-1) rose from 7.0 (0.7) to 26.6 (2.5) in patients and from 9.3 (1.2) to 17.8 (1.8) in healthy subjects (reference range 7.5-20.0 mg l-1). No changes were observed in either group in plasma creatinine, bicarbonate, haemoglobin, or erythrocyte 2,3,diphosphoglycerate (2,3 DPG) after the 3 week supplementation period. Before supplementation lactate generation (area under curve, mmol min l-1) in the 5 min following a 60 s period of standardized ischaemic forearm exercise was significantly (P = 0.026) greater in patients [69.1 (4.7)] than in healthy subjects [46.9 (6.7)]; no significant change in lactate generation occurred in either group after ascorbate-induced hyperoxalaemia. We conclude that changes in plasma oxalate of the order of 20 mumol l-1 have no significant effect on lactate generation or 2,3,DPG levels in uraemic subjects.

Topics: 2,3-Diphosphoglycerate; Adult; Ascorbic Acid; Diphosphoglyceric Acids; Erythrocytes; Forearm; Humans; Ischemia; Lactates; Lactic Acid; Male; Middle Aged; Oxalates; Oxalic Acid; Peritoneal Dialysis, Continuous Ambulatory; Physical Exertion; Renal Dialysis; Uremia

Primary oxalosis is a rare inborn error of oxalate metabolism. Most cases are discovered in children, but occasionally symptoms begin later in life. Since early deaths in the past were from renal failure, prolonged survival obtained with chronic dialysis allows oxalosis to develop. This paper presents a 38-year-old man with an atypical history of type-I primary hyperoxaluria, not diagnosed until after 5 years of dialysis. Bone biopsy was performed because the biochemical and radiologic features did not seem consistent with a putative diagnosis of secondary hyperparathyroidism. This case emphasizes the clinical heterogeneity of this disorder, and the need for its considerations in the spectrum of dialysis-related bone diseases. It also stresses that bone oxalosis may mimic hyperparathyroidism, especially radiologically. Differential diagnosis is therefore mandatory.

Topics: Adult; Biopsy; Bone and Bones; Diagnosis, Differential; Glycolates; Humans; Hyperoxaluria, Primary; Hyperparathyroidism, Secondary; Male; Oxalates; Oxalic Acid; Renal Dialysis; Time Factors; Uremia

Oxalate nephrotoxicosis was determined, by renal biopsy, to be the cause of azotemia in a goat. The origin of the oxalate was determined to be a high concentration of ascorbic acid that had been administered parenterally to the goat. Ascorbic acid has been documented as a cause of oxalate nephrotoxicosis in human beings.

Topics: Animals; Ascorbic Acid; Biopsy; Female; Goat Diseases; Goats; Kidney; Mastitis; Oxalates; Ultrasonography; Uremia

Topics: Adult; Ascorbic Acid; Endothelium, Vascular; Humans; Middle Aged; Oxalates; Oxalic Acid; Peritoneal Dialysis, Continuous Ambulatory; Renal Dialysis; Uremia; von Willebrand Factor

Ten of 100 mature ewes were afflicted with acute oxalate toxicosis within 40 hours after being temporarily penned in a lot that contained considerable growing Rumex crispus (curly dock). Clinical signs of toxicosis included excess salivation, tremors, ataxia, and recumbency. Affected ewes were markedly hypocalcemic and azotemic. Oxalate crystals were not observed in urine. Gross postmortem lesions were minimal and nondiagnostic in 2 ewes that died peracutely, but perirenal edema and renal tubular degeneration were clearly observable in ewes euthanatized on the third day of toxicosis. Diagnosis of oxalate toxicosis was confirmed by histopathologic findings. Samples of Rumex spp contained 6.6 to 11.1% oxalic acid on a dry-weight basis, a concentration comparable with that in other oxalate-containing plants that have caused acute oxalate toxicosis.

Topics: Acute Kidney Injury; Animals; Female; Hypocalcemia; Kidney; Kidney Tubular Necrosis, Acute; Oxalates; Plant Poisoning; Sheep; Sheep Diseases; Uremia

An enzymatic assay for the determination of oxalate in plasma was developed which is specific, simple, rapid and requires no specialised equipment; interference from vitamin C was removed by incubation of acidified plasma ultrafiltrate with ascorbate oxidase prior to oxalate estimation. Recoveries were 93 +/- 11% and the inter-batch coefficient of variation for 31 determinations at an oxalate level of 24 mumol/l was 10%. The assay is linear up to 300 mumol/l with a detection limit of 2 mumol/l. The reference range, based on results from 25 healthy volunteers, was defined as less than 2-5 mumol/l which is similar to levels established for the in vivo isotope dilution technique. The assay has an added advantage over the latter method, which requires a urine collection, in that it can be applied to plasma from anuric patients. A linear correlation (r = 0.68, p less than 0.001) was found between plasma oxalate and serum creatinine in individuals with varying degrees of renal failure.

Topics: Ascorbic Acid; Creatinine; False Positive Reactions; Humans; Hydrogen-Ion Concentration; Methods; Oxalates; Oxidoreductases; Ultrafiltration; Uremia

Human platelet aggregation induced by ADP was studied after incubation with urea, methylguanidine, creatinine and oxalic acid. Oxalic acid significantly (p less than 0.05) inhibits human thrombocyte aggregation. Physiopathological implications are discussed.

Topics: Adenosine Diphosphate; Adolescent; Creatinine; Humans; Methylguanidine; Oxalates; Oxalic Acid; Platelet Aggregation; Urea; Uremia

The mean plasma oxalic acid level is increased in renal failure. The mean plasma oxalic acid level was 74.8 +/- 18.5 mumol/l in 15 patients with chronic renal failure and 129.9 +/- 47.7 mumol/l in 31 patients on chronic haemodialysis which are several times higher than the normal range (16.8 +/- 6.0 mumol/l). During haemodialysis oxalic acid showed a behaviour similar to that of creatinine. The increased plasma oxalic acid levels are due to the accumulation of oxalic acid in renal insufficiency and additional metabolic factors increasing endogenous synthesis of oxalic acid. The administration of pyridoxine caused a decrease of the mean plasma oxalic acid level by 46% (32.0 to 56.1%) in 6 out of 8 chronic haemodialysis patients. This occurred most probably by correcting a vitamin B6 deficiency. Investigations of the intraerythrocyte glutamic oxalacetic transaminases showed, that the action of pyridoxine therapy on the endogenous oxalic acid synthesis can be explained by an increase of available pyridoxal-5-phosphate, the active metabolite of vitamin B6. The administration of vitamin B1, however, caused no statistically significant decrease of the plasma oxalic acid levels. Other influences on plasma oxalic acid synthesis result from the diminished excretion of the precursors of oxalic acid glycolic acid and ascorbic acid. The conversion of glycolic acid to glycine is probably increased in uraemia. The administration of 1 g ascorbic acid after each haemodialysis caused a striking increase of the plasma oxalic acid levels up to 240% of the initial value within 2 weeks, as a consequence of an increased metabolism of accumulated ascorbic acid. Increased plasma oxalic acid levels seem to be an important factor for calcium oxalate deposits in uraemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Ascorbic Acid; Aspartate Aminotransferases; Combined Modality Therapy; Erythrocytes; Glycolates; Humans; Kidney Failure, Chronic; Kidney Function Tests; Oxalates; Oxalic Acid; Pyridoxine; Renal Dialysis; Thiamine; Uremia

An enzyme/bioluminescent assay for the determination of oxalate in plasma is described in which NADH, a reaction product of the enzymic degradation of oxalate by oxalate decarboxylase and formate dehydrogenase, is determined using a commercially available bioluminescent system. In contrast to most previously documented methods, this sensitive and specific assay requires minimal sample preparation allowing oxalate concentrations to be determined within 2 h of sample collection. The limit of detection for plasma samples is 0.8 mumol/l. The recovery of oxalate added to plasma averaged 99%. The inter-batch coefficient of variation, calculated by analysis of a plasma sample from a uraemic patient (oxalate concentration = 45.8 mumol/l) on 8 occasions, over a period of 5 wk, was 3.2%. Plasma oxalate concentrations in 35 normal subjects ranged from less than 0.8-1.5 mumol/l, which is in excellent agreement with values obtained by in vivo isotope dilution studies. Plasma oxalate was found to be strikingly elevated in a group of uraemic patients maintained on regular haemodialysis.

Topics: Adult; Calibration; Carboxy-Lyases; Female; Formate Dehydrogenases; Humans; Luciferases; Luminescent Measurements; Male; Middle Aged; NAD; Oxalates; Oxalic Acid; Renal Dialysis; Specimen Handling; Temperature; Uremia

Accumulation of oxalic acid resulting in elevated plasma levels is a common finding in uraemic patients. Since vitamin B6 is an important coenzyme in oxalic acid metabolism the influence of vitamin B6 administration on plasma oxalic acid levels was investigated. Vitamin B6 was administered to eight chronic haemodialysis patients with secondary hyperoxalaemia. Mean plasma oxalic acid concentration decreased from 149.5 +/- 67 mumol/l to 99.0 +/- 36.4 mumol/l within 2 weeks and to 93.8 +/- 33.1 mumol/l after 4 weeks of pyridoxine treatment (P less than 0.01) the mean reduction being 46% (32.0-56.1%). The decrease in plasma oxalic acid levels was most pronounced in patients with the highest pretreatment values. Two patients who received pyridoxine therapy prior to the beginning of the study had low initial values of plasma oxalic acid concentrations and showed no further decline.

Topics: Administration, Oral; Creatinine; Depression, Chemical; Humans; Injections, Intravenous; Oxalates; Oxalic Acid; Pyridoxine; Renal Dialysis; Uremia

Topics: Blood; Calcinosis; Calcium Oxalate; Creatinine; Humans; Kidney Failure, Chronic; Oxalates; Oxalic Acid; Pyridoxine; Renal Dialysis; Ultrafiltration; Uremia

The concentration of oxalic acid was determined in the plasma of 15 patients with conservatively treated chronic renal insufficiency and 17 dialysis patients. A cumulation of oxalic acid was found in connection with uraemia. The extent to which plasma oxalic acid concentrations were raised depended on the degree of renal insufficiency and was directly related to the plasma creatinine values in all patients with or without dialysis. In the patients with chronic renal insufficiency the median plasma oxalic acid concentration was 74.4-18.5 (control group 27.0 +/- 7.4) mumol/l. In the dialysis patients the levels were even higher, at 137.5 +/- 56.0 mumol. By means of haemodialysis it was possible to lower the plasma oxalic levels by about the same amount as creatinine concentrations. The higher plasma oxalic acid concentrations seem to be an important pathogenetic factor in the formation of uraemic calcification in various organs. The therapeutic consequences are to increase the duration and frequency of dialysis and to remedy possible vitamin B6 deficiency.

Topics: Adult; Creatinine; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Oxalates; Oxalic Acid; Renal Dialysis; Uremia

The clinical features of eight cases of primary hyperoxaluria have been summarized. The possibility of different phenotypes is discussed. A reduction, but no normalization, of the oxalate formation during pyridoxine therapy was found. A renal transplantation performed in one of the patients failed because of the formation of nephrocalcinosis.

Topics: Adolescent; Adult; Child; Child, Preschool; Female; Follow-Up Studies; Glycolates; Glyoxylates; Humans; Infant; Kidney Calculi; Male; Middle Aged; Nephrocalcinosis; Oxalates; Pedigree; Uremia; Ureteral Calculi

In the fragmented sarcoplasmic reticulum from skeletal muscle of rabbits with experimental uremia, defective calcium ion transport is found. An impairment of all parameters is observed (initial rate of uptake, storing capacity with and without oxalate, and concentrating ability). In vivo administration of 1,25-dihydroxycholecalciferol (1,25-(OH)2-vitamin D3)(2 X 27 ng X kg of body wt-1 X day-1 and 6 X 27 ng X kg-1 X day-1, respectively) improved the kinetic parameters. The low dose improved storing capacity, and the higher dose, in addition to the storing capacity, also corrected concentrating ability and the initial rate of uptake. It is concluded that active calcium transport in the sarcoplasmic reticulum is impaired by uremia and that this defect is responsive to the administration of 1,25-(OH)2-vitamin D3.

Topics: Animals; Biological Transport, Active; Calcium; Dihydroxycholecalciferols; Female; Hydroxycholecalciferols; Kidney Concentrating Ability; Kinetics; Male; Muscles; Oxalates; Rabbits; Sarcoplasmic Reticulum; Uremia; Vitamin D

Histological and biochemical studies were carried out in a total of 300 patients who had died in the recovery room, and in rabbits, to investigate the frequency of deposits of calcium oxalte crystals in the kidneys, the influence of infusion therapy and the pathological significance of such deposits on the kidney tissue and on renal function. - Quite independent of any infusions, however, deposits of calcium oxalate crystals were found in the presence of kidney-specific diseases, in particular uraemia and anuric conditions. Xylitol infusions of 0.4 g/kg body weight or, in individual cases, of not more than 500 g total in 7 days, had no infllence on the appearance of calcium oxalate deposits. The blockage of the tubular system by the calcium oxalate deposits leads to a temporary reversible increase in serum urea and serum creatinine. With time, and uninfluenced by infusions, the deposits disappear out of the kidney again without having caused any organic renal damage. In the presence of a temporary excess of serum oxalate, the kidneys temporarily act like a cloaca.

Topics: Animals; Anuria; Autopsy; Calcium; Humans; Injections, Subcutaneous; Kidney; Kidney Calculi; Kidney Diseases; Oxalates; Parenteral Nutrition; Rabbits; Uremia; Xylitol

In a patient suffering from primary hyperoxaluria with oxalosis a progressive peripheral neuropathy was associated with intra-axonal deposition of microcrystals of calcium oxalate. Probably his neuropathy was the result of mechanical obstruction of axoplasmic flow.

Topics: Adult; Autopsy; Axonal Transport; Heart Arrest; Humans; Male; Metabolism, Inborn Errors; Muscles; Oxalates; Paresthesia; Peripheral Nerves; Peripheral Nervous System Diseases; Renal Dialysis; Uremia

Topics: Adams-Stokes Syndrome; Adult; Humans; Kidney Tubules; Male; Myocardium; Oxalates; Uremia

Topics: Arm; Arteries; Autopsy; Calcinosis; Child; Female; Gangrene; Humans; Ischemia; Kidney; Kidney Tubules; Leg; Metabolic Diseases; Microscopy, Polarization; Oxalates; Radiography; Uremia

Topics: Autopsy; Crystallization; Female; Glycols; Glyoxylates; Histocytochemistry; Humans; Kidney; Liver; Metabolic Diseases; Methods; Microscopy, Electron, Scanning; Middle Aged; Myocarditis; Myocardium; Nephrosis; Oxalates; Pancreas; Spectrophotometry, Infrared; Thyroid Gland; Uremia; X-Ray Diffraction

Topics: Adult; Aged; Aspergillosis; Aspergillus; Aspergillus flavus; Aspergillus fumigatus; Bronchitis; Bronchopneumonia; Calcium; Female; Humans; Lung; Lung Diseases; Lymph Nodes; Male; Mediastinum; Mycetoma; Oxalates; Prostatic Neoplasms; Sarcoidosis; Uremia

Topics: Autopsy; Child, Preschool; Humans; Kidney; Male; Metabolism, Inborn Errors; Myocarditis; Myocardium; Oxalates; Uremia

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Calcium; Child; Child, Preschool; Endomyocardial Fibrosis; Humans; Infant; Kidney; Kidney Failure, Chronic; Kidney Tubules; Metabolic Diseases; Middle Aged; Myocardium; Oxalates; Peritoneal Dialysis; Renal Dialysis; Spine; Splenic Artery; Uremia

Topics: Acute Kidney Injury; Adult; Arterial Occlusive Diseases; Autopsy; Coronary Vessels; Female; Humans; Metabolic Diseases; Nephrocalcinosis; Oxalates; Peritoneal Dialysis; Plethysmography; Uremia

Topics: Acidosis; Adolescent; Adult; Aged; Anuria; Bicarbonates; Calcium; Carbon Dioxide; Chemical and Drug Induced Liver Injury; Chemical Phenomena; Chemistry; Female; Humans; Hydrogen-Ion Concentration; Liver; Male; Middle Aged; Neurologic Manifestations; Nitrogen; Oxalates; Parenteral Nutrition; Solutions; Uremia; Uric Acid; Water-Electrolyte Balance; Xylitol

Topics: Acute Kidney Injury; Aged; Anuria; Calcium; Child; Female; Humans; Kidney Calculi; Kidney Tubules; Male; Methoxyflurane; Middle Aged; Oxalates; Postoperative Complications; Uremia

Topics: Adult; Animals; Cattle; Chromatography, Thin Layer; Erythrocytes; Humans; Imidazoles; L-Lactate Dehydrogenase; Male; Methods; Oxalates; Plasma; Rabbits; Renal Dialysis; Urea; Uremia

Topics: Acute Kidney Injury; Anesthesia, Inhalation; Autopsy; Biopsy; Creatinine; Histocytochemistry; Humans; Kidney; Kidney Diseases; Methoxyflurane; Nitrogen; Oxalates; Postoperative Complications; Uremia

Topics: Acute Kidney Injury; Anesthesia, Inhalation; Autopsy; Biopsy; Calcium; Humans; Kidney; Kidney Diseases; Methoxyflurane; Nitrogen; Oxalates; Time Factors; Uremia

Topics: Adolescent; Candidiasis; Digestive System; Glyoxylates; Heart Conduction System; Histocompatibility; Humans; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Male; Metabolism, Inborn Errors; Myocardium; Oxalates; Transplantation, Homologous; Uremia

Topics: Adult; Calcium Phosphates; Humans; Infrared Rays; Kidney Tubules; Kidneys, Artificial; Oxalates; Spectrophotometry; Uremia; Urinary Calculi

Topics: Adult; Aged; Female; Humans; Kidney; Male; Metabolism, Inborn Errors; Middle Aged; Myocardium; Oxalates; Uremia

Topics: Adult; Anuria; Female; Humans; Kidney; Kidney Diseases; Metabolic Diseases; Metabolism, Inborn Errors; Myocarditis; Myocardium; Oxalates; Uremia

Topics: Consanguinity; Heart Block; Humans; Hyperoxaluria; Kidney Calculi; Metabolism, Inborn Errors; Nephrocalcinosis; Oxalates; Pancreatitis; Pathology; Skin Diseases; Uremia; Urine

Topics: Enzymes; Humans; Hydroxybutyrate Dehydrogenase; Kidneys, Artificial; L-Lactate Dehydrogenase; Oxalates; Urea; Uremia

Topics: Acute Kidney Injury; Glomerulonephritis; Heart Diseases; Hyperkalemia; Hyperoxaluria; Kidney; Kidneys, Artificial; Oxalates; Pyelonephritis; Renal Insufficiency; Shock, Hemorrhagic; Shock, Traumatic; Toxicology; Uremia

Topics: Calcium; Calcium Oxalate; Chemical Phenomena; Chemistry; Humans; Kidney; Kidney Diseases; Kidney Tubules; Oxalates; Pathology; Uremia

Topics: Humans; Hyperoxaluria; Oxalates; Uremia; Urologic Diseases

Topics: Humans; Hyperoxaluria; Oxalates; Uremia

Topics: Humans; Oxalates; Oxalic Acid; Uremia; Urologic Diseases

Topics: Adult; Humans; Hyperoxaluria; Oxalates; Uremia

Topics: Adult; Humans; Hyperoxaluria; Oxalates; Uremia; Urologic Diseases

Topics: Humans; Kidney; Kidney Diseases; Necrosis; Oxalates; Uremia; Urologic Diseases