oxalates and Kidney-Diseases

Topics: Ascorbic Acid; Humans; Hyperoxaluria; Kidney; Kidney Diseases; Kidney Transplantation; Oxalates

Solute-linked carrier 26 (SLC26) isoforms constitute a conserved family of anion transporters with 10 distinct members. Except for SLC26A5 (prestin), all can operate as multifunctional anion exchangers, with three members (SLC26A7, SLC26A9, and SLC26A11) also capable of functioning as chloride channels. Several SLC26 isoforms can specifically mediate Cl(-)/HCO(3)(-) exchange. These include SLC26A3, A4, A6, A7, A9, and A11, which are expressed in the kidney except for SLC26A3 (DRA), which is predominantly expressed in the intestine. SLC26 Cl(-)/HCO(3)(-) exchanger isoforms display unique nephron segment distribution patterns with distinct subcellular localization in the kidney tubules. Together with studies in pathophysiologic states and the examination of genetically engineered mouse models, the evolving picture points to important roles for the SLC26 family in health and disease states. This review summarizes recent advances in the characterization of the SLC26 Cl(-)/HCO(3)(-) exchangers in the kidney with emphasis on their essential role in diverse physiological processes, including chloride homeostasis, oxalate excretion and kidney stone formation, vascular volume and blood pressure regulation, and acid-base balance.

Topics: Acid-Base Equilibrium; Animals; Antiporters; Chloride-Bicarbonate Antiporters; Chlorides; Disease Models, Animal; Homeostasis; Humans; Kidney; Kidney Diseases; Membrane Transport Proteins; Mice; Oxalates; Sulfate Transporters

Drug and xenobiotic toxicity is an important cause of kidney injury, especially in vulnerable patients. Nephrotoxic syndromes include functional disorders; vascular injury, such as thrombotic microangiopathy; glomerular injury resulting in nephrotic syndrome or glomerulonephritis; acute tubular necrosis; acute interstitial nephritis; and crystalopathy/nephrolithiasis. Recently reported nephrotoxins are reviewed in the context of these syndromes of kidney injury.

Topics: Adenine; Alcohols; Angiogenesis Inhibitors; Anticonvulsants; Antipsychotic Agents; Dasatinib; Diphosphonates; Glutamates; Guanine; HIV Protease Inhibitors; Humans; Indoles; Kidney Diseases; Organophosphonates; Oxalates; Pamidronate; Pemetrexed; Phenindione; Plants, Toxic; Proton Pump Inhibitors; Pyrimidines; Pyrroles; Selective Serotonin Reuptake Inhibitors; Sunitinib; Tenofovir; Thiazoles; Triazines

The hypoxia-inducible factor (HIF) family of transcription factors is responsible for coordinating the cellular response to low oxygen levels in animals. By regulating the expression of a large array of target genes during hypoxia, these proteins also direct adaptive changes in the hematopoietic, cardiovascular, and respiratory systems. They also play roles in pathological processes, including tumorogenesis. In recent years, several oxygenases have been identified as key molecular oxygen sensors within the HIF system. The HIF hydroxylases regulate the stability and transcriptional activity of the HIF-alpha subunit by catalyzing hydroxylation of specific proline and asparaginyl residues, respectively. They require oxygen and 2-oxoglutarate (2OG) as co-substrates, and depend upon non-heme ferrous iron (Fe(II)) as a cofactor. This article summarizes current understanding of the biochemistry of the HIF hydroxylases, identifies targets for their pharmacological manipulation, and discusses their potential in the therapeutic manipulation of the HIF system.

Topics: Anemia; Animals; Brain Ischemia; Enzyme Inhibitors; Gastrointestinal Diseases; Humans; Hypertension, Pulmonary; Hypoxia-Inducible Factor 1; Iron; Iron Chelating Agents; Ketoglutaric Acids; Kidney Diseases; Mice; Myocardial Ischemia; N-substituted Glycines; Neoplasms; Oxalates; Oxygen; Procollagen-Proline Dioxygenase; Rats

The multifunctional anion exchanger family (Slc26) encompasses 11 identified genes, but only 10 encode real proteins (Slc26a10 is a pseudogene). Most of the Slc26 proteins function primarily as anion exchangers, exchanging sulfate, iodide, formate, oxalate, hydroxyl ion, and bicarbonate anions, whereas other Slc26 proteins function as chloride ion channels or anion-gated molecular motors. The aim of this review is to present recent studies on the molecular function of the Slc26 family and its role in renal physiology and pathophysiology.. In proximal tubules, Slc26a1 (Sat-1) mediates sulfate and oxalate transport across the basolateral membrane, while Slc26a6 (CFEX, Pat-1) mediates a variety of anion exchange at the apical membrane to facilitate transcellular sodium chloride absorption. Targeted deletion of murine Slc26a6 leads to intestinal hyperabsorption of oxalate, hyperoxaluria, and kidney stones. Slc26a4 (pendrin) and Slc26a7 are expressed in intercalated cells, and are involved in acid-base homeostasis and blood pressure regulation. Messenger RNA for Slc26a2, Slc26a9, and Slc26a11 is also present in the kidney, yet the roles of these family members in renal physiology or pathophysiology are not clear.. Members of this multifunctional anion transporter family play evolving roles in the etiology of nephrolithiasis (Slc26a6) and hypertension (Slc26a4 and Slc26a6). Other Slc26 family members (Slc26a2, Slc26a9, Slc26a11) express mRNA in the kidney but their roles in renal physiology are not yet known.

Topics: Animals; Anion Transport Proteins; Anions; Antiporters; Chlorides; Humans; Kidney; Kidney Diseases; Kidney Tubules; Membrane Transport Proteins; Models, Biological; Oxalates; RNA, Messenger; Sulfate Transporters

Topics: Acute Disease; Agaricales; Cyanides; Encephalitis; Excitatory Amino Acids; Humans; Japan; Kidney Diseases; Mushroom Poisoning; Oxalates

Nephrocalcinosis may be defined as a generalized increase in the calcium content of the kidneys. This renal calcification may occur at a molecular, microscopic or macroscopic level leading to progressive amounts of renal damage. The major causes include those associated with an increase in urinary levels of calcium, oxalate and phosphate. Under these conditions, urine concentration and supersaturation leads to calcium crystal precipitation, which may be an intratubular event or initiate within the renal interstitium. The focus of discussion concerning renal calcification is often limited to factors that lead to renal stones (calculi and nephrolithiasis); however, nephrocalcinosis is a more sinister event, and often implies a serious metabolic defect. This review will discuss the hypotheses concerning initiating lesions of nephrocalcinosis using available laboratory and clinical studies and will examine whether new understanding of the molecular basis of tubulopathies, that lead to nephrocalcinosis, has given further insights.

Topics: Bartter Syndrome; Biological Transport; Calcium; Chemical Precipitation; Humans; Hyperoxaluria; Kidney; Kidney Diseases; Kidney Medulla; Kidney Tubules; Nephrocalcinosis; Oxalates; Phosphates

There are many challenges in oxalosis, including prompt, clinical recognition of this inborn error of metabolism, management of its many medical problems, provision of adequate care at end-stage kidney disease, and optimizing both the timing and results of liver and kidney allografts. This review provides a framework for the interested clinician to understand the many problems, and to begin to assimilate knowledge about an increasingly recognized, metabolic disorder. It ends with potential, innovative therapies that are not yet at the patient's bedside.

Topics: Child; Humans; Kidney Diseases; Male; Metabolic Diseases; Oxalates

Topics: Alcohol Oxidoreductases; Biomarkers; Diagnosis, Differential; Glyceric Acids; Humans; Hyperoxaluria; Kidney Diseases; Oxalates; Oxalic Acid; Prognosis; Sugar Alcohol Dehydrogenases

Topics: Aluminum; Humans; Hyperoxaluria; Kidney Diseases; Oxalates; Oxalic Acid

Topics: Disease Susceptibility; Humans; Kidney; Kidney Calculi; Kidney Diseases; Oxalates; Oxalic Acid

Recurrence of the original disease in the transplanted kidney is observed in 5.6%-9.3% of the patients. However, the clinical significance of recurrence is often minor. Diagnosis is easy in diseases with specific renal lesions, e.g., in dense deposit disease and IgA-nephropathy, but may be difficult if such a marker is missing. Recurrence is of special clinical importance in the following conditions: Membranoproliferative GN type I (in 33%, often severe) and type II (= dense deposit disease, recurrence in 90%, often minor), focal segmental glomerulosclerosis (in 48% of patients with a rapid course (less than 3 years) and in 12% of patients with a longer duration of the original disease; often severe), membranous nephropathy (recurrence rather rare, but often serious), and primary hyperoxaluria (in 100%). Mesangial IgA deposits recur in half of the patients with IgA-nephropathy and anaphylactoid purpura, but clinical findings are often minimal. Recurrence in anti-GBM-nephritis and SLE is rare. The study of recurrence may contribute to a better understanding of many renal diseases.

Topics: Anti-Glomerular Basement Membrane Disease; Glomerulonephritis; Glomerulosclerosis, Focal Segmental; Humans; IgA Vasculitis; Kidney Diseases; Kidney Transplantation; Lupus Erythematosus, Systemic; Metabolism, Inborn Errors; Nephritis, Hereditary; Oxalates; Oxalic Acid; Recurrence

Topics: Calcium Oxalate; Cations; Cholestyramine Resin; Diet; Food Analysis; Humans; Intestinal Absorption; Intestinal Diseases; Kidney Calculi; Kidney Diseases; Lipid Metabolism; Malabsorption Syndromes; Oxalates

Oxalosis is the histological manifestation of a number of diverse clinicopathological states involving abnormalities of both endogenous and exogenous oxalate. Crystalline deposits of calcium oxalate, usually first detected by their birefringence, may be characterised by a combination of their physical and tinctorial properties.

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Crystallization; Female; Glyoxylates; Hot Temperature; Humans; Infant; Intestinal Diseases; Kidney Diseases; Male; Metabolic Diseases; Metabolism, Inborn Errors; Middle Aged; Oxalates; Solubility; Staining and Labeling

The identification of a disease entity as one that is the result of a heritable defect offers the physician an opportunity to intervene in a variety of ways. As emphasized, knowledge of the heritable pattern of a particular disease allows the physician an opportunity to counsel family members in personal disease risk and the offspring. Such genetic counseling results in a reduction of affected cases for many inherited diseases. There is every expectation that similar approaches would be effective for inherited renal diseases. The heritable diseases are a favored group for investigative purposes since these diseases result from a single gene defect no matter how plieotropic the effects of that defect. Thus the investigator is capable of constant probing with tools available for identifying that one event or component that lies at the basis of the disease. The emphasis of this chapter is on those inherited renal diseases for which we have reached a high level of understanding of this single defect. In many of these diseases a single enzyme is identified as deficient and is the presumed genetic defect. In others (cystinuria, RTA, and cystinosis) the precise biochemical answers appear close at hand. Thus a variety of therapeutic approaches to overcome either the gene defect or ill effects of the gene defect emerge for diseases involving the kidney and are listed in Table 7. For some of these diseases the new diagnostic technique of prenatal diagnosis can be used (Table 8). This genetic option provides couples at risk for bearing affected offspring with reduced risk. For a number of other diseases that are not identified by amniocentesis, this risk can be effectively lowered to acceptable levels by use of artificial insemination. Thus the inherited diseases of the kidney are amenable to medical intervention at a variety of levels. Such intervention can predictably lead to a lowering of both the incidence and consequences of these gene defects.

Topics: Acidosis, Renal Tubular; Adult; Child; Chromosome Aberrations; Chromosome Disorders; Cystinosis; Cystinuria; Diabetes Insipidus; Fanconi Syndrome; Female; Genes, Dominant; Genes, Recessive; Glycosphingolipids; Humans; Infant, Newborn; Kidney; Kidney Diseases; Kidney Diseases, Cystic; Lesch-Nyhan Syndrome; Lipid Metabolism, Inborn Errors; Male; Metabolism, Inborn Errors; Middle Aged; Nephritis; Orotic Acid; Oxalates; Polycystic Kidney Diseases; Pseudohypoparathyroidism; Sex Chromosome Aberrations; Xanthines

Topics: Acidosis, Renal Tubular; Alkaptonuria; Cystinuria; Diabetes Insipidus; Female; Glycine; Gout; Humans; Hyperlipidemias; Hyperparathyroidism; Kidney Diseases; Lesch-Nyhan Syndrome; Male; Metabolism, Inborn Errors; Nephritis, Hereditary; Oxalates; Porphyrias; Uric Acid; Urologic Diseases; Xanthines

Topics: Animals; Chickens; Citrinin; Female; Horse Diseases; Horses; Kidney Diseases; Male; Mycotoxins; Ochratoxins; Oxalates; Polyuria; Poultry Diseases; Swine; Swine Diseases; Thirst

Topics: Animals; Calcinosis; Calcium; Ethylenes; Glycols; Humans; Kidney Calculi; Kidney Diseases; Metabolic Diseases; Methoxyflurane; Oxalates; Uric Acid; Urinary Bladder Calculi

Topics: Central Nervous System Diseases; Ethylenes; Glycols; Humans; Kidney Diseases; Lung Diseases; Oxalates; Poisoning; Propylene Glycols

Topics: Ascorbic Acid; Bone and Bones; Calcium; Cell Membrane Permeability; Erythrocytes; Feces; Glycine; Humans; Intestinal Absorption; Intestinal Mucosa; Kidney; Kidney Diseases; Kidney Function Tests; Liver; Metabolism, Inborn Errors; Microsomes; Mitochondria; Muscles; Oxalates; Plants, Edible; Urinary Calculi

Lumasiran reduces urinary and plasma oxalate (POx) in patients with primary hyperoxaluria type 1 (PH1) and relatively preserved kidney function. ILLUMINATE-C evaluates the efficacy, safety, pharmacokinetics, and pharmacodynamics of lumasiran in patients with PH1 and advanced kidney disease.. Phase 3, open-label, single-arm trial.. Lumasiran administered subcutaneously; 3 monthly doses followed by monthly or quarterly weight-based dosing.. Primary end point: percent change in POx from baseline to month 6 (cohort A; not receiving hemodialysis at enrollment) and percent change in predialysis POx from baseline to month 6 (cohort B; receiving hemodialysis at enrollment). Pharmacodynamic secondary end points: percent change in POx area under the curve between dialysis sessions (cohort B only); absolute change in POx; percent and absolute change in spot urinary oxalate-creatinine ratio; and 24-hour urinary oxalate adjusted for body surface area.. All patients (N = 21; 43% female; 76% White) completed the 6-month primary analysis period. Median age at consent was 8 (range, 0-59) years. For the primary end point, least-squares mean reductions in POx were 33.3% (95% CI, -15.2% to 81.8%) in cohort A (n = 6) and 42.4% (95% CI, 34.2%-50.7%) in cohort B (n = 15). Improvements were also observed in all pharmacodynamic secondary end points. Most adverse events were mild or moderate. No patient discontinued treatment or withdrew from the study. The most commonly reported lumasiran-related adverse events were injection-site reactions, all of which were mild and transient.. Single-arm study without placebo control.. Lumasiran resulted in substantial reductions in POx with acceptable safety in patients with PH1 who have advanced kidney disease, supporting its efficacy and safety in this patient population.. Alnylam Pharmaceuticals.. Registered at ClinicalTrials.gov with study number NCT04152200 and at EudraCT with study number 2019-001346-17.. Primary hyperoxaluria type 1 (PH1) is a rare genetic disease characterized by excessive hepatic oxalate production that frequently causes kidney failure. Lumasiran is an RNA interference therapeutic that is administered subcutaneously for the treatment of PH1. Lumasiran has been shown to reduce oxalate levels in the urine and plasma of patients with PH1 who have relatively preserved kidney function. In the ILLUMINATE-C study, the efficacy and safety of lumasiran were evaluated in patients with PH1 and advanced kidney disease, including a cohort of patients undergoing hemodialysis. During the 6-month primary analysis period, lumasiran resulted in substantial reductions in plasma oxalate with acceptable safety in patients with PH1 complicated by advanced kidney disease.

Topics: Adolescent; Adult; Child; Child, Preschool; Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Infant; Infant, Newborn; Kidney Diseases; Male; Middle Aged; Oxalates; Young Adult

Primary hyperoxaluria is characterized by severe urolithiasis, nephrocalcinosis, and early renal failure. As treatment options are scarce, we aimed for a new therapeutic tool using colonic degradation of endogenous oxalate by Oxalobactor formigenes. Oxalobacter was orally administered for 4 weeks as frozen paste (IxOC-2) or as enteric-coated capsules (IxOC-3). Nine patients (five with normal renal function, one after liver-kidney transplantation, and three with renal failure) completed the IxOC-2 study. Seven patients (six with normal renal function and one after liver-kidney transplantation) completed the IxOC-3 study. Urinary oxalate or plasma oxalate in renal failure was determined at baseline, weekly during treatment and for a 2-week follow-up. The patients who showed >20% reduction both at the end of weeks 3 and 4 were considered as responders. Under IxOC-2, three out of five patients with normal renal function showed a 22-48% reduction of urinary oxalate. In addition, two renal failure patients experienced a significant reduction in plasma oxalate and amelioration of clinical symptoms. Under IxOC-3 treatment, four out of six patients with normal renal function responded with a reduction of urinary oxalate ranging from 38.5 to 92%. Although all subjects under IxOC-2 and 4 patients under IxOC-3 showed detectable levels of O. formigenes in stool during treatment, fecal recovery dropped directly at follow up, indicating only transient gastrointestinal-tract colonization. The preliminary data indicate that O. formigenes is safe, leads to a significant reduction of either urinary or plasma oxalate, and is a potential new treatment option for primary hyperoxaluria.

Topics: Administration, Oral; Adolescent; Adult; Capsules; Child; Child, Preschool; Chromatography, Gas; Creatinine; Feces; Female; Flame Ionization; Follow-Up Studies; Humans; Hyperoxaluria, Primary; Kidney; Kidney Diseases; Kidney Failure, Chronic; Kidney Function Tests; Kidney Transplantation; Male; Middle Aged; Oxalates; Oxalobacter formigenes; Time Factors; Treatment Outcome; Ultrasonography

Ethylene glycol poisoning causes metabolic acidosis and renal failure and may cause death. The standard treatment is inhibition of alcohol dehydrogenase with ethanol, given in intoxicating doses, and adjunctive hemodialysis. We studied the efficacy of fomepizole, a new inhibitor of alcohol dehydrogenase, in the treatment of ethylene glycol poisoning.. We administered intravenous fomepizole to 19 patients with ethylene glycol poisoning (plasma ethylene glycol concentration, > or =20 mg per deciliter [3.2 mmol per liter]). Patients who met specific criteria also underwent hemodialysis. Treatment was continued until plasma ethylene glycol concentrations were less than 20 mg per deciliter. Acid-base status, renal function, the kinetics of fomepizole, and ethylene glycol metabolism were assessed at predetermined intervals.. Fifteen of the patients initially had acidosis (mean serum bicarbonate concentration, 12.9 mmol per liter). Acid-base status tended to normalize within hours after the initiation of treatment with fomepizole. One patient with extreme acidosis died. In nine patients, renal function decreased during therapy; at enrollment, all nine had high serum creatinine concentrations and markedly elevated plasma glycolate concentrations (> or =97.7 mg per deciliter [12.9 mmol per liter]). None of the 10 patients with normal serum creatinine concentrations at enrollment had renal injury during treatment; all 10 had plasma glycolate concentrations at or below 76.8 mg per deciliter (10.1 mmol per liter). Renal injury was independent of the initial plasma ethylene glycol concentration. The plasma concentration of glycolate and the urinary excretion of oxalate, the major metabolites of ethylene glycol, uniformly fell after the initiation of fomepizole therapy. Few adverse effects were attributable to fomepizole.. In patients with ethylene glycol poisoning, fomepizole administered early in the course of intoxication prevents renal injury by inhibiting the formation of toxic metabolites.

Topics: Adult; Aged; Antidotes; Ethylene Glycol; Female; Fomepizole; Glycolates; Humans; Keratolytic Agents; Kidney Diseases; Male; Middle Aged; Oxalates; Poisoning; Prospective Studies; Pyrazoles; Treatment Outcome

Topics: Acute Disease; Acute Kidney Injury; Colonoscopy; Humans; Hyperoxaluria; Kidney Diseases; Oxalates

Since plasma oxalate (POx) concentrations increase at lower glomerular filtration rate (GFR) levels, even among those without enteric (EH) or primary hyperoxaluria (PH), the appropriate thresholds for considering a disorder of oxalate metabolism are poorly defined. The current study was completed to establish relationships between POx, GFR, and urine oxalate excretion (UOx) among patients with PH, EH, and routine urinary stone disease (USD).. The most recent POx measurement on all Mayo Clinic patients between 2005 and 2015 were electronically pulled from the Lab Information System together with the closest serum creatinine within 14days and 24h urine study within 60days. After exclusion of patients not in steady state at the time of blood draw, 270 patients were available for study. Records were reviewed for clinical diagnoses to categorize patients as PH, EH, or USD. Waste plasma for Pox was also obtained from controls without USD undergoing clinical GFR testing.. In all 3 groups POx increased as eGFR fell. For any given eGFR, POx was highest in the PH group and lowest in the USD and control groups (p<0.0001). POx was also influenced by UOx excretion (reflecting total body oxalate burden, absorption from diet and endogenous production). Generalized estimating equations of POx vs eGFR revealed higher average POx levels in PH compared to EH,USD or control, and for EH compared to USD or control. GEE prediction models were created that use POx, UOx, age, and serum creatinine to estimate the probability of a PH diagnosis.. New models were developed to help interpret POx when considering PH in clinical practice even when it was not previously suspected and/or eGFR is reduced.

Topics: Adult; Calcium Oxalate; Female; Glomerular Filtration Rate; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Diseases; Kidney Failure, Chronic; Male; Metabolic Diseases; Middle Aged; Oxalates; Urinary Calculi

To report a case of acute oxalate nephropathy related to vitamin C intake within the intensive care unit (ICU).. Case report.. ICU and nephrology department of a French university hospital.. A 57-year-old woman with septic shock related to Legionella pneumophila pneumonia complicated by acute respiratory distress syndrome and acute kidney injury who required renal replacement therapy for 75 days.. A renal biopsy was performed on day 72 because of persistent anuria and because the patient showed characteristic features of severe acute oxalate nephropathy. The only cause identified was vitamin C intake received during hospitalization within the ICU (~ 30 g over 2.5 months). At month 6 after ICU admission, estimated glomerular filtration rate was 24 mL/min/1.73m. Compelling evidence obtained from in-vitro and animal studies suggest that vitamin C, a circulating antioxidant, may be a valuable adjunctive therapy in critically-ill patients. Data from humans are more conflicting. Oxalate, a well-known metabolite of vitamin C, is excreted by the kidneys and can exert a toxic effect on epithelial cells and causes direct tubular damage, and/or it can crystallize within the tubular lumen. This case highlights an under-recognized secondary adverse event from vitamin C given to critically-ill patients. The use of high-dose vitamin C should be prescribed with caution in this population.
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Topics: Acute Kidney Injury; Ascorbic Acid; Critical Illness; Female; Humans; Intensive Care Units; Kidney Diseases; Middle Aged; Oxalates; Renal Replacement Therapy

Topics: Animals; Cyanides; Dogs; Humans; Hydroxocobalamin; Kidney Diseases; Oxalates; Smoke Inhalation Injury

In February 2014, wild American bullfrog Lithobates catesbeianus tadpoles from an artificial pond in the Kyusyu region, Japan, presented with coelomic and subcutaneous edema and erythema within the skin. A pathological examination of 57 tadpoles of American bullfrogs in the region was conducted to evaluate the disease. Crystal deposition of varying degrees was found in the kidneys of 35 tadpoles (61.4%). The crystals were transparent, pleomorphic in shape, highly birefringent in polarized light, and arranged in a radial pattern within the renal tubular lumen. Using Alizarin Red S stain and liquid chromatography, these crystals were identified as calcium oxalate. Severe coelomic and subcutaneous edema was observed in 7 of these 35 tadpoles (20.0%). Ammonia levels in coelomic fluid were extremely elevated (>1000 µg dl(-1)) in 4 tadpoles examined. These findings suggest that oxalate deposition in kidneys causes metabolic disorder with renal nephropathy. The source of the oxalate could not be determined; however, the presence of calcium oxalates in pond sediments, as revealed by liquid chromatography, suggested that the deposition was most likely due to ingestion of oxalate materials from the environment. This is the first report of oxalate nephropathy in free-living amphibians.

Topics: Animals; Calcium Oxalate; Geologic Sediments; Kidney Diseases; Larva; Oxalates; Rana catesbeiana

Topics: Anti-Obesity Agents; Canada; Chemical and Drug Induced Liver Injury; Databases, Factual; France; Humans; Kidney Diseases; Lactones; Obesity; Orlistat; Oxalates

We report a 29 year old male cystic fibrosis patient with end stage lung disease and normal renal function who underwent a sequential double lung transplant. Medical history included: an ileal resection and pancreatic exocrine dysfunction. The postoperative period was complicated with haemorrhage and repeat surgery, requiring multiple blood transfusions and extensive antibiotic cover. Pancreatic supplements were interrupted. Acute renal failure attributed to haemodynamically-mediated acute tubular necrosis was managed expectantly. He remained dialysis dependent 8 weeks post surgery and was maintained on triple immunosuppression with tacrolimus, mycophenolate and prednisolone. A DTPA study was consistent with ATN. Renal biopsy revealed features consistent with tubular injury due to acute oxalate nephropathy (AON). Further biochemical characterization excluded primary hyperoxaluria but confirmed increased 24 hour urinary oxalate. He was maintained on enhanced frequency HDF and subsequently received an uncomplicated live related renal transplant 10 months post lung transplant with only additional basiliximab. Calcium carbonate was continued to manage post transplant hyperoxaluria and an early renal biopsy excluded recurrent oxalate injury. Enteric hyperoxaluria due to malabsorption in patients with CF especially with ileal resection, in addition to loss of gut Oxalobacter formigenes due to prolonged antimicrobials, increases the risk of AON. Increased awareness of this condition and screening prior to lung transplant is recommended.

Topics: Adult; Anti-Infective Agents; Biomarkers; Biopsy; Cystic Fibrosis; Humans; Hyperoxaluria; Ileum; Immunosuppressive Agents; Intestinal Absorption; Kidney Diseases; Kidney Transplantation; Living Donors; Lung Transplantation; Male; Oxalates; Oxalobacter formigenes; Reoperation; Risk Factors; Treatment Outcome

Decreased kidney function from kidney deposition of calcium oxalate has been described previously in inflammatory bowel disease and after jejuno-ileal and Roux-en-Y gastric bypass surgeries. Although celiac disease is the most prevalent bowel abnormality associated with intestinal malabsorption, its relationship to high kidney oxalate burden and decreased kidney function has not been established. We report a case of subclinical celiac disease and hyperoxaluria that presented with loss of kidney function as a result of high oxalate load in the absence of overt diarrhea, documented intestinal fat malabsorption, and nephrolithiasis. Subclinical celiac disease is commonly overlooked and hyperoxaluria is not usually investigated in kidney patients. We propose that this entity should be suspected in patients with chronic kidney disease in which the cause of kidney damage has not been clearly established.

Topics: Celiac Disease; Creatinine; Female; Humans; Hyperoxaluria; Immunohistochemistry; Kidney Diseases; Kidney Transplantation; Kidney Tubules; Malabsorption Syndromes; Membrane Transport Proteins; Middle Aged; Oxalates; Sulfate Transporters

Seven common marmoset monkeys (Callithrix jacchus) from a laboratory colony of 17 died over a period of eight months. Death of six of these monkeys was attributed to kidney failure from an oxalate-induced nephropathy. The epidemiology of this outbreak suggested an exogenous source and there was strong evidence that the source was bark and leaves from an Eucalyptus viminalis tree. Branches of this tree were introduced one month before the first death. The branches were removed one month after deaths commenced, but deaths continued for another five months. Urinalysis of all surviving marmosets at 80 and 122 days after initial contact with the E viminalis branches suggested that these monkeys had renal impairment. In the cases described here, the eating behaviour of common marmosets apparently exposed the animals to toxic levels of oxalate in the bark and leaves of an E viminalis tree.

Topics: Animal Husbandry; Animals; Animals, Laboratory; Callithrix; Eucalyptus; Fatal Outcome; Female; Kidney Calculi; Kidney Diseases; Male; Monkey Diseases; Oxalates; Plant Poisoning

Topics: Animals; Fatal Outcome; Female; Kidney Calculi; Kidney Diseases; Male; Oxalates; Sex Factors; Sheep; Sheep Diseases

We present here the anatomy and histopathology of kidneys from 11 patients with renal stones following small bowel resection, including 10 with Crohn's disease and 1 resection in infancy for unknown cause. They presented predominantly with calcium oxalate stones. Risks of formation included hyperoxaluria (urine oxalate excretion greater than 45 mg per day) in half of the cases, and acidic urine of reduced volume. As was found with ileostomy and obesity bypass, inner medullary collecting ducts (IMCDs) contained crystal deposits associated with cell injury, interstitial inflammation, and papillary deformity. Cortical changes included modest glomerular sclerosis, tubular atrophy, and interstitial fibrosis. Randall's plaque (interstitial papillary apatite) was abundant, with calcium oxalate stone overgrowth similar to that seen in ileostomy, idiopathic calcium oxalate stone formers, and primary hyperparathyroidism. Abundant plaque was compatible with the low urine volume and pH. The IMCD deposits all contained apatite, with calcium oxalate present in three cases, similar to findings in patients with obesity bypass but not an ileostomy. The mechanisms for calcium oxalate stone formation in IMCDs include elevated urine and presumably tubule fluid calcium oxalate supersaturation, but a low calcium to oxalate ratio. However, the mechanisms for the presence of IMCD apatite remain unknown.

Topics: Abdomen; Adult; Apatites; Biopsy; Calcium Oxalate; Calculi; Digestive System Surgical Procedures; Female; Humans; Hyperoxaluria; Hyperparathyroidism, Primary; Ileostomy; Intestine, Small; Intestines; Kidney; Kidney Calculi; Kidney Cortex; Kidney Diseases; Male; Obesity; Oxalates; Young Adult

Topics: Acute Kidney Injury; Chronic Disease; Comorbidity; Gastric Bypass; Humans; Incidence; Kidney; Kidney Diseases; Obesity, Morbid; Oxalates; Risk Factors; Treatment Outcome

In PH, PLTX, although ideal in theory, is rarely achieved. Patients usually have reached end-stage kidney disease while requiring combined liver and kidney transplantation. In this combined procedure, the sudden high oxalates mobilization from blood and tissue stores jeopardizes the success of the kidney graft, with a high risk of post-transplant early kidney necrosis or chronic graft damage. Here, we report the case of a three-yr-old girl with PH and ESRF in whom we performed sequentially deceased donor liver transplantation followed four months later by living donor kidney transplant, after normalization of blood oxalate levels and improvement of urinary oxalate output. After this two-step transplantation, our patient showed normalization of renal function with good urinary output and maintained normal blood oxalate levels. This strategy seems to be a reasonable approach in order to avoid acute renal tubular injury because of oxalate excretion in these patients.

Topics: Cadaver; Child, Preschool; Female; Graft Survival; Humans; Hyperoxaluria, Primary; Kidney Diseases; Kidney Transplantation; Liver Diseases; Liver Transplantation; Oxalates; Risk; Treatment Outcome

Despite advances in the enzymology, molecular genetics, and clinical knowledge of the primary hyperoxalurias, few treatments are available. Oxalobacter formigenes is a promising new therapy with potential to induce secretion of oxalate into the intestinal lumen, where it can be degraded by the bacteria.

Topics: Administration, Oral; Animals; Humans; Hyperoxaluria, Primary; Kidney Diseases; Kidney Function Tests; Kidney Transplantation; Oxalates; Oxalobacter formigenes; Rats; Time Factors; Treatment Outcome

Urinary oxalate is commonly measured with an enzymatic assay that is specific but requires a manual clean-up step to reduce ascorbic acid interference. We developed a urinary oxalate assay that uses liquid chromatography-tandem mass spectrometry (LC-MS/MS) with anion exchange chromatography and simple sample preparation.. We added calibrator or urine sample (10 microL) to 10 microL of (13)C2 oxalate and 400 microL of water and performed separation on a Waters OASIS WAX column, flow rate 0.6 mL/min, and then elution for 0.3 min with water containing 2 mmol/L ammonium acetate and 1 mL/L formic acid and for 1.0 min with 750 mL/L methanol containing 20 mL/L ammonia. We detected multiple reaction monitoring transitions m/z 88.6 > 60.5 and m/z 90.5 > 61.5 for oxalic acid and 13C2-oxalate, respectively, with a Quattro micro tandem mass spectrometer in electrospray-negative mode.. Oxalate and 13C2-oxalate eluted at 1.2 min. Mean recovery was 95%, limit of detection 3.0 micromol/L, lower limit of quantification 100.0 micromol/L, linearity to 2212 micromol/L, imprecision <6%, and bias <3% at 166, 880, and 1720 micromol/L. Oxalate eluted after the main area of ion suppression. Mean response ratios for urine and aqueous samples, enriched at 200 and 1000 micromol/L, were 3.7% and 5.4%, respectively. No interference was observed from other organic acids. Passing and Bablock regression analysis comparing the Trinity Biotech enzymatic reagent set and LC-MS/MS showed LC-MS/MS = 1.06 (enzymatic assay) -21.2, r = 0.964, n = 110. Bland Altman analysis showed general agreement, with a mean bias of -1.9 mumol/L.. This LC-MS/MS assay is applicable for quantifying urinary oxalate excretion.

Topics: Anion Exchange Resins; Chromatography, Ion Exchange; Chromatography, Liquid; Humans; Kidney Diseases; Mass Spectrometry; Oxalates; Recurrence

C-phycocyanin, a biliprotein pigment found in some blue green algae (Spirulina platensis) with nutritional and medicinal properties, was investigated for its efficacy on sodium oxalate-induced nephrotoxicity in experimentally induced urolithic rats.. Male Wistar rats were divided into four groups. Hyperoxaluria was induced in two of these groups by intraperitoneal infusion of sodium oxalate (70 mg/kg), and a pretreatment of phycocyanin (100 mg/kg) as a single oral dosage was given to one of these groups by 1 h prior to sodium oxalate infusion challenges. The study also encompasses an untreated control group and a phycocyanin-alone treated drug control group. The extent of lipid peroxidation (LPO) was evaluated in terms of renal concentrations of MDA, conjugated diene and hydroperoxides. The following assay was performed in the renal tissue (a) antioxidant enzymes such as superoxide dismutase (SOD) and catalase, (b) glutathione metabolizing enzymes such as glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) and glucose 6-phosphate dehydrogenase (G6PD), (c) the low molecular weight antioxidants (GSH, vitamins E and C) and protein carbonyl content.. The increased concentrations of MDA, conjugated diene and hydroperoxide (index of the lipid peroxidation) were controlled (P < 0.001) in the phycocyanin-pretreated group. At the outset, the low molecular weight antioxidants were appreciably increased (P < 0.001), whereas the tissue protein carbonyl concentration was decreased (P < 0.001), suggesting that phycocyanin provides protection to renal cell antioxidants. It was noticed that the activities of antioxidant enzymes and glutathione metabolizing enzymes were considerably stabilized in rats pretreated with phycocyanin.. We suggest that phycocyanin protects the integrity of the renal cell by stabilizing the free radical mediated LPO and protein carbonyl, as well as low molecular weight antioxidants and antioxidant enzymes in renal cells. Thus, the present analysis reveals that the antioxidant nature of C-phycocyanin protects the renal cell against oxalate-induced injury and may be a nephroprotective agent.

Topics: Animals; Antioxidants; Hyperoxaluria; Injections, Intraperitoneal; Kidney; Kidney Diseases; Lipid Peroxidation; Male; Oxalates; Phycocyanin; Protective Agents; Rats; Rats, Wistar

Topics: Adult; Bone Marrow; Chronic Disease; Crystallization; Female; Humans; Kidney Diseases; Oxalates

Tracer experiments in rats mimicking type II primary hyperoxaluria, with an expanded intracellular pool of hydroxypyruvate, showed that the excess formation of oxalate did not originate from its immediate precursor glyoxylate. In these animals, the hepatic and kidney activities of oxalate synthesising enzymes such as lactate dehydrogenase and glycolate oxidase were normal, but tissue lipid peroxidation was significantly higher. In vitro experiments established that in a mild alkaline solution, hydroxypyruvate underwent auto-oxidation to form oxalate and H2O2 and also inhibited lactate dehydrogenase and glycolate oxidase from oxidising glyoxylate to oxalate. On the basis of the experimental evidence, we suggest that in type II primary hyperoxaluria, the accumulating hydroxypyruvate could reduce the intracellular pool of glyoxylate and on ageing, give rise to excess oxalate and H2O2, to cause oxalosis in the former and free radical mediated-cell injuries in the latter.

Topics: Animals; Glyceric Acids; Glyoxylates; Hyperoxaluria; Kidney Diseases; L-Lactate Dehydrogenase; Lipid Peroxides; Liver; Male; Oxalates; Oxalic Acid; Rats; Rats, Wistar

Topics: Acute Disease; Humans; Iatrogenic Disease; Kidney Diseases; Oxalates; Pyridoxine

The paper presents the results of clinical and laboratory examination made in 3 groups of children: populational, hospital and control (a total of 176 patients). The children were diagnosed to have variants of dysmetabolic nephropathy (DN) which had become a problem not only for urolithiasis-endemic regions, but also for the Middle Russia. The study involving characterization of cytomembranes, renal tissue biopsy allowed conclusion on nonspecific DN symptoms. Obligatory symptoms were those of OCC, microhematuria and/or mild proteinuria, changes in cytomembranes, weak tubular function, tubulo-interstitial changes. DN genesis is thought multifactorial, involving genetic predisposition, biochemical defects, ecological hazards.

Topics: Adolescent; Biopsy; Child; Child, Preschool; Chronic Disease; Crystallization; Humans; Incidence; Infant; Kidney; Kidney Calculi; Kidney Diseases; Lipids; Moscow; Oxalates; Terminology as Topic

The authors reported ten cases of familial nephropathy (two cystinosis, three Senior and Loken syndrome, one Alport's syndrome and four Oxalosis) associated to ocular manifestations. Aetiologic diagnosis was known from ocular symptoms in five cases (all cases of cystinosis and Senior and Loken syndrome). The authors undertook this study to analyse the value of ocular manifestations in determining the right aetiologic diagnosis in familial nephropathies. The results of this study showed that ocular manifestations are helpful for aetiologic diagnosis in the first diseases. Indeed, corneal injury is synonym of cystinosis and retinitis pigmentosa is usually associated with Senior and Loken syndrome. In Alport's syndrome, ocular manifestations: antcrior lenticonus cataractous and perimacular white points only have orientation value in the diagnosis of this disease. Oxalosis ocular manifestations which consist of retinal oxalate deposits appear late and are concomitant to familial renal insufficiency. They cannot help in the diagnostic search.

Topics: Adolescent; Child; Corneal Diseases; Cystinosis; Eye Diseases; Humans; Kidney Diseases; Nephritis, Hereditary; Oxalates; Renal Insufficiency; Retinal Diseases; Retinitis Pigmentosa

The authors describe the results of the follow-up of children of the early age (n-68) and senior age (n-42) with different allergic diseases and 77 children with metabolic nephropathies (oxalate nephropathy, pyelonephritis associated with metabolic disorders, interstitial nephritis). In both age groups, an interrelationship was established between renal pathology in the form of metabolic nephropathies and allergo-pathology. Children with different allergies manifested the high incidence of metabolic disorders, with crystalluria and erythrocyturia being mostly encountered in respiratory allergies whereas leukocyturia largely occurred in skin allergies. At the same time the high incidence of allergic reactions was revealed in children with metabolic nephropathies. A relationship was established between the signs of atopy with graver varieties of nephropathies. The presence of the common pathogenetic components in the development of allergic and renal pathology requires the inclusion of immunologic and nephrologic methods into the complex of those patients' examination and the consideration of those factors in the treatment policy.

Topics: Age Factors; Asthma; Child, Preschool; Dermatitis, Atopic; Food Hypersensitivity; Humans; Hypersensitivity; Infant; Kidney Diseases; Neurodermatitis; Oxalates; Pyelonephritis; Rhinitis, Allergic, Seasonal; Urticaria

A 39-year-old man with a 13-year history of hemodialysis was hospitalized with left back pain in May 1989. The plain radiograph showed a calcification in the left kidney. Ct scan demonstrated a round high density area. We could not exclude the possibility of malignancy, therefore, we performed left nephrectomy. Pathological examination revealed that a tumorous mass in the renal parenchyma and renal adenocarcinoma was confined to the mass intermingled with the deposition of the oxalate crystals. It was difficult to diagnose. Therefore we recommend nephrectomy when the diagnosis is uncertain.

Topics: Adenocarcinoma; Adult; Calcinosis; Humans; Kidney Diseases; Kidney Failure, Chronic; Kidney Neoplasms; Male; Oxalates; Renal Dialysis

Topics: Child, Preschool; Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Infant; Kidney; Kidney Diseases; Malabsorption Syndromes; Male; Oxalates

Topics: Adolescent; Adult; Carbon Radioisotopes; Creatinine; Humans; Kidney Diseases; Male; Middle Aged; Oxalates

Topics: Calcium; Child; Crystallization; Humans; Kidney Diseases; Kidney Function Tests; Metabolism, Inborn Errors; Oxalates; Oxalic Acid

In twenty-one patients (sixteen male, five female) with various kidney diseases including primary hyperoxaluria type I (four patients), the plasma oxalate level was calculated from the isotopically determined oxalate clearance and the chemically determined urinary oxalate excretion. The apparent oxalate distribution volume was assessed as well. In patients with impaired kidney function (n = 12), the oxalate clearance was lower and the biological half-life and plasma concentration were higher than in patients with normal kidney function (n = 10). No differences were found in the oxalate-to-creatinine clearance ratio (mean value 1.93), urinary oxalate excretion and apparent oxalate distribution volume. A linear relation was found between the oxalate and creatinine clearance, while the clearance ratio was independent of the degree of renal failure. The apparent oxalate distribution volume was 1.45 times the estimated extracellular fluid volume. Because the isotopically determined plasma oxalate levels are lower than chemically measured ones, a quick and better estimation of plasma oxalate can be made from the urinary oxalate excretion and the creatinine clearance.

Topics: Adolescent; Adult; Creatinine; Extracellular Space; Female; Half-Life; Humans; Kidney; Kidney Diseases; Male; Middle Aged; Oxalates

The 14C-oxalate clearance was determined in 13 healthy subjects and 22 patients with various diseases and varying degrees of renal function impairment, including 5 patients with primary hyperoxaluria (PH). The clearances of oxalate (Cox) and creatinine (Ccr) were correlated (r = 0.95). The regression line intersects the ordinate at the origin, while the regression coefficient is 2.0. This implies that the fractional Cox is constant, irrespective of the underlying disease and the degree of renal failure. Plasma oxalate (Pox), as calculated from the urinary oxalate excretion (Uox) and Cox, was elevated in patients with severely impaired kidney function and those with PH. Plasma creatinine (Pcr) and Pox were correlated as well (r = 0.83). Pox values of patients with PH were above the 95% confidence limits of the regression line. It is of practical importance that Pox can be estimated from Uox and Ccr when a 14C-oxalate clearance test cannot be performed. The reasons for the constancy of the Cox/Ccr ratio are discussed, and it is suggested that the effective renal plasma flow (ERPF) is the regulating factor for the tubular secretion of oxalate.

Topics: Adolescent; Adult; Creatinine; Female; Humans; Kidney Calculi; Kidney Diseases; Male; Middle Aged; Oxalates; Oxalic Acid

Topics: Humans; Infant; Kidney Diseases; Kidney Transplantation; Oxalates

Topics: Adult; Child; Female; Humans; Kidney Diseases; Male; Metabolic Diseases; Oxalates

Topics: Humans; Kidney Diseases; Oxalates; Ultrasonography

A gas chromatographic procedure for determining oxalate in plasma is described, in which the trimethylsilyl derivative of oxalate is analyzed on a 25-m capillary SE-30 column. In addition the effects of standing of whole blood or plasma and the effect of added glyoxalate on the oxalate concentration were studied. The present method offers good specificity and sensitivity and is easy to perform, in contrast to most methods hitherto described. The normal value of plasma oxalate was found to be 2.8 +/- 1.1 mumol/l (mean +/- 1 SD), which is close to the values obtained with in vivo tracer studies. Plasma oxalate values before and after haemodialysis are presented. By introducing a few minor modifications the method is also applicable to urine samples and in principle it should be possible to determine the glycollic acid concentration as well, both in urine and plasma.

Topics: Adolescent; Adult; Child; Child, Preschool; Chromatography, Gas; Drug Stability; Glyoxylates; Humans; Hydrogen-Ion Concentration; Kidney Diseases; Middle Aged; Oxalates; Oxalic Acid; Reference Values; Renal Dialysis

Patients suffering from primary hyperoxaluria show elevated plasma concentrations of oxalic acid and glyoxylic acid. The in vitro adsorption of these compounds into activated charcoal, a series of neutral and ion exchange resins and onto hydrous zirconium oxide has been investigated. Hydrous zirconium oxide was the most effective sorbent studied for the removal of both oxalic acid and glyoxylic acid. In batch experiments, the zirconium oxide was capable of binding 5.5 mu mol oxalic acid and 8 mu mol glyoxylic acid per gram sorbent using 0.5 gram sorbent and 50 ml of solutions with initial concentrations of 100 mu mol . L-1 and an ionic composition resembling that of plasma. Recirculation of 2 L of the same solutions through 12 gram of a mixture of hydrous zirconium oxide and alumina for 6 hours at a flow rate of 12 ml . min-1, resulted in a final concentration of 70 mu mol . L-1 of oxalic acid and 50 mu mol . L-/ of glyoxylic acid.

Topics: Adsorption; Binding Sites; Charcoal; Glyoxylates; Hemoperfusion; Humans; Kidney Diseases; Microscopy, Electron; Oxalates; Oxalic Acid; Polystyrenes; Polyvinyls; Resins, Plant; Zirconium

Six out of seven patients with primary hyperoxaluria showed various degrees of oxalosis. The radiographic manifestations differ between patients younger than 15 years and those older than 45 years. The mild manifestations in children, only urolithiasis, can be explained by the, as yet, unimpaired renal function. The renal function in the older patients, with extensive pathologic changes like nephrocalcinosis, urolithiasis, soft-tissue calcification, and osseous changes, is very poor. The findings of extensive soft-tissue calcification and the bony changes are not in complete agreement with those in the literature.

Topics: Adolescent; Adult; Age Factors; Calcinosis; Humans; Kidney Diseases; Middle Aged; Nephrocalcinosis; Oxalates; Radiography; Urinary Calculi

Topics: Acidosis, Renal Tubular; Adult; Calcinosis; Female; Humans; Kidney Cortex Necrosis; Kidney Diseases; Kidney Medulla; Kidney Papillary Necrosis; Male; Medullary Sponge Kidney; Nephritis, Hereditary; Oxalates; Oxalic Acid; Radiography; Tuberculosis, Renal

Topics: Acute Kidney Injury; Female; Humans; Infant; Kidney Diseases; Oxalates; Ultrasonography

Topics: Fluorescent Antibody Technique; Humans; Intestines; Kidney; Kidney Diseases; Kidney Glomerulus; Obesity; Oxalates; Oxalic Acid; Postoperative Complications

Renal failure secondary to oxalate interstitial nephritis developed in three patients with malabsorption and steatorrhea following a jejunoileal bypass, extensive small intestine resection and a partial gastrectomy. Hyperoxaluria was documented in two of the cases. The possibility that this complication can occur in patients after a jejunoileal bypass operation is now recognized. This report shows that it can also occur in patients with other bowel disorders that cause malabsorption and steatorrhea. Since the prognosis for patients with oxalate nephropathy is poor, renal function should be closely monitored in patients who are at risk because of these disorders. Therapy should be directed at correcting malabsorption, steatorrhea and hyperoxaluria. When the renal function of patients with a jejunoileal bypass continues to decline despite intensive medical therapy, restoration of bowel continuity is strongly recommended.

Topics: Female; Gastrectomy; Gastrointestinal Diseases; Humans; Kidney Calculi; Kidney Diseases; Kidney Tubules; Male; Middle Aged; Nephrocalcinosis; Oxalates; Postoperative Complications

Topics: Humans; Kidney Diseases; Oxalates

Topics: Adolescent; Anemia; Child; Child, Preschool; Europe; Female; Follow-Up Studies; Graft Survival; Growth; Hospitals, Pediatric; Humans; Infant; Kidney Diseases; Kidney Transplantation; Male; Oxalates; Puberty; Renal Dialysis; Transplantation, Homologous

Topics: Adolescent; Child; Diet; Diet Therapy; Humans; Kidney; Kidney Diseases; Magnesium; Oxalates; Time Factors; Vitamin B Complex

Direct tubular damage, hypersensitivity reaction, metabolically mediated kidney disturbances, and chronic nephropathies are important sequelae of several drugs or their metabolites. In this review the drug-induced kidney disease is discussed from a clinical, histological, and pathogenetic point of view. The knowledge of possible nephrotoxic reactions and their underlying toxins are essential for prevention of this kidney disease.

Topics: Analgesics; Drug Hypersensitivity; Ethylene Glycols; Glomerulonephritis; Humans; Hypercalcemia; Kidney Concentrating Ability; Kidney Diseases; Kidney Failure, Chronic; Kidney Tubular Necrosis, Acute; Methicillin; Methotrexate; Nephritis, Interstitial; Oxalates

In summary it can be stated that clinically and radiologically, nephrolithiasis und nephrocalcinosis are not uncommonly encountered together. It is the aim of x-ray diagnostic to detect stones and parenchymal calcification, to assess localisation, size and numer or extent, to recognise secondary changes in the renal parenchyma and urinary-tract resulting from stones and to aid the search for the primary disease. In addition there are readiographic methods valuable for the initiation of treatment, e. g. percutaneous antegrade pyelography and nephrostomy.

Topics: Adolescent; Glomerulonephritis; Humans; Hypercalcemia; Hyperparathyroidism; Kidney Calculi; Kidney Cortex Necrosis; Kidney Diseases; Male; Metabolic Diseases; Nephrocalcinosis; Oxalates; Phenacetin; Radiography

Oxalate nephrosis resulted in progressive renal failure in 4 patients after jejunoileal bypass for morbid obesity. In general, increased levels of oxalates in the blood and urine of such patients result from enhanced absorption of exogenous oxalates. Urinary calculous formation is determined further by concomitant deficiency of inhibitor substances, whereas oxalate nephrosis probably occurs as a result of oxalate deposition in renal interstitium via the blood stream. Clinical manifestations of oxalate nephrosis include pain, infection, hematuria and renal failure. Routine postoperative renal function studies and early renal biopsy in suspicious cases are urged to establish early diagnosis. Continued deterioration of renal function, despite therapy with oxalate restruction and oxalate binding agents, indicates a reversal of the bypass to preserve unaffected renal substance.

Topics: Adult; Female; Humans; Ileum; Jejunum; Kidney; Kidney Diseases; Male; Middle Aged; Nephrosis; Obesity; Oxalates; Postoperative Complications

Topics: Adult; Brain; Brain Diseases, Metabolic; Crystallization; Female; Humans; Infusions, Parenteral; Kidney; Kidney Diseases; Oxalates; Xylitol

Topics: Adult; Autopsy; Chromosome Aberrations; Chromosome Disorders; Female; Humans; Kidney; Kidney Diseases; Middle Aged; Oxalates

Topics: Animals; Birds; Carcinogens; Citrinin; Food Contamination; Haplorhini; Humans; Kidney Diseases; Lethal Dose 50; Mice; Mycotoxins; Ochratoxins; Oxalates; Swine; Teratogens

Topics: Crystallization; Diagnosis, Differential; Humans; Infant; Kidney Diseases; Male; Nephrocalcinosis; Oxalates; Radiography

Kidney tissures were collected from 142 calves during a study of pre- and perinatal mortality. Fifty-six calves had oxalate crystals in their renal tissue. Thirty-four of the 56 had either single or multiple congenital defects, mostly of the skeleton. Twenty-two of the 56 died of causes other than congenital defects. The renal oxalosis was more pronounced in those calves affected with congenital anomalies.

Topics: Abnormalities, Multiple; Animals; Animals, Newborn; Cattle; Cattle Diseases; Kidney; Kidney Diseases; Oxalates

Topics: Amyloidosis; Bile Acids and Salts; Celiac Disease; Cholelithiasis; Cholestyramine Resin; Colitis, Ulcerative; Crohn Disease; Gastrointestinal Diseases; Glycine; Hepatic Encephalopathy; Humans; Kidney Calculi; Kidney Diseases; Kidney Failure, Chronic; Malabsorption Syndromes; Oxalates; Proteinuria

Topics: Adult; Female; Humans; Kidney Diseases; Oxalates

Topics: Brain Diseases, Metabolic; Cerebrovascular Disorders; Glycerol; Humans; Infusions, Parenteral; Kidney; Kidney Diseases; Male; Middle Aged; Oxalates

Topics: Adult; Amyloidosis; Cadaver; Child; Cystinosis; Diabetic Nephropathies; Fabry Disease; Female; HLA Antigens; Humans; Kidney Diseases; Kidney Transplantation; Male; Metabolic Diseases; Middle Aged; Oxalates; Registries; Transplantation, Homologous

Topics: Adolescent; Adult; Amyloidosis; Child; Cystinosis; Diabetic Nephropathies; Fabry Disease; Female; Gout; Humans; Kidney Diseases; Kidney Failure, Chronic; Kidney Transplantation; Male; Metabolic Diseases; Middle Aged; Nephritis; Nephritis, Hereditary; Oxalates; Renal Dialysis; Retrospective Studies; Transplantation, Homologous

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 total of 45 deceased persons, 33 cases showed no intrarenal crystal deposition and in 12 cases morphological investigation revealed intrarenal crystal deposition of varying intensity. All patients with crystal deposition had received considerable quantities of xylitol infusions within a period of 10 days. The possible connection between infusion of xylitol-containing solutions and intrarenal crystal deposition is discussed in detail.

Topics: Adolescent; Autopsy; Humans; Kidney Calculi; Kidney Diseases; Kidney Tubules; Nephrosis; Oxalates; Parenteral Nutrition; Xylitol

Topics: Acidosis, Renal Tubular; Humans; Ileum; Jejunum; Kidney Diseases; Kidney Failure, Chronic; Nephritis, Interstitial; Obesity; Oxalates; Postoperative Complications; Renal Aminoacidurias

Topics: Child, Preschool; Female; Humans; Kidney; Kidney Diseases; Metabolic Diseases; Oxalates; Radiography

Investigations of methoxyflurane-induced nephrotoxicity in man have been extensively aided by the use of an animal model. To be of value the animal model must share similar metabolic pathways with man and have the same clinical manifestations of the diseases process. The Fischer 344 rat appears to meet these criteria. The predominant factors in the production of methoxyflurane nephrotoxicity appear to be high methoxyflurane dosage and serum inorganic fluoride concentration. It is likely that secondary factors include: (1) a high rate of methoxyflurane metabolism and sepsitivity of the kidney to inorganic fluoride toxicity: (2) concurrent treatment with other nephrotoxic drugs; (3) preexisting renal disease; (4) surgery of the urogenital tract, aorta, or renal vasculative; (5) repeat administration of methoxyflurane due to accumulation of inorganic fluoride and, perhaps, methoxyflurane induction of its own metabolism: and (6) concurrent treatment with enzyme-inducing drugs such as phenobarbital.

Topics: Age Factors; Animals; Child; Dose-Response Relationship, Drug; Fluorides; Gentamicins; Humans; Kidney Diseases; Kidney Tubules; Methoxyflurane; Oxalates; Rats

A patient with normal preoperative hepatic and renal laboratory findings was exposed to relatively low concentrations of methoxyflurane during a routine anaesthetic procedure. For at least 12 postoperative days, the patient showed unusually high level of inorganic serum fluoride; his urinary excretion of fluoride and oxalic acid were also increased. However, he had no clinical signs of nephrotoxicity. This observation suggests that some patients with presumably normal renal function may have a low threshhold for the nephrotoxic effects of methoxyflurane.

Topics: Anesthesia, Inhalation; Drug Hypersensitivity; Female; Humans; Kidney Diseases; Methoxyflurane; Middle Aged; Oxalates

The radiological changes in a patient with endogenous oxalosis are correlated with their pathological and anatomical counterparts. These involve particulary the kidneys (nephrolithiasis, calcium oxalate nephrosis with scarring), the skeleton (combination of renal osteodystrophy, secondary hyperparathyroidism and oxalate deposition), and soft tissues (generalised oxalate deposition). The pathological aspects described in the literature are mentioned and possible forms of treatment are stressed.

Topics: Adult; Bone and Bones; Humans; Hyperparathyroidism; Kidney Calculi; Kidney Diseases; Metabolic Diseases; Nephrocalcinosis; Nephrosclerosis; Nephrosis; Oxalates; Radiography

The results of kidney transplantation in a variety of renal diseases have been analyzed. The diseases causing end-stage kidney failure in recipients were Alport syndrome, amyloidosis, cystinosis, diabetes mellitus, Fabry disease, familial nephritis, gout, medullary cystic disease, oxalosis, and systemic lupus erythematosus. The data indicate that renal transplantation is justifiable and parallels functional results for the more common causes of end-stage renal disease in all but Fabry disease and oxalosis. Although Fabry disease did not recur in any grafted kidney, only three patients have a functioning graft one year after transplantation. From a group of ten patients with oxalosis who received a total of 14 kidneys, only one survives. In no other metabolic disease, except one instance of primary amyloidosis, did the metabolic disease notably affect the transplant as it did in oxalosis.

Topics: Adolescent; Adult; Amyloidosis; Cystinosis; Diabetes Complications; Evaluation Studies as Topic; Fabry Disease; Female; Follow-Up Studies; Gout; Humans; International Cooperation; Kidney Diseases; Kidney Transplantation; Lupus Erythematosus, Systemic; Male; Middle Aged; Nephritis; Nephritis, Hereditary; Oxalates; Registries; Transplantation, Homologous

Obstruction is rarely accepted as the sole cause of calculi. We have reviewed 106 cases of nephrolithiasis for which surgery was performed at the St. Luke's Hospital Center during the past ten years. In 17 of these cases, obstruction of the ureteropelvic junction was demonstrated, an incidence of 16 per cent. We propose the theory that too frequently the responsible ureteropelvic junction obstruction goes undetected when a "routine" pyelolithotomy or nephrolithotomy is performed.

Topics: Adolescent; Adult; Aged; Calcium; Child; Female; Humans; Kidney; Kidney Calculi; Kidney Diseases; Kidney Pelvis; Male; Middle Aged; Oxalates; Ureteral Obstruction

Topics: Anesthesia; Enzyme Inhibitors; Fluorides; Humans; Kidney Diseases; Methoxyflurane; Oxalates

Type I hyperoxaluria results from reduced activity of alpha-ketoglutarate: glyoxylate carboligase, which is necessary for the synergistic decarboxylation of glyoxylate and alpha-ketoglutarate to alpha-hydroxy-beta-keto-adipate. Since thiamine pyrophosphate is a cofactor in the reaction, thiamine deficiency might be expected to result in tissue oxalosis. However, there was no significant increase in the incidence of renal oxalosis in 15 patients with Wernicke's encephalopathy at necropsy compared with controls. It is possible that hyperoxaluria was present in these thiamine-deficient patients but at a urine concentration below that necessary for calcium oxalate deposition. It is also possible that the severity of the thiamine deficit required for hyperoxaluria exceeds that for the neuronal and cardiac manifestations.

Topics: Acute Kidney Injury; Adipates; Adult; Carboxy-Lyases; Diphosphates; Glyoxylates; Humans; Ketoglutaric Acids; Kidney Diseases; Metabolic Diseases; Middle Aged; Oxalates; Thiamine; Thiamine Deficiency; Wernicke Encephalopathy

Topics: Animals; Fluorides; Kidney; Kidney Diseases; Kidney Tubules, Proximal; Liver; Male; Methoxyflurane; Microscopy, Electron; Mitochondria; Mitochondrial Swelling; Osmolar Concentration; Oxalates; Phenobarbital; Proadifen; Rats; Rats, Inbred Strains

Topics: Adolescent; Bone Diseases; Calcinosis; Calcium; Humans; Hydroxyapatites; Hyperparathyroidism, Secondary; Kidney Diseases; Male; Metabolic Diseases; Oxalates; Urinary Calculi; Urography

Topics: Animals; Cattle; Cattle Diseases; Female; Fetal Diseases; Kidney Diseases; Liver Diseases; Metabolic Diseases; Oxalates; Pregnancy

Topics: Abortion, Veterinary; Animals; Cattle; Cattle Diseases; Female; Fetal Diseases; Kidney Diseases; Oxalates; Pregnancy

Topics: Adult; Ascorbic Acid; Calcinosis; Humans; Kidney Diseases; Male; Oxalates

Topics: Adolescent; Animals; Biopsy; Chick Embryo; Child; Child, Preschool; Humans; Infant; Kidney; Kidney Calculi; Kidney Diseases; Microscopy, Polarization; Nephrectomy; Oxalates; Tajikistan; Urinary Tract Infections

Topics: Adult; Amino Acid Metabolism, Inborn Errors; Basement Membrane; Biopsy; Chronic Disease; Crystallization; Female; Glycine; Humans; Inclusion Bodies; Kidney Cortex; Kidney Diseases; Kidney Glomerulus; Kidney Medulla; Kidney Tubules; Male; Microscopy, Electron; Middle Aged; Oxalates

Topics: Angiography; Female; Humans; Kidney Diseases; Metabolic Diseases; Middle Aged; Oxalates

Topics: Angiography; Arteriovenous Shunt, Surgical; Autopsy; Female; Humans; Kidney; Kidney Diseases; Kidney Transplantation; Metabolism, Inborn Errors; Microradiography; Necrosis; Nephritis; Oxalates; Postoperative Complications; Thrombosis; Transplantation, Homologous; Vascular Diseases

Topics: Autopsy; Calcium; Crystallography; Cystine; Diagnosis, Differential; Histological Techniques; Humans; Kidney; Kidney Diseases; Oxalates; Solvents; Tyrosine; Uric Acid

Topics: Amides; Animals; Diet; Female; Humans; Ischemia; Kidney; Kidney Diseases; Magnesium; Male; Oxalates; Rabbits; Time Factors; Urinary Calculi

Topics: Animals; Kidney Diseases; Liver Diseases; Oxalates; Proteinuria; Swine; Swine Diseases; Urea

Topics: Biotransformation; Fluorides; Humans; Kidney Calculi; Kidney Diseases; Methoxyflurane; Oxalates

Topics: Adult; Female; Health Resorts; Humans; Kidney Diseases; Male; Metabolic Diseases; Middle Aged; Oxalates; Phosphates; Uric Acid

Topics: Animals; Aspergillosis; Deer; Kidney Diseases; Lung; Male; Oxalates

Topics: Animal Feed; Animals; Female; Flavonoids; Food Contamination; Food Microbiology; Kidney; Kidney Diseases; Kidney Tubules; Oxalates; Penicillium; Rats; Swine; Zea mays

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: Anesthesia; Humans; Kidney; Kidney Diseases; Methoxyflurane; Oxalates

Topics: Humans; Kidney Diseases; Kidney Transplantation; Male; Metabolism, Inborn Errors; Oxalates; Postoperative Complications; Transplantation, Homologous

Topics: Animals; Blood Chemical Analysis; Calcium; Female; Glycols; Haplorhini; Kidney Diseases; Kidney Glomerulus; Kidney Tubules; Male; Necrosis; Oxalates

Topics: Calcinosis; Hearing Disorders; Humans; Kidney Diseases; Male; Metabolism, Inborn Errors; Middle Aged; Oxalates

Topics: Adolescent; Adult; Carbohydrate Metabolism, Inborn Errors; Carbon Isotopes; Child; Coenzymes; Dialysis; Erythrocytes; Female; Flavin-Adenine Dinucleotide; Freezing; Glyoxylates; Humans; In Vitro Techniques; Kidney Diseases; Leukocytes; Male; Methods; NAD; Oxalates; Oxidation-Reduction; Ultrasonics

Topics: Adult; Humans; Kidney; Kidney Diseases; Male; Nephritis, Interstitial; Nephrocalcinosis; Oxalates; Renal Tubular Transport, Inborn Errors

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

1. The metabolism of [1-(14)C]glyoxylate to carbon dioxide, glycine, oxalate, serine, formate and glycollate was investigated in hyperoxaluric and control subjects' kidney and liver tissue in vitro. 2. Only glycine and carbon dioxide became significantly labelled with (14)C, and this was less in the hyperoxaluric patients' kidney tissue than in the control tissue. 3. Liver did not show this difference. 4. The metabolism of [1-(14)C]glycollate was also studied in the liver tissue; glyoxylate formation was demonstrated and the formation of (14)CO(2) from this substrate was likewise unimpaired in the hyperoxaluric patients' liver tissue in these experiments. 5. Glycine was not metabolized by human kidney, liver or blood cells under the conditions used. 6. These observations show that glyoxylate metabolism by the kidney is impaired in primary hyperoxaluria.

Topics: Adult; Carbon Dioxide; Carbon Isotopes; Child; Child, Preschool; Chromatography, Ion Exchange; Female; Glycine; Glycolates; Glyoxylates; Humans; Kidney; Kidney Diseases; Liver; Male; Oxalates; Time Factors

Topics: Humans; Infant; Kidney Diseases; Male; Nephrocalcinosis; Oxalates; Urine

Topics: Animals; Cattle; Cattle Diseases; Isoenzymes; Kidney Diseases; L-Lactate Dehydrogenase; Oxalates

Topics: Calcium; Calcium Oxalate; Cell Biology; Chemistry Techniques, Analytical; Crystallography; Electrons; Humans; Kidney; Kidney Diseases; Kidney Tubules; Liver Diseases; Microscopy; Microscopy, Electron; Neoplasms; Oxalates; X-Ray Diffraction

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

Topics: Amino Acid Metabolism, Inborn Errors; Calcinosis; Glycine; Glycolates; Humans; Hyperoxaluria, Primary; Kidney Calculi; Kidney Diseases; Oxalates; Transaminases; Urine; Vitamin B 6 Deficiency

Topics: Calcification, Physiologic; Calcinosis; Child; Humans; Hyperoxaluria; Infant; Kidney Diseases; Oxalates; Urinary Calculi

Topics: Humans; Kidney; Kidney Diseases; Kidney Failure, Chronic; Nephrectomy; Oxalates; Oxalic Acid; Renal Insufficiency, Chronic

Topics: Calcium Oxalate; Humans; Hyperoxaluria; Kidney; Kidney Diseases; Oxalates

Topics: Calcium Oxalate; Humans; Hyperoxaluria, Primary; Kidney Diseases; Nephrocalcinosis; Oxalates

Topics: Acidosis; Alkalosis; Diagnostic Techniques, Urological; Humans; Kidney; Kidney Diseases; Oxalates

Topics: Humans; Hyperoxaluria; Kidney; Kidney Diseases; Oxalates

Topics: Calcium Oxalate; Humans; Kidney; Kidney Diseases; Nephrosis; Oxalates

Topics: Humans; Hyperoxaluria, Primary; Kidney Diseases; Nephrocalcinosis; Oxalates

Topics: Humans; Kidney Diseases; Oxalates

Topics: Humans; Kidney; Kidney Diseases; Metabolic Diseases; Oxalates

Topics: Calcinosis; Calcium; Calcium Oxalate; Calcium, Dietary; Humans; Hyperoxaluria; Kidney Diseases; Oxalates

Topics: Calcification, Physiologic; Calcinosis; Kidney Diseases; Nephrocalcinosis; Oxalates

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