oxalates and Acute-Disease

The kidney is particularly vulnerable to toxins due to its abundant blood supply, active tubular reabsorption, and medullary interstitial concentration. Currently, calcium phosphate-induced and calcium oxalate-induced nephropathies are the most common crystalline nephropathies. Hyperoxaluria may lead to kidney stones and progressive kidney disease due to calcium oxalate deposition leading to oxalate nephropathy. Hyperoxaluria can be primary or secondary. Primary hyperoxaluria is an autosomal recessive disease that usually develops in childhood, whereas secondary hyperoxaluria is observed following excessive oxalate intake or reduced excretion, with no difference in age of onset. Oxalate nephropathy may be overlooked, and the diagnosis is often delayed or missed owning to the physician's inadequate awareness of its etiology and pathogenesis. Herein, we discuss the pathogenesis of hyperoxaluria with two case reports, and our report may be helpful to make appropriate treatment plans in clinical settings in the future.. We report two cases of acute kidney injury, which were considered to be due to oxalate nephropathy in the setting of purslane (portulaca oleracea) ingestion. The two patients were elderly and presented with oliguria, nausea, vomiting, and clinical manifestations of acute kidney injury requiring renal replacement therapy. One patient underwent an ultrasound-guided renal biopsy, which showed acute tubulointerstitial injury and partial tubular oxalate deposition. Both patients underwent hemodialysis and were discharged following improvement in creatinine levels.. Our report illustrates two cases of acute oxalate nephropathy in the setting of high dietary consumption of purslane. If a renal biopsy shows calcium oxalate crystals and acute tubular injury, oxalate nephropathy should be considered and the secondary causes of hyperoxaluria should be eliminated.

Topics: Acute Disease; Acute Kidney Injury; Aged; Calcium Oxalate; Humans; Hyperoxaluria; Oxalates; Portulaca

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

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

Oxalate kidney injury can manifest as oxalate nephropathy or nephrolithiasis and present as acute kidney injury or even as end-stage renal disease. There are several known causes for acute oxalate nephropathy; however, the combination of exocrine pancreatic insufficiency with overconsumption of vitamin C has not been described before. In this case, a man in his early 80s presented with anorexia and extreme fatigue for 1 week. He had a history of myalgic encephalomyelitis, also known as chronic fatigue syndrome, for which he took several supplements, including high doses of vitamin C. Furthermore, several years ago, he was diagnosed elsewhere with exocrine pancreatic insufficiency. On admission, acute kidney injury was diagnosed. The kidney biopsy showed oxalate nephropathy as the cause. We diagnosed acute oxalate nephropathy due to high vitamin C doses and exocrine pancreatic insufficiency. Within 14 days, his kidney function got worse and he required renal replacement therapy.

Topics: Acute Disease; Acute Kidney Injury; Aged, 80 and over; Ascorbic Acid; Exocrine Pancreatic Insufficiency; Humans; Hyperoxaluria; Kidney; Kidney Failure, Chronic; Male; Oxalates; Renal Replacement Therapy

Topics: Acute Disease; Humans; Oxalates

Topics: Acute Disease; Animals; Antineoplastic Agents; Calcium Channels; Chronic Disease; Humans; Mice; Nerve Tissue Proteins; Organoplatinum Compounds; Oxalates; Oxaliplatin; Peripheral Nervous System Diseases; Transient Receptor Potential Channels; TRPA1 Cation Channel

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

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

Topics: Acute Disease; Artifacts; Calcium Oxalate; Diagnosis, Differential; Equipment and Supplies; Ethylene Glycol; Humans; Hyperoxaluria, Primary; Meningitis; Oxalates

The aim of this study was to evaluate possible changes in renal hemodynamic and urodynamic parameters in rats with chronic hyperoxaluria and after acute oxalate challenge. We also evaluated the possible association between free radical (FR) production, hyperoxaluria, and calcium oxalate (CaOx) calculi formation.. Chronic hyperoxaluria was induced by adding 0.75% ethylene glycol (EG) to the drinking water of male Wistar rats. After 7, 21, and 42 days of treatment, urinary biochemistry, oxalate levels, and lipid peroxides were measured. Kidney calculi were examined by polarizing microscopy. In the second part of the experiments, 1, 10, 20, and 30 mg kg(-1) hr(-1) oxalate was infused, by means of an intrarenal arterial catheter (IRA), into normal rats sequentially. Superoxide dismutase (SOD) infusion by means of IRA, in addition to oxalate, was also performed to check its influence on the altered renal function after oxalate infusion. In both the acute and chronic groups, renal blood flow (RBF), cortical microvascular blood flow (CMVBF), glomerular filtration rate (GFR), urine flow (UV), and urinary sodium excretion (U(Na)V) were measured, and chemiluminescence (CL) was examined in the renal venous blood.. Levels of urinary lipid peroxides and enzymuria had increased since day 7, and increased the size of numbers of CaOx crystals in the kidney were noted beginning on day 21, but elevated CL was detectable only on day 7 after 0.75% EG treatment. Decreased UV and U(Na)V were noted in the 42-day EG group, although the 24-hr creatinine clearance values were normal in all experimental groups. On the other hand, RBF, GFR, and CMVBF were attenuated with elevated FR when the oxalate concentration was higher than 10 mg kg(-1) hr(-1) in the acute oxalate infusion group. With SOD pretreatment, the decreased RBF, GFR, and CMVBF could be reversed at 10 mg kg(-1) hr(-1) of oxalate, and be partially reversed at 20. FR also could be reduced significantly at 10 and 20 mg kg(-1) hr(-1) of oxalate.. Decreased urine flow and sodium excretion were the main renal functions affected by chronic hyperoxaluria. However, that only the 42-day EG group had a decreased tubular function cannot be fully explained by the persistent tubular enzymuria and increased lipid peroxides that began on day 7 after EG treatment. With acute oxalate infusion, the major insult to renal function was renal hemodynamics. Pretreated SOD could reverse the attenuated hemodynamics and reduce the elevated FR partly, which suggested that FR is responsible for oxalate toxicity.

Topics: Acute Disease; Animals; Chronic Disease; Ethylene Glycol; Free Radicals; Glomerular Filtration Rate; Hyperoxaluria; Injections, Intra-Arterial; Luminescent Measurements; Male; Oxalates; Rats; Rats, Wistar; Renal Artery; Renal Circulation; Superoxide Dismutase; Urodynamics

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

Topics: Acute Disease; Acute Kidney Injury; Adenocarcinoma; Anuria; Ascorbic Acid; Humans; Infusions, Intravenous; Kidney Calculi; Male; Middle Aged; Oxalates; Prostatic Neoplasms

Single intraperitoneal injections of three, seven, or 10 mg. of sodium oxalate per 100 gm. of rat body weight were administered to male Sprague-Dawley rats. At various times after the injection, urine samples were analyzed for oxalate, and urinary enzymes, alkaline phosphatase, leucine aminopeptidase, gamma-glutamyl transpeptidase, and N-acetyl-beta-glucosaminidase. The kidneys were processed for light microscopy and renal calcium and oxalate determination. Oxalate administration resulted in an increase in urinary oxalate and formation of calcium oxalate crystals in the kidneys. The amount and duration of urinary excretion of excess oxalate and retention of crystals in the kidneys correlated with the dose of sodium oxalate administered. At a low oxalate dose of three mg./100 gm., crystals moved rapidly down the nephron and cleared the kidneys. At higher doses crystals were retained in kidneys and at a dose of 10 mg./100 gm. were still there seven days post-injection. Crystal retention was associated with enhanced excretion of urinary enzymes indicating renal tubular epithelial injury.

Topics: Acute Disease; Animals; Calcium; Calcium Oxalate; Histocytochemistry; Hyperoxaluria; Kidney; Kidney Calculi; Male; Oxalates; Rats; Rats, Inbred Strains

Mice were made acutely hypocalcemic by injection of sodium oxalate. After the transient drop of plasma calcium marked changes in erythroblastic proliferation, number of erythroblasts and 59Fe kinetics were observed. The probable mechanism of this response that may reflect increased erythropoiesis is discussed.

Topics: Acute Disease; Animals; Bone Marrow Cells; Calcium; Erythroblasts; Erythropoiesis; Female; Hypocalcemia; Iron; Iron Radioisotopes; Mice; Mice, Inbred C3H; Mitosis; Oxalates; Oxalic Acid

Topics: Acidosis, Renal Tubular; Acute Disease; Analgesics; Calcium; Chronic Disease; Cystinuria; Female; Humans; Hyperparathyroidism; Infrared Rays; Kidney Calculi; Male; Oxalates; Radiography; Spectrum Analysis; Ureteral Calculi; Urinary Calculi; Urinary Tract Infections; X-Ray Diffraction

Topics: Accidents, Home; Acute Disease; Acute Kidney Injury; Glycols; Humans; Male; Middle Aged; Neurologic Manifestations; Oxalates; Peritoneal Dialysis

Topics: Acute Disease; Animals; Chromatography, Gas; Citrates; Citric Acid Cycle; Drug Synergism; Glyoxylates; Injections, Intraperitoneal; Kidney Calculi; Male; Oxalates; Rats

Topics: Acid-Base Equilibrium; Acute Disease; Aged; Anuria; Autopsy; Brain; Calcium; Dehydration; Glycols; Humans; Hydrogen-Ion Concentration; Kidney Tubules; Male; Oxalates; Peritoneal Dialysis; Poisoning