oxalates and Calcinosis

Topics: Calcinosis; Humans; Hyperoxaluria, Primary; Oxalates; Oxalic Acid

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

Nephrolithiasis is a common disease that seriously affects the health and life quality of patients. Despite the reported effect of hyperoside (Hyp) against nephrolithiasis, the specific mechanism has not been clarified. Therefore, this study is aimed at investigating the effect and potential mechanism of Hyp on renal injury and calcium oxalate (CaOx) crystal deposition.. Rat and cell models of renal calculi were constructed by ethylene glycol (EG) and CaOx induction, respectively. The renal histopathological damage, CaOx crystal deposition, and renal function damage of rats were assessed by HE staining, Pizzolato staining, and biochemical detection of blood and urine parameters. MTT and crystal-cell adhesion assays were utilized to determine the activity of HK-2 cells and crystal adhesion ability, biochemical detection and enzyme-linked immunosorbent assay (ELISA) to measure the levels of oxidative stress-related substances and inflammatory factors, and western blot to test the expression levels of proteins related to the AMPK/Nrf2 signaling pathway.. Hyp can improve renal pathological and functional damage, decrease CaOx crystal deposition, and inhibit oxidative stress and inflammatory response. Such effects may be achieved by activating the AMPK/Nrf2 signaling pathway.

Topics: AMP-Activated Protein Kinases; Animals; Calcinosis; Calcium Oxalate; Kidney; Kidney Calculi; NF-E2-Related Factor 2; Oxalates; Oxidative Stress; Rats; Signal Transduction

Calcium oxalate (CaOx) stones are among the most common types of kidney stones and are associated with renal tubular damage, interstitial fibrosis, and chronic kidney disease. The mechanism of CaOx crystal-induced renal fibrosis remains unknown. Ferroptosis, a type of regulated cell death, is characterised by iron-dependent lipid peroxidation, and the tumour suppressor p53 is a key regulator of ferroptosis. In the present study, our results demonstrated that ferroptosis was significantly activated in patients with nephrolithiasis and hyperoxaluric mice as well as verified the protective effects of ferroptosis inhibition on CaOx crystal-induced renal fibrosis. Moreover, the single-cell sequencing database, RNA-sequencing, and western blot analysis revealed that the expression of p53 was increased in patients with chronic kidney disease and the oxalate-stimulated human renal tubular epithelial cell line, HK-2. Additionally, the acetylation of p53 was enhanced by oxalate stimulation in HK-2 cells. Mechanistically, we found that the induction of p53 deacetylation, owing to either the SRT1720-induced activation of deacetylase sirtuin 1 or the triple mutation of p53, inhibited ferroptosis and alleviated renal fibrosis caused by CaOx crystals. We conclude that ferroptosis is one of the critical mechanisms contributing to CaOx crystal-induced renal fibrosis, and the pharmacological induction of ferroptosis via sirtuin 1-mediated p53 deacetylation may be a potential target for preventing renal fibrosis in patients with nephrolithiasis.

Topics: Animals; Calcinosis; Calcium Oxalate; Ferroptosis; Fibrosis; Humans; Kidney; Kidney Calculi; Mice; Oxalates; Renal Insufficiency, Chronic; Sirtuin 1; Tumor Suppressor Protein p53

To investigate whether ADSC-derived miR-23-enriched exosomes could protect against calcium oxalate stone formation in a hyperoxaluria rat model.. An ethylene glycol- (EG-) induced hyperoxaluria rat model and an in vitro model of COM-induced HK-2 cells coculturing with RAW264.7 cells were established to explore the protective mechanisms of ADSC-derived miR-23-enriched exosomes.. The results showed that treatment with miR-23-enriched exosomes from ADSCs protected EG-induced hyperoxaluria rats, and cell experiments confirmed that coculturing with miR-23-enriched exosomes alleviated COM-induced cell autophagy. Overexpressed miR-23 suppressed M1 macrophage polarization by inhibiting IRF1 expression. Furthermore, the predicted binding site between the IRF1 messenger RNA 3'-untranslated region (3'-UTR) and miR-23 was confirmed by the dual-luciferase reporter assay.. In conclusion, our research gave the first evidence that ADSC-derived miR-23-enriched exosomes affected the polarization of M1 macrophages by directly inhibiting IRF1 and protecting against calcium oxalate stone formation in a hyperoxaluria rat model.

Topics: Animals; Calcinosis; Calcium Oxalate; Exosomes; Hyperoxaluria; Macrophages; MicroRNAs; Oxalates; Rats; Stromal Cells

Patients with primary hyperoxaluria type I (PH I) are prone to develop early kidney failure. Systemic deposition of calcium-oxalate (CaOx) crystals starts, when renal function declines and plasma oxalate increases. All tissue, but especially bone, heart and eyes are affected. However, liver involvement, as CaOx deposition or chronic hepatitis/fibrosis has never been reported. We examined liver specimen from 19 PH I patients (aged 1.5 to 52 years at sample collection), obtained by diagnostic biopsy (1), at autopsy (1), or transplantation (17). With polarization microscopy, birefringent CaOx crystals located in small arteries, but not within hepatocytes were found in 3/19 patients. Cirrhosis was seen in one, fibrosis in 10/19 patients, with porto-portal and nodular fibrosis (n = 1), with limitation to the portal field in 8 and/or to central areas in 5 patients. Unspecific hepatitis features were observed in 7 patients. Fiber proliferations were detectable in 10 cases and in one sample transformed Ito-cells (myofibroblasts) were found. Iron deposition, but also megakaryocytes as sign of extramedullary erythropoiesis were found in 9, or 3 patients, respectively. Overall, liver involvement in patients with PH I was more pronounced, as previously described. However, CaOx deposition was negligible in liver, although the oxalate concentration there must be highest.

Topics: Calcinosis; Calcium; Calcium Oxalate; Fibrosis; Humans; Hyperoxaluria, Primary; Iron; Kidney; Liver Diseases; Oxalates

This study assesses the differences in the presentations, complications and metabolic abnormalities of children with renal calyceal microlithiasis (RCM) and overt urolithiasis in different pediatric ages.. A total of 465 children with urolithiasis were investigated retrospectively. Patients were categorized based on their ages to infancy, early childhood, middle childhood and adolescence. When the hyperechogenic spots on ultrasound imaging were <3 mm, they were considered RCM, and if they were ≥3 mm, they were considered overt urolithiasis.. Metabolic abnormalities were detected in 71%; hyperuricosuria in infants, hyperoxaluria in younger children and hypocitraturia in older children were the most common metabolic abnormalities. Hypercalciuria was the only metabolic abnormality that was significantly associated with overt urolithiasis in all pediatric ages (OR 2.25, 95% CI 1.21-4.19). The clinical presentations were not significantly different between RCM and overt urolithiasis; however, complications such as urinary tract infection was significantly higher with overt urolithiasis in infancy (p = 0.01), early childhood (p = 0.02), middle childhood (p = 0.007) and adolescence (p = 0.01). Also, growth retardation was significantly higher with overt urolithiasis in infancy and early childhood (p = 0.02).. Most children with urolithiasis have underlying urinary metabolic abnormalities that differ according to the child's age. Despite these differences, hypercalciuria is significantly associated with overt urolithiasis in all pediatric ages. Clinical and laboratory features cannot differentiate RCM and overt urolithiasis; however, complications are significantly higher with overt urolithiasis.

Topics: Adolescent; Age Factors; Calcinosis; Calcium; Child; Child, Preschool; Citric Acid; Female; Humans; Infant; Kidney Calices; Male; Nephrology; Oxalates; Pediatrics; Retrospective Studies; Risk Factors; Uric Acid; Urinary Tract Infections; Urolithiasis

Microcalcifications can be the early and only presenting sign of breast cancer. One shared characteristic of breast cancer is the appearance of mammographic mammary microcalcifications that can routinely be used to detect breast cancer in its initial stages, which is of key importance due to the possibility that early detection allows the application of more conservative therapies for a better patient outcome. The mechanism by which mammary microcalcifications are formed is still largely unknown but breast cancers presenting microcalcifications are more often associated with a poorer prognosis.. We combined Capillary Electrochromatography, histology, and gene expression (qRT-PCR) to analyze patient-matched normal breast tissue vs. breast tumor. Potential carcinogenicity of oxalate was tested by its inoculation into mice. All data were subjected to statistical analysis.. To study the biological significance of oxalates within the breast tumor microenvironment, we measured oxalate concentration in both human breast tumor tissues and adjoining non-pathological breast tissues. We found that all tested breast tumor tissues contain a higher concentration of oxalates than their counterpart non-pathological breast tissue. Moreover, it was established that oxalate induces proliferation of breast cells and stimulates the expression of a pro-tumorigenic gene c-fos. Furthermore, oxalate generates highly malignant and undifferentiated tumors when it was injected into the mammary fatpad in female mice, but not when injected into their back, indicating that oxalate does not induce cancer formation in all types of tissues. Moreover, neither human kidney-epithelial cells nor mouse fibroblast cells proliferate when are treated with oxalate.. We found that the chronic exposure of breast epithelial cells to oxalate promotes the transformation of breast cells from normal to tumor cells, inducing the expression of a proto-oncogen as c-fos and proliferation in breast cancer cells. Furthermore, oxalate has a carcinogenic effect when injected into the mammary fatpad in mice, generating highly malignant and undifferentiated tumors with the characteristics of fibrosarcomas of the breast. As oxalates seem to promote these differences, it is expected that a significant reduction in the incidence of breast cancer tumors could be reached if it were possible to control oxalate production or its carcinogenic activity.

Topics: Animals; Breast Neoplasms; Calcinosis; Cell Line, Tumor; Cell Transformation, Neoplastic; Female; Humans; Mammary Glands, Human; Mammary Neoplasms, Animal; Mice; Mice, Inbred BALB C; Neoplasms, Experimental; Oxalates; Prognosis

Topics: Adult; Bone Diseases; Bone Resorption; Calcinosis; Fingers; Giant Cells; Hand; Humans; Hyperoxaluria, Primary; Male; Middle Aged; Osteosclerosis; Oxalates; Radiography

A pathological study on 5 of 21 cats affected naturally with systemic calcinosis was performed. The animals ranged in age from 1 to 9 years. Hematology and serum chemistry analyses showed the elevated values of phosphorus, blood urea nitrogen and serum creatinine. X-ray examination disclosed the increased density of systemic bones. Histologically, marked calcification was present at the vascular walls of almost all the organs including the lungs, trachea, kidneys, heart, aorta, alimentary tracts, choroid plexus and bones. In the lungs, kidneys and stomach, the calcified lesions were associated with deposition of oxalate crystals. Serum chemistry showed more elevated values of 25-hydroxycholecalciferol (vitamin D) of the affected cats than the normal level. Retrospective examination revealed that these cats had been fed the commercial pet foods containing a large amount of vitamin D (6,370 IU/100 g diet) from their young age, and its value was about ten times as much as that of the control food (680 IU/100 g diet). Pathological changes found in the cats from the experimental vitamin D3 toxicosis were similar to those in the natural cases. In addition, tissue levels of calcium, phosphorous and zinc in the lungs and kidneys were markedly elevated in both natural and vitamin D-intoxicated cases. These findings suggest that long-term feeding of the pet food containing excessive vitamin D was responsible for the outbreak of the systemic calcinosis in the cats.

Topics: Animals; Aorta; Blood Urea Nitrogen; Bone and Bones; Calcifediol; Calcinosis; Calcium; Cat Diseases; Cats; Choroid Plexus; Creatinine; Disease Outbreaks; Drug Overdose; Female; Japan; Kidney; Lung; Male; Oxalates; Phosphorus; Stomach; Trachea; Vitamin D; Zinc

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: Adult; Ascorbic Acid; Calcinosis; Calcium Oxalate; Cardiomyopathies; Humans; Kidney Failure, Chronic; Male; Oxalates; Oxalic Acid; Renal Dialysis

Primary hyperoxaluria is a rare metabolic disorder characterized by excessive synthesis and urinary excretion of oxalate. Nephrocalcinosis with or without calcium oxalate nephrolithiasis leads to renal failure in infancy through young adulthood. Oxalosis is the condition in which the highly insoluble calcium oxalate crystals are deposited in extrarenal tissues including bone, blood vessels, heart, and the male urogenital system. The radiographic abnormalities in 14 patients with primary hyperoxaluria are described. These abnormalities include nephrolithiasis, nephrocalcinosis, dense vascular calcifications, abnormal bone density, and characteristic metaphyseal abnormalities. Changes of renal osteodystrophy and pathologic fractures are common. Radiographic bone abnormalities are dependent on the age of the patient when renal failure occurred and the degree of success of renal transplantation. Characteristic skeletal changes are present in six of seven patients who developed renal failure when less than 7 years of age.

Topics: Adolescent; Adult; Calcinosis; Child; Child, Preschool; Female; Fractures, Spontaneous; Humans; Infant; Kidney Calculi; Male; Metabolism, Inborn Errors; Nephrocalcinosis; Oxalates; Radiography; Vascular Diseases

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

Topics: Aldehyde-Ketone Transferases; Calcinosis; Carbohydrate Metabolism, Inborn Errors; Child; Child, Preschool; Chronic Kidney Disease-Mineral and Bone Disorder; Female; Glyoxylates; Humans; Ketoglutaric Acids; Kidney Calculi; Kidney Failure, Chronic; Male; Oxalates; Oxo-Acid-Lyases

Topics: Calcinosis; Humans; Kidney Calculi; Metabolic Diseases; Metabolism, Inborn Errors; Oxalates

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

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

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

Topics: Animals; Calcinosis; Chlorides; Ergocalciferols; Infertility, Male; Lanthanum; Male; Nitrates; Oxalates; Rats; Testis; Thorium; Time Factors; Trace Elements; Uranium; Yttrium

Topics: Animals; Bone and Bones; Calcinosis; Calcium; Calcium Phosphates; Crystallization; Histocytochemistry; Humans; Indicators and Reagents; Mercury; Mice; Nitrates; Oxalates; Solutions; Staining and Labeling

Topics: Adult; Calcinosis; Crystallography; Gout; Humans; Infant, Newborn; Infant, Newborn, Diseases; Infarction; Kidney; Male; Metabolism, Inborn Errors; Methods; Microscopy, Electron; Middle Aged; Oxalates; Uric Acid

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

Topics: Adolescent; Axilla; Calcinosis; Humans; Kidney Calculi; Male; Oxalates; Skin Diseases; Thigh

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

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