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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Oxalate is a metabolite excreted in urine. Hyperoxaluria can arise from metabolic disorders, excess dietary oxalate intake in foods such as spinach, rhubarb and chocolate, and ileal disease.
Envisioning Utilization of Super Grains for Healthcare
Published in Megh R. Goyal, Preeti Birwal, Santosh K. Mishra, Phytochemicals and Medicinal Plants in Food Design, 2022
Oxalates are harmful substances and potential risk for the human body. It is not metabolized in human body and excrete through urine. The higher consumption of the oxalates results in the reduced availability of the certain elements, which can lead to hyperoxaluria. This can cause a risk of calcium oxalate stone formation in the kidneys since oxalate and divalent ions are capable of forming insoluble complex in the gut [87, 107, 159]. Moreover, the presence of the oxalic acid in the human diet leads to various harmful effects such as gastrointestinal irritation, reduced minerals availability, impaired blood clotting, and contraction of muscles mainly attributed to the higher amounts of crystalline calcium contents deposits in the cells (Table 10.6). The recommended levels of oxalates in the human diet are estimated to be 50–200 mg per day [107].
Urolithiasis
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Thomas Johnston, James Armitage, Oliver Wiseman
Patients should be advised to eat a healthy and balanced diet. However, foods rich in oxalate (for example, chocolate, nuts, rhubarb, tea) should be limited or avoided particularly in those patients with hyperoxaluria. Excessive dietary animal protein may cause hypocitraturia, hyperuricosuria, hyperoxaluria and acidic urine thereby encouraging stone formation. High salt intake increases the risk of urolithiasis by causing increased tubular calcium excretion and hypocitraturia. Therefore, not more than 3–5 g sodium should be consumed per day.
Opportunities for future therapeutic interventions for hyperoxaluria: targeting oxidative stress
Published in Expert Opinion on Therapeutic Targets, 2019
Hyperoxaluria is a multifactorial disease. It may result from overconsumption of oxalate-rich food or lack of specific oxalate degrading gut bacteria or gene mutations responsible for enzymes that control glyoxylate metabolism mainly in the liver. Genetic diseases are called primary hyperoxaluria (PH) [92,93]. Current therapies for PH are limited to supra-physiologic doses of vitamin B6 which is a cofactor in alanine-glyoxylate aminotransferase (AGT), or citrate as an inhibitor of CaOx crystallization. Patients are advised high fluid intake and avoidance of the oxalate-rich food. None of these lead to acceptable levels of endogenous oxalate production with eventual combined liver kidney transplantation in most PH patients. Reduction of urinary oxalate through orally administered oxalate degrading bacteria has been unsuccessful in long-term trials. A number of other therapies such as recombinant enzymes that degrade oxalate in the gut are being currently tested in animal models. Review of various studies, however, indicate that reduction of urinary oxalate is possible but in cases with severe hyperoxaluria, not to levels where CaOx crystallization is totally prevented.
From pathogenesis to novel therapies in primary hyperoxaluria
Published in Expert Opinion on Orphan Drugs, 2019
Gill Rumsby, Sally-Anne Hulton
All three types of hyperoxaluria are similar in terms of age of presentation [18] and urine oxalate excretion [19], consequently one might expect that they have a similar prognosis although this does not appear to be the case. This finding may reflect misdiagnosis or ascertainment bias and certainly, there is now evidence that PH3, previously regarded as a ‘mild’ disease, can lead to renal impairment [3,18,20]. In addition, there may be marked differences in presentation even within family members with the same genetic defects suggesting that there may be other genes or environmental influences on phenotype. There is some evidence that the degree of hyperoxaluria has a bearing on renal function, with those in the highest quartile of urine oxalate excretion (>1.87 mmol/1.73m2 per 24 h) with a worse renal outcome [21]. The presence of nephrocalcinosis at presentation is also a predictor of renal impairment [22].
Oral administration of oxalate-enriched spinach extract as an improved methodology for the induction of dietary hyperoxaluric nephrocalcinosis in experimental rats
Published in Toxicology Mechanisms and Methods, 2018
Abhishek Albert, Vidhi Tiwari, Eldho Paul, Sasikumar Ponnusamy, Divya Ganesan, Rajkumar Prabhakaran, Selvi Mariaraj Sivakumar, Selvam Govindan Sadasivam
Urolithiasis, a multifactorial disorder affecting about 12% of the world population is influenced by diet, genetic and environmental factors (Scales et al. 2012). Calcium oxalate (CaOx) is the most prevalent type of kidney stone. The increased level of oxalate in the urine is the major risk factor for CaOx crystallization and stone formation. Humans acquire oxalate from both dietary sources and endogenous synthesis. Hyperoxaluria normally results from either excessive endogenous production of oxalate or by increased dietary intake of oxalates, or by a combination of these factors. Oxalate synthesized by liver and erythrocytes is not further metabolized by humans and thereby contribute to the body burden of endogenous oxalate (Smith et al. 1972; Farinelli et al. 1983). The free oxalate in the diet absorbed majorly by the colon accounts for almost 50% of the daily urinary oxalate excretion (Hautmann et al. 1993; Holmes et al. 2001; Hatch et al. 2005; Freel et al. 2006; Jiang et al. 2006). The excessive ingestion of dietary oxalate increases urinary oxalate excretion in individuals with high rate of oxalate absorption and has significant impact on CaOx crystal formation. Although the consumption of oxalate rich food caused a significant increase in urinary oxalate excretion, the underlining factor for CaOx stone formation is not clear (Chiangjong and Thongboonkerd 2016). Moreover, the existing treatments have limitations including recurrence of stone, hematuria and renal insufficiency.