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Intestinal Failure
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Rashmi Patil, Elizabeth King, Jeffrey Rudolph
Long-chain triglycerides (LCTs) are of special consideration as they are a major trophic factor for intestinal adaptation, but require micelle formation and are not absorbed well in the small intestine. The optimal fat source to facilitate optimal absorption in patients who have undergone significant intestinal resection may be a combination of medium-chain triglycerides (MCTs, which do not require micelle formation) and LCTs. Patients without a colon tolerate diets that are high in fat (30%–40% of total energy intake). Those with an intact colon may experience steatorrhea and magnesium/calcium loss with high-fat intake due to the process of saponification. Saponification occurs when the unabsorbed fat combines with calcium and/or magnesium to form soaps. The soaps prevent these ions from interacting with oxalate as they would in normal individuals. This, in turn, enhances oxalate absorption in the colon and needs excretion by the kidneys, increasing risk for oxalate renal stone formation. It may be necessary to restrict oxalate intake or provide calcium supplements to reduce the risk of oxalate renal stone formation.
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].
The Role of the Clinical Laboratory in Nutritional Assessment
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Calcium oxalate kidney stones are the leading type of kidney stones. Oxalate is naturally found in many foods, including fruits and vegetables, nuts and seeds, grains, legumes, and even chocolate and tea. Some examples of foods that contain high levels of oxalate include peanuts, rhubarb, spinach, beets, chocolate, and sweet potatoes. Another common type of kidney stone is a uric acid stone. Red meat and shellfish have high concentrations of a natural chemical compound known as a purine. High purine intake leads to a higher production of uric acid, which then accumulates as crystals in the joints or as stones in the kidneys. Again, based on the type of kidney stone, different diets and medication are prescribed. Monitoring 24-hour urine is often used in patient management to reduce reoccurrence.52
Calcium-sensing receptor promotes calcium oxalate crystal adhesion and renal injury in Wistar rats by promoting ROS production and subsequent regulation of PS ectropion, OPN, KIM-1, and ERK expression
Published in Renal Failure, 2021
Xiaoran Li, Siyu Chen, Demei Feng, Yuqiang Fu, Huang Wu, Jianzhong Lu, Junsheng Bao
In addition, we found that rats with nephrolithiasis showed low urinary calcium and citrate and high urinary oxalate compared to control animals. Oxalate is a more important promoter of kidney stones and exhibits 15-fold greater efficacy on urinary calcium oxalate saturation than calcium [43]. Notably, we observed low urinary oxalate in our rat nephrolithiasis model treated with GdCl3 compared with group B; one possible explanation for this finding is that CaSR increased free calcium, which binds to oxalate and thus reduces urinary oxalate. In addition, the main risk factor for recurrence of calcium oxalate stones is thought to be urinary citrate deficiency. Urinary citrate inhibits the formation of stones by inhibiting nucleation and growth [44]. Our results showed that urinary citrate levels decreased in the rat nephrolithiasis model. The CaSR inhibitor NPS-2390 increased the urinary citrate concentration and reduced crystal deposition in the rat nephrolithiasis model compared with group B. Therefore, we speculated that NPS-2390 might be a potential drug for the treatment of nephrolithiasis, especially when exposed to ethylene glycol, but the effect must be further verified by animal experiments and clinical trials before introducing it in clinical practice.
Novel therapeutic approaches in primary hyperoxaluria
Published in Expert Opinion on Emerging Drugs, 2018
Alexander Weigert, Christina Martin-Higueras, Bernd Hoppe
Current research mainly focuses on ways to eliminate oxalate not only via the kidneys but also by the intestine, so that the harmful effect of increased urinary oxalate can be decreased. This can be achieved by degrading oxalate in the intestine (dietary and endogenous oxalate), thus reducing oxalate uptake (ALLN-177) and/or promoting endogenous oxalate removal into the intestine (O. formigenes). A second topic is substrate reduction treatment. By manipulating the glyoxylate metabolism via RNA-interference mechanisms (Lumisaran, DCR-PHXC), hepatic oxalate production is significantly decreased. Another approach is delaying the process of kidney fibrosis, by preventing CaOx-induced inflammation (CRID 3, R-7050) achieving a prolonged kidney function and thus increasing the quality of life for PH patients. Most recently, therapeutic approaches with gene therapy, replacing the defective gene in PH I (AAV, SVac-vectors), have been started, possibly presenting the first non-transplantation curative approach for PH I patients (Table 1).
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
Increased urinary excretion of oxalate is derived from dietary and endogenous sources. Common dietary sources with high oxalate content include green leafy vegetables, beets, strawberries, nuts, cocoa, dark chocolates and tea infusions (Ritter and Savage 2007; Schroder et al. 2011; Mahdavi et al. 2013). Oxalic acid is a non-essential dietary component available at varying concentrations in all plant species. Reports from previous studies demonstrate that oxalate rich leafy vegetables such as spinach can accumulate oxalate between 800 and 12 576 mg/100 g dry matter (Siener et al. 2006; Savage and Martensson 2010). Spinach extract used in this study showed maximum oxalate content among various dietary sources. Minor variations in oxalate content observed among spinach extracts harvested from different regions can be attributed to the subtle environmental and growth conditions.