Oxalate Homeostasis in Non-Stone-Forming Chronic Kidney Disease: A Review of Key Findings and Perspectives
Abstract
:1. Introduction to Health Oxalate Homeostasis
1.1. Dietary Oxalate Intake
1.2. Endogenous Oxalate Metabolism
1.3. Intestinal Oxalate Absorption and Bacterial Degradation
1.4. Oxalate Excretion
2. Oxalate Implications in Health and Disease
3. The Interplay between Oxalate and CKD: A Vicious Cycle of Shared Risk Factors
4. Oxalate’s Role in the Pathogenesis of CKD: From Silent Culprit to Active Player
5. Gut-Kidney Axis in CKD Oxalate Homeostasis
6. Oxalate as a Clinical Marker for CKD Progression and Prognosis
7. Targeting Oxalate Homeostasis to Reduce CKD Progression and the Risk of Cardiovascular Events
7.1. Dialysis Treatment for Management Oxalate Burden in Patients with Kidney Failure
7.2. Modifying the Shared Risk Factors to Prevent CKD Progression
7.3. Medication Adjustments
- Calcium-based phosphate binders. Calcium-based phosphate binders, including calcium acetate and calcium carbonate, are commonly used to prevent mineral-bone disorders associated with CKD and are also considered to prevent CaOx stone formation [23,128]. These supplements work by binding with phosphate in the intestine, thus reducing its bioavailability and absorption, resulting in lower urinary oxalate excretion and a decreased risk of hyperoxaluria and CaOx stone formation [23]. To achieve a neutral calcium balance and avoid the adverse effects of either negative or positive calcium balance, a calcium intake of around 1000 mg/day is recommended [128,129]. However, calcium supplementation, especially if administered between meals, can raise urinary calcium excretion without any positive impact on oxalate, thereby elevating the risk of stone formation [23]. Moreover, caution should be exercised when using calcium supplements in patients with advanced CKD because they may cause hypercalcemia and vascular calcification [128,130]. Therefore, the decision to use calcium-based phosphate binders in patients with advanced CKD should be made on a case-by-case basis, balancing the individual needs and risks of each patient against the risk of worsening vascular calcification.
- Noncalcium phosphate binders. Noncalcium phosphate binders, such as lanthanum carbonate, have also been shown to reduce UOx excretion in CKD patients by decreasing gut absorption of dietary oxalate [131,132]. This is thought to be due to the ability of lanthanum to form insoluble complexes with oxalate, thus reducing its bioavailability for absorption [131,133]. However, more extensive studies are needed to establish the efficacy and safety of noncalcium phosphate binders in preventing hyperoxalemia/hyperoxaluria and CKD progression.
- Calcium channel blockers. Verapamil has been shown to increase urinary oxalate excretion and reduce the risk of CaOx stone formation in animal models [134]. However, their efficacy in patients with hyperoxalemia/hyperoxaluria has not been established, and the risk-benefit ratio for the individual patient should determine the treatment option.
- Thiazide and thiazide-like diuretics. Thiazide diuretics have been found to be effective in treating hypertension in patients with ESKD [135] and in reducing the formation of CaOx kidney stones. Thiazide-type diuretics (hydrochlorothiazide, chlorthalidone, and indapamide) act on the distal tubule of the kidney, increasing calcium reabsorption and decreasing the excretion of calcium in the urine, resulting in a decrease in UOx excretion [136,137]. However, the use of thiazide and thiazide-like diuretics in CKD patients is often restricted due to concerns regarding their safety and effectiveness, such as the risk of electrolyte imbalances, volume depletion, and a decline in eGFR [138].
- Magnesium. Magnesium has been recognized as a potent inhibitor of calcium oxalate (CaOx) crystals due to its ability to bind with oxalate, forming a soluble complex. This inhibitory effect is particularly significant when magnesium is combined with citrate and remains effective even in acidic environments [139]. Magnesium also inhibits the absorption of dietary oxalate from the gut lumen, as well as citrate-rich food [140]. Furthermore, magnesium plays a multifaceted role in the management of CKD. It has been shown to suppress the secretion of parathyroid hormones, activate the calcium-sensing receptor, promote osteoblast activity, and reduce intestinal phosphate absorption. These mechanisms contribute to the regulation of mineral metabolism and prevent the development of secondary hyperparathyroidism and vascular calcification in CKD patients. Additionally, magnesium has been associated with a decrease in the incidence of vascular calcification and improvements in cardiac function [141,142,143]. Incorporating magnesium supplementation as a medical adjustment in patients with CKD may not only help address oxalate burden but also maintain mineral balance, reduce the risk of complications, and improve overall cardiac health. However, further studies are needed to determine optimal dosing strategies and assess the long-term effects of magnesium supplementation in CKD populations.
- Vitamins B6 and D. Extensive research has been conducted on the association between deficiencies in vitamins B6 and D and the development of CaOx urolithiasis [23,144,145,146]. However, the effectiveness of vitamin supplementation in preventing hyperoxalemia/hyperoxaluria is still a controversial issue [122,145,146]. Additionally, there is a lack of knowledge regarding the potential of these vitamins to prevent the oxalate burden in CKD patients. More research is required to ascertain the potential benefits of these vitamins in managing disrupted oxalate homeostasis in CKD.
7.4. Enhancement of Intestinal Oxalate Handling with Promising New Pharmacological Targets
- ODB. ODB have been extensively studied as a potential treatment option for patients with hyperoxaluria and urolithiasis [147]. By degrading oxalate in the gut, ODB may prevent the absorption of oxalate into the bloodstream and reduce the burden of oxalate in CKD patients. Studies have shown that probiotics and synbiotics can be considered good sources of naturally occurring oxalate-degrading agents in the human colon. Pro- and/or synbiotics supplements containing O. formigenes, Bifidobacterium lactis, Lactobacillus strains, and others have been found to decrease hyperoxalemia/hyperoxaluria [21,147,148,149,150], but the results of in vitro and experimental studies do not always reflect the ability of bacteria to degrade oxalate in humans [18,147,151]. Specific clinical studies are scarce, and further research is needed to determine the optimal dosages and benefits of ODB supplementation in the management of the oxalate burden in CKD.
- Oxalate-degrading enzymes. Oxalate-degrading enzymes represent a new class of enzymes that can effectively degrade oxalate into nontoxic compounds [150,151]. As described above, enzymes, such as OxdC and Oxc, have been found naturally in the gut microbiota [18]. Two promising oxalate-degrading enzymes, reloxaliase and Oxazyme®, are currently under investigation as potential treatments for oxalate-related diseases. Reloxaliase, also known as ALLN-177, is a recombinant OxdC enzyme derived from Bacillus subtilis and expressed in Escherichia coli and developed for the treatment of enteric hyperoxaluria [152]. Clinical trials have demonstrated the safety and efficacy of reloxaliase, showing a significant reduction in UOx levels in patients with enteric hyperoxaluria [152,153]. Notably, reloxaliase has also shown promising results in lowering urine and plasma oxalate in patients with CKD, including those with moderate to severe kidney dysfunction. Specifically, it has led to a ~30% decrease in UOx in two patients with grade 3b CKD and a similar reduction in POx in seven patients with grade 5 CKD [154]. Oxazyme® is a synthetic enzyme engineered to effectively degrade oxalate in the gastrointestinal tract [155]. Although clinical trials for Oxazyme® are still in the early stages, preclinical studies have demonstrated its ability to degrade oxalate in laboratory settings [155]. Further research and clinical trials are needed to establish their efficacy, safety, and optimal dosing regimens for the CKD patient population.
- Small-molecule inhibitor. A small-molecule inhibitor of the intestinal anion exchanger SLC26A3 has been identified for the treatment of hyperoxaluria [151]. The small-molecule SLC26A3 inhibitor (DRAinh-A270) selectively inhibits SLC26A3-mediated chloride/bicarbonate exchange and oxalate/chloride exchange [13,17]. In colonic closed loops in mice, luminal DRAinh-A270 inhibited oxalate absorption by 70% [17]. By selectively inhibiting SLC26A3-mediated oxalate absorption, this inhibitor has the potential to alleviate the burden of oxalate-related complications and improve the management of hyperoxaluria. Continued research and clinical investigations are necessary to fully explore the therapeutic potential of this small-molecule inhibitor and advance its translation into clinical practice.
8. Conclusions and Future Directions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Stepanova, N. Oxalate Homeostasis in Non-Stone-Forming Chronic Kidney Disease: A Review of Key Findings and Perspectives. Biomedicines 2023, 11, 1654. https://doi.org/10.3390/biomedicines11061654
Stepanova N. Oxalate Homeostasis in Non-Stone-Forming Chronic Kidney Disease: A Review of Key Findings and Perspectives. Biomedicines. 2023; 11(6):1654. https://doi.org/10.3390/biomedicines11061654
Chicago/Turabian StyleStepanova, Natalia. 2023. "Oxalate Homeostasis in Non-Stone-Forming Chronic Kidney Disease: A Review of Key Findings and Perspectives" Biomedicines 11, no. 6: 1654. https://doi.org/10.3390/biomedicines11061654
APA StyleStepanova, N. (2023). Oxalate Homeostasis in Non-Stone-Forming Chronic Kidney Disease: A Review of Key Findings and Perspectives. Biomedicines, 11(6), 1654. https://doi.org/10.3390/biomedicines11061654