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Kidney Stones
Published in Charles Theisler, Adjuvant Medical Care, 2023
Magnesium is a known inhibitor of the formation of calcium oxalate crystals in the urine and was proposed for prophylactic treatment in kidney stone disease as early as the 17th and 18th centuries.2 Magnesium oxide (400-500 mg/day) increases the solubility of calcium oxalate and thus decreases rates of stone recurrence.3 Fifty-five patients with recurrent renal calcium stone disease without signs of magnesium deficiency were given 500 mg of magnesium hydroxide daily for up to four years. The authors concluded that magnesium treatment in renal calcium stone disease is effective with few side effects. No clinical signs of magnesium excess were observed.2
Urolithiasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Hypercalciuria: ~50% of calcium stone formers.Excretion of >7 mmol/day in men and >6 mmol/day in women.
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
Hypercalciuria is defined as >4 mg/kg/24 hours or >7 mmol (men) or >6 mmol (women). Hypercalciuria can classified into idiopathic (50%), absorptive (from gut), renal leak or resorptive (from bone). In absorptive hypercalciuria, excessive calcium is absorbed from the gut leading to increased renal filtration and reduced renal reabsorption due to low parathyroid hormone and associated raised urinary phosphate (fasting urinary calcium is normal). Impaired tubular reabsorption of calcium (renal leak) occurs in 5%–10% of calcium stone formers and is characterised by fasting hypercalciuria with secondary hyperparathyroidism (raised PTH) but without hypercalcaemia. Resorptive hypercalciuria is almost always due to primary hyperparathyroidism which accounts for 3%–5% of all cases of hypercalciuria. The increased PTH levels leads to release of calcium from the bones as well as increasing calcium and vitamin D absorption from the bone and reducing calcium renal excretion from the distal tubule resulting in hypercalciuria (Table 16.1). Excess salt intake can result in hypercalciuria, as sodium and calcium are co-transported in the kidney. Hypercalciuria is most commonly associated with calcium oxalate dihydrate stones.
Established and recent developments in the pharmacological management of urolithiasis: an overview of the current treatment armamentarium
Published in Expert Opinion on Pharmacotherapy, 2020
Mohamed Abou Chakra, Athanasios E. Dellis, Athanasios G. Papatsoris, Mohamad Moussa
A RCT designed to evaluate the effect of treatment with febuxostat and allopurinol in recurrent calcium stone formers with higher urinary uric acid excretion. The results showed that febuxostat (80 mg) once daily lowered 24-hour urinary uric acid excretion significantly more than allopurinol (300 mg) in recurrent stone formers with higher urinary uric acid excretion. Despite the greater reduction in 24-hour urinary uric acid level when compared to allopurinol, there was no change in stone size or number at six months [102]. High-dose allopurinol 600 mg/day acted as an antioxidant, reducing the vascular oxidative stress, and improving the endothelial function. To compare this result to a similar levels of urate lowering agents, investigators used probenecid (at 1,000 mg/day), a uricosuric drug used in the treatment of gout and hyperuricemia. Despite causing similar reduction of serum urate as allopurinol, probenecid had no effect on endothelial function. This experiment suggests that there are context specific effects of allopurinol therapy, beyond its ability to lower serum or urine uric acid. These other effects may relate to other hypotheses regarding calcium stone formation. A vascular etiology for initiation of stones has been proposed [103].
Impact of food quantity and quality on the biochemical risk of renal stone formation
Published in Scandinavian Journal of Urology, 2018
Francesco Esperto, Roberto Miano, Martino Marangella, Alberto Trinchieri
In conclusion, the overweight and obese patients in this study did not show an increased biochemical risk of calcium stone formation, but only a limited group of them was at risk of uric acid stone formation. Overweight and obesity are not related to a specific food pattern but rather to the imbalance between the energy intake from food and the energy expenditure linked to physical activity. An increased intake of food, by itself, does not imply urinary modifications that could lead to an increased risk of calcium stone formation. The quality of foods consumed, specifically their acid load, has a more relevant impact on the risk of calcium stone formation. The risk of stone formation in obese patients is modulated by the pattern of their diets, where a diet rich in meat and poor in vegetables and fruits may lead to an increased risk of calcium stone formation owing to the high acid load associated with this specific dietary pattern. In contrast, a dietary pattern associated with a lower acid load, such as the Mediterranean diet of this population, could imply a lower risk of calcium stones, even in the presence of overweight and obesity.
Rising occurrence of hypocitraturia and hyperoxaluria associated with increasing prevalence of stone disease in calcium kidney stone formers
Published in Scandinavian Journal of Urology, 2020
Ramy F. Youssef, Jeremy W. Martin, Khashayar Sakhaee, John Poindexter, Sharmin Dianatnejad, Charles D. Scales, Glenn M. Preminger, Michael E. Lipkin
We also describe an increase in hyperoxaluria in the contemporary cohort, which was significant in males. A recent study reported that urinary oxalate excretion was also increased in calcium stone formers from 1980 to 2015 [14]. We recently demonstrated in a systematic review that hyperoxaluria has increased significantly over the past two decades, with the effect more prominent in Asian populations [27]. The mechanism underlying this rise in hyperoxaluria is likely multifactorial. Hyperoxaluria has been associated with obesity in large retrospective studies, although the mechanisms underlying this association are complex and require further investigation [28].