Kidney Stones

[brentipold]

Hello,

Completely out of the blue, I started having what I believe to be kidney stones. Totally unsure how this is possible considering I take about 3-4mg of K2 everyday. I wasn't sure what was going on till I just noticed in the toliet that I passed them. They broke up almost on touch, and sort of felt grainy. I'm not sure how or why this is happening to me. I was experiencing almost like a bloated lower abdomen, and when I would pee, I would have micro-second interruptions, but I wasn't seeing any stones. When I looked closer, I did find some.

Can salt cause stones? I have about 1/4 tsp of salt with 1.5 cups of OJ 2-3x a day. So 3/4tsp total of salt. Not a lot by RP standards I would think? I consume roughly 1000-1500mg of calcium a day, so not overconsumption and right on point.

 

[Mito]

Peat might disagree with some of these ideas, but some things to consider.

 

[brentipold]

Peat might disagree with some of these ideas, but some things to consider.

TY!

 

[stsfut]

I have been having some prostate dull pain, but thought that perhaps it is kidney stones since I am now consuming so much dairy (calcium). Wonder if that,s my case.

 

[tca300]

High phosphate or bad calcium to phosphorus ratio, and low vitamin D.


Vitamin D and kidney stone disease.
Tang J(1), Chonchol MB.
(1)Division of Renal Disease and Hypertension, University of Colorado School of
Medicine, Aurora, Colorado 80045, USA.
PURPOSE OF REVIEW: Vitamin D is important in maintaining calcium homeostasis, but its role in kidney stone disease and its effect on stone formation are still not clear.
RECENT FINDINGS: Kidney stone formers tend to experience enhanced intestinal calcium absorption, increased urinary calcium excretion, and excessive bone mineral loss. Although direct actions of active vitamin D have been implicated in all these processes, the effect of nutritional vitamin D (vitamin D2 or vitamin D3) use on calcium balance among stone formers is still not clear. In addition, the safety of nutritional vitamin D use in the stone forming population is also not established, considering the potential effect of its use on raising urinary calcium. However, most of the observational studies do not support a significant association between higher nutritional vitamin D store and increased risk of stone formation. Short-term nutritional vitamin D repletion in stone formers with vitamin D deficiency also does not appear to increase urinary calcium excretion.
SUMMARY: The effect of nutritional vitamin D use in stone formers is still not clear. As vitamin D deficiency is highly prevalent among stone formers, future prospective studies are needed to establish the biological effect, as well as the safety and efficacy of nutritional vitamin D therapy in this unique patient population.

Nephron Clin Pract. 2012;122(3-4):134-8.
Vitamin D status in patients with recurrent kidney stones.
Pipili C(1), Oreopoulos DG.
(1)Kidney Stone Clinic, University Health Network, Toronto, Ont., Canada.
J Urol. 2014 Mar;191(3):679.
Data regarding the prevalence of 25-hydroxyvitamin D (25(OH)D) insufficiency in patients with nephrolithiasis, and the effects of vitamin D supplementation on parathyroid hormone (PTH) are few and conflicting. In this article, we examined the prevalence of vitamin D insufficiency and deficiency in 236 recurrent kidney stone formers and the correlation of vitamin D levels with other parameters of stone formation. The prevalent stone composition was calcium oxalate (80.4%) and uric acid (16.45%). One third of stone formers had vitamin D insufficiency and a quarter of them high PTH levels (PTH >7.5 pmol/l) with normal serum (total and ionized) calcium values. Predictor of high PTH was low 25(OH)D level (r = 0.989, r(2) = 0.977, p < 0.001). Stone formers with hypercalciuria had higher 25(OH)D values (72.26 ± 4.21 vs. 59.29 ± 1.76, p = 0.0013) compared to stone formers with urine calcium within normal ranges. Further studies are needed in order to better define the consequences of vitamin D insufficiency and to evaluate the impact of the therapeutic interventions in this cohort.
Copyright © 2013 S. Karger AG, Basel.

Clin Nephrol. 2012 May;77(5):352-7.
Normocalcemic hyperparathyroidism in patients with recurrent kidney stones: a disease entity or vitamin D deficiency?
Pipili C(1), Sekecioglu N, Oreopoulos DG.
(1)Kidney Stone Clinic, Toronto Western Hospital, Division of Nephrology, University
Health Network and University of Toronto, Toronto, Canada.
This retrospective data analysis was undertaken to examine the biochemical differences between renal stone formers with normocalcemic hyperparathyroidism (NHPT) and those with normal parathyroid hormone (PTH) levels. Our goal was to ascertain whether 25-hydroxyvitamin D (25(OH)D) status related to PTH levels in this patient cohort. Our findings among 74 patients with NHPT indicate that stone formers with NHPT had significantly lower 25(OH)D levels compared to 192 controls (p = 0.0001) and that 25(OH)D is positively correlated with 1,25-dihydroxyvitamin D values (R = 0.736, p = 0.015). Sequential measurements (after 3 - 5 years), among 11 patients with NHPT who did not receive vitamin D (VitD) preparations, showed a significant increase in urinary calcium (3.43 ± 1.96 vs. 5.72 ± 3.95, p = 0.0426) without a significant change in PTH levels. VitD supplementation, to 3 patients resulted in significant PTH decrease (11.8 ± 1.8 vs. 9.8 ± 1.3, p = 0.003). Prospective studies are needed to confirm the role of vitamin
supplementation in renal stone formers with NHPT.

Clin J Am Soc Nephrol. 2012 May;7(5):829-34.
Effect of vitamin D repletion on urinary calcium excretion among kidney stone formers.
Leaf DE(1), Korets R, Taylor EN, Tang J, Asplin JR, Goldfarb DS, Gupta M, Curhan GC.
(1)Department of Medicine, Columbia University, New York, New York, USA.
BACKGROUND AND OBJECTIVES: Despite the important role of vitamin D in maintaining bone health, many clinicians are reluctant to treat vitamin D deficiency in kidney stone formers because of the theoretical risk of increasing urinary
calcium excretion. This study examined the effect of vitamin D repletion on
urinary calcium excretion among stone formers.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Participants (n=29)
were recruited from urology clinics affiliated with New York Presbyterian Hospital. Enrollment criteria included a history of nephrolithiasis, urinary calcium excretion between 150 and 400 mg/d, and a serum 25-hydroxyvitamin D level <30 ng/ml. Participants were given oral ergocalciferol (50,000 IU/wk) for 8 weeks. Serum and 24-hour
urine tests were repeated after 8 weeks.
RESULTS: Levels of 25-hydroxyvitamin D increased significantly after vitamin D repletion (17±6 and 35±10 ng/ml, P<0.001), but mean 24-hour urinary calcium excretion did not change (257±54 and 255±88 mg/d at baseline and follow-up, respectively, P=0.91). However, 11 participants had an increase in urinary calcium excretion ≥20 mg/d; these participants also had an increase in urine sodium excretion, likely reflecting dietary variability. No participant experienced adverse effects from vitamin D, including hypercalcemia.
CONCLUSIONS: Among stone formers with vitamin D deficiency, a limited course of vitamin D repletion does not seem to increase mean urinary calcium excretion, although a subset of individuals may have an increase. These data suggest that vitamin D therapy, if indicated, should not be withheld solely on the basis of stone disease, but 24-hour urinary calcium excretion should be monitored after repletion.

 

[brentipold]

High phosphate or bad calcium to phosphorus ratio, and low vitamin D.


Vitamin D and kidney stone disease.
Tang J(1), Chonchol MB.
(1)Division of Renal Disease and Hypertension, University of Colorado School of
Medicine, Aurora, Colorado 80045, USA.
PURPOSE OF REVIEW: Vitamin D is important in maintaining calcium homeostasis, but its role in kidney stone disease and its effect on stone formation are still not clear.
RECENT FINDINGS: Kidney stone formers tend to experience enhanced intestinal calcium absorption, increased urinary calcium excretion, and excessive bone mineral loss. Although direct actions of active vitamin D have been implicated in all these processes, the effect of nutritional vitamin D (vitamin D2 or vitamin D3) use on calcium balance among stone formers is still not clear. In addition, the safety of nutritional vitamin D use in the stone forming population is also not established, considering the potential effect of its use on raising urinary calcium. However, most of the observational studies do not support a significant association between higher nutritional vitamin D store and increased risk of stone formation. Short-term nutritional vitamin D repletion in stone formers with vitamin D deficiency also does not appear to increase urinary calcium excretion.
SUMMARY: The effect of nutritional vitamin D use in stone formers is still not clear. As vitamin D deficiency is highly prevalent among stone formers, future prospective studies are needed to establish the biological effect, as well as the safety and efficacy of nutritional vitamin D therapy in this unique patient population.

Nephron Clin Pract. 2012;122(3-4):134-8.
Vitamin D status in patients with recurrent kidney stones.
Pipili C(1), Oreopoulos DG.
(1)Kidney Stone Clinic, University Health Network, Toronto, Ont., Canada.
J Urol. 2014 Mar;191(3):679.
Data regarding the prevalence of 25-hydroxyvitamin D (25(OH)D) insufficiency in patients with nephrolithiasis, and the effects of vitamin D supplementation on parathyroid hormone (PTH) are few and conflicting. In this article, we examined the prevalence of vitamin D insufficiency and deficiency in 236 recurrent kidney stone formers and the correlation of vitamin D levels with other parameters of stone formation. The prevalent stone composition was calcium oxalate (80.4%) and uric acid (16.45%). One third of stone formers had vitamin D insufficiency and a quarter of them high PTH levels (PTH >7.5 pmol/l) with normal serum (total and ionized) calcium values. Predictor of high PTH was low 25(OH)D level (r = 0.989, r(2) = 0.977, p < 0.001). Stone formers with hypercalciuria had higher 25(OH)D values (72.26 ± 4.21 vs. 59.29 ± 1.76, p = 0.0013) compared to stone formers with urine calcium within normal ranges. Further studies are needed in order to better define the consequences of vitamin D insufficiency and to evaluate the impact of the therapeutic interventions in this cohort.
Copyright © 2013 S. Karger AG, Basel.

Clin Nephrol. 2012 May;77(5):352-7.
Normocalcemic hyperparathyroidism in patients with recurrent kidney stones: a disease entity or vitamin D deficiency?
Pipili C(1), Sekecioglu N, Oreopoulos DG.
(1)Kidney Stone Clinic, Toronto Western Hospital, Division of Nephrology, University
Health Network and University of Toronto, Toronto, Canada.
This retrospective data analysis was undertaken to examine the biochemical differences between renal stone formers with normocalcemic hyperparathyroidism (NHPT) and those with normal parathyroid hormone (PTH) levels. Our goal was to ascertain whether 25-hydroxyvitamin D (25(OH)D) status related to PTH levels in this patient cohort. Our findings among 74 patients with NHPT indicate that stone formers with NHPT had significantly lower 25(OH)D levels compared to 192 controls (p = 0.0001) and that 25(OH)D is positively correlated with 1,25-dihydroxyvitamin D values (R = 0.736, p = 0.015). Sequential measurements (after 3 - 5 years), among 11 patients with NHPT who did not receive vitamin D (VitD) preparations, showed a significant increase in urinary calcium (3.43 ± 1.96 vs. 5.72 ± 3.95, p = 0.0426) without a significant change in PTH levels. VitD supplementation, to 3 patients resulted in significant PTH decrease (11.8 ± 1.8 vs. 9.8 ± 1.3, p = 0.003). Prospective studies are needed to confirm the role of vitamin
supplementation in renal stone formers with NHPT.

Clin J Am Soc Nephrol. 2012 May;7(5):829-34.
Effect of vitamin D repletion on urinary calcium excretion among kidney stone formers.
Leaf DE(1), Korets R, Taylor EN, Tang J, Asplin JR, Goldfarb DS, Gupta M, Curhan GC.
(1)Department of Medicine, Columbia University, New York, New York, USA.
BACKGROUND AND OBJECTIVES: Despite the important role of vitamin D in maintaining bone health, many clinicians are reluctant to treat vitamin D deficiency in kidney stone formers because of the theoretical risk of increasing urinary
calcium excretion. This study examined the effect of vitamin D repletion on
urinary calcium excretion among stone formers.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Participants (n=29)
were recruited from urology clinics affiliated with New York Presbyterian Hospital. Enrollment criteria included a history of nephrolithiasis, urinary calcium excretion between 150 and 400 mg/d, and a serum 25-hydroxyvitamin D level <30 ng/ml. Participants were given oral ergocalciferol (50,000 IU/wk) for 8 weeks. Serum and 24-hour
urine tests were repeated after 8 weeks.
RESULTS: Levels of 25-hydroxyvitamin D increased significantly after vitamin D repletion (17±6 and 35±10 ng/ml, P<0.001), but mean 24-hour urinary calcium excretion did not change (257±54 and 255±88 mg/d at baseline and follow-up, respectively, P=0.91). However, 11 participants had an increase in urinary calcium excretion ≥20 mg/d; these participants also had an increase in urine sodium excretion, likely reflecting dietary variability. No participant experienced adverse effects from vitamin D, including hypercalcemia.
CONCLUSIONS: Among stone formers with vitamin D deficiency, a limited course of vitamin D repletion does not seem to increase mean urinary calcium excretion, although a subset of individuals may have an increase. These data suggest that vitamin D therapy, if indicated, should not be withheld solely on the basis of stone disease, but 24-hour urinary calcium excretion should be monitored after repletion.

I had my D tested this summer and it was 41. I’ve been taking about 1000-2000 ius since this started over last few days. I don’t know how fast it could drop from that point on, but I live in Chicago and haven’t seen sun in months..

Frustrating as hell. I’m going to try and reduce salt, only thing I’ve got at the moment... sigh..

 

[brentipold]

Now that I think about it, could low D cause this? Due to its ability to increase calcium absorption?

 

[Giraffe]

Calcium intake and urinary stone disease

This review article discusses whether dietary calcium or calcium supplementation have impact on stone formation.

They conclude that "dietary calcium intake is a protective factor against stone formation" while "dietary calcium restriction [...] may lead to increased stone formation potentially through increased oxalate absorption, and may cause bone demineralization."

"When calcium and oxalate are consumed at the same meal, a calcium oxalate subsequent urinary excretion of free oxalate (36,43)." If calcium supplementation is medically necessary, they advise to take the calcium supplements with meals.

..........

Effects of magnesium hydroxide in renal stone disease.

From the abstract:

Magnesium is a known inhibitor of the formation of calcium oxalate crystals in the urine and was proposed for prophylactic treatment in renal stone disease as early as the 17th and 18th centuries. We have treated 55 patients with recurrent renal calcium stone disease without signs of magnesium deficiency [...] for up to four years with 500 mg Mg2+, in the form of Mg(OH)2, daily.

The mean stone episode rate decreased from 0.8 to 0.08 stones/year on treatment and 85% of the patients remained free of recurrence during follow-up, whereas 59% of the patients in the control group continued their stone formation. Side effects were few. Magnesium treatment in renal calcium stone disease is effective with few side effects.

..........

Changes in urinary stone risk factors in hypocitraturic calcium oxalate stone formers treated with dietary sodium supplementation.

This study contradicts the usual recommendation to limit salt intake.

From the abstract:

Dietary sodium supplementation resulted in an increased voided urine volume and decreased the relative risk supersaturation ratio for calcium oxalate stones in patients with a history of hypocitraturic calcium oxalate nephrolithiasis. [...] Sodium restriction may be inappropriate in patients with hypocitraturia and recurrent urinary stones. Sodium supplementation may be beneficial in these patients because it results in voluntary increased fluid intake.

..........

While the articles and studies above discuss calcium oxalate stones, the following one is about uric acid stones:

Uric Acid Nephrolithiasis: Recent Progress and Future Directions

I was particularly looking for information about the use of baking soda.

The usual adult dose of sodium bicarbonate is 650 to 1000 mg 3 to 4 times daily. Commercial baking soda is a source of sodium bicarbonate, and the usual adult dose is 1 to 2 teaspoons 3 to 4 times daily.79

......

WARNING: Do not overdo with alkalizing substances... milk-alkali syndrome