Calcium Malabsorption->>Kidney Stones->>Procedures

Spiky Bugger

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Had the first of 1-3 procedures to get rid of some stones. Doctor is pleased as punch at what a good job he did with the ESWL. I'm still too sore to be pleased. In a week, I go for stent removal and ?imaging? To see how much more has to be done.

I survived. Or, I'm in the process of attempting to survive.

Not sure if I'm yet at the place where we can call me "pleased."
 
Query: why is this post titled "Calcium Malabsorption"? I thought is was more of an issue of oxalate (assuming that your stones are calcium oxalate) OVER absorption (from the gut, because you aren't taking enough calcium to get the oxalates bound to calcium in your gut BEFORE it is absorbed, so you can just poop it out without ever absorbing the oxalates at all), or overproduction of oxalates IN your body, which your body then tries to excrete through the kidneys, where the oxalates bind to serum calcium and unfortunately form stones, and thus suggesting that this is more of a problem of INSUFFICIENT citric acid IN your kidneys.

Can you (or someone else who actually has this problem, and thus pays careful attention) please explain?
 
Had the first of 1-3 procedures to get rid of some stones. Doctor is pleased as punch at what a good job he did with the ESWL. I'm still too sore to be pleased. In a week, I go for stent removal and ?imaging? To see how much more has to be done.

I survived. Or, I'm in the process of attempting to survive.

Not sure if I'm yet at the place where we can call me "pleased."
I hope you are recovering and get through this quickly. You are tough and act like it is no big deal but we know it isn'darling so hang in there darling. I Feel for you
 
Query: why is this post titled "Calcium Malabsorption"? I thought is was more of an issue of oxalate (assuming that your stones are calcium oxalate) OVER absorption (from the gut, because you aren't taking enough calcium to get the oxalates bound to calcium in your gut BEFORE it is absorbed, so you can just poop it out without ever absorbing the oxalates at all), or overproduction of oxalates IN your body, which your body then tries to excrete through the kidneys, where the oxalates bind to serum calcium and unfortunately form stones, and thus suggesting that this is more of a problem of INSUFFICIENT citric acid IN your kidneys.

Can you (or someone else who actually has this problem, and thus pays careful attention) please explain?


Do I have it back-asswards again?

Uhm...because post-op Calcium Malabsorption is where it starts?

You are technically correct, of course. (As usual.) But, so far, every uro I've been to--a lot, because we move a lot--says it starts, for RnY patients and us, with lowered absorption of calcium, giving (what could or could not be a normal amount of) oxalates an insufficient quantity of calcium to bond with. A highly increased amount of citrate is needed to make it all work correctly. (And we are all told to supplement calcium and I was never told to supplement citrate as part of my post-DS routine.)

So...my understanding is that we ARE citrate deficient, but primarily because post-op we need a lot more citrate due to calcium malabsorption. (I think.)

It can be fixed, for many, with four ounces of pure lemon juice every day. (Of course, all citrus fruits are on the Intertitial Cystitis no-no list.)

Is the title misleading?
 
Last edited:
I was advised to take calcium citrate with the first bite of food. The citrate is important in preventing kidney stones. Small doses are available and the rest of your calcium requirements can be adjusted.
 
I was advised to take calcium citrate with the first bite of food. The citrate is important in preventing kidney stones. Small doses are available and the rest of your calcium requirements can be adjusted.


Me, too.

But...And this may be why I'm confused...

Years ago, I called manufacturers to try to learn how much citrate I was ingesting. I was told by the manufacturers of Calcium Citrate and Magnesium Citrate, that isn't actual measurable citrate, as in what we need for stones. Rather it refers to the way the product is formulated, which is why citrate, per se, is not listed as a measured ingredient. As in, in calcium citratae and calcium carbonate, you are getting calcium...not citrate, not carbonate. Just calcium.

For some reason, potassium citrate is the formulation of citrate (not potassium?) we need for stones. However...those labels ALSO show "potassium citrate," not just "citrate." Yet that's the prescribed version...the one that changes the pH of the kidney.

Given what I was told, I'd assume that I'm actually potassium deficient, since what fixes this problem is potassium citrate.

Either way, I'm drinking lemon juice right now.
 
I took a stroll through PubMed ....

http://www.ncbi.nlm.nih.gov/pubmed/26439475
Cochrane Database Syst Rev. 2015 Oct 6;10:CD010057. doi: 10.1002/14651858.CD010057.pub2.
Citrate salts for preventing and treating calcium containing kidney stones in adults.
Phillips R1, Hanchanale VS, Myatt A, Somani B, Nabi G, Biyani CS.
Author information

Abstract
BACKGROUND:
Kidney stones affect people worldwide and have a high rate of recurrence even with treatment. Recurrences are particularly prevalent in people with low urinary citrate levels. These people have a higher incidence of calcium phosphate and calcium oxalate stones. Oral citrate therapy increases the urinary citrate levels, which in turn binds with calcium and inhibits the crystallisation thus reduces stone formation. Despite the widespread use of oral citrate therapy for prevention and treatment of calcium oxalate stones, the evidence to support its clinical efficacy remains uncertain.

OBJECTIVES:
The objective of this review was to determine the efficacy and adverse events associated with citrate salts for the treatment and prevention of calcium containing kidney stones.

SEARCH METHODS:
We searched the Cochrane Kidney and Transplant Specialised Register to 29 July 2015 through contact with the Trials' Search Co-ordinator using search terms relevant to this review.

SELECTION CRITERIA:
We included randomised controlled trials (RCTs) that assessed the efficacy and adverse events associated with citrate salts for the treatment and prevention of calcium containing kidney stones in adults treated for a minimum of six months.

DATA COLLECTION AND ANALYSIS:
Two authors assessed studies for inclusion in this review. Data were extracted according to predetermined criteria. Summary estimates of effect were obtained using a random-effects model, and results were expressed as risk ratios (RR) and their 95% confidence intervals (CI) for dichotomous outcomes, and mean difference (MD) and 95% CI for continuous outcomes.

MAIN RESULTS:
We included seven studies that included a total of 477 participants, most of whom had oxalate stones. Of these, three studies (247 participants) compared potassium citrate with placebo or no intervention; three (166 participants) compared potassium-sodium citrate with no intervention; and one (64 participants) compared potassium-magnesium citrate with placebo. Overall, quality of the reporting of the included studies was considered moderate to poor, and there was a high risk of attrition bias in two studies.Compared with placebo or no intervention,citrate therapy significantly reduced the stone size (4 studies, 160 participants: RR 2.35, 95% CI 1.36 to 4.05). New stone formation was significantly lower with citrate therapy compared to control (7 studies, 324 participants: RR 0.26, 95% CI 0.10 to 0.68). The beneficial effect on stone size stability was also evident (4 studies, 160 participants: RR 1.97, 95% CI 1.19 to 3.26). Adverse events were reported in four studies, with the main side effects being upper gastrointestinal disturbance and one patient reported a rash. There were more gastrointestinal adverse events in the citrate group; however this was not significant (4 studies, 271 participants: RR 2.55, 95% CI 0.71 to 9.16). There were significantly more dropouts due to adverse events with citrate therapy compared to control (4 studies, 271 participants: RR 4.45, 95% CI 1.28 to 15.50). The need for retreatment was significantly less with citrate therapy compared to control (2 studies, 157 participants: RR 0.22, 95% CI 0.06 to 0.89).

AUTHORS' CONCLUSIONS:
Citrate salts prevent new stone formation and reduce further stone growth in patients with residual stones that predominantly contain oxalate. The quality of reported literature remains moderate to poor; hence a well-designed statistically powered multi-centre RCT is needed in order to answer relevant questions concerning the efficacy of citrate salts.


http://www.pagepressjournals.org/index.php/aiua/article/view/aiua.2015.2.105/4756
Arch Ital Urol Androl. 2015 Jul 7;87(2):105-20. doi: 10.4081/aiua.2015.2.105.
Dietary treatment of urinary risk factors for renal stone formation. A review of CLU Working Group.
Prezioso D1, Strazzullo P, Lotti T, Bianchi G, Borghi L, Caione P, Carini M, Caudarella R, Gambaro G, Gelosa M, Guttilla A, Illiano E, Martino M, Meschi T, Messa P,Miano R, Napodano G, Nouvenne A, Rendina D, Rocco F, Rosa M, Sanseverino R, Salerno A, Spatafora S, Tasca A, Ticinesi A, Travaglini F, Trinchieri A,Vespasiani G, Zattoni F; CLU Working Group.
Author information

Abstract
OBJECTIVE:
Diet interventions may reduce the risk of urinary stone formation and its recurrence, but there is no conclusive consensus in the literature regarding the effectiveness of dietary interventions and recommendations about specific diets for patients with urinary calculi. The aim of this study was to review the studies reporting the effects of different dietary interventions for the modification of urinary risk factors in patients with urinary stone disease.

MATERIALS AND METHODS:
A systematic search of the Pubmed database literature up to July 1, 2014 for studies on dietary treatment of urinary risk factors for urinary stone formation was conducted according to a methodology developed a priori. Studies were screened by titles and abstracts for eligibility. Data were extracted using a standardized form and the quality of evidence was assessed.

RESULTS:
Evidence from the selected studies were used to form evidence-based guideline statements. In the absence of sufficient evidence, additional statements were developed as expert opinions.

CONCLUSIONS:
General measures: Each patient with nephrolithiasis should undertake appropriate evaluation according to the knowledge of the calculus composition. Regardless of the underlying cause of the stone disease, a mainstay of conservative management is the forced increase in fluid intake to achieve a daily urine output of 2 liters. HYPERCALCIURIA: Dietary calcium restriction is not recommended for stone formers with nephrolithiasis. Diets with a calcium content ≥ 1 g/day (and low protein-low sodium) could be protective against the risk of stone formation in hypercalciuric stone forming adults. Moderate dietary salt restriction is useful in limiting urinary calcium excretion and thus may be helpful for primary and secondary prevention of nephrolithiasis. A low-normal protein intake decrease calciuria and could be useful in stone prevention and preservation of bone mass. Omega-3 fatty acids and bran of different origin decreases calciuria, but their impact on the urinary stone risk profile is uncertain. Sports beverage do not affect the urinary stone risk profile. HYPEROXALURIA: A diet low in oxalate and/or a calcium intake normal to high (800-1200 mg/day for adults) reduce the urinary excretion of oxalate, conversely a diet rich in oxalates and/or a diet low in calcium increase urinary oxalate. A restriction in protein intake may reduce the urinary excretion of oxalate although a vegetarian diet may lead to an increase in urinary oxalate. Adding bran to a diet low in oxalate cancels its effect of reducing urinary oxalate. Conversely, the addition of supplements of fruit and vegetables to a mixed diet does not involve an increased excretion of oxalate in the urine. The intake of pyridoxine reduces the excretion of oxalate. HYPERURICOSURIA: In patients with renal calcium stones the decrease of the urinary excretion of uric acid after restriction of dietary protein and purine is suggested although not clearly demonstrated. HYPOCITRATURIA: The administration of alkaline-citrates salts is recommended for the medical treatment of renal stone-formers with hypocitraturia, although compliance to this treatment is limited by gastrointestinal side effects and costs. Increased intake of fruit and vegetables (excluding those with high oxalate content) increases citrate excretion and involves a significant protection against the risk of stone formation. Citrus (lemons, oranges, grapefruit, and lime) and non citrus fruits (melon) are natural sources of dietary citrate, and several studies have shown the potential of these fruits and/or their juices in raising urine citrate levels.
 
I took a stroll through PubMed ....

http://www.ncbi.nlm.nih.gov/pubmed/26439475
Cochrane Database Syst Rev. 2015 Oct 6;10:CD010057. doi: 10.1002/14651858.CD010057.pub2.
Citrate salts for preventing and treating calcium containing kidney stones in adults.
Phillips R1, Hanchanale VS, Myatt A, Somani B, Nabi G, Biyani CS.
Author information

Abstract
BACKGROUND:
Kidney stones affect people worldwide and have a high rate of recurrence even with treatment. Recurrences are particularly prevalent in people with low urinary citrate levels. These people have a higher incidence of calcium phosphate and calcium oxalate stones. Oral citrate therapy increases the urinary citrate levels, which in turn binds with calcium and inhibits the crystallisation thus reduces stone formation. Despite the widespread use of oral citrate therapy for prevention and treatment of calcium oxalate stones, the evidence to support its clinical efficacy remains uncertain.

OBJECTIVES:
The objective of this review was to determine the efficacy and adverse events associated with citrate salts for the treatment and prevention of calcium containing kidney stones.

SEARCH METHODS:
We searched the Cochrane Kidney and Transplant Specialised Register to 29 July 2015 through contact with the Trials' Search Co-ordinator using search terms relevant to this review.

SELECTION CRITERIA:
We included randomised controlled trials (RCTs) that assessed the efficacy and adverse events associated with citrate salts for the treatment and prevention of calcium containing kidney stones in adults treated for a minimum of six months.

DATA COLLECTION AND ANALYSIS:
Two authors assessed studies for inclusion in this review. Data were extracted according to predetermined criteria. Summary estimates of effect were obtained using a random-effects model, and results were expressed as risk ratios (RR) and their 95% confidence intervals (CI) for dichotomous outcomes, and mean difference (MD) and 95% CI for continuous outcomes.

MAIN RESULTS:
We included seven studies that included a total of 477 participants, most of whom had oxalate stones. Of these, three studies (247 participants) compared potassium citrate with placebo or no intervention; three (166 participants) compared potassium-sodium citrate with no intervention; and one (64 participants) compared potassium-magnesium citrate with placebo. Overall, quality of the reporting of the included studies was considered moderate to poor, and there was a high risk of attrition bias in two studies.Compared with placebo or no intervention,citrate therapy significantly reduced the stone size (4 studies, 160 participants: RR 2.35, 95% CI 1.36 to 4.05). New stone formation was significantly lower with citrate therapy compared to control (7 studies, 324 participants: RR 0.26, 95% CI 0.10 to 0.68). The beneficial effect on stone size stability was also evident (4 studies, 160 participants: RR 1.97, 95% CI 1.19 to 3.26). Adverse events were reported in four studies, with the main side effects being upper gastrointestinal disturbance and one patient reported a rash. There were more gastrointestinal adverse events in the citrate group; however this was not significant (4 studies, 271 participants: RR 2.55, 95% CI 0.71 to 9.16). There were significantly more dropouts due to adverse events with citrate therapy compared to control (4 studies, 271 participants: RR 4.45, 95% CI 1.28 to 15.50). The need for retreatment was significantly less with citrate therapy compared to control (2 studies, 157 participants: RR 0.22, 95% CI 0.06 to 0.89).

AUTHORS' CONCLUSIONS:
Citrate salts prevent new stone formation and reduce further stone growth in patients with residual stones that predominantly contain oxalate. The quality of reported literature remains moderate to poor; hence a well-designed statistically powered multi-centre RCT is needed in order to answer relevant questions concerning the efficacy of citrate salts.


http://www.pagepressjournals.org/index.php/aiua/article/view/aiua.2015.2.105/4756
Arch Ital Urol Androl. 2015 Jul 7;87(2):105-20. doi: 10.4081/aiua.2015.2.105.
Dietary treatment of urinary risk factors for renal stone formation. A review of CLU Working Group.
Prezioso D1, Strazzullo P, Lotti T, Bianchi G, Borghi L, Caione P, Carini M, Caudarella R, Gambaro G, Gelosa M, Guttilla A, Illiano E, Martino M, Meschi T, Messa P,Miano R, Napodano G, Nouvenne A, Rendina D, Rocco F, Rosa M, Sanseverino R, Salerno A, Spatafora S, Tasca A, Ticinesi A, Travaglini F, Trinchieri A,Vespasiani G, Zattoni F; CLU Working Group.
Author information

Abstract
OBJECTIVE:
Diet interventions may reduce the risk of urinary stone formation and its recurrence, but there is no conclusive consensus in the literature regarding the effectiveness of dietary interventions and recommendations about specific diets for patients with urinary calculi. The aim of this study was to review the studies reporting the effects of different dietary interventions for the modification of urinary risk factors in patients with urinary stone disease.

MATERIALS AND METHODS:
A systematic search of the Pubmed database literature up to July 1, 2014 for studies on dietary treatment of urinary risk factors for urinary stone formation was conducted according to a methodology developed a priori. Studies were screened by titles and abstracts for eligibility. Data were extracted using a standardized form and the quality of evidence was assessed.

RESULTS:
Evidence from the selected studies were used to form evidence-based guideline statements. In the absence of sufficient evidence, additional statements were developed as expert opinions.

CONCLUSIONS:
General measures: Each patient with nephrolithiasis should undertake appropriate evaluation according to the knowledge of the calculus composition. Regardless of the underlying cause of the stone disease, a mainstay of conservative management is the forced increase in fluid intake to achieve a daily urine output of 2 liters. HYPERCALCIURIA: Dietary calcium restriction is not recommended for stone formers with nephrolithiasis. Diets with a calcium content ≥ 1 g/day (and low protein-low sodium) could be protective against the risk of stone formation in hypercalciuric stone forming adults. Moderate dietary salt restriction is useful in limiting urinary calcium excretion and thus may be helpful for primary and secondary prevention of nephrolithiasis. A low-normal protein intake decrease calciuria and could be useful in stone prevention and preservation of bone mass. Omega-3 fatty acids and bran of different origin decreases calciuria, but their impact on the urinary stone risk profile is uncertain. Sports beverage do not affect the urinary stone risk profile. HYPEROXALURIA: A diet low in oxalate and/or a calcium intake normal to high (800-1200 mg/day for adults) reduce the urinary excretion of oxalate, conversely a diet rich in oxalates and/or a diet low in calcium increase urinary oxalate. A restriction in protein intake may reduce the urinary excretion of oxalate although a vegetarian diet may lead to an increase in urinary oxalate. Adding bran to a diet low in oxalate cancels its effect of reducing urinary oxalate. Conversely, the addition of supplements of fruit and vegetables to a mixed diet does not involve an increased excretion of oxalate in the urine. The intake of pyridoxine reduces the excretion of oxalate. HYPERURICOSURIA: In patients with renal calcium stones the decrease of the urinary excretion of uric acid after restriction of dietary protein and purine is suggested although not clearly demonstrated. HYPOCITRATURIA: The administration of alkaline-citrates salts is recommended for the medical treatment of renal stone-formers with hypocitraturia, although compliance to this treatment is limited by gastrointestinal side effects and costs. Increased intake of fruit and vegetables (excluding those with high oxalate content) increases citrate excretion and involves a significant protection against the risk of stone formation. Citrus (lemons, oranges, grapefruit, and lime) and non citrus fruits (melon) are natural sources of dietary citrate, and several studies have shown the potential of these fruits and/or their juices in raising urine citrate levels.


And the translations?
 
I'm not sure - drink melon juice?
"Citrus (lemons, oranges, grapefruit, and lime) and non citrus fruits (melon) are natural sources of dietary citrate, and several studies have shown the potential of these fruits and/or their juices in raising urine citrate levels."
 
Sue, just wanted to say I hope you get to the place where you are pleased soon. Feel better!
 
Sue, just wanted to say I hope you get to the place where you are pleased soon. Feel better!

Thanks, Hil. My aged uro (he's 42...lol) was REALLY pleased with the stone smashing. It's the first time I had to do it under a general. But he said it made for a more stationary target. Thing is... I'm not peeeing sand. I always pee sand after this procedure. Uro said the stones looked flat as pancakes. So...maybe they went to powder and dissolved? Who knows? He says he smashed them. Maybe I need to do a handstand or something?
 
I'm not sure - drink melon juice?
"Citrus (lemons, oranges, grapefruit, and lime) and non citrus fruits (melon) are natural sources of dietary citrate, and several studies have shown the potential of these fruits and/or their juices in raising urine citrate levels."

Maybe....watermelon is a no-no. But cantaloupe isn't on the list.
 
@Spiky Bugger you're gonna need to pick more carefully the people you talk to one line. You always check up on me and report back to the crew but now it seems like my plethora of health and family issues has worn off on you and you have been going through. I'm gonna need for my rain cloud to stop following and harassing you and the rest of your clan.
 
Why is watermelon a no-no? It's almost all water as it is ...

I have to go check my compendium of forbidden foods. Could be from the "No FODMAPS Diet," or the "Interstitial Cystitis Diet," or the "Low Oxalate Diet," or any one of my diets that are so restrictive that I ignore them all.
 

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