Kidney Stones AGAIN!!!!!!!!

Once again I have kidney stones....So I had to go to the ER at Glens Falls this morning and come to find out they are not stuck THANK GOD, BUT I have many in my kidney so I will have to pas them!  I am so freaked out about this.  I have had two surgeries to remove them B4 cause they always get stuck and won't come out....So I have never had to physically pass them........I am so very scared to feel that pain........I guess I should be glad that I do not need another surgery BUT I really do not look forward to passing the little B@#$!@DS!!!!!   I guess I am prone to getting them and taking all the calcium that I do everyday doesn't help.  So I am damed if I do and damed if I don't  So if anyone has any input on what I should do or what it is going to feel like please send me a message back so I know what I am in for.    Thanks Bridgit

Have you been to a urologist? I have had to pass ONE small stone, the pain was unbelievable. I wouldn't wish that pain on my worst enemy. How did you know you had another stone that sent you to the ER, if you didn't have pain? Just curious. I also am prone to stones, and have had 8 lithotripsies over 10 years. I was never asked to just pass them, unless they were microscopic. Blast them away is the answer, even if they aren't stuck.

UHMMMM I did have pain that is why I went to the ER........I have been to ER twice in 5 months for stones.  i know have tp pass these one.  The 2 I had in march ere stuck in my ututer and I had to have sugery to remove.  The dr thinks that I can pass these ones.  I hope so.  Yes i do have a urologist.  1 in glens falls and a specialist in Alabny who did my bladder sugery in April 2007.  So yes I called the Urolgist in GF Tuesday B4 going to ER.  The nurse there said to go to ER.  I am prone to them too.  yes the pain is awlful and I won't ever wish them on anyone!!!!!!!!!!!!!!!!!!!

Hi! i too am one of the fortunate who has had the joy of kidney stones. WOW THEY SUCK!!!!! I had to pass one a few years ago because it was a week before Christmas and my sons birthday and i re fussed to go to the hospital. Finally Christmas Eve it was over. I have to be honest although yes it sucks i cant say the pain was any worse then the pain i was in just from the stupid thing. If the doctor didn't have me straining all my pee i might not have even realized. So dotn freak out just try to relax it doesn't get any worse then the pain you are in now. 
I hope this helps

Thanks that is good news to hear.  I think that I can handle what i am now cause of pain meds BUT it if gets any worse i will be back at ER.  OMG it is awful.  So thanks again XXOO

oh and im sure you know this but  the one thing that they told me would help and i did it is DRINK WATER drink like you have never drank before. Envision yourself as a camel and GO

Yes I hear ya....I am drinking so much I feel like I am floating LOL.   I went to the Urologist today and I have 2 in my left kidney and 2 in my right....Great I thought.  He said that they are small enough to pass so he thinks....I hope so...But my history they never have B4....But I trust this dr and he really in nice so I hope he is right.   I do NOT want to have another sugery!!!!!  Thanks for everyone who has written my back..  I appreciate all the input  XXOO    I just wish they would leave my body already.....I feel so sick of the pain.....I wouldn't wish this on my worst enemy LOL 

Bridgit:
Hello, I apologize for the dealy, I have not been as responsive to email and the internet lately. (You know you can call me anytime!)

Wow, it sounds as if things are really a challenge right now! May I ask what TYPE of calcium you are taking?
http://bariatrictimes.com/2007/09/10/urinary-calculi-and-bariatric-surgery/
Urinary Calculi and Bariatric Surgery

September 2007

by Carolyn F. Langford, DO; Verena Mueller; and Gamal M. Ghoniem, MD, FACS

All from Cleveland Clinic Florida


Introduction

Urolithiasis is a common disease, with a prevalence of 3 to 5 percent in the US. It causes considerable morbidity, occasional mortality, and costs over $1 billion per year for hospital treatment of stones alone and up to $2 billion when including costs associated with lost employment.[1] Patients who have undergone bariatric surgery have an increased incidence of stone formation. Older techniques such as jejunal ileal bypass (JIB) have reported rates of renal oxalate calculi ranging from 4 to 30 percent.[2,10,12]

Modern procedures, such as laparoscopic Roux-en-Y gastric bypass (RYGB) and laparoscopic adjustable gastric banding (LAGB), are suspected to have lower rates of stone formation due to decreased malabsorptive consequences. Studies regarding the newer procedures and urinary calculi are limited; therefore, much of the information must be extrapolated from procedures like the JIB. In order to understand the relationship of stone formation to weight reduction surgery, it is first necessary to understand how stones are formed in other groups, such as obese and non-obese patients, as well as those who have undergone non-surgical weight loss.

THEORIES OF CALCULI FORMATION IN NON-OBESE PATIENTS

Generally speaking, urinary calculi are formed due to excess urinary concentration of stone-forming substances (calcium, oxalate, urate, cystine, phosphate), a decreased concentration of inhibitory substances (citrate, magnesium, certain urinary proteins), and/or super concentrated urine.[3] However, the exact etiologic cascade of events leading to urolithiasis is unknown.

Hypotheses ranging from oxalate-induced renal injury to insufficient urinary inhibitors of calculogenesis, to nidus formation with epitaxy, have been proposed.[4] Crystal formation and growth are common events in the urinary tract of humans. Urine in most humans is saturated with various breakdown products and substances (calcium, oxalate, urate, cystine, phosphate) that can form stones if the upper limit of saturation for a substance is surpassed.[5]

Urinary calculi are comprised of a large variety and combination of different substances. Calcium oxalate and calcium phosphate make up the most common type (75%) of urinary calculi. The next most prevalent types of urinary calculi are struvite or infection stones (15%), uric acid (5-10%), cystine (1%), or some combination of these substances.[6]

Various medical illnesses, such as hyperparathyroidism, renal tubular acidosis, malabsorptive bowel diseases, metabolic disturbances in oxalate, and purine metabolism, may cause stone formation in non-obese patients. Obese patients who have undergone weight loss surgery and subsequently developed urinary calculi should also be evaluated for these illnesses, as their propensity for stone formation may have been a preexisting condition. The individual mechanisms of stone formation for each of these conditions are beyond the scope of this article, but malabsorption and enteric hyperoxaluria are key to stone formation in surgical weight loss.

Enteric hyperoxaluria may occur from certain malabsorptive bowel diseases and cause calcium oxalate stone formation. Chronic diarrheal states, such as Crohn's disease, alter oxalate metabolism. Malabsorption leads to increased intraluminal fat and bile. Intraluminal calcium readily binds to fat, resulting in a saponification process. Urinary calcium levels are usually low (<100mg/24hr), and intraluminal gut calcium that normally would have bound to oxalate is decreased. The unbound oxalate is readily absorbed by a diffusion mechanism that is unaffected by the usual metabolic inhibitors of energy-dependant pumps. Bile salts may increase in oxalate absorption, and subsequent urinary excretion dramatically increases the formation product of calcium-oxalate. This increases the potential for heterogeneous nucleation and crystal growth in the metastable environment. Interestingly, oral calcium treatment is effective and binds to the intraluminal oxalate, limiting its absorption.[6]

THEORIES OF CALCULI FORMATION IN OBESE PATIENTS

Obesity alone has been shown to put men and women at increased risk for kidney stone formation. In a study of three large observational databases of more than 240,000 men and women, obese men (BMI>30) had a relative risk for stone formation of 1.33 compared to men who are not obese. Obese women were found to have a relative risk of up to 2.09.[7]

Obesity, as a result of dietary indiscretion, probable purine gluttony, and possible type 2 diabetes, appears to have a significant role in recurrent stone formation.[8] Individuals with type 2 diabetes mellitus have insulin resistance affecting ammonia synthesis and lowering urinary pH. Dietary intake may have a significant influence on stone formation. Purine and oxalate intake are well known to increase stone formation and may be ingested in excess in obese patients. Urine volume and concentration is varied in obese patients, and high concentration urine may contribute to stone formation.

Recent studies have also shown obesity to be associated with unique changes in serum and urinary excretion of calcium, phosphate, oxalate, uric acid, cystine, and low urinary pH.[9] It has also been demonstrated that stone recurrence among obese stone formers was significantly higher than in non-obese stone formers.[10] In a small study of 83 obese patients, the most common presenting metabolic abnormalities included hypercalciuria (59%), low urinary volume (58%), and hypocitraturia (54%). This was significantly higher than nonobese nonstone formers and suggested a positive correlation between hypercalciuria, hyperuricosuria, and obesity severity.[3]

An elevated BMI may also present an independent risk factor in IgA nephropathy for progression of vascular, tubular and interstitial lesions.[11] It is known that renal tubular acidosis is associated with stone formation in both obese and non-obese stone formers.

THEORIES OF CALCULI FORMATION IN WEIGHT LOSS WITHOUT SURGERY

Little is documented regarding the impact of rapid or medical weight loss on stone formation. The metabolic consequences are dependant upon the method of weight loss as well as dietary intake during weight loss. High protein diets such as the Atkins diet have been associated with excess purine intake and at times gluttony, which can predispose patients to uric acid stone formation. This diet also can cause ketoacidosis, which lowers urinary pH increasing the possibility of stone formation. In theory, any diet or medication that causes drastic changes in metabolism may create a situation conducive to stone formation.

THEORIES OF CALCULI FORMATION IN BYPASS PATIENTS

It has estimated that the incidence of urinary calculi formation after intestinal bypass surgery such as JIB is 4 to 30 percent.[10,11] On long-term analysis, the interval between JIB and stone formation has a median of four years with a range from one month to nine years. It is interesting to note that the male to female ratio of stone formation is also affected by JIB. In the general population, stone formers have a higher male to female ratio, which reverses after JIB.[13]

Histologic changes have been noted within the kidney of calcium oxalate stone formers. Randall's plaques are interstitial crystal deposition at or near the papillary tip of the kidney and are seen nearly twice as mu*****alcium oxalate stone formers as in normal kidneys. In a small study evaluating the histology of post-gastric bypass kidneys there were no Randall's plaques noted. Instead these patients had small nodular deposits that appeared to project off the urothelium near the ducts of Bellini.[3] This may indicate a different mechanism of stone formation in these post bypass patients.

One study compares urinary oxalate excretion in patients that have undergone modern weight loss surgery, such as gastric banding or bypass, stone formers who have not had gastric surgery, normal subjects, and those who have had JIB. Patients treated with modern bariatric surgery had oxalate excretions that were 2 to 3 times higher than stone formers and normal subjects of the same gender, and were not significantly different from those found in patients who had undergone JIB. In this study, the mean time from surgery to stone formation was 3.6 years but has been reported from 4 to 42 months.[14,15]

In light of the fact that JIB is no longer performed as the standard of care for weight loss, much can be learned from the effects this procedure has had on these patients' renal function. It has been mentioned that JIB increases urinary oxalate excretion and increases stone formation in these patients. Renal oxalate calculi develop at a rate of between 4 to 30 percent in patients who have undergone JIB. A study by Streem, et al., shows that JIB reversal can normalize 24-hour urinary oxalate levels. Interestingly, it did not normalize urinary citrate, and this may have contributed to recurrent stone formation in these patients until the citrate levels were increased.[15]

Another less understood theory of post-bypass stone formation suggests glycine may contribute to this process. Glycine is an important oxalate precursor and has been shown to increase after bypass surgery. This has been theorized to lead to an increase in endogenous oxalate production and subsequent stone production in these patients.[16]

The literature on malabsorptive procedures clearly shows that both weight loss and adverse metabolic consequences vary with the length of the alimentary and common intestinal limbs.[17] This would suggest that less malabsorptive procedures would have less metabolic consequences and therefore less stone formation.

Nelson, et al., looked at the Roux-en-Y gastric bypass in 1,436 patients at the Mayo clinic. He found that 23 patients (14 men and 9 women) developed enteric hyperoxaluria. In these patients, enteric hyperoxaluria was defined by calcium oxalate nephrolithiasis in 21 patients or oxalate nephropathy leading to renal failure in two patients. Although a small number of patients developed renal failure, preoperative evaluation for enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy is an important consideration when performing gastric bypass surgery.[18]

In another paper by Nelson, et al., the malabsorptive consequences of the "very, very long limb Roux-en-Y" gastric bypass for super obesity was evaluated. This bypass has a much longer Roux limb of 300 to 500cm and a 100cm common channel of distal ileum. They looked at 257 patients with a BMI of greater than 50Kg/m2. One hundred eight-eight patients returned questionnaires with a mean follow-up of 43 months. All patients lost and maintained 35 to 50 percent of excess body weight. Sixteen percent (31) of these patients formed nephrolithiasis postoperatively. Of these patients, 21 had a prior history of urinary calculi, most commonly calcium oxalate. Oxalate nephropathy occurred in two patients, resulting in irreversible renal failure. The exact mechanism of stone formation is unknown but assumed to be similar to other malabsorptive procedures.[19]

See Table 1.

CONCLUSION

It takes a number of complex factors in order to form urinary calculi. It is also known that malabsorptive procedures, such as JIB, significantly increase the risk of stone formation. It is apparent that more research must be done to determine what effect the modern, less malabsorptive techniques of surgical weight loss have on urinary calculi formation. It will also be important to determine the metabolic effects of rapid as well as non-surgical weight loss on calculi formation. It should be considered that obesity itself increases the chance of stone formation and that most patients undergoing weight loss surgery are at a peak of stone formation in the third to fifth decades of life.

References
1. Shuster J, Schaeffer RL. Economic impact of kidney stones in white male adults. Urology 1984;24:327.
2. Taylor EN, Stampfer MJ, and Curran GC. Obesity, weight gain, and the risk of kidney stones. JAMA 2005;293:455.
3. Evan AP, Coe FL, Lingeman JE, Worcestrer E. Urol Res 2005;33:383-9.
4. Khan SR. Pathogenesis of oxalate urolithiasis: lessons from experimental studies with rats. Am J Kidney Dis 1991;17:398.
5. Randall A. The origin and growth of renal calculi. Ann Surg 1937;105:1009.
6. Stoller ML, Bolton DM. Smith's General Urology, Third Edition. McGraw-Hill; New York, 1995;296.
7. Taylor EN, Stampfer MJ, Curhan GC. Obesity, weight gain and the risk of kidney stones. JAMA 2005, 293(4):455-62.
8. Ekeruo WO, Tan YH, Young M, et al. Metabolic risk factors and the impact of medical therapy on the management of Nephrolithiasis in obese patients. J of Urol 2004;172:159-63.
9. Powell C, Yokoyama M, Iwata H, et al. Impact of body weights on urinary electrolytes in urinary stone formers. Urology 2000;55:825.
10. Nishio S, Yokoyana M, Iwata H, et al. Obesity as one of the risk factors for urolithiasis. Nippon Hinyokika Gakkai Zasshi 1998;89:573.
11. Soto FC, Higa-Sansone G, Copley JB, et al. Renal failure, glomerulonephritis and morbid obesity: Improvement after rapid weight loss following laparoscopic gastric bypass. Obes Surg 2005;15,137-40.
12. Drenick EJ, Stanley TM, Border WA, Zawada, et al. Renal damage with intestinal bypass. Ann Intern Med 1978;89:594-9.
13. Annuk M, Backman U, Holmgren K, Vessby B. Urinary calculi and jejunoileal bypass operation: A long-term follow-up. Scand J Urol Nephrol 1998;32(3):177-80.
14. Asplin JR, Coe FL. Hyperoxaluria in kidney stone formers treated with modern bariatric surgery. Urolithiasis/Endourology 2007;177,565-9.
15. Dhar NB, Grundfest S, Jones JS, Streem SB. Jejunoileal bypass reversal: Effect on renal function, metabolic parameters and stone formation. J Urol 2005;174 (5):1844-6.
16. Nordenvall B, Backman L, Larson L, Vessby B. Oxalate metabolism after intestinal bypass operation. Scand J Gastroenterol 1981;16(3):395-9.
17. Lynch RJ, Eisenberg D, Bell RL. Metabolic consequences of bariatric surgery. J Clin Gastroenterology 2006;40:8.
18. Nelson W, Houghton S, Milliner D. Enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy: Potentially serious and unappreciated complications of Roux-en-Y gastric bypass. SOARD 2005;481-5.
19. Nelson W, Fatima J, Houghton S, et al. The malabsorptive very, very long limb Roux-en-Y gastric bypass for super obesity: Results in 257 patients. Surgery 2006: 517-23.

Posted in 2007 September, Surgical Perspective |




http://www.medicalnewstoday.com/printerfriendlynews.php?newsid=56495

Gastric Bypass Surgery May Lead To Increased Kidney Stone Risk
13 Nov 2006

Patients who have undergone gastric bypass surgery for morbid obesity have increased risk factors for the formation of kidney stones, according to a paper being presented at the American Society of Nephrology's 39th Annual Meeting and Scientific Exposition in San Diego.

"Gastric bypass surgery appears to lead to changes in the chemical composition of urine that could favor the formation of kidney stones," comments Dr. Rajiv Kumar of Mayo Clinic College of Medicine in Rochester, Minnesota, one of the study authors. "Based upon this information, we suggest that patients take appropriate measures to reduce the potential for kidney stone formation."

From 21 patients who had undergone gastric bypass surgery 6 or 12 months previously, the researchers obtained urine samples to measure biochemical risk factors for kidney stones. All patients had undergone the "Roux-en-Y" procedure, which is the most common type of gastric bypass surgery. The same risk factors were measured in a group of 20 obese patients who were being evaluated for gastric bypass surgery.

The group who had bypass surgery 12 months previously showed several chemical changes that have been linked to an increased risk of kidney stones. These included a significant increase in the level of oxalate-a chemical that increases kidney stone risk by binding to calcium.

The patients also had reduced urine levels of citrate, which normally plays an important role in dissolving crystals that can lead to kidney stones. The combination of high oxalate and low citrate levels led to an increase in calcium oxalate supersaturation"-a strong risk factor for stones formed by binding of oxalate to calcium.

Patients who underwent gastric bypass surgery 6 months previously did not yet have significant changes in oxalate or citrate levels. Levels of other chemicals that can contribute to kidney stones-such as uric acid and potassium-were unaltered from before to after surgery. There were no changes in standard kidney function indicators after gastric bypass.

As the problem of obesity continues to increase in the United States and around the world, more patients are undergoing gastric bypass operations. "Although these procedures have several possible complications, an increased incidence of kidney stones was not believed to be one of them," says Dr. Kumar.

Previous, more extensive gastric bypass operations did lead to increased urinary oxalate levels, and thus to an increased risk of kidney stones. The new study is the first to specifically examine the risk of similar abnormalities following the "Roux-en-Y" procedure, which has become the standard approach to gastric bypass.

"Our results suggest that individuals undergoing such procedures are potentially at increased risk for developing kidney stones," Dr. Kumar concludes. Gastric bypass patients may want to talk to their doctors about dietary changes and other steps they can take to reduce their risk of kidney stones, the researchers suggest.

The study abstract, "Increased Lithogenic Risk Factors Following Roux-en-Y Gastric Bypass Surgery for Morbid Obesity" (TH-F-DS871) will be presented as part of a Poster Discussion Session on the topic of "Nephrolithiasis" on Thursday, November 16 at 10:00 am in Room 3 of the San Diego Convention Center and also discussed during a News Briefing on the topic of "Obesity and the Kidney" on Friday, November 17 beginning at 12:15 pm in Room 12 of the San Diego Convention Center by a co-author, Dr. John C. Lieske.

The ASN is a not-for-profit organization of 9,500 physicians and scientists dedicated to the study of nephrology and committed to providing a forum for the promulgation of information regarding the latest research and clinical findings on kidney diseases. ASN's Renal Week 2006, the largest nephrology meeting of its kind, will provide a forum for 10,000 nephrologists, to discuss the latest findings in renal research and engage in educational sessions relating advances in the care of patients with kidney and related disorders from November 14-19 at the San Diego Convention Center in San Diego, CA.

American Society of Nephrology (ASN)
1725 I St., NW, Ste 510
Washington, DC 20006
United States
http://www.asn-online.org/
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Article URL: http://www.medicalnewstoday.com/articles/56495.php

Main News Category: Urology / Nephrology

Also Appears In: Obesity / Weight Loss / Fitness, Cosmetic Medicine / Plastic Surgery,


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Hey girly...I am taking Calcium Citrate plus d 315 mg twice a day...I hope that is the right one......I guess per the uroligist I am prone to them and these ones he thinks I can pass.  I am still very wearly of apssing any..  I HAVE NEVER passed any I have had.  I was always knocked out and when I wake up all gone.  So I am freaking out everytime I go to the bathroom think am I going to pass one now?????  So if you you know that I am taking the wronge kind let me know.......Thanks and I did not want to bother ya...I know you are always there for me and any of us that need ya BUT I really wasn't up to chatting .....I feel miserable and I keep working even though I want to stay home....I need the $ after being out of work so much B4 with all the other sugeries.....Once again thanks I miss ya and think of you often.  I plan on being at meeting on Monday if i feel OK to go.   XXOO Bridgit

Bridgit Citrate is the right kind we need about 1,500mg minimum a day for most folks (FDA for normies is 1,000-1,200mg) we malabsorb..So do you take TWo of the 315mg tabs twice a day or one? if one you arent probably getting enough but then again with your issues best to check with clinical nutrition MD! Be well hope to see you 9/1 at group!