Urinary Calculi and Bariatric Surgery

| September 10, 2007

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

All from Cleveland Clinic Florida


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.


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]


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.


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.


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 much in calcium 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.


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.

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