epidemiology and pathophysiology of kidney stones

Dyad 6 guomanman and chenya



Although naturally occurring urolithiasis is rare in animals, spontaneously hypertensive rats are prone to develop kidney stones [1]. In humans, the rst report of an association between hypertension and kidney stones can be traced back to 1761 [2] when Giovan Battista Morgagni described a patient with clinical and anatomical ndings suggestive of long-standing hypertension and the presence of kidney stones. More recently, cross-sectional epidemiological surveys have described an independent association between hypertension and a history of kidney stone disease [3±6]. However, given the retrospective nature of the assessment of urolithiasis, the time sequence of events is unclear, and, in particular, the possibility that hypertension may result from renal damage caused by kidney stones could not be ruled out. Prospective investigations are therefore needed to establish whether hypertension precedes the development of kidney stones and may therefore be considered as a possible cause of this condition.

Madore et al. [6] have recently reported prospective analyses of the Health Professionals Follow-up Study suggesting that prior occurrence of kidney stones increases the risk of subsequent hypertension. We report
the results of a prospective study of middle-aged men without evidence of urolithiasis at the baseline and followed-up for 8 years to establish the incidence of kidney stone disease and its relation to hypertension. The present study assesses both exposure and outcome by direct measurement and verication and is based on the `a priori' hypothesis that hypertension would precede the development of kidney stones. It also provides measures of renal function and other potential confounders.

countries are renal stones [9]. Men were classied as incident cases of kidney stones if, within the period of follow-up, they experienced any of the following: spontaneous passage of one or more stones, X-ray or
echographic evidence of one or more stones in the upper urinary tract, lithotripsy or surgical removal of stones from kidney or ureter. The self-reported occurrence of kidney stones was checked against available
medical records.

Research appraisal

This research through a prospective cohort study to examine whether hypertension predicts the incidence of kidney stone disease in men or not. Based on this study have five hundred and three male workers, aged 21 to 68 years, with no evidence of kidney stone disease at baseline. To endorse these preventive strategies, however, we need to confirm the cost-effectiveness of such early diagnosis and the beneficial effect of sodium restriction not only on the reduction of urinary calcium excretion but on the overall reduction of the incidence of kidney stones or their recurrence rate using a randomized controlled clinical trial at the Olivetti factory in Southern Italy. During research time we use sphygmomanometer, Anthropometer, Weight instrument measure our participants, the outcome of measures are Anthropometry, blood pressure, biochemistry and history of kidney stone disease were evaluated at the baseline examination. Occurrence of kidney stone disease was evaluated again in recent year. Hypertension was defined as systolic blood pressure > 160 or diastolic blood pressure, > 95 mmHg or both, or being on drug therapy for hypertension. Occurrence of kidney stone disease was defined as radiological or echo graphic evidence of calculi or documented passage of one or more stones.

Research results

Hypertensive men had a greater risk of developing kidney stones than normotensive ones (RR 1.96; 95% confidence interval 1.16±3.32). The risk was unaffected by the exclusion of treated hypertensive’s (2.01; 1.13±3.59) and after adjustment for age (1.89; 1.12±3.18), body weight (1.78; 1.05±3.00) or height (2.00; 1.19±3.38).

Reviewer’s conclusion

Hypertension in middle-aged men is a significant predictor of kidney stone disease rather than a consequence of renal damage caused by the kidney stones.

Epidemiology
In humans, the first report of an association between hypertension and kidney stones can be traced back to 1761 when Giovan Battista Morgagni described a patient with clinical and anatomical ndings suggestive of long-standing hypertension and the presence of kidney stones. More recently, cross-sectional epidemiological surveys have described an independent association between hypertension and a history of kidney stone disease.

Within the United States, about 10–15% of adults will be diagnosed with a kidney stone, and the total cost for treating this condition was US$2 billion in 2003. The incidence rate increases to 20–25% in the Middle East, because of increased risk of dehydration in hot climates. (The typical Arabian diet is also 50% lower in calcium and 250% higher in oxalates compared to Western diets, increasing the net risk.)Recurrence rates are estimated at about 10% per year, totaling 50% over a 5–10 year period and 75% over 20 years. Men are affected approximately 4 times more often than women. Recent evidence has shown an increase in pediatric cases.

Based on this study, the incidence of kidney stones is increasing worldwide [29±33]. It is estimated that 12±15% of the population will develop kidney stones over their life-time [29,30]. Moreover, stone-formers are at a much greater risk of recurrence (as high as 80%) [29]. Although kidney stone disease is seldom fatal, it does lead to substantial morbidity from pain, urinary tract infections and obstructive uropathy, with a considerable economic burden on healthcare provision for an effective treatment (mostly removal, fragmentation or extracorporeal shockwave lithotripsy) [34]. Primary prevention and prevention of recurrence would therefore be an important aspect of the population approach to the overall control of urolithiasis. Despite early reports of cross-sectional associations between hypertension and kidney stones [3±5], very little attention has so far been paid to consideration of hypertension as a risk factor (or a marker of risk) for urolithiasis [28,35], nor has a reduction of the intake of sodium ± a major determinant of urinary calcium excretion ± been seriously implemented as a dietary approach to the management of hypercalciuria [28,35]. The present prospective study highlights the importance of hypertension as a marker of kidney stone risk.

Pathophysiology
1. Stone formation is inhibited by Citrate
2. Women have much higher levels of citrate than men
3. Low citrate levels are related to most stone forms
Kidney stone are crystalline mineral deposits that form in the kidney. They develop from microscopic crystals in the loop of Henle, the distal tubule, or the collecting duct, and they can enlarge to form visible fragments. The process of stone formation depends on urinary volume; concentrations of calcium, phosphate, oxalate, sodium, and uric acid ions; concentrations of natural calculus inhibitors; and urinary pH.4 High ion levels, low urinary volume, low pH, and low citrate levels favor calculus formation.
stones are classified into five categories based on their composition: calcium oxalate (70 percent), calcium phosphate (5 to 10 percent), uric acid (10 percent), struvite (15 to 20 percent) and cystine (1 percent). stones can be classified more broadly into calcareous stones and noncalcareous stones. Calcareous stones usually are visible on radiographic imaging (Figure 1), whereas noncalcareous stonesoften are radiolucent or poorly visualized on plain film radiography. Many calculi have a mixed composition, with one type of crystal becoming a nidus for heterogeneous crystallization.

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Dyad 4
Balajadia, Bond
Zaño, Alexis

Epidemiology of paediatric renal stone disease in the UK

The previous epidemiological study of paediatric nephrolithiasis in Britain was conducted more than 30 years ago. In order to examine the presenting features, predisposing factors, and treatment strategies used in
paediatric stones presenting to a British centre over the past five years. The researchers utilized a total sample of 121 children presented with a urinary tract renal stone, to one adult and one paediatric centre, over a five year period (1997–2001). All children were reviewed in a dedicated stone clinic and had a full infective and metabolic stone investigative work up. Treatment was assessed by retrospective hospital note review.

A metabolic abnormality was found in 44% of children, 30% were classified as infective, and 26% idiopathic. Bilateral stones on presentation occurred in 26% of the metabolic group compared to 12% in
the infective/idiopathic group (odds ratio 2.7, 95% CI 1.03 to 7.02). Coexisting urinary tract infection was common (49%) in the metabolic group. Surgically, minimally invasive techniques (lithotripsy, percutaneous
nephrolithotomy, and endoscopy) were used in 68% of patients.

There has been a shift in the epidemiology of paediatric renal stone disease in the UK over the past 30 years. We therefore conclude that the underlying metabolic causes are now the most common but can be masked by coexisting urinary tract infection. Through the years, treatment of kidney stones has progressed, especially surgically, with sophisticated minimally invasive techniques are now employed. Also, all children with renal stones should have a metabolic screen for early detection and management of the condition.

Reference: Coward R J M et. al. Epidemiology of paediatric renal stone disease in the UK. PMC. March 2003

RESPONSE- Kidney Stones
By: D2- Gil Legarda/ Joanalyn Balino

Type 2 Diabetes Increases the Risk for Uric Acid Stones
Michel Daudon,* Olivier Traxer,† Pierre Conort,‡ Bernard Lacour,* and Paul Jungers§



The research design of this study is quasi-experimental. The goal of this research study was to evaluate the distribution of stone components in stone formers with versus without type 2 diabetes, with the hypothesis that type 2 diabetes may be associated with an increased risk for formation of UA stones. The researcher wanted to know the effect of having a DM in increasing the uric acid stones. The researcher compared type 1 and type 2 DM if which between the two is the most contributor in uric acid stone formation. There are 2464 patients, 1760 men and 704 women also the researcher included 272 patients with type 2 diabetes and 2192 patients without type 2 diabetes. The researcher used a random cluster separating those patients with diabetes to those patients without diabetes. Included in this study were calculi from patients for whom information on diabetes status, body height, and body weight had been provided and who had idiopathic Ca or UA nephrolithiasis. Excluded from the study were cystine stones and struvite, whose occurrence depends on specific factors that are not known to be influenced by diabetes or body size. This research study was held in Laboratoire CRISTAL in Hosptal Necker-Enfants in Paris, France. This research study used laboratory tests and findings to compare the effect of having a type 2 diabetes in the formation of uric acid stone. The researcher used a logistic regression analysis to determine the relative contribution of diabetes, BMI, gender and age on the risk for uric acid stone formation. In using univariate analysis, increasing age, presence of diabetes, increasing body mass index and male gender were significantly and positively associated with risk for uric acid stones. In multivariate analysis in the whole series, only presence of diabetes, increasing BMI, and male gender still were independent significant risk factors.

All in all, 272 or 11% of the patients had type 2 diabetes, whereas 2192 or 89% did not. Those stone formers who are younger than 50 years were 3 times more frequent among patients with type 2 diabetes. The proportion of recurrent stone formers was significantly higher in patients with than without type 2 diabetes, and this was apparent especially for UA nephrolithiasis. The findings of this study confirmed the hypothesis on an epidemiologic basis showing for the first time that the proportion of Uric Acid stones is strikingly higher in stone formers with than without type 2 diabetes and the type 2 diabetes constitutes a strong independent factor of uric acid nephrolithiasis with overweight/obesity acting as an additional risk factor. This data show that the prevalence of type 2 diabetes is more than 3 times higher among UA stone formers than among CA stone formers.

Two epidemiologic studies showed a relationship between diabetes and urolithiasis. This two studies recently provided an arguments in support of a preferential relationship between type 2 diabetes and Uric Acid stone formation. Based on Sakhee et. all the one who first showed that 21 patients with pure UA nephroiathiasis were overweight and hypertriglyceridemic. Pak et all specifically tested the hypothesis that patients with type 2 diabetes may exhibit a high prevalence of UA stones. This research data is helpful in providing an epidemiologic evidence that type 2 diabetes is significantly associated with an increased risk for Uric acid stone formation.



References:
Michel Daudon, Olivier Traxer, Pierre Conort, Bernard Lacour, and Paul Jungers (2006) Type 2 Diabetes Increases the Risk for Uric Acid Stones. Journal of American Society Nephrology Vol 17: pages 2026–2033 Retrieved June 23,2009 from http://jasn.asnjournals.org/cgi/reprint/17/7/2026?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&minscore=5000&resourcetype=HWCIT

resonpse by
Yang ChunHua and Yuan ShuHui
Kidney Stones as a Systemic Disease
Dr. Gary Curhan
Kidney stone disease is a common and painful health
problem in the U.S. It is also a growing problem: the
number of people in the U.S. with kidney stones has
increased significantly over the past 30 years. White
Americans are more prone to develop kidney stones
than African Americans, and men are more likely to
develop stones than women. For unknown reasons,
some individuals are prone to repeatedly developing
stones. Each year, people make almost three million
visits to health care providers and more than half a
million people go to emergency rooms for kidney
stone problems.1

The first symptom of a kidney stone typically
appears when the stone moves from the kidney
into the ureter, causing irritation or blockage and
resulting in extreme pain. Most kidney stones can
pass harmlessly—though not painlessly—through
the urinary system. In such cases, medication
to alleviate the pain may be the only medical
intervention needed. Stones that cause lasting
symptoms or other complications may be treated
by various techniques, most of which do not involv
major surgery. In severe cases, however, surgery
may be required to remove the stone.

In addition to being extremely painful, kidney stones
also are costly to treat. According to the 2007 edition
of Urologic Diseases in America, kidney stones are
the second-costliest urologic disease, accounting for
over $2 bil ion spent on medical care,2 with another
$4 mil ion to $14 mil ion spent on prescription drugs.3
These numbers do not include costs not associated
with direct medical expenditures, such as time lost
from work.

Composition of Kidney Stones
Kidney stones can consist of a number of different
components. The most common type of stone,
accounting for two-thirds of al stones, is a combi
nation of calcium and oxalate. Less common types
of stones include stones caused by urinary tract
infections, and stones made of uric acid or the amino
acid cystine. “Nephrolithiasis” is the medical term
used to describe stones occurring in the kidney, while
stones in the urinary tract are formal y designated as
“urolithiasis.” For the sake of simplicity, “kidney stone”
is often used to designate stones regardless of their
location in the kidney or urinary tract.

Urine is a liquid with various substances dissolved
in it, and there is a finite amount of material that can
be dissolved in a given quantity of water. If this limit
is exceeded, material wil fal out of solution and
crystal ize. Once this process starts, the nascent
crystals attract other dissolved elements in the water,
and the crystal grows in size. Although the precise
steps that lead to kidney stone formation are not
known, one way to think about crystal formation is
as a problem of too much material trying to remain
dissolved in too little water.
Risk factors for kidney stones encompass gastro
intestinal, skeletal, and metabolic factors, as well
as obesity. At first glance, the connection of most
of these factors to the kidney may not be obvious.
However, closer examination reveals clues that
implicate kidney stone disease as an organ-specific
manifestation of more general systemic disturbances.
Risk Factors: Gastrointestinal
Risk Factors: Obesity
Risk Factors: Bone
Risk Factors: Endocrine and Metabolic Pathways
Risk Factors: Genetics
Conclusion
Kidney stone disease should be thought of as a
systemic disorder and not just a disease of the
kidneys. In the past several years, significant progress
has been made in understanding the causes of the
disease, but much work remains to be done. Moving
forward, new paradigms regarding the underlying
causes of the disease wil shape the research agenda,
especial y regarding the origins of stones and the risk
factors that contribute to their formation. Future large
studies of genetics and gene-environment interactions
wil further our understanding of this complex disorder.

Unenhanced MDCT in Patients with Suspected Urinary Stone Disease:
Do Coronal Reformations Improve Diagnostic Performance?
Mazda Memarsadeghi; Cornelia Schaefer-Prokop; Mathias Prokop; Thomas H. Helbich; Christian C. Seitz; Iris M. Noebauer-Huhmann; Gertraud Heinz-Peer
Published: 08/21/2007

The use of Computed tomography (CT scan) has already become a standard technique in evaluating clients with suspected renal stone (Miller OF, 2000). In the time when Multidetector Computed Tomography Scan (MDCT) was discovered, the availability of high-quality multiplanar reformations is used in displaying the urinary tract in its longitudinal axis. This is a retrospective study in order to asses if the coronal reformations will improve the diagnostic performance of MDCT in patients with suspected urinary stone disease. 147 patients who underwent MDCT during 9-month period were included in the study. The data gathered from the study were analyzed using SAS statistical package. The results were conveyed in whole numbers and gathered their means thru standard deviation. The level of significance is at less than 0.05 the statistical method used is McNemar test.

Results revealed that there about 71 patients have uroliths. There were no significant difference between axial sections and coronal reformations with regards to the number of stones detected. However, the time in order to review the result findings was significantly shorter for coronal reformations compared to axial sections. The advantage of using axial section was it is more sensitive in determination of additional findings suggestive of other diagnosis. In conclusion, the use of coronal reformations from the findings of MDCT does not significantly improve the urolith detection but may reduce the time for evaluation. The use of coronal reformation from the findings of axial sections is disregarded due to risks of missed detection of small stones in the renal pelvis.

Finding from this study would provide additional information to health care provider about improvements with regards to detection of kidney stones among patients with suspected cases. Axial section gathered from CT scan is still the best diagnostic method in confirming the diagnosis. It should be avoided that coronal reformations be directly reconstructed from axial sections. However, the use of coronal reformations may speed up the detection in patients with suspected cases. The physicians should be aware that risks of missing small stone formation takes place when coronal reformations are use alone and not in conjunction with axial sections, and should guide interpreting radiologist whom are not yet familiar with the use of coronal reformations as a primary tool for evaluation.

References:
Miller OF, Kane CJ. Unenhanced helical computed tomography in the evaluation of acute flank pain. Curr Opin Urol
2000; 10:123 -129.

Authors and Disclosures
Mazda Memarsadeghi,1 Cornelia Schaefer-Prokop,2 Mathias Prokop,3 Thomas H. Helbich,1 Christian C. Seitz,4 Iris M. Noebauer-Huhmann,1 Gertraud Heinz-Peer 1

1Department of Radiology, Medical University of Vienna, General Hospital of Vienna, Vienna, Austria
2Department of Radiology, University of Amsterdam, Amsterdam, The Netherlands
3Department of Radiology, University Medical Center Utrecht, Utrecht, The Netherlands
4Department of Urology, Medical University of Vienna, Vienna, Austria

Dyad Three (3)
Byron Webb A. Romero
Von Deneb H. Vitto
Raymond C. Ursal

Pathophysiology
According to Cameron and Sakhaee (2007), three primary factors contribute to the development of uric acid nephrolithiasis: low urinary volume, hyperuricosuria, and acidic urine pH. Evaluation of a uric acid stone former should therefore include assessment for these three factors mentioned, which should then guide the treatment plan. Low pH is the most prevalent feature in idiopathic uric acid nephrolithiasis. However, all three predisposing causes should never be disregarded.

In low urinary volume, by increasing the relative saturation of stone-forming constituents is pathophysiologic in the development of all kidney stones. In patients with nephrolithiasis, a urinary volume less than 2 L/d would be considered stone promoting. Any form of volume depletion, such as excessive perspiration or chronic diarrheal states, may all contribute to uric acid stones. Typically, a low urine volume is insufficient to fully account for uric acid lithiasis, but in the context of low urine pH low urine volume may exacerbate stone-promoting risks.

Hyperuricosuria is a condition typically defined as urinary uric acid excretion in excess of 700 mg/d. There are various genetic and environmental factors that may augment urinary uric acid excretion. Urate overproduction and, consequently, hyperuricosuria have both been proposed as mechanisms for uric acid stone formation in primary gout. However, more recent studies have demonstrated that uric acid excretion is not really elevated in patients with gout. Such results suggest alternative causative mechanisms, instead of hyperuricosuria in gouty patients (Alvarez-Nemegyei, et.al., 2005; and Sakhaee, et.al., 2002).

The overriding pathogenic factor in uric acid nephrolithiasis is an unduly acidic urine pH (low urine pH), whereas hyperuricosuria is a relatively rare cause of uric acid stones. The acidic environment causes titration of more soluble urate to relatively insoluble uric acid, which predisposes to uric acid precipitation. In most uric acid stone formers, the etiology of the acidic urine remain unknown. However, secondary causes should also be considered before the etiology is then defined as idiopathic. Conditions that contribute to acidic urine include base loss and increased acid generation either endogenously or via ingestion of an acidic diet. Diarrhea results in stool loss of bicarbonate, making the urine more acidic. It further contributes to lithogenic risk because of the associated volume loss & increased urinary saturation. Similarly, strenuous physical activities can result in lactic acidosis, contributing to a low urine pH, which is further complicated by volume depletion from perspiration. Diet rich in proteins (especially animal proteins) provides an acidogenic load, in addition to providing a purine load that contributes to hyperuricosuria. Acidic urine has also been associated with primary gout, regardless of the presence of kidney stones. In their review of 325 gout patients, including those with and without a nephrolithiasis history,Yu and Gutman found that 92% of the subjects had a urine pH less than 5.6. A recent study of 140 gout patients revealed similar findings with a mean urine pH of 5.4 in stone formers and 5.6 in non-stone formers. In the absence of an identifiable cause therefore, such as in gouty patients, an acidic urine pH is defined as idiopathic.

Epidemiology
Uric acid nephrolithiasis comprises approximately 10% of the total stone burden in the United States. However, this value exhibits considerable geographic and racial diversity as mentioned in the study conducted by Cameron and Sakhaee (2007). The proportion of uric acid stones is significantly higher in Middle Eastern countries, such as Israel (40%); in Okinawa, Japan (16%); and in some European countries, including regions in Germany (25%). In the United States, there is a high prevalence of uric acid nephrolithiasis reported in the Hmong population, an ethnic group with Chinese ancestry who emigrated from Laos. When compared with a non-Hmong population, the Hmong patients demonstrated increased stone risk with over 50% of the stones containing uric acid. Factors related to these global and ethnic variations in uric acid stone risk have not been identified or explored.

Recent studies have described metabolic factors that affect the epidemiology of uric acid nephrolithiasis. An epidemiologic study that included over 200,000 subjects from three cohorts found that type 2 diabetes mellitus is associated with kidney stone disease (Taylor, Stampfer and Curhan, 2005). Stone composition was not assessed in their study. However, smaller studies have demonstrated increased prevalence of uric acid stones in type 2 diabetics, suggesting that uric acid stones contribute to the higher stone risk in this population (Pak, Sakhaee & Moe, 2003; Daudon, Lacour, & Jungers, 2005). An initial report by Pak and colleagues (2003) found an association of uric acid stones with type 2 diabetes mellitus. This finding was confirmed in another study of 4718 kidney stones, of which 631 were obtained from patients with diabetes mellitus and 4087 from nondiabetic stone formers (Daudon, Lacour, & Jungers, 2005). A significantly higher proportion of pure uric acid stones was found in diabetic patients than in nondiabetics (28.5% versus 13%, with P<.0001). This difference was even greater when mixed uric acid–calcium stones were included in the proportion of uric acid–containing stones (35.4% vs 16.8%, with P<.0001). Additionally, a comparison of diabetic and nondiabetic stone formers found that 35.7% of stones in diabetics were composed of uric acid versus 11.3% in nondiabetic stone formers. Similarly, obesity has been associated with a higher prevalence of uric acid nephrolithiasis. A report of 32 obese stone formers found that 63% of their stones were composed of uric acid (Ekeruo, et.al, 2004). Additionally, a French study compared the proportion of uric acid stones in lean nephrolithiasis patients (body mass index (BMI) < 25 kg/m2) with that of obese patients (BMI R 30 kg/m2) (Daudon, Lacour, & Jungers, 2005). Uric acid stones constituted 6.8% of the total stone burden in lean patients, and 24.1% accounted in obese subjects. The increased prevalence of uric acid stones in obese and diabetics would suggest that a common underlying mechanism, such as insulin resistance, may influence stone risk. This mechanism may be considered as contributor to the ethnic and geographic variations in stone prevalence.

Diagnostic Evaluation
The initial evaluation of a uric acid stone former should include a complete history and physical with a focus on secondary factors, described above, that contribute to stone formation (Cameron & Pak, 2004) including a review of medications and diet should be included. Identification of the underlying cause will guide future management of the condition. The definitive diagnosis depends upon stone analysis that would reveal complete or partial uric acid content.

If the calculus is not available for the evaluation, radiographic and metabolic features may suggest the presence of uric acid lithiasis. These stones appear radiolucent on evaluation by roentgenography, but are portrayed by Computed Tomography. In addition, an acidic urine pH suggests that a uric acid component may be present. A 24-hour urine collection should be obtained on all patients to evaluate for predisposing abnormalities, including low urine volume, hyperuricosuria, high urinary sulfate, hypocitraturia, and low urine pH.

According to Cameron and Sakhaee (2007) stone analysis distinguishes uric acid lithiasis from other stones in the differential diagnosis. Both xanthine and 2,8-dihydroxyadenine (2,8-DHA) stones appear radiolucent on radiographic evaluation and therefore may be mistaken for uric acid stones. Xanthine calculi typically would develop in patients receiving allopurinol or in patients with congenital conditions, such as Lesch-Nyhan syndrome or hereditary xanthinuria, an autosomal recessive deficiency of xanthine oxidase. 2,8-DHA stones occur in patients with autosomal recessive disorder, adenine phosphoribosyltransferase deficiency. Both stone types are extremely insoluble and that they do not respond to alkali therapy; thus providing a diagnostic clue. Serum uric acid would be low in hereditary xanthinuria. The differential diagnosis also includes calcium calculi, such as hyperuricosuric calcium stones and mixed uric acid–calcium oxalate stones. Hyperuricosuria is a risk factor that is common to both calcium and uric acid stones. However, calcium nephrolithiasis is more commonly associated with hyperuricosuria than in uric acid nephrolithiasis. A report evaluating metabolic abnormalities and related kidney stones found that 78% of hyperuricosuric stone formers have calcium oxalate stones and 10% have calcium phosphate stones (Pak, et.al, 2003). Hyperuricosuria would usually results from dietary indiscretion and purine gluttony. Other features that distinguish these patients from uric acid stone formers would include a normal serum uric acid concentration and a normal urine pH. In contrast, in patients with mixed uric acid–calcium oxalate stones the main metabolic derangement is a low urine pH.

References:

Alvarez-Nemegyei, J., Medina-Escobedo, M., Villanueva-Jorge, S., et al. (2005). Prevalence and risk factors for urolithiasis in primary gout: is a reappraisal needed?. Journal of Rheumatology 32(11):2189–91.

Cameron, M.A., & Pak, C.Y.C. (2004). Approach to the patient with the first episode of nephrolithiasis. Clinical Review: Bone Mineral Metabolism. 2(3):265–78.

Cameron, M.A., & Sakhaee, K. (2007). Uric Acid Nephrolothiasis. Urologic Clinics of North America. 34 (2007): 335-346.

Daudon, M., Lacour, B., & Jungers, P. (2005). High prevalence of uric acid calculi in diabetic stone formers. Nephrology Dialysis & Transplant. 20(2):468–9.

Ekeruo, W.O., Tan, Y.H., Young, M.D, et al. (2004). Metabolic risk factors and the impact of medical therapy on the management of nephrolithiasis in obese patients. Journal of Urology. 172(1):159–63.

Pak, C.Y.C., Poindexter, J.R., Adams-Huet, B., et al. (2003). Predictive value of kidney stone composition in the detection of metabolic abnormalities. American Journal of Medicine. 115:26–32.

Pak, C.Y.C, Sakhaee, K., Moe, O.W, et al. (2003). Biochemical profile of stone-forming patients with diabetes mellitus. Urology. 61:523–7.

Sakhaee., K, Adams-Huet, B., Moe, O.W., et al. (2002). Pathophysiologic basis for normouricosuric uric acid nephrolithiasis. Kidney International. 62:971–9.

Taylor, E.N., Stampfer, M.J., & Curhan, G.C. (2005). Diabetes mellitus and the risk of nephrolithiasis. Kidney International. 68(3):1230–5.