Uric Acid Stone Disease Research Articles

Urinary Risk Profile, Impact of Diet, and Risk of Calcium Oxalate Urolithiasis in Idiopathic Uric Acid Stone Disease.

The role of diet in the pathogenesis of uric acid (UA) nephrolithiasis is incompletely understood. This study investigated the effect of dietary intervention on the risk of UA stone formation under standardized conditions. Twenty patients with idiopathic UA stone disease were included in the study. Dietary intake and 24 h urinary parameters were collected on the usual diet of the patients and a standardized balanced mixed diet. Although urinary UA excretion did not change, the relative supersaturation of UA decreased significantly by 47% under the balanced diet primarily due to the significant increase in urine volume and pH. Urinary pH was below 5.8 in 85% of patients under the usual diet, and in 60% of patients under the balanced diet. The supersaturation of calcium oxalate declined significantly under the balanced diet due to the significant decrease in urinary calcium and oxalate excretion and the increase in urine volume. Dietary intervention is a key component in the management of UA nephrolithiasis. Urinary calcium and oxalate excretion should also be monitored in patients with pure UA calculi to reduce the risk of mixed stone formation with calcium oxalate. Lower urinary pH in UA stone patients can only be partially explained by diet.

Differences of Uric Acid Transporters Carrying Extracellular Vesicles in the Urine from Uric Acid and Calcium Stone Formers and Non-Stone Formers.

Background: Low urine pH and volume are established risk factors for uric acid (UA) stone disease (UASD). Renal tubular epithelial cells exposed to an acidic pH and/or UA crystals can shed extracellular vesicles (EVs) into the tubular fluid, and these EVs may be a pathogenic biomarker of UASD. Methods: Urinary EVs bearing UA transporters (SLC2A9, SLC17A3, SLC22A12, SLC5A8, ABCG2, and ZNF365) were quantified in urine from UA stone formers (UASFs), calcium stone formers (CSFs), and age-/sex-matched non-stone formers (NSFs) using a standardized and published method of digital flow cytometry. Results: Urinary pH was lower (p < 0.05) and serum and urinary UA were greater (p < 0.05) in UASFs compared with NSFs. Urinary EVs carrying SLC17A3 and SLC5A8 were lower (p < 0.05) in UASFs compared with NSFs. Urinary EVs bearing SLC2A9, SLC22A12, SLC5A8, ABCG2, and ZNF365 were lower (p < 0.05) in CSFs than UASFs, while excretion of SLC17A3-bearing EVs did not differ between groups. Conclusion: EVs bearing specific UA transporters might contribute to the pathogenesis of UASD and represent non-invasive pathogenic biomarkers for calcium and UA stone risk.

Uric acid stone disease: lessons from recent human physiologic studies.

An overly acidic urine resulting in supersaturation of urine with respect to uric acid is the major mechanism responsible for uric acid nephrolithiasis. The present review summarizes findings from recent human physiologic studies examining the pathophysiology and reversibility of low urine pH in uric acid stone formers. Epidemiologic and metabolic studies have confirmed an increase in the prevalence of uric acid nephrolithiasis and reported its association with several features of the metabolic syndrome including dyslipidemia, hyperglycemia, hepatic steatosis, and greater visceral adiposity. Physiologic studies in uric acid stone formers have identified diet-independent excessive net acid excretion and concomitant reduction in urinary buffering from impaired renal ammoniagenesis as the two causes underlying the greater aciduria. Administration of the insulin sensitizer pioglitazone to uric acid stone formers reduced the acid load presented to the kidney and enhanced ammoniagenesis and ammonium excretion, resulting in significantly higher urine pH. Recent human physiologic studies have identified greater acid excretion and reduced urinary buffering by ammonia as two culprits of aciduria in uric acid nephrolithiasis that can be reversed by pioglitazone, raising new questions regarding the origin of the aciduria and opening the door to pathophysiology-based treatment of uric acid stones.

An innovative bio-tissue network signal amplifier activated by high-N-doped carbon for uric acid detection

We herein report the first attempt to engineer an innovative bio-tissue network signal amplifier transduced by a novel natural N-doped carbon material. In order to prevent kidney uric acid (UA) stone disease in advance, based on the excretion of most UA through the kidney, as well as the high nitrogen content in animal tissues, and considering the biocompatibility, a high-N-doped carbon was firstly prepared by in situ carbonization and chemical activation method with the mouse kidney as precursor. The activated mouse kidney transformed carbon (AMKC) had a large specific surface area and network hierarchical pore structure, and played the biological transduction for signal enrichment to vastly increase sensitivity to detect UA, which may be due to the multi-circuitry performance of bio-tissue. Under the optimized conditions, AMKC as a network signal amplifier expressed a linear relationship to UA concentrations from 0.5 to 300 μM, with a high sensitivity of 0.1195 μA μM−1 and a low detection limit of 0.15 μM (3σ). Furthermore, the bio-tissue multi-circuitry signal amplifier exhibited a high selectivity for UA even with interference of other biological inorganic salts and small organic molecules, which has broad application prospects in clinical diagnosis and detection.

Pathophysiology and Treatment of Uric Acid Stones

Uric acid is the third most common stone composition and comprises 7 to 10% of all kidney stones sent for analysis. These stones are more common with increasing age and in men. Uric acid stone disease is associated with conditions such as the metabolic syndrome and type 2 diabetes mellitus. Uric acid is produced by the enzyme, xanthine oxidase and is the final product of purine metabolism in humans. Three main factors contribute to the formation of uric acid stones: low urine pH (the most important), hyperuricosuria (rare, includes conditions such as myeloproliferative disorders and Lesch-Nyhan syndrome), and low urine volume. Uric acid stones appear radiolucent on plain radiographs and are ultimately diagnosed via stone analysis. These stones may be treated with medical expulsive therapy, dissolution therapy, or surgical intervention depending on the size, location, and clinical presentation. Urine pH manipulation therapy with potassium citrate is the first-line treatment for the prevention of uric acid stones and attempts at dissolution. Allopurinol should not be offered as the first-line therapy for uric acid stones. This review contains 3 figures, 1 table and 38 references Key Words: ammonium, diabetes mellitus, epidemiology, management, metabolic syndrome, nephrolithiasis, pathophysiology, potassium citrate, uric acid, urine pH

Obesity and kidney stone disease: a systematic review.

Currently, abdominal obesity has reached an epidemic stage and obesity represents an important challenge for worldwide health authorities. Epidemiologic studies have demonstrated that the stone risk incidence increases with Body Mass Index, through multiple pathways. Metabolic syndrome and diabetes are associated with an increased renal stones disease incidence. The aim of this systematic review was to investigate the prevalence, morbidity, risk factors involved in the association between obesity and urolithiasis. The search involved finding relevant studies from MEDLINE, EMBASE, Ovid, the Cochrane Central Register of Controlled Trials, CINAHL, Google Scholar, and individual urological journals between January 2001 and May 2017. The inclusion criteria were for studies written in the English language, reporting on the association between obesity and urinary stones. The underlying pathophysiology of stone formation in obese patients is thought to be related to insulin resistance, dietary factors, and a lithogenic urinary profile. Uric acid stones and calcium oxalate stones are observed frequently in these patients. Insulin resistance is thought to alter the renal acid-base metabolism, resulting in a lower urine pH, and increasing the risk of uric acid stone disease. Obesity is also associated with excess nutritional intake of lithogenic substances and with an increase in urinary tract infection incidence. Recent studies highlighted that renal stone disease increases the risk of myocardial infarction, progression of chronic kidney disease, and diabetes. Contemporary, bariatric surgery has been shown to be associated with hyperoxaluria and oxalate nephropathy. Certainly, the many health risks of obesity, including nephrolithiasis, will add more burden on urologists and nephrologists. Obesity related nephrolithiasis seems to necessitate weight loss as primary treatment, but the recognition of the associated complications is necessary to prevent induction of new and equally severe medical problems. The optimal approach to obesity control that minimizes stone risk needs to be determined in order to manage obesity-induced renal stones disease.

Effectiveness of Treatment Modalities on Kidney Stone Recurrence.

Nephrolithiasis is highly prevalent across all demographic groups in the Western world and beyond, and its incidence rates are rising. In addition to the morbidity of the acute event, stone disease often becomes a lifelong problem that requires preventative therapy to diminish ongoing morbidity. Across the majority of stone types, increased fluid intake and targeted dietary modifications are mainstays of therapy. Specific dietary interventions associated with reduced calcium stone risk include adequate dietary calcium intake and restriction of sodium, protein, and oxalate intake, among others. Pharmaceutical therapy may be required if lifestyle changes are insufficient to minimize risk of stone recurrence, and must be targeted to the specific metabolic abnormalities portending risk for a given patient. Therapeutic options for idiopathic calcium stone disease include thiazides, citrate salts, and uric acid-lowering agents. Alkali salts are also the treatment of choice for uric acid stone disease. Management of struvite stone disease is largely surgical, but acetohydroxamic acid is a proven second line therapy. Cystinuria requires lifestyle modifications and may call for thiol-binding agents. Significant heterogeneity of the clinical population with stone disease has previously limited opportunities for large randomized controlled trials. However, as clinical phenotypes and genotypes are increasingly clarified, there are mounting opportunities for targeted randomized controlled trials in stone prevention. In the meantime, the currently available evidence for both lifestyle and pharmacologic interventions is reviewed herein.

Update on Nephrolithiasis

Many recent papers analyze the association between renal stone disease and other diseases that are typical of industrialized countries. Epidemiology studies from large series indicate that the prevalence of nephrolithiasis is higher among patients with metabolic syndrome, diabetes, and hypertension. Patients with nephrolithiasis also have an increased risk of myocardial infarction and stroke. It has been hypothesized that the common underlying defect could be insulin resistance. This, in turn, alters the urine biochemistry (i.e. more acidic pH and less urine citrate) thereby increasing the propensity of stone forming. In the diabetic rat renal steatosis has been implicated in the reduced production of ammonia, which has been shown to be reversible after PPARγ administration. Furthermore, pioglitazone was shown to be effective in reducing ethylene glycol-induced renal injury. Another significant association concerns gout. Two recent papers report that both calcium and uric acid stone disease are more prevalent among patients with gout. The metabolic derangements found in gouty and non-gouty patients were quite similar. CT imaging in patients with gout indicates that the incidence of nephrolithiasis is underestimated if only based on stone history. Finally, stone episodes may occur many years before the first gouty attack. Another interesting issue is that of a potential adverse effect of calcium and vitamin D supplementation on the risk of stone formation. It has been shown that treated post-menopausal women have a slight but significantly higher risk of forming stones, independently of other interfering variables. From this the recommendation to evaluate the actual benefit of supplementation, even more in the face of its ineffectiveness to prevent fractures in older women. Bariatric surgery is increasingly proposed for managing severe obesity, and in the last few years it has shown a widespread use in the US. Previous procedures of digestive diversion were often complicated by hyperoxaluria and renal oxalosis. More recent techniques, including Roux-en-Y gastric bypass and gastric bending, seem to give better outcomes. Hyperoxaluria and hypocitraturia following these procedures induce only minor increases in the risk of forming stones, but some recent reports of renal oxalosis after gastric bypass deserve attention.

2089 INCIDENCE OF URIC ACID STONES AND HIGH VISCERAL FAT AREA ARE ELEVATED IN CAUCASIAN VERSUS HISPANIC AND AFRICAN AMERICAN PATIENTS

You have accessJournal of UrologyStone Disease: Evaluation & Medical Management (I)1 Apr 20132089 INCIDENCE OF URIC ACID STONES AND HIGH VISCERAL FAT AREA ARE ELEVATED IN CAUCASIAN VERSUS HISPANIC AND AFRICAN AMERICAN PATIENTS Tian Zhou, Kara Watts, Joseph DiVito, and David Hoenig Tian ZhouTian Zhou Bronx, NY More articles by this author , Kara WattsKara Watts Bronx, NY More articles by this author , Joseph DiVitoJoseph DiVito Bronx, NY More articles by this author , and David HoenigDavid Hoenig Bronx, NY More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.1998AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Patients with uric acid stone disease are more obese than patients without. Recent review of a series of percutaneous stone removal (PCNL) patients demonstrated that visceral fat area (VFA) is statistically significantly different among patients with uric acid stones, but Body Mass Index (BMI) is not. In addition, we found a higher incidence of uric acid stones in Caucasian patients than in other ethnic groups. We hypothesized that there may be a difference by ethnic group in fat distribution between Caucasian (C), Hispanic (H), and African American (AA) patients with uric acid stones. METHODS Retrospective review of an IRB-approved database of patients who underwent PCNL was performed. VFA and BMI measurements among all patients were obtained, with VFA calculated on a CT scan slice at the umbilicus (TeraRecon, Aquarius iNuition workstation). Comparison of the incidence of uric acid stones, BMI, and VFA was made between each ethnic group. RESULTS Uric acid stone material was found in 11/71 AA (15.5%), 14/93 H (15.1%), and 15/55 C (27.3%) (Chi square value 6.5, p=0.011). Mean BMI was 30.3 kg/m2 in AA, 30.0 kg/m2 in H, and 31.4 kg/m2 in C patients, while VFA was 148.0 cm2 in AA, 170.0 cm2 in H, and 207.0 cm2 in C patients. Post Hoc multiple comparison tests (Games-Howell) demonstrated a statistically significant difference in mean VFA (C versus AA: p=0.001, C versus H: p= 0.039). CONCLUSIONS A significantly higher incidence of uric acid stones was present in Caucasian patients compared to either African American or Hispanic patients undergoing PCNL. While BMI does not differ significantly between groups, VFA does, indicating a strong association between visceral adiposity and uric acid stones. It also appears that, among obese stone-forming patients, Caucasians have a significantly higher visceral fat distribution than either African American or Hispanic patients. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e857 Peer Review Report Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Tian Zhou Bronx, NY More articles by this author Kara Watts Bronx, NY More articles by this author Joseph DiVito Bronx, NY More articles by this author David Hoenig Bronx, NY More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

127 MANAGEMENT PATTERNS OF MEDICARE PATIENTS UNDERGOING TREATMENT FOR UPPER URINARY TRACT CALCULI

You have accessJournal of UrologyGeneral & Epidemiological Trends & Socioeconomics: Practice Patterns, Cost Effectiveness (I)1 Apr 2013127 MANAGEMENT PATTERNS OF MEDICARE PATIENTS UNDERGOING TREATMENT FOR UPPER URINARY TRACT CALCULI Brian Matlaga, Lisa Meckley, Thomas Byrne, and Jessica Perhanidis Brian MatlagaBrian Matlaga Baltimore, MD More articles by this author , Lisa MeckleyLisa Meckley Marlborough, MA More articles by this author , Thomas ByrneThomas Byrne Marlborough, MA More articles by this author , and Jessica PerhanidisJessica Perhanidis Marlborough, MA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.1506AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Given the rising prevalence of stone disease in the United States coupled with the fact that Medicare is the single largest healthcare payer in the United States, a better understanding of resource utilization in stone management within the Medicare population is urgently needed. At present, ureteroscopy (URS) and shock wave lithotripsy (SWL) are the two most commonly performed stone management procedures; yet our understanding of the re-treatments and ancillary procedures is limited and dated. We conducted this study to identify differences in resource utilization for SWL and URS in a recent sampling of the Medicare population. METHODS A retrospective claims analysis of the Medicare 5% sample was conducted to identify patients undergoing treatment of renal or ureteral calculi with a principal diagnosis of urinary lithiasis between 2009 and 2010. The index date was the date of first fragmentation procedure. Patients were excluded if they had a prior stone treatment within 6 months of the index stone treatment or prior uric acid or cystine stone disease. Outcomes evaluated were (1) a subsequent stone removal procedure within 120 days post index procedure, and (2) stent placement procedures 30 days prior to and 120 days post index date, as well as on the index date. Treatment groups were compared using Chi-Squared tests, T-tests, and relative risks. RESULTS We identified 3885 Medicare eligible patients, of which 2165 (56%) underwent SWL and 1720 (44%) underwent URS. SWL patients were 1.73 times (p=<.0001) more likely to undergo at least one repeat procedure than URS patients, and twice as likely (p=<.0001) to require multiple re-treatments compared to URS. SWL patients were 1.41 times (p=<.0001) more likely than URS patients to have a stent placed prior to index procedure, and 1.33 times (p=0.003) more likely to have a stent placed subsequent to the index procedure. The majority of URS patients (77.8%) had a stent placed at the time of index procedure. CONCLUSIONS Medicare patients undergoing SWL are significantly more likely to require multiple treatments than those undergoing URS. SWL patients are also significantly more likely to require ureteral stent placement as a separate event. As the Medicare program transitions from a volume to value driven system, these procedural trends will be subject to increasing scrutiny. This analysis of Medicare claims data demonstrates the need to characterize optimal treatment patterns, and better understand their economic effects. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e51 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Brian Matlaga Baltimore, MD More articles by this author Lisa Meckley Marlborough, MA More articles by this author Thomas Byrne Marlborough, MA More articles by this author Jessica Perhanidis Marlborough, MA More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Renal Stone Disease and Obesity: What is Important for Urologists and Nephrologists?

Currently, obesity has reached an epidemic stage and represents a challenge for health authorities across the globe. Certainly, with emergence of obesity epidemic, we started to see an increase in the prevalence of chronic kidney disease (CKD) and nephrolithiasis. Interestingly, epidemiologic studies have shown that the incident stone risk increases with body mass index (BMI), and no further increase in risk is noticed when the BMI > 30 kg/m2. Furthermore, metabolic syndrome and diabetes are also associated with an increase in the incidence of renal stones disease. The shared links between these metabolic disorders are insulin resistance. Furthermore, insulin resistance is thought to alter renal acid–base metabolism, resulting in a lower urine pH and increased risk of uric acid stone disease. Obesity is also associated with excess nutritional intake of lithogenic substances such as refined sugars, low fluid intake, calcium, oxalate, and purine-rich foods. Obesity is also associated with an increase in incidence of urinary tract infection. Recent reports suggested that renal stone disease carries risk of myocardial infarction, progression of CKD, and diabetes. Alarmingly, orlistat (obesity medication) and bariatric surgery are associated with hyperoxaluria and associated stone formation and even oxalate nephropathy. Certainly, the many health risks of obesity, including nephrolithiasis, will add more burden on urologists and nephrologists. Shockwave lithotripsy, percutaneous nephrolithotomy, and ureteroscopy are all safe procedures in obese individuals. Further research is urgently needed to address the pathophysiology and management of obesity-induced renal stones disease.

Urine alkalinization may be enough for the treatment of bilateral renal pelvis stones associated with Lesch–Nyhan syndrome

Lesch-Nyhan syndrome is a rare sex-linked disorder of purine metabolism that is caused by a mutation in the hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene which causes marked hyperuricemia and hyperuricosuria, with signs of gouty arthritis and uric acid stone disease in early childhood. We report a case of renal pelvis calculi which was dissolved within 10 days of urine alkalinization and hydration.

Percutaneous Nephrolithotripsy in Patients with Diabetes Mellitus

To compare the surgical outcomes in a cohort of patients with diabetes who were undergoing percutaneous nephrolithotripsy (PCNL) for renal stone disease to a nondiabetic group of patients at a single center. Between July 1990 and December 2005, all patients scheduled for PCNL were prospectively included in a single-center database. Preoperative, intraoperative, and postoperative data were prospectively collected and analyzed. Primary outcomes evaluated were stone-free rates and complications, including the need for blood transfusion, while the secondary outcome was length of hospital stay. This report specifically reviews these outcomes in patients known to have diabetes at the time of surgery. Both outcomes were compared with those obtained in our nondiabetic patient population. Analysis of the data from 183 (13.7%) patients with diabetes of the 1338 patients undergoing PCNL revealed that patient age (63.1 years), surgical time (90.8 minutes), and complications (major 2.2%), including need for transfusion (0.5%) and stone-free rate (94.5%), were not significantly different from those observed in our nondiabetic patients. The average length of hospital stay was significantly longer in the diabetic group (4.4 days vs 3.9 days, P = 0.022). Uric acid stone composition was found to be the most common stone composition among the patients with diabetes in this study (41%). PCNL can be performed with excellent stone-free rates and with an acceptable complication risk in the diabetic population. The incidence of uric acid stone disease appears to be significantly higher than previously reported and warrants heightened efforts directed toward stone prevention in this population.

Obesity and Urolithiasis

The current obesity epidemic in the United States has deleterious effects on the health of the population. Temporally related to the increase in obesity is an increase in the prevalence of urolithiasis. Epidemiologic studies have shown that the incident stone risk increases with body mass index. Obesity can increase stone risk in multiple ways. Excess nutritional intake increases traffic of lithogenic substances such as calcium, oxalate, and uric acid. Metabolic syndrome, commonly associated with obesity, alters renal acid-base metabolism, resulting in a lower urine pH and increased risk of uric acid stone disease. The low urine pH is caused by deficient ammonia production, which appears to be related to insulin resistance. Even weight-loss programs to combat obesity can influence stone risk. Contemporary bariatric surgery has been shown to frequently cause hyperoxaluria with associated stone formation and even oxalate nephropathy. Commonly used low-carbohydrate diets increase the risk of both calcium and uric acid stones. Certainly, the many health risks of obesity, including urolithiasis, necessitate weight loss, but recognition of the potential complications of such therapies is required to prevent induction of new and equally severe medical problems. The optimal approach to weight control that minimizes stone risk needs to be determined.

Preventive treatment of nephrolithiasis with alkali citrate—a critical review

Using the keywords "urolithiasis and citrate treatment", "nephrolithaisis and citrate treatment", "kidney stones and citrate treatment", a Medline search revealed 635 articles published between 1 January 1966 and 1 December 2004. For the present analysis, only studies meeting all of the following criteria were included: (1) publications in English or German, (2) studies on preventive alkali citrate treatment in patients with calcium oxalate, uric acid and infection stone disease, (3) clinical studies including at least ten subjects, and (4) treatment phases of at least 1 week duration. A total of 43 studies met the inclusion criteria and were further subclassified according to intermediate or ultimate endpoints as well as to study design. With stone recurrence as the ultimate endpoint, 21 uncontrolled studies in almost 1,000 patients demonstrated a reduction in stone forming rate by 47-100%. In four randomized controlled trials including 227 patients, 53.5% on alkali citrate vs 35% on placebo remained stone-free after at least 1 year of treatment (P<0.0005). Similar values (66% vs 27.5% for alkali citrate vs placebo, P<0.0005) were obtained in 104 patients from two randomized trials with dissolution/clearance of residual stones as endpoint. Unfortunately, up to 48% of alkali citrate treated patients left the studies prematurely, primarily due to adverse effects such as eructation, bloating, gaseousness or frank diarrhea.

ESRD caused by nephrolithiasis: Prevalence, mechanisms, and prevention

The contribution of nephrolithiasis-related end-stage renal disease (ESRD) to patients requiring renal replacement therapy has never been specifically evaluated. Of the entire cohort of 1,391 consecutive patients who started maintenance dialysis therapy at our nephrology department between January 1989 and December 2000, a total of 45 patients (21 men) had renal stone disease as the cause of ESRD and constitute the study material. Type and cause of renal stone disease was determined in the 45 patients, as well as the change in prevalence of nephrolithiasis-related ESRD with time during this 12-year period. The overall proportion of nephrolithiasis-related ESRD was 3.2%. Infection (struvite) stones accounted for 42.2%; calcium stones, 26.7%; uric acid nephrolithiasis, 17.8%; and hereditary diseases (including primary hyperoxaluria type 1 and cystinuria), 13.3% of cases. Women were predominant among patients with infection and calcium stones, whereas men were predominant among patients with uric acid or hereditary stone disease. The proportion of patients with nephrolithiasis-related ESRD decreased from 4.7% in the triennial period 1989 to 1991 to 2.2% in the most recent period, 1998 to 2000 ( P = 0.07). This tendency to a decreasing prevalence mainly was caused by a rarefaction of infection and calcium stones with time, whereas frequencies of uric acid and hereditary stone disease remained essentially unchanged. Severe forms of nephrolithiasis remain an underestimated cause of potentially avoidable ESRD and need for renal replacement therapy. These findings highlight the crucial importance of accurate stone analysis and metabolic evaluation to provide early diagnosis and proper therapy for conditions that may lead to ESRD through recurrent stone formation and/or parenchymal crystal infiltration.

Rapid Communication: Stone Disease in the Hmong of Minnesota: Initial Description of a High-Risk Population

The Hmong are an ethically distinct refugee population from the highlands of Laos. Metropolitan Minneapolis-St. Paul, Minnesota is home to the largest population of Hmong ( 40,000) outside Asia. A clinical impression that the Hmong have a high rate of uric acid stone disease was evaluated. A retrospective chart review was performed. All adult Hmong patients seen between January 1, 2000, and December 31, 2001, by a large urology group practice (N = 205) were compared with a similar number of non-Hmong patients (N = 204). Of these patients, 94 Hmong (46%) and 23 non-Hmong (11%) patients had stone disease (P < 0.001). After addition of 75 non-Hmong stone patients to create a suitable comparison group, a total of 86 Hmong and 88 non-Hmong stone patients had complete records. Sex (57% v 60% male) and mean age (47.9 v 47.3 years) were similar. Staghorn calculi were found in 21 Hmong (24%) and 0 non-Hmong patients (P < 0.001). Surgical treatments differed between Hmong and non-Hmong (P = 0.004): SWL (16 v 35), ureteroscopy (24 v 29), percutaneous nephrolithotomy (19 v 7), and nephrectomy (5 v 0). Treatment for staghorn calculi was refused by 9 Hmong patients (43%). Stone composition was available in 40 Hmong and 39 non-Hmong. Uric acid (>10%) was found in 50% of Hmong and 10% of non-Hmong stones (P < 0.001). Hmong patients who come to urologic attention tend to do so for stone disease and tend to have uric acid calculi. The frequent requirement for invasive therapy, including nephrectomy, in the Hmong is of concern.

Diagnostik und Prävention des Harnsäuresteins

Uric acid stones occur in 10% of all kidney stones and are the second most-common cause of urinary stones after calcium oxalate and calcium phosphate calculi. The most important risk factor for uric acid crystallization and stone formation is a low urine pH (below 5.5) rather than an increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrhea or severe dehydration. Uric acid stone disease can be prevented and these are one of the few urinary tract stones that can be dissolved successfully. The treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml daily), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary alkalization with potassium citrate or sodium bicarbonate is a highly effective treatment, resulting in dissolution of existing stones. Urinary uric acid excretion can be reduced by a low-purine diet. Potassium citrate is the treatment of choice for the prevention of recurrence of uric acid calculi. Allopurinol reduces the frequency of stone formation in hyperuricosuric patients with recurrent uric acid stones and/or gout.

Novel insights into the pathogenesis of uric acid nephrolithiasis.

The factors involved in the pathogenesis of uric acid nephrolithiasis are well known. A low urinary pH is the most significant element in the generation of stones, with hyperuricosuria being a less common finding. The underlying mechanism(s) responsible for these disturbances remain poorly characterized. This review summarizes previous knowledge and highlights some recent developments in the pathophysiology of low urine pH and hyperuricosuria. Epidemiological and metabolic studies have indicated an association between uric acid nephrolithiasis and insulin resistance. Some potential mechanisms include impaired ammoniagenesis caused by resistance to insulin action in the renal proximal tubule, or substrate competition by free fatty acids. The evaluation of a large Sicilian kindred recently revealed a putative genetic locus linked to uric acid stone disease. The identification of novel complementary DNA has provided an interesting insight into the renal handling of uric acid, including one genetic cause of renal uric acid wasting. The recognition of metabolic, molecular, and genetic factors that influence urinary pH, and uric acid metabolism and excretion, will provide novel insights into the pathogenesis of uric acid stones, and open the way for new therapeutic strategies.

Recurrence prevention in patients with urinary tract stone disease.

Formation of urinary tract concrements is a common disease and steps should be taken in order to elucidate the underlying mechanisms and to give the patients appropriate advice and medical treatment. This present article summarizes the principles for recurrence preventive measures in patients with uric acid, infection, cystine and calcium stone disease. Categories of stone formers are identified with the aim of providing a basis for an individualised treatment with a reasonable patient's compliance. The recommendations are in line with those given by the EAU guideline group for urolithiasis.