The purpose of this guideline is to provide a clinical framework for the diagnosis, prevention and follow-up of adult patients with kidney stones based on the best available published literature. The primary source of evidence for this guideline was the systematic review conducted by the Agency for Healthcare Research and Quality on recurrent nephrolithiasis in adults. To augment and broaden the body of evidence in the AHRQ report, the AUA conducted supplementary searches for articles published from 2007 through 2012 that were systematically reviewed using a methodology developed a priori. In total, these sources yielded 46 studies that were used to form evidence-based guideline statements. In the absence of sufficient evidence, additional statements were developed as Clinical Principles and Expert Opinions. Guideline statements were created to inform clinicians regarding the use of a screening evaluation for first-time and recurrent stone formers, the appropriate initiation of a metabolic evaluation in select patients and recommendations for the initiation and follow-up of medication and/or dietary measures in specific patients. A variety of medications and dietary measures have been evaluated with greater or less rigor for their efficacy in reducing recurrence rates in stone formers. The guideline statements offered in this document provide a simple, evidence-based approach to identify high-risk or interested stone-forming patients for whom medical and dietary therapy based on metabolic testing and close follow-up is likely to be effective in reducing stone recurrence.

Research from JAMA — Effect of Homocysteine Lowering on Mortality and Vascular Disease in Advanced Chronic Kidney Disease and End-stage Renal Disease — A Randomized Controlled Trial — ContextHigh plasma homocysteine levels are a risk factor for mortality and vascular disease in observational studies of patients with chronic kidney disease. Folic acid and B vitamins decrease homocysteine levels in this population but whether they lower mortality is unknown.ObjectiveTo determine whether high doses of folic acid and B vitamins administered daily reduce mortality in patients with chronic kidney disease.Design, Setting, and ParticipantsDouble-blind randomized controlled trial (2001-2006) in 36 US Department of Veterans Affairs medical centers. Median follow-up was 3.2 years for 2056 participants aged 21 years or older with advanced chronic kidney disease (estimated creatinine clearance ≤30 mL/min) (n = 1305) or end-stage renal disease (n = 751) and high homocysteine levels (≥ 15 μmol/L).InterventionParticipants received a daily capsule containing 40 mg of folic acid, 100 mg of pyridoxine hydrochloride (vitamin B6), and 2 mg of cyanocobalamin (vitamin B12) or a placebo.Main Outcome MeasuresThe primary outcome was all-cause mortality. Secondary outcomes included myocardial infarction (MI), stroke, amputation of all or part of a lower extremity, a composite of these 3 plus all-cause mortality, time to initiation of dialysis, and time to thrombosis of arteriovenous access in hemodialysis patients.ResultsMean baseline homocysteine level was 24.0 μmol/L in the vitamin group and 24.2 μmol/L in the placebo group. It was lowered 6.3 μmol/L (25.8%; P < .001) in the vitamin group and 0.4 μmol/L (1.7%; P = .14) in the placebo group at 3 months, but there was no significant effect on mortality (448 vitamin group deaths vs 436 placebo group deaths) (hazard ratio [HR], 1.04; 95% CI, 0.91-1.18). No significant effects were demonstrated for secondary outcomes or adverse events: there were 129 MIs in the vitamin group vs 150 for placebo (HR, 0.86; 95% CI, 0.67-1.08), 37 strokes in the vitamin group vs 41 for placebo (HR, 0.90; 95% CI, 0.58-1.40), and 60 amputations in the vitamin group vs 53 for placebo (HR, 1.14; 95% CI, 0.79-1.64). In addition, the composite of MI, stroke, and amputations plus mortality (P = .85), time to dialysis (P = .38), and time to thrombosis in hemodialysis patients (P = .97) did not differ between the vitamin and placebo groups.ConclusionTreatment with high doses of folic acid and B vitamins did not improve survival or reduce the incidence of vascular disease in patients with advanced chronic kidney disease or end-stage renal disease.Trial Registrationclinicaltrials.gov Identifier: NCT00032435

Mammalian species have co-evolved with intestinal microbial communities that can shape development and adapt to environmental changes, including antibiotic perturbation or nutrient flux. In humans, especially children, microbiota disruption is common, yet the dynamic microbiome recovery from early-life antibiotics is still uncharacterized. Here we use a mouse model mimicking paediatric antibiotic use and find that therapeutic-dose pulsed antibiotic treatment (PAT) with a beta-lactam or macrolide alters both host and microbiota development. Early-life PAT accelerates total mass and bone growth, and causes progressive changes in gut microbiome diversity, population structure and metagenomic content, with microbiome effects dependent on the number of courses and class of antibiotic. Whereas control microbiota rapidly adapts to a change in diet, PAT slows the ecological progression, with delays lasting several months with previous macrolide exposure. This study identifies key markers of disturbance and recovery, which may help provide therapeutic targets for microbiota restoration following antibiotic treatment.

In the past two decades, major breakthroughs that improve our understanding of the pathophysiology and therapy of kidney stones (KS) have been lacking. The disease continues to be challenging for patients, physicians, and healthcare systems alike. In this context, epidemiological studies are striving to elucidate the worldwide changes in the patterns and the burden of the disease and identify modifiable risk factors that contribute to the development of kidney stones. Our expanding knowledge of the epidemiology of kidney stones is of paramount importance and largely upgrades the modern management of the disease. In this paper, we review the variables affecting prevalence and incidence, including age, gender, race, ethnicity, occupation, climate, geography, systemic diseases, diabetes, vascular disease, chronic kidney disease, and dietary risk factors relevant to kidney stones.

Nephrolithiasis is a complex phenotype that is influenced by both genetic and environmental factors. Stone disease has a lifetime risk of 10% to 15% in the United States. The disorder causes acute, painful, and recurrent episodes of renal colic that lead to costly medical visits, procedures, and hospitalizations¹ x 1 Parks, J.H. and Coe, F.L. The financial effects of kidney stone prevention. Kidney Int. 1996; 50: 1706–1712 Abstract | Full Text PDF | PubMed | Scopus (93) | Google Scholar See all References . The cause of calcium stone disease in the general population is unknown but it may in part be heritable. One study demonstrated that nearly 40% of patients in a stone clinic had a first-degree relative with a positive history of stones² x 2 Ljunghall, S., Danielson, B.G., Fellstrom, B. et al. Family history of renal stones in recurrent stone patients. Br J Urol. 1985; 57: 370–374 Crossref | PubMed | Scopus (37) | Google Scholar See all References . More recently, in the population-based Nurses Health Cohort II, 36% of those with kidney stones reported a family history of stones³ x 3 Curhan, G.C., Willett, W.C., Knight, E.L., and Stampfer, M.J. Dietary factors and the risk of incident kidney stones in younger women: Nurses' Health Study II. Arch Intern Med. 2004; 164: 885–891 Crossref | PubMed | Scopus (279) | Google Scholar See all References . Mutations in a human gene homologous to a rat soluble adenylate cyclase are associated with familial absorptive hypercalciuria and decreased bone mineral density⁴ x 4 Reed, B.Y., Gitomer, W.L., Heller, H.J. et al. Identification and characterization of a gene with base substitutions associated with the absorptive hypercalciuria phenotype and low spinal bone density. J Clin Endocrinol Metab. 2002; 87: 1476–1485 https://doi.org/10.1210/jc.87.4.1476 Crossref | PubMed | Scopus (102) | Google Scholar See all References . An animal model, the genetic hypercalciuric rat, is known to form calcium stones⁵ x 5 Bushinsky, D.A. Genetic hypercalciuric stone-forming rats. Curr Opin Nephrol Hypertens. 1999; 8: 479–488 Crossref | PubMed | Scopus (39) | Google Scholar See all References . Progressive generations of these rats have successively higher levels of calciuria, suggesting the involvement of multiple genes.