BackgroundRecently published guidelines on the medical management of renal stone disease did not address relevant topics in the field of idiopathic calcium nephrolithiasis, which are important also for clinical research.DesignA steering committee identified 27 questions, which were proposed to a faculty of 44 experts in nephrolithiasis and allied fields. A systematic review of the literature was conducted and 5216 potentially relevant articles were selected; from these, 407 articles were deemed to provide useful scientific information. The Faculty, divided into working groups, analysed the relevant literature. Preliminary statements developed by each group were exhaustively discussed in plenary sessions and approved.ResultsStatements were developed to inform clinicians on the identification of secondary forms of calcium nephrolithiasis and systemic complications; on the definition of idiopathic calcium nephrolithiasis; on the use of urinary tests of crystallization and of surgical observations during stone treatment in the management of these patients; on the identification of patients warranting preventive measures; on the role of fluid and nutritional measures and of drugs to prevent recurrent episodes of stones; and finally, on the cooperation between the urologist and nephrologist in the renal stone patients.ConclusionsThis document has addressed idiopathic calcium nephrolithiasis from the perspective of a disease that can associate with systemic disorders, emphasizing the interplay needed between urologists and nephrologists. It is complementary to the American Urological Association and European Association of Urology guidelines. Future areas for research are identified.

Objective-Proton magnetic resonance spectroscopy ( 1 H-MRS) has been increasingly used to examine striatal neurochemistry in adult major depressive disorder. This study extends the use of this modality to pediatric major depression to test the hypothesis that adolescents with major depression have elevated concentrations of striatal choline and creatine and lower concentrations of N-acetylaspartate.Method-Fourteen adolescents (ages 12-19 years, eight female) who had major depressive disorder for at least 8 weeks and a severity score of 40 or higher on the Children's Depression Rating Scale -Revised and 10 healthy comparison adolescents (six female) group-matched for gender, age, and handedness were enrolled. All underwent three-dimensional 3-T 1 H-MRS at high spatial resolution (0.75-cm 3 voxels). Relative levels of choline, creatine, and N-acetylaspartate in the left and right caudate, putamen, and thalamus were scaled into concentrations using phantom replacement, and levels were compared for the two cohorts.Results-Relative to comparison subjects, adolescents with major depressive disorder had significantly elevated concentrations of choline (2.11 mM versus 1.56 mM) and creatine (6.65 mM versus 5.26 mM) in the left caudate. No other neurochemical differences were observed between the groups.Conclusions-These findings most likely reflect accelerated membrane turnover and impaired metabolism in the left caudate. The results are consistent with prior imaging reports of focal and lateralized abnormalities in the caudate in adult major depression.Rates of major depressive disorder rise dramatically in adolescence, with an estimated lifetime prevalence of 15% in adolescents by ages 15-18. Major depression is associated with significant morbidity, including deterioration in academic functioning, increased risk of substance use, and attempted and completed suicides (1,2). Furthermore, adolescent major depression is a strong predictor of major depression in adulthood, which carries its own burden of disadvantage (3). These findings highlight the need for specific neurobiological research in adolescent major depression.Converging lines of evidence suggest that the pathophysiology of depression entails impairment of cellular resilience and neuroplasticity in specific cortical, subcortical, and limbic brain regions. The relationship between the basal ganglia and depression has been inferred from the high comorbidity between depression and Parkinson's disease as well as Huntington's NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript disease, both basal ganglia-related disorders. In addition, morphometric studies (but not all) and functional neuroimaging studies have documented smaller caudate, putamen, and thalamus as well as impaired metabolism and blood flow in the striatum and thalamus in depression (4-10).Proton magnetic resonance spectroscopy ( 1 H-MRS) has provided additional evidence for the involvement of the striatum in adult major depression. 1 H-MRS provides metabolic assay of ne...

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Background Impaired renal H+ ion secretion causes acid retention which is known to promote bone dissolution Objectives To prospectively assess the prevalence of distal renal tubular acidosis (dRTA) in low bone mass patients (LBM) and the effects of alkali treatment. Methods Between January 1, 2006, and December 31, 2010, we screened all LBM referred for metabolic evaluation of T-Scores ≤ -1.0 at lumbar spine and/or hip (measured by Hologic or Lunar) for dRTA. Calcium intake (mineral waters and dairy products) was assessed by food content tables. In fasting venous blood, Ca++, venous bicarbonate (VenBic) and creatinine (Crea) were measured by blood gas analyzer, 25-OH-vitamin D (25-OH-D) by immunoassay. LBM with hypercalcemic disorders were excluded. In fasting urines, calcium (Ca), citrate (Cit) and Crea were measured, and renal calcium reabsorption (CaR) was calculated as filtered calcium (Ca++) - excreted calcium (CaE). In all 182 LBM (156 F, 26 M, age 17-86 ys.), pH was measured (Metrohm pH-meter) in 2nd morning urines (U-pH) after 12 hrs. of fasting. If U-pH remained >5.80, LBM underwent 1-day acid loading by ammonium chloride (NH4Cl, 50 mg/kg BW in 3 oral doses), and U-pH and venous blood were remeasured the next morning. Normal values for acid loading were obtained from 21 healthy controls (C, 11 F, 10 M, age 25-80 yrs.). The acidifying effect of NH4Cl was assessed by measuring urine Ca, Cit and Crea in 17 C and 35 LBM. All LBM with dRTA were recommended alkali citrate (K-Cit), and follow-up DXAs were obtained until 1/2014. Paired and unpaired t-tests were used for statistics, values are mean±SD. Results 84 LBM with U-pH >5.80 underwent NH4Cl loading; this caused U-pH to drop from 6.64±0.54 to 5.62±0.69 (p<0.0001) vs. from 5.71±0.55 to 5.09±0.17 in C (p<0.001). The fall in U-Cit/Crea (p<0.0001 in all subjects) proved the systemic effects of NH4Cl. If U-pH remained >5.44 (mean + 2 SDs of C) after NH4Cl, dRTA was diagnosed; this was found in 42 LBM (39 F, 3 M), i.e. 23.1%. Since VenBic was normal, all cases had incomplete dRTA (idRTA) by definition. Daily calcium intake and 25-OH-D were not different between subgroups. At baseline, CaR (mmol/l) was reduced in idRTA (1.17±0.04 vs. 1.22 + 0.03 in C, p=0.005). NH4Cl lowered VenBic (mEq/l) by 1.35±1.75 in C (p<0.005) and 1.44±2.60 in Non-RTA (p<0.05), but only by 0.71±2.59 in idRTA (NS). After NH4Cl, urine CaE rose insignificantly and equally in all subgroups, whereas blood Ca++ (mmol/l) increased only in idRTA (0.023±0.057, p=0.042), suggesting enhanced Ca release from bone. Baseline bone mineral densities were equal in Non-RTA and idRTA. Among idRTA, 15 were lost for follow-up. In idRTA adherent to K-Cit for 1.6-7 years (n=19), T-scores rose from -2.14±0.81 to -1.72±0.88 (p<0.001) at lumbar spine, but did not change at total hip and femoral neck. In idRTA not taking K-Cit (n=7), T-scores at all sites were unchanged. Conclusions 1) The prevalence of idRTA in LBM is surprisingly high, i.e. 23%; 2) Upon acid loading, idRTA do not lower VenBic and U-pH nor...