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Parathyroidectomy (PTX) is routinely performed in hypercalciuric renal stone patients with primary hyperparathyroidism (PHPT). However, some data indicate a persistent stone activity following PTX, raising the issue of the link between PHPT and stone disease. We performed an observational study on 30 renal stone patients diagnosed with PHPT. Patients were selected among 1448 hypercalciuric patients referred in our department for a diagnostic evaluation. Patients with no parathyroid surgery or any biological follow-up were excluded. Clinical and biological data (including 24-h urine collection and a calcium load test) were collected before and within 12 months following surgery. Stone recurrence was evaluated by direct phone contact (median 43 months). Comparison of biological data before and after surgery showed a significant decrease of ionized calcium and serum parathyroid hormone after PTX. All stones contained calcium-dependent species such as carbapatite, brushite or dihydrate calcium oxalate. Urine saturation indexes and calciuria significantly decreased after surgery (from 9.9 to 5.9 mmol/d, p < 0.0001), but a persistent hypercalciuria was detected in 47% of patients. The other stone risk factors including diuresis stayed similar. Stone activity that was increasing (from 0.20–0.30 to 0.50–0.75/year) the 2 years before PTX, significantly decreased after surgery [0.05–0.15/year (p < 0.001)]. PTX in calcium-dependent renal stone formers with PHPT significantly decreases both stone recurrence and urine saturation indexes. However, PTX unmasked an underlying renal stone disease related to idiopathic hypercalciuria in half of patients with a remaining stone activity, testifying the need for patient's follow-up to prevent stone recurrence. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency is frequent in pediatric nephrology. The 2017 European guidelines recommend keeping 25OH vitamin D (25-D) levels within the 75-120 nmol/L range, ideally with daily supplementation. Intermittent supplementation with D3 has also been proposed. We aimed to assess the influence of our local protocol of intermittent vitamin D supplementation on the evolution of 25-D levels between baseline and 2 months. VITATOL is a prospective single-center study performed in our tertiary unit in children and teenagers followed for chronic kidney disease (CKD), kidney transplantation, or stable chronic nephrotic syndrome with 25-D levels below 75 nmol/L. Intermittent oral cholecalciferol (100,000 IU) was administered depending on baseline vitamin D levels and body weight. The primary outcome was the change in 25-D levels between baseline and 2 months. Secondary outcomes were the evolution of the main mineral biomarkers. Thirty-seven patients were included. Two months after beginning supplementation, corresponding to a median(min-max) of 46 (14-79) days after the last dose of vitamin D, 25-D levels increased from 50 to 76 nmol/L (p < 0.001), 18 patients having 25-D levels within the target range and 2 above. All patients displayed 25-D levels above 50 nmol/L. There were no significant changes in phosphate, PTH, alkaline phosphatase, and FGF23 levels before and after supplementation. Calcium levels increased from 2.39 to 2.44 mmol/L (p = 0.017), but no differences in calciuria and urinary calcium/creatinine ratio were observed.Conclusion: This vitamin D supplementation protocol using intermittent moderate doses of cholecalciferol seems efficient in 54% of cases, with neither significant overdose nor hypercalciuria. What is Known: • Vitamin D deficiency is frequent in pediatric nephrology. • The 2017 European guidelines recommend keeping 25OH vitamin D levels within the 75-120 nmol/L range ideally with daily supplementation, but intermittent supplementation with D3 has also been proposed. What is New: • We assessed the influence of a local protocol of intermittent vitamin D supplementation on the evolution of 25-D levels between baseline and 2 months in children and teenagers followed in pediatric nephrology. • The intermittent cholecalciferol supplementation protocol seems efficient in 54% of cases, with neither significant overdose nor hypercalciuria. [ABSTRACT FROM AUTHOR]

Background: There is a paucity of data on blood pressures (BP), urinary albumin, and mineral excretion in early childhood in contemporary cohorts of extremely low gestational age (GA) neonates. Our aim was to compare BPs and the urinary excretion of albumin, calcium, and phosphate in preterm and term-born cohorts in early childhood. Methods: This was a prospective observational study conducted at a single center, involving children <5 years age, born preterm (GA <30 weeks) or at term (≥37 weeks' GA). Urinary albumin (mg/L), calcium and phosphate levels indexed to creatinine (mg/dL), and BP were measured. Results: The median (IQR) follow-up age of our cohort ( n = 106) was 30 (16-48) months. Preterm-born children ( n = 55) had a significantly lower mean GA and birth weight and higher mean systolic, diastolic, and mean BPs, compared with term ( n = 51) controls. A significantly higher proportion of preterm-born children weighed <10th centile and had systolic BP >95th centile at follow-up. Albumin and calcium excretion did not differ between the groups; median urine-phosphate creatinine ratios were higher in the preterm group. On logistic regression, lower GA and younger age at follow-up were significantly associated with an increased risk of systolic and diastolic BP above the 95th centile; male gender was associated with decreased risk of diastolic hypertension. Conclusions: Even in early childhood, children born preterm had significantly elevated BP, compared with their term-born counterparts. Closer monitoring of BPs in this population may be warranted. [ABSTRACT FROM AUTHOR]

The aim of this study was to analyze the presence of lithogenic metabolic factors in the blood and urine of patients with osteopenia versus osteoporosis. This is a cross-sectional study including 67 patients who were divided into two groups according to the presence of either osteopenia or osteoporosis as measured by bone densitometry: group 1-40 patients with osteopenia (22 men and 18 women) and group 2-27 patients with osteoporosis (13 men and 14 women). Metabolic studies were performed on the blood and urine; statistical analysis was performed comparing means and conducting linear correlation and multivariate analyses with SPSS. Statistical significance was considered to be p ≤ 0.05. The mean age of patients in group 1 was 52.9 ± 12.8 years versus 50.3 ± 11.4 in group 2; the difference was not statistically significant. In group 2, higher levels of osteocalcin, β-crosslaps, urinary calcium, fasting urine calcium/creatinine, 24 h urine calcium/creatinine and 24 h oxaluria were observed compared to group 1. In the multivariate analysis, only the β-crosslaps and urinary calcium were independently associated with osteoporosis. It would be advisable to determine the urinary calcium levels in patients with osteoporosis since altered levels may necessitate modifying the diagnostic and therapeutic approach to osteoporosis. [ABSTRACT FROM AUTHOR]

Background: Hypercalciuria and hypocitraturia are considered the most important risk factors for urolithiasis. Citrate binds to urinary calcium to form a soluble complex which decreases the availability of ionized calcium (Ca) necessary for calcium oxalate formation and phosphate crystallization. The aims of this study were to assess the Ca fraction in relation to total calciuria, citraturia and urinary pH and to determine whether urinary Ca concentration is a helpful biomarker in metabolic evaluation of children with urolithiasis. Methods: We collected 24-h urine samples from 123 stone-forming children and adolescents with hypocitraturia and from 424 healthy controls. Total calciuria (total calcium, Ca), Ca, pH, citrate, oxalate and Bonn Risk Index (BRI) were assessed and compared between the two groups. Results: Total calciuria and Ca content were higher in stone-formers than in the healthy children. In both stone-formers and controls, Ca content was inversely related to citraturia and urinary pH, whereas the Ca/Ca ratio differed slightly between the groups. A large variability in Ca level was found across individuals in both groups. The BRI increased with increasing calciuria and urine acidity. Conclusions: Compared to controls, stone-formers with hypocitraturia demonstrated a higher urinary Ca concentration, but this was proportional to calciuria. The large individual variability in urinary Ca content limits its practical use in metabolic evaluation of children with urolithiasis. However, the Ca/Citrate ratio may be a useful clinical tool in evaluating children with urolithiasis. [ABSTRACT FROM AUTHOR]

Background: Renal complications in acromegaly include glomerular hyperfiltration, insulin resistance, hypercalciuria and urolithiasis. The aim of this study was to investigate whether urinary calcium (U) excretion is a direct consequence of growth hormone secretion or secondary to hyperfiltration and/or insulin resistance. Methods: We performed a cross-sectional study of 58 patients diagnosed with acromegaly. Demographic data were obtained, serum analysis was performed, including insulin-like growth factor (IGF)-1, and 24-h urine collection, to measure urinary protein excretion, U and phosphate excretion, as well as fractional excretion of sodium and potassium. We also calculated the homeostasis model assessment of insulin resistance (HOMA-IR). Results: Patients were predominantly male (60.3%), and their mean age was 45.9 ± 14 years. Hypercalciuria was present in 24% of patients. Patients with higher HOMA-IR had higher IGF-1 levels, a trend toward higher body mass index and higher U excretion. In univariate analysis, U excretion was associated with HOMA-IR ( r = 0.472, P = 0.001), phosphaturia ( r = 0.457, P = 0.001), IGF-1 ( r = 0.398, P = 0.002) and creatinine clearance ( r = 0.394, P = 0.001). HOMA-IR and phosphaturia were independently associated with U excretion. No independent associations were found between phosphaturia and HOMA-IR or IGF-1. Conclusions: The present study revealed an association between hypercalciuria and insulin resistance in patients with acromegaly. Further studies are required to fully understand the pathogenesis of these abnormalities in patients with acromegaly. [ABSTRACT FROM AUTHOR]

The effects of glucose, sorbitol and xylitol ingestion on calciuria, oxaluria and phosphaturia in healthy black and white males on a standardized diet were investigated. After ingestion, they collected urine hourly for 3 h. Glucose decreased phosphaturia in blacks. Sorbitol decreased phosphaturia in both groups and increased oxaluria in whites. Xylitol increased oxaluria in blacks. Decreases in phosphaturia are attributed to penetration by phosphate into cells leading to decreases in phosphatemia and the renal filtered load. We suggest that this mechanism is more sensitive in blacks. We speculate that the increase in oxaluria after sorbitol ingestion occurs via its conversion to glyoxylate and that this pathway may be blocked in blacks. For the increase in oxaluria after xylitol ingestion, it is hypothesized that ketohexokinase and aldolase may be more active in blacks. Our results demonstrate, for the first time, a urinary effect due to sorbitol ingestion and an ethnic dependency of these and other effects. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated reduced bone mineral density (BMD) and biochemical changes of excessive bone resorption in some patients with idiopathic hypercalciuria (IH). Consequently, bisphosphonates have been successfully employed in research animals and adults with IH and reduced BMD. We evaluated the effect of treatment with bisphosphonates in seven patients ages 10–16 years with persistent IH and reduced BMD. In five children, preceding traditional therapy failed. All children received oral alendronate and one also IV Zoledronic acid for 6–18 (median 9.0, mean 10.7) months. With treatment, BMD Z scores in the lumbar spine improved from −2.0 ± 0.3 to −0.8 ± 0.8 ( p = 0.002) and in the femoral neck from −1.8 ± 0.4 to −0.7 ± 0.9 ( p = 0.01); urine N-telopeptides/creatinine decreased from 372 ± 289 to 72 ± 39 nmol/mmol ( p = 0.05) and calcium/creatinine from 0.29 ± 0.12 to 0.13 ± 0.06 mg/mg ( p = 0.009). Height Z scores, normal at baseline in all, remained unaffected, and no new stones or fractures were documented throughout the treatment period. Serum creatinine, electrolytes, calcium, phosphorus and parathyroid hormone remained normal as well. In summary, in children with IH and decreased BMD, treatment with bisphosphonates normalized urine calcium excretion, eliminated urinary symptoms, and significantly improved reduced BMD. These short-term beneficial effects indicate the need for larger prospective studies on the potential of bisphosphonates to serve as a new tool in treating children with IH and reduced BMD. [ABSTRACT FROM AUTHOR]

Idiopathic hypercalciuria is a defect occurring in 5–10% of the general population and most commonly detected in patients with calcium kidney stones or osteoporosis. Although high-penetrance autosomal dominant inheritance cannot be ruled out, hypercalciuria is probably a polygenic phenomenon. Findings obtained in monogenic disorders characterized by renal calcium stones, and/or hypercalciuria, and/or nephrocalcinosis, have suggested a number of genes as candidate genes in the pathogenesis of idiopathic hypercalciuria, i.e. soluble adenylate cyclase, calcium sensing receptor, vitamin D receptor and 1-alpha hydroxylase, sodium-phosphate co-transporter-2, claudin-16, chloride channel 5, etc. All the genetic findings obtained so far do not support the idea of different types of idiopathic hypercalciuria, i.e. absorptive, renal, and resorptive. On the contrary, they support clinical observations, which suggest idiopathic hypercalciuria as a single disorder characterized by altered calcium transport in the intestine, kidney and bone, due to various different combinations of multiple genetic and dietary players. [ABSTRACT FROM AUTHOR]

Coexpression studies in Xenopus oocytes revealed the ability of the serum- and glucocorticoid-inducible kinase 1 (SGK1) to stimulate the renal epithelial Ca2+ channel TRPV5. SGK1 increases the abundance of the channel protein in the plasma membrane, an effect requiring the participation of the Na+/H+ exchanger regulating factor 2 (NHERF2). The present study was performed to explore the role of SGK1 in the regulation of renal Ca2+ handling in vivo. To this end, TRPV5, calbindin D-28K abundance, and renal Ca2+ excretion were analyzed in gene-targeted mice lacking functional SGK1 ( sgk1 −/− ) and their age- and sex-matched littermates ( sgk1 +/+ ). Immunohistochemistry revealed lower abundance of TRPV5 and calbindin D-28K protein in sgk1 −/− mice than in sgk1 +/+ mice, both fed with control diet. Feeding the mice a Ca2+-deficient diet marked ly increased TRPV5 protein abundance in both genotypes. Renal Ca2+ excretion under control diet was significantly lower in sgk1 −/− than in sgk1 +/+ mice. The Ca2+-deficient diet decreased renal excretion of Ca2+ to the same levels in both phenotypes. Furosemide increased fractional Ca2+ excretion and dissipated the difference between phenotypes. We conclude that lack of SGK1 may lead to decrease in TRPV5 abundance in connecting tubules but does not abrogate TRPV5 regulation. The decrease in abundance of TRPV5 in connecting tubules of sgk1 −/− mice is presumably compensated for by enhanced Ca2+ reabsorption in upstream nephron segments such as the loop of Henle, which may indirectly result from impaired SGK1-dependent Na+ reabsorption in the aldosterone-sensitive distal part of the nephron, salt loss, and enhanced Na+ (and Ca2+) reabsorption in those upstream nephron segments. [ABSTRACT FROM AUTHOR]

Effect of pyridoxine (Vitamin-B6) supplementation on calciuria and oxaluria levels of 20 normal healthy persons and 17 urinary stone patients has been studied. Mean 24 hr urinary calcium and oxalate levels of controls (healthy persons) and stone patients were estimated in presupplementation period and at every 20 days interval during supplementation. Stone patients were divided into two groups viz., mild hyperoxaluriacs and moderate hyperoxaluriacs, based on their pre-supplementation (base line) oxaluria levels. 60 days of pyridoxine supplementation, at the rate of 10 mg/day, resulted in a significant decrease (p<0.01 for mild hyperoxaluriacs and p<0.001 for moderate hyperoxaluriacs) in mean 24 hr urinary oxalate levels of urinary stone patients. The corresponding decrement in mean oxaluria level of controls was, however, only mild. The decrease of mean calciuria level of controls as well as stone patients, upon pyridoxine supplementation, were also found to be only mild and not significant. Utility of pyridoxine therapy in oxalate urolithiasis has been discussed in the light of results. [ABSTRACT FROM AUTHOR]

We investigated the changes in renal excretion of calcium, sodium, and potassium in asthmatic children treated with inhaled budesonide, an inhaled glucocorticoid. Twenty-two asthmatic patients (7 female, 15 male, mean age 10.1±4.3 years) treated with 400-600 μg/day inhaled budesonide and 23 healthy children (6 female, 17 male, mean age 10.2±2.8 years) were enrolled in the study. The parameters recorded were serum sodium, potassium, calcium, phosphorus, alkaline phosphatase (ALP), type I collagen carboxyterminal telopeptide (ICTP), osteocalcin, intact parathyroid hormone (PTH) levels, first spot morning urine calcium/creatinine ratio, sodium/potassium ratio, and daily renal calcium excretion rate (UCa-ER). These parameters were measured in the control group and pre- and post-budesonide treatment in asthmatic children. Serum electrolytes, ALP, PTH, ICTP, and UCa-ER were in the normal ranges and were not significantly different between controls and asthmatic children. Serum levels of ICTP increased, while levels of osteocalcin decreased after budesonide therapy in the asthmatic group (P=0.001, P=0.005). UCa-ER was decreased after budesonide therapy in asthmatics (P=0.000). In conclusion, moderate doses of inhaled budesonide cause hypocalciuria and decreased bone turnover. These results may be attributed to a mechanism compensating for decreased absorption of calcium in the gut due to the topical effect of swallowed budesonide rather than the systemic effects of the drug. Increased bone metabolism and decreased turnover may have an important role in this compensatory mechanism. [ABSTRACT FROM AUTHOR]

The objective of the study was to update the evaluation and treatment of idiopathic urolithiasis in children in Western society. A secondary goal was to evaluate patients' compliance with high fluid intake. Over 2 years we prospectively studied children referred to us for idiopathic urolithiasis confirmed radiographically, excluding those with secondary disorders. A metabolic urinalysis, which included calcium, citrate, uric acid, oxalate, cystine, and creatinine, was ordered in all patients. Hypercalciuric patients were first treated with a low-sodium (Na)/high-potassium (K) diet and if hypercalciuria persisted, thiazides or potassium citrate was added. Follow-up ultrasound scans were scheduled every 10-12 months. Urine specific gravity (SG) measured during clinic visits was used to assess compliance with high fluid intake. A survey was sent to pediatric urologists and nephrologists to establish a recommended maximal SG value. Thirty healthy school-aged children served as controls. There were 45 children (24 males, 21 females) aged 10.4±2.0 years (median 11.0) studied. Stones were retrieved and analyzed in 28 showing calcium composition in all. Urine chemistry analysis was incomplete in 3, and in the others showed hypercalciuria in 33 (78.6%), hypocitraturia in 1 (2.4%), and normal values in 8 (19.0%). Treatment of 33 hypercalciuric patients consisted of diet alone in 13, potassium citrate in 17, thiazides in 2, and potassium citrate and thiazide in 1. All 33 achieved normocalciuria, apart from 2 who remained mildly hypercalciuric on diet alone. The 12 normocalciuric children were treated by diet modification alone. Followup ultrasonography showed no new stones in 36 of 39 patients. In 3, new stone formation was associated with recurrence of hypercalciuria after the potassium citrate dose was lowered or discontinued. Upon their first clinic visit, the urine SG of stone formers (1.021±0.007) was significantly higher than the maximum SG recommended by 18 physicians of 1.010±0.003 (P<0.001), and not different from the SG in the control group (1.018±0.007). Urine SG at follow-up visits was unchanged in stone formers. We therefore propose a step-wise approach in evaluating children with idiopathic urolithiasis in Western society, in which first only urine calcium is studied. Only if urine calcium is normal, should other chemistries be studied. In many hypercalciuric children, low-Na/high-K diet alone is effective, while in most others the addition of potassium citrate is well tolerated, normalizes calciuria, and protects against new stone formation. Children rarely comply with the recommendation of high fluid intake. [ABSTRACT FROM AUTHOR]

: The urine-acidifying properties of food constituents depend on their content of non-oxidizable acids or precursors. Acidifying constituents such as animal proteins may negatively affect calcium metabolism and accelerate bone resorption, thus representing an aggravating factor for osteoporosis. This four-period, double-crossover study investigated whether a diet intervention specifically focused on acid load could modify calcium metabolism in humans. Eight healthy volunteers underwent a four-day metabolic preparation with two types of diets, one rich in acid ash-forming nutrients, and one providing base-forming nutrients (including bicarbonate-rich mineral water), both having similar contents of calcium, phosphate, sodium, proteins and calories. On the fourth day, a single oral dose of 1 g calcium was given, either as carbonate or as gluconolactate. Serial blood and urine samples revealed that the diet affected blood pH (average difference 0.014, p = 0.002) and urine pH (average difference 1.02, p<0.0001) in the expected direction, but had no influence on the absorption of the calcium supplement. The acid-forming diet increased urinary calcium excretion by 74% when compared with the base-forming diet (p<0.0001), both at baseline and after the oral calcium load, and C-telopeptide excretion by 19% (p = 0.01), suggesting a skeletal origin for the excess calcium output. This observation confirms that renally excreted acids derived from food influence calcium metabolism, and that alkalizing nutrients inhibit bone resorption. Further studies are needed to determine the clinical impact of dietary counseling for avoiding diet acids as a preventive measure against osteoporosis. [ABSTRACT FROM AUTHOR]

Male rats weighing approximately 250 g were given streptozotocin (STZ), 60 mg/kg, i.p., on two successive days. Six h after the last STZ injection, some STZ-diabetic rats began receiving daily injections of insulin (NPH, 1.5 U, s.c.). At various times after the above treatments the following studies were performed: control rats, STZ-diabetic rats and NPH-treated STZ-diabetic rats were injected s.c. with calcium-45 and housed individually in metabolic cages. Urine from each rat was collected at 24 h intervals for two weeks. Volumes, osmolalities, glucose concentrations, total calcium and radioactivity due to calcium-45 were measured. The results of the studies showed that: STZ-diabetes caused rapid urinary excretion of the injectedCa and increased renal excretion ofCa; the increased urinary excretion of calcium was not due to an osmotic effect or to a direct nephrotoxic action of STZ; and insulin therapy instituted early, but insufficient to control blood glucose, significantly reduced the diabetes-induced calcium loss. [ABSTRACT FROM AUTHOR]

Gallium nitrate (GaN) reduces cancer-related hypercalcemia and inhibits bone resorption in vitro. This study investigated the effects of chronic GaN administration on bone, kidney, and parathyroid gland activity of growing rats. Experimental animals received GaN (1.75 mg elemental gallium i.p. QOD X 8, Ga+), and controls received the solvent (Ga-). In the bone of Ga+ rats the number of osteoclasts was increased (Ga+: 70.4 +/- 2.31 osteoclasts/mm2; Ga-: 46.5 +/- 1.61 osteoclasts/mm2, P less than 0.001), and apposition rate and osteoid width were unchanged. Ga was concentrated in bone (2.4 mumol/g cortical bone) and detected by electron microprobe on the surface of a few trabeculae. Alkaline (Alp) and acid (Acp) phosphatase activities were higher in Ga+ than in Ga- calvaria (Ga+: Alp 223 +/- 23.4 U/mg prot, Ga-: Alp 145 +/- 13.3 U/mg prot, P less than 0.02; Ga+: Acp 69.5 +/- 4.7 U/mg prot, Ga-: 57.5 +/- 2.8 U/mg prot, P less than 0.05). Serum iPTH was increased (Ga+: 112.9 +/- 17.6 pg/ml, Ga-: 41.4 +/- 7.4 pg/ml, P less than 0.01), serum calcium was reduced (Ga+: 2.4 +/- 0.02 mmol/l, Ga-: 2.6 +/- 0.03 mmol/l, P less than 0.001); calciuria remained comparable to controls. Relative to the hypocalcemia this suggests renal loss of Ca. The calcemic response to hPTH 1-34 (i.v. 50 micrograms/kg) was decreased 2 hours after injection of the hormone (delta Ca: TPTX Ga+: 0.11 +/- 0.04 mmol/l, Ga-: 0.33 +/- 0.03 mmol/l P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) [ABSTRACT FROM AUTHOR]

Pharmacological inhibition of parathyroid hormone (PTH) secretion has been the object of several experimental and clinical trials in the past. It is only recently that a drug, WR-2721 [S-,2-(3-aminopropylamino)-,ethylphosphorothioic acid], has been shown to effectively inhibit PTH secretion in euparathyroid subjects and in parathyroid cancer patients within a few hours after its administration. In the present study we tested its long term efficacy as a PTH inhibitor in a model of nephrocalcinosis resulting from secondary hyperparathyroidism. Intact and thyroparathyroidectomized (TPTX) rats were pair-fed on a low Ca (0.2%)-high phosphorus (1.6%) diet (nephrocalcinotic diet) or on a normal Ca (1.1%)-normal phosphorus (0.8%) diet for 7 days. Simultaneously, either 0.2 mmol/kg of WR-2721 or its solvent was injected subcutaneously twice daily. The intact animals on the nephrocalcinotic diet had an increased urinary cyclic AMP excretion and important renal Ca accumulation. This nephrocalcinosis was markedly reduced by WR-2721 treatment. The kidney Ca content of the WR-2721-treated rats was 58 +/- 6% lower than that of the nontreated animals. The low Ca-high phosphorus diet did not cause nephrocalcinosis in the TPTX rats. WR-2721 failed to reduce the nephrocalcinosis induced by 1,25 dihydroxyvitamin D3 intoxication in TPTX rats fed the normal Ca-normal phosphorus diet. In conclusion, the present study suggests that chronic treatment with WR-2721, a potent inhibitor of PTH secretion, may be effective for preventing the deleterious consequences of hyperparathyroidism, such as nephrocalcinosis. [ABSTRACT FROM AUTHOR]

The effects of dietary supplementation with granulated guar gum (21 g/day in three divided doses at the main meals), were compared with placebo response during three months in a doubleblind, cross-over trial in 11 Type 2 (insulin-independent) diabetics. The nine patients who completed the study (two dropped out because of side-effects) showed a significant reduction in both basal and postprandial hyperglycaemia as well as of urinary excretion of glucose during guar gum supplementation. No change in mean bodyweight was observed during the study. Mean fasting and post-prandial plasma insulin levels were similar during both study periods, but the two subjects who received no oral hypoglycaemic agents had lower insulin levels during the guar gum period. Mean serum total- and LDL-cholesterol concentrations were significantly lower during the guar gum period, whereas the HDL-cholesterol level remained unchanged. Long-term administration of guar gum induced a sustained improvement in diabetic control in Type 2 diabetes. [ABSTRACT FROM AUTHOR]

Nephrocalcinosis was demonstrated by computerized tomography (CT) in all five children with Bartter's syndrome followed at our institution. In three of these five patients, nephrocalcinosis was also noted on ultrasound examination. Hypercalciuria was present in only one case. The mechanism leading to renal calcification remains unclear in this disease. It is noteworthy, however, that Bartter's syndrome is associated with such a high incidence of nephrocalcinosis. [ABSTRACT FROM AUTHOR]

Twelve male farmers (38 ± 14 years of age, mean ± SD) were exposed to 7.3 ± 2.2 mg formic acid/m for 8 h in the silage making (mean ± SD, N=12). Each gave urine samples immediately, 15 h and 30 h after the end of the exposure. The excretion of formate was linearly related to the exposure 15 and 30 h after the exposure. Exposure increased renal ammoniagenesis and urinary calcium at 30 h post-exposure. Both biochemical effects may be explained by the interaction of formic acid with the oxidative metabolism of renal tubular cells, as formic acid is a known inhibitor of the cytochrome oxidase. In view of these renal effects, the current hygienic limits may not entirely protect exposed individuals. [ABSTRACT FROM AUTHOR]