Urinary N-acetyl-β-D-glucosaminidase activity in rabbits with experimental hypercalciuria

Routinely used renal function tests remain normal in uncomplicated hypercalciuria. The aim of this study was to assess the value of N-acetyl-β-D-glucosaminidase (NAG), a sensitive marker of renal proximal tubular damage, in experimental hypercalciuria. Oral calcium providing 75 mg/kg per day elementary calcium and 20,000 IU/day vitamin D₃ was administered for 15 days to 7 rabbits (Orytolagus cuniculus-New Zealand white) and 7 rabbits were given placebo as a control group. Serum calcium, phosphorus, and alkaline phosphatase, daily urinary calcium excretion and NAG/creatinine ratio were measured before and after drug administration. Kidneys were examined macroscopically and microscopically following the study period. Serum calcium, phosphorus and urinary calcium excretion increased, while alkaline phosphatase decreased significantly in response to drug treatment [10.8±1.5 vs. 12.2±1.3 mg/dl, 4.6±0.6 vs. 6.7±0.7 mg/dl, 22.3±8.3 vs. 46.8±22.5 mg/kg per day, and 138.0±57.1 vs. 70.1±33.1 IU/l, respectively (P <0.05)]. The NAG/creatinine ratio prior to the study (0.5±0.1 mU/mg) was significantly different from that after the study (5.4±1.5 mU/mg, P <0.01). In the control group, changes in serum and urinary parameters were not significant (P >0.05). The relationship between the urinary NAG/creatinine ratio and the daily urinary calcium excretion was statistically significant (r = 0.67, P <0.05). In the study group, nephrocalcinosis was present in all rabbits except 1 (85.7%), whereas none of the control group rabbits had nephrocalcinosis. In conclusion, in rabbits urinary NAG excretion increases significantly in nephrocalcinosis induced by hypercalciuria. Received February 12, 1996; received in revised form November 25, 1996; accepted November 27, 1996     

Effect of combined supplementation of magnesium oxide and pyridoxine in calcium-oxalate stone formers

A combined supplement of magnesium oxide (300 mg/day) and pyridoxine·HCl (10 mg/day) was given p.o. to 16 recurrent calcium oxalate (CaOx) stone formers, and its therapeutic efficacy was biochemically evaluated by measuring various parameters of blood (Na, K, Mg, urea, creatinine, calcium, phosphate, uric acid, alanine transaminase, aspartate transaminase and alkaline phosphatase) and urine (volume, pH, creatinine, Na, K, Mg, uric acid, calcium, phosphate, oxalate and citrate) at 0, 30, 60, 90 and 120 days of treatment. Serum Mg significantly (P<0.01) increased after 30 days of treatment and remained constant thereafter while other blood parameters were unaltered. Combined treatment led to a significant increase in the urinary excretion of Mg and citrate over pretreatment values while oxalate excretion showed a gradual and significant decline during the therapy. The results confirmed the efficacy of MgO-pyridoxine supplementation in terms of changes in urinary excretion of lithogenic and inhibitory components, leading to a significant (P<0.01) decrease in CaOx risk index from 0.09±0.04 at 0 day to 0.05±0.02 after 120 days of treatment.     

Clinical and biochemical profile of patients with “pure” uric acid nephrolithiasis compared with “pure” calcium oxalate stone formers

The purpose of the present study was to compare the clinical characteristics of “pure” uric acid (UA) stone formers with that of “pure” calcium oxalate (CaOx) stone formers and to determine whether renal handling of UA, urinary pH, and urinary excretion of promoters and inhibitors of stone formation were different between the two groups. Study subjects comprised 59 patients identified by records of stone analysis: 30 of them had “pure” UA stones and 29 had “pure” CaOx nephrolithiasis. Both groups underwent full outpatient evaluation of stone risk analysis that included renal handling of UA and urinary pH. Compared to CaOx stone formers, UA stone formers were older (53.3 ± 11.8 years vs. 44.5 ± 10.0 years; P = 0.003); they had higher mean weight (88.6 ± 12.5 kg vs. 78.0 ± 11.0 kg; P = 0.001) and body mass index (29.5 ± 4.2 kg/m² vs. 26.3 ± 3.5 kg/m²; P = 0.002) with a greater proportion of obese subjects (43.3% vs. 16.1%; P = 0.01). Patients with “pure” UA lithiasis had significantly lower UA clearance, UA fractional excretion, and UA/creatinine ratio, with significantly higher serum UA. The mean urinary pH was significantly lower in UA stone formers compared to CaOx stone formers (5.17 ± 0.20 vs. 5.93 ± 0.42; P < 0.0001). Patients with CaOx stones were a decade younger, having higher 24-h urinary calcium excretion (218.5 ± 56.3 mg/24 h vs. 181.3 ± 57.1 mg/24 h; P = 0.01) and a higher activity product index for CaOx [AP (CaOx) index]. Overweight/obesity and older age associated with low urine pH were the principal characteristic of “pure” UA stone formers. Impairment in urate excretion associated with increased serum UA was also another characteristic of UA stone formers that resembles patients with primary gout. Patients with pure CaOx stones were younger; they had a low proportion of obese subjects, a higher urinary calcium excretion, and a higher AP index for CaOx.     

Pediatric urolithiasis in southern Israel: the role of uricosuria

We describe three cases of severe obstructive uropathy in children under 2 years of age, due to radio-lucent renal stones. Metabolic work-up revealed only normouricemic hyperuricosuria (HU) as the single identifiable risk factor for urolithiasis (UL) in these infants. We reviewed records of 66 cases of pediatric UL seen in our service over an 8-year period. UL prevalence was greater for Bedouin than for Jewish children (1.02 vs. 0.13 cases/1,000 inhabitants at risk respectively, P<0.01). HU (>0.6 mg uric acid/dl GFR) was the only biochemical risk factor that differed between Bedouin and Jewish children (mean uric acid excretion index 0.8±0.39 vs. 0.55±0.26 mg/dl GFRrespectively, P<0.05). Bedouin children comprised 85% of patients in the HU group versus 59% in the non-hyperuricosuric group (P<0.05). The mean age of onset of UL was 38±44 months and 93±52 months in the HU and the non-HU group, respectively (P<0.05). The UA excretion index in the HU group was inversely correlated with age (r=0.41, P<0.01) and its slope and constant were different from an age-matched non-UL control population. In conclusion, pediatric UL in southern Israel is predominant in Bedouin toddlers. HU was the only identifiable biochemical risk factor that could explain this difference. Received: 3 November 1999 / Revised: 8 February 2000 / Accepted: 9 February 2000     

Effect of heavy exercise on mineral metabolism and calcium regulating hormone in humans

Summary The relationship between acid base status and mineral metabolism after heavy exercise has been examined in 12 healthy subjects. Following burst exercise (duration 60–130 sec) to the point of exhaustion, blood pH had decreased (7.42±0.01 vs. 7.18±0.02,P<0.001) and plasma ionized calcium had increased (1.09±0.01 vs. 1.22±0.02 mmol/liter,P<0.001). Log ionized calcium concentration showed a significant negative correlation with pH (r=−0.90). Although plasma total calcium increased after exercise (2.47±0.05 vs. 2.67±0.04 mmol/liter,P<0.001), this change was not seen if the observed values were corrected for the accompanying increase in plasma protein concentration, suggesting that hemoconcentration accounted for these increments. Significant increases were also seen in plasma inorganic phosphate concentration, though not in plasma magnesium. Radioimmunoassay of parathyroid hormone using two different region-specific assays, one directed at the mid-region/carboxy-terminal and the other at the amino-terminal portion of the molecule, and of calcitonin, showed no change during exercise-induced hypercalcemia. The results do not suggest significant skeletal buffering of this type of acidosis and indicate that the changes in ionized calcium associated with short bursts of intense exercise are directly related to acidosis and that those in total calcium are a consequence of hemoconcentration.     

Effects of buffering in hypercapnia and hypercapnic hypoxemia

Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (Paco_2-20 kPa) at Fio₂ 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 ±0.01 vs 7.01±0.01 (mean ± s.e.mean, P < 0.01). Serum osmolality and Paco₂ did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 ± 6 vs 189±12 min^-1 (P < 0.01), mean arterial pressure (MAP) 109 ± 4 vs 124 ± 4 mmHg (14.5 ± 0.5 vs 16.5 ± 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16±1 vs 23 ± 1 mmHg (2.1 ±0.1 vs 3.1 ±0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 ± 21 vs 343 ± 20 dyn s-cm^-5 (2490±210 vs 3430±200 μN-s-cm^-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in Fio₂ (0.15, 0.10, 0.05) at 30-min intervals, while Fico₂ was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At Fio₂ 0.15, buffered animals had higher arterial oxygen saturation (73 ± 5%) than the controls (55 ± 5%), (P < 0.05). The control animals died after 1–29 min (mean 14 min) at Fio₂ 0.10, while all buffered animals survived Fio₂ 0.10 with stable MAP (122 ± 14 mmHg (16.3 ± 1.9 kPa). The buffered animals died after 4–22 min (mean 15 min) at Fio₂ 0.05. We conclude that buffering to a pH of 7.21 attenuates the observed hemodynamic response in extreme hypercapnia and improves survival in hypercapnic hypoxemia.     

Potassium citrate supplementation results in sustained improvement in calcium balance in older men and women

The dietary acid load created by the typical Western diet may adversely impact the skeleton by disrupting calcium metabolism. Whether neutralizing dietary acid with alkaline potassium salts results in sustained improvements in calcium balance remains controversial. In this randomized, double‐blind, placebo‐controlled study, 52 men and women (mean age 65.2 ± 6.2 years) were randomly assigned to potassium citrate 60 mmol/d, 90 mmol/d, or placebo daily with measurements of bone turnover markers, net acid excretion, and calcium metabolism, including intestinal fractional calcium absorption and calcium balance, obtained at baseline and at 6 months. At 6 months, net acid excretion was significantly lower in both treatment groups compared to placebo and it was negative, meaning subjects' dietary acid was completely neutralized (?11.3 mmol/d on 60 mmol/d; ?29.5 mmol/d on 90 mmol/d, p < 0.001 compared to placebo). At 6 months, 24‐hour urine calcium was significantly reduced in persons taking potassium citrate 60 mmol/d (?46 ± 15.9 mg/d) and 90 mmol/d (?59 ± 31.6 mg/d) compared with placebo (p < 0.01). Fractional calcium absorption was not changed by potassium citrate supplementation. Net calcium balance was significantly improved in participants taking potassium citrate 90 mmol/d compared to placebo (142 ± 80 mg/d on 90 mmol/d versus ?80 ± 54 mg/d on placebo; p = 0.02). Calcium balance was also improved on potassium citrate 60 mmol/d, but this did not reach statistical significance (p = 0.18). Serum C‐telopeptide decreased significantly in both potassium citrate groups compared to placebo (?34.6 ± 39.1 ng/L on 90 mmol/d, p = 0.05; ?71.6 ± 40.7 ng/L on 60 mmol/d, p = 0.02) whereas bone‐specific alkaline phosphatase did not change. Intact parathyroid hormone was significantly decreased in the 90 mmol/d group (p = 0.01). Readily available, safe, and easily administered in an oral form, potassium citrate has the potential to improve skeletal health. Longer‐term trials with definitive outcomes such as bone density and fracture are needed. © 2013 American Society for Bone and Mineral Research.     

Urinary calcium excretion in healthy school children

Two hundred and twenty Argentinian primary school children (122 boys, 98 girls, aged 6 – 13 years) were studied to establish reference values of 24-h urinary calcium excretion (UCa) and calcium/creatinine ratio (Ca/Cr) in 24-h urine collections and in first-morning urine samples. Mean UCa excretion was 2.05±1.40 mg/kg per day and the 95th percentile was 4.74 mg/kg per day. UCa excretion was higher in boys than girls (2.33±1.47 and 1.70±1.24 mg/kg per day respectively, P <0.001). Statistically significant differences were found between the 6- to 9-year and the 10- to 13-year age groups (2.37±1.49 vs. 1.73±1.25 mg/kg per day, P <0.001). Mean Ca/Cr ratios in 24-h collections and in first-morning urine samples were 0.129±0.086 and 0.105±0.079 for the group overall (P <0.001). The Ca/Cr ratio in the first-morning urine sample correlated poorly with the 24-h calcium excretion, suggesting that the Ca/Cr ratio in first-morning urine samples cannot replace the 24-h measurement. Received December 22, 1995; received in revised form June 17, 1996; accepted June 18, 1996     

Long-term nephrotoxicity of cisplatin, ifosfamide, and methotrexate in osteosarcoma

The acute renal effects of chemotherapy are known, but long-term nephrotoxicity has rarely been investigated. The aim of the present study was to assess long-term renal function in children and adolescents who received at-risk chemotherapy, including cisplatin, ifosfamide, and methotrexate, to treat an osteosarcoma. Renal function tests [creatinine clearance, microalbuminuria, and renal excretion of sodium, potassium, chloride, calcium, magnesium (Mg), phosphorus (P), and uric acid] were prospectively performed 5.4±2.2 (±SD) years after chemotherapy (total cumulative dose: methotrexate 41±31 g/m², ifosfamide 39±14 g/m², cisplatin 674±188 mg/m²) in 18 children and adolescents. The results were compared with 13 normal volunteers matched for age and sex. Creatinine clearance, which was greater than 80 ml/min per 1.73 m² in all patients, correlated with the total dose of ifosfamide (r=0.55, P<0.05) and cisplatin (r=0.48, P<0.05). Microalbuminuria was noted in 4 patients. Hypomagnesemia was present in 4 and hypercalciuria in 3 patients; renal excretion of P, Mg, and uric acid was higher in patients than in controls. Glomerular function was not significantly altered and only mild tubular dysfunction was present. Since renal excretion of P and Mg were increased in patients compared with normal volunteers and hypercalciuria was occasionally seen, divalent ion disorders are the most-likely potential complications. Received September 29, 1997; received in revised form December 12, 1997; accepted February 18, 1998     

Fibroblast Growth Factor–23 Levels Are Associated With Uric Acid But Not Carotid Intima Media Thickness in Renal Transplant Recipients

IntroductionCardiovascular disease (CVD) is the leading cause of mortality in chronic kidney disease (CKD) patients. Fibroblast growth factor–23 (FGF-23) is associated with atherosclerosis and cardiovascular mortality in CKD patients and healthy subjects. However, data in renal transplant recipients (RTR) are scarce. We aimed to determine factors associated with FGF-23 and to explore its relationship to atherosclerosis.MethodsForty-six patients and 44 controls were included. FGF-23 was measured from plasma. Carotid intima media thickness (CIMT) was evaluated ultrasonographically.ResultsPatients had higher waist circumference (WC; 92.2 ± 14.9 vs 85.3 ± 11.0 cm; P < .05), glucose (99.8 ± 17.2 vs 90.3 ± 6.5 mg/dL; P < .01), creatinine (1.43 ± 0.6 vs 0.86 ± 0.1 mg/dL; P < .01), triglyceride (160.4 ± 58.9 vs 135.6 ± 59.8 mg/dL; P < .05), white blood cells (WBC; 7938.6 ± 2105.2 vs 6715.7 ± 1807.5 WBC/mm³; P < .01), ferritin (217.0 ± 255.8 vs 108.3 ± 142.4 ng/mL; P < .05), uric acid (6.5 ± 1.6 vs 4.7 ± 1.3 mg/dL; P < .01), C-reactive protein (CRP; 8.2 ± 18.2 vs 5.3 ± 7.9 mg/L; P < .01), parathyroid hormone (PTH; 89.7 ± 59.2 vs 44.1 ± 16.7 pg/mL; P < .01), and alkaline phosphatase (ALP; 162.5 ± 86.6 vs 74.2 ± 21.9 U/L; P < .01). FGF-23 was higher in patients (11.7 ± 7.2 vs 9.6 ± 6.8 pg/mL; P < .05). CIMT was similar (0.58 ± 0.09 vs 0.57 ± 0.1 mm; P > .05). WC, creatinine, and uric acid were positively correlated with FGF-23, whereas albumin showed negative correlation. On multivariate analysis only creatinine and uric acid were determinants of FGF-23.ConclusionFGF-23 levels are associated with uric acid in RTR. Larger studies are needed to confirm this finding.     

Zinc transport by the heart lymphatic system after acute myocardial infarction

Open-chest dog preparations were used to determine divalent cation transport following acute myocardial infarction. Cardiac lymph flow, lymph and plasma protein, zinc, calcium, and magnesium content and hemodynamic measurements were recorded every 20 min before and after coronary artery occlusion in sham operated (N = 4), infarcted (N = 6), and lymph-ablated animals (N = 4). During the 4-hr occlusion period, with constant blood pressure, lymph flow increased from 1.53 ± 0.25 to 2.15 ± 0.44 mg/hr (SEM), P < 0.01. Zinc decreased in plasma from 0.69 ± 0.10 to 0.41 ± 0.08 μg/ml, P < 0.01, and in lymph from 0.69 ± 0.08 to 0.40 ± 0.02 μg/ml, P < 0.01. Zinc to protein ratio decreased similarly to total zinc in plasma and lymph. Changes in calcium and magnesium were insignificant. Lymph to plasma concentration ratios increased for protein from 0.57 ± 0.05 to 0.62 ± 0.02, P < 0.05, and for zinc from 1.10 ± 0.26 to 1.21 ± 0.14, P < 0.05. Heart lymph clearance (lymph:plasma ratio × lymph flow) steadily rose for protein from 0.31 to 0.06 to 0.50 ± 0.08, P < 0.05, and for zinc from 0.59 ± 0.18 to 0.92 ± 0.15, P < 0.05. Lymph and plasma measurements did not change significantly in shamoperated animals. Plasma zinc remained unchanged from baseline after coronary occlusion in all lymphablated animals. The increased clearance of protein and zinc suggests that plasma proteins are zinc carriers after acute myocardial infarction and that the reduction of plasma zinc is dependent upon an intact cardiac lymphatic circulation.     

Diurnal Rhythm of Urinary Calcium Excretion in Adults

Twenty-four-hour urinary calcium excretion is normally the equivalent of daily calcium intake, and varies between 200–300 mg/dL with a calcium/creatinine ratio of 0.07–0.15. In this study, we aimed to investigate the diurnal rhythm of calcium excretion in healthy individual. Forty subjects (30 male, 10 female) were involved into the study. The spot urine samples were taken at 08:00, 14:00, and 22:00 together with a 24-hour collection. Mean spot urinary calcium levels at 08:00, 14:00, and 22:00 were 12.39 ± 8.19, 12.97 ± 8.37, and 16.95 ± 10.39 mg/dL, with calcium/creatinine ratios of 0.104 ± 5.26l, 0.119 ± 7.85, and 0.133 ± 8.17, respectively. Twenty-four-hour urinary calcium excretion was 12.74 ± 7.31 mg/dL with a calcium/creatinine ratio of 0.111 ± 5.41. The values at 08:00, 14:00, and of 24-hour collection were statistically similar (p > 0.05), but the nighttime values were significantly elevated (p < 0.05). In conclusion, calcium excretion is increased at night, and urinary calcium measurements should be interpreted accordingly.     

Effects of phosphorus-containing calcium preparation (bone meal powder) and calcium carbonate on serum calcium and phosphorus in young and old healthy volunteers: a double-blinded crossover study

To evaluate the effects of bone meal powder (BEC) on calcium and phosphorus metabolism, a calcium absorption test was conducted using a preparation of calcium carbonate (CAC) as the control drug. A total of 12 healthy volunteers, consisting of 6 younger (aged 20–29 years, 3 men and 3 women) and 6 older (aged 60–69 years, 3 men and 3 women) persons, were subjected to a double-blinded crossover study. Serum calcium (s-Ca) level significantly increased to 105.3% ± 1.9% (P < 0.01 vs the basal value; mean ± SD) from the basal value in the BEC group and to 104.4% ± 2.7% (P < 0.01) in the CAC group at 3 h post load. Urinary excretions of calcium (u-Ca/glomerular filtration rate, u-Ca/GF) after BEC and CAC load rose to 226.6% ± 154.5% (P < 0.05) and 211.1% ± 148.0% (P < 0.05), respectively. Serum phosphorus (s-P) levels after BEC load increased to 110.0% ± 15.1% (P < 0.05), whereas that after CAC load showed no significant change (99.3% ± 7.9%). On the other hand, urinary excretion of phosphorus (u-P/GF) after CAC load decreased to 60.0% ± 32.4% (P < 0.01) and that in the BEC group showed no significant change (92.5% ± 49.5%). The increase in s-Ca led to decrease in serum intact parathyroid hormone (i-PTH) level [77.3% ± 33.4% (P < 0.05) for BEC and 69.5% ± 20.3% (P < 0.01) for CAC] although s-P was increased by the BEC load. The responses to BEC and CAC administration were compared in the younger and the older groups. The responses in the younger and the older group showed fundamentally the same trends and to the same extent. However, the changes in serum ionized calcium (i-Ca) and i-PTH levels at 1.5 h post load were significantly smaller in the older group than in the younger group (P < 0.01; P < 0.05). The increment in s-P level after BEC load in the older group was larger than that in the younger group. In conclusion, BEC can modulate not only calcium but also phosphorus metabolism in both younger and older subjects. Further investigations are required to evaluate the effects of BEC on bone density and safety for renal function in long-term observations. Received: January 31, 2000 / Accepted: April 17, 2000     

Cystinuria: the South Indian experience

Gout is well known to be produced by increased uric acid level in blood. The objective of this paper is to assess the relationship between gout and calcium oxalate stone formation in the humans. 48 patients with combination of gout and calcium oxalate stone problem were included. The biochemical values of this group were compared with 38 randomly selected uric acid stone patients with gout, 43 stone patients with gout alone, 100 calcium oxalate stone patients without gout and 30 controls, making a total of 259 patients. Various biochemical parameters, namely serum calcium, phosphorus and uric acid and 24-h urine calcium, phosphorus, uric acid, oxalate, citrate and magnesium were analysed. ANOVA and Duncan’s multiple-range tests were performed to assess statistical significance of the variations. The promoters of stone formation, namely serum calcium (P < 0.05), phosphorus (P < 0.05) and uric acid (P < 0.05) and urine calcium (P < 0.05), uric acid (P < 0.05) and oxalate (P < 0.05) were significantly variable in the different groups. The inhibitor citrate (P < 0.05) was also significantly variable. Multiple-range test showed that the promoters, namely serum calcium (P < 0.05) and urine uric acid (P < 0.05) were in a significantly higher range in the gouty patients, gouty uric acid stone patients and gouty calcium oxalate stone patients compared to the non-gouty patients and controls. Urine oxalate (P < 0.0001) was in the highest range in the gouty calcium oxalate or gouty uric acid stones patients. The inhibitor urine citrate (P < 0.001) was significantly lower in the gouty, gouty uric acid and gouty calcium oxalate patients. Serum uric acid was highest in the non-stone gouty patients, followed by the gouty uric acid stone formers and gouty calcium oxalate stone patients. The high values of promoters, namely uric acid and calcium in the gouty stone patients indicate the tendency for urinary stone formation in the gouty stone patients. There is probably a correlation between gout and calcium oxalate urinary stone. We presume this mechanism is achieved through the uric acid metabolism. The findings point to the summation effect of metabolic changes in development of stone disease.     

The effects of muscle-building exercise on bone mineral density of the radius,spine, and hip in young men

Summary We previously demonstrated that muscle-building exercise is associated with increases in serum Gla-protein, serum 1,25(OH)₂D, and urinary cyclic AMP. These studies were interpreted to mean that this form of exercise increases bone formation and modifies the vitamin D-endocrine system to provide more calcium for bone. The present investigation was carried out in normal young adult white men to determine the effects of exercise on bone mineral density at weight-bearing and nonweight-bearing sites. Twelve men who had regularly engaged in muscle-building exercises (use of weights, exercise machines, or both) for at least 1 year and 50 age-matched controls (aged 19–40 years) were studied. The body weights of the two groups were not different from each other (78±2 vs. 74±1 kg, NS). Bone mineral density (BMD) of the lumbar spine, trochanter, and femoral neck was measured by dual-photon absorptiometry, and BMD of the midradius was measured by single-photon absorptiometry. It was found that muscle-building exercise was associated with increased BMD at the lumbar spine (1.35±0.03 vs. 1.22±0.02 g/cm²,P<0.01), trochanter (0.99±0.04 vs. 0.86±0.02 g/cm²,P<0.01), and femoral neck (1.18 ±0.03 vs. 1.02±0.02 g/cm²,P<0.001) but not at the midradius (0.77±0.02 vs. 0.77±0.01 g/cm², NS). These studies provide additional evidence that muscle-building exercise is associated with increases in BMD at weight-bearing sites but not at nonweight-bearing sites.     

Calcium oxalate stone and gout

Gout is well known to be produced by increased uric acid level in blood. The objective of this paper is to assess the relationship between gout and calcium oxalate stone formation in the humans. 48 patients with combination of gout and calcium oxalate stone problem were included. The biochemical values of this group were compared with 38 randomly selected uric acid stone patients with gout, 43 stone patients with gout alone, 100 calcium oxalate stone patients without gout and 30 controls, making a total of 259 patients. Various biochemical parameters, namely serum calcium, phosphorus and uric acid and 24-h urine calcium, phosphorus, uric acid, oxalate, citrate and magnesium were analysed. ANOVA and Duncan’s multiple-range tests were performed to assess statistical significance of the variations. The promoters of stone formation, namely serum calcium (P < 0.05), phosphorus (P < 0.05) and uric acid (P < 0.05) and urine calcium (P < 0.05), uric acid (P < 0.05) and oxalate (P < 0.05) were significantly variable in the different groups. The inhibitor citrate (P < 0.05) was also significantly variable. Multiple-range test showed that the promoters, namely serum calcium (P < 0.05) and urine uric acid (P < 0.05) were in a significantly higher range in the gouty patients, gouty uric acid stone patients and gouty calcium oxalate stone patients compared to the non-gouty patients and controls. Urine oxalate (P < 0.0001) was in the highest range in the gouty calcium oxalate or gouty uric acid stones patients. The inhibitor urine citrate (P < 0.001) was significantly lower in the gouty, gouty uric acid and gouty calcium oxalate patients. Serum uric acid was highest in the non-stone gouty patients, followed by the gouty uric acid stone formers and gouty calcium oxalate stone patients. The high values of promoters, namely uric acid and calcium in the gouty stone patients indicate the tendency for urinary stone formation in the gouty stone patients. There is probably a correlation between gout and calcium oxalate urinary stone. We presume this mechanism is achieved through the uric acid metabolism. The findings point to the summation effect of metabolic changes in development of stone disease.     

Urinary calcium excretion in healthy Thai children

The objective of this study was to determine age-specific reference values for urinary calcium/creatinine ratios (UCa/Cr) of children in southern Thailand. Non-fasting urine samples were collected from a random population of 488 healthy children (282 males, 206 females) ranging in age from 17 days to 15 years. Samples were divided into six groups by age. Subjects whose calcium levels exceeded the 95th percentile within each age group were classified as having hypercalciuria. Pyuria, hematuria, proteinuria, urinary sodium, and potassium levels in children with normal UCa/Cr were compared with levels in children with high UCa/Cr. The 95th percentiles for UCa/Cr (mg/mg) by age were: <6 months, 0.75; 6 months to <12 months, 0.64; 12 months to <2 years, 0.40; 2 years to <5 years, 0.38; 5 years to <10 years, 0.29; and 10 years to <15 years, 0.26. Pyuria, hematuria, and proteinuria were no more prevalent in the 22 children with hypercalciuria than in children with normal urinary calcium levels. Urinary sodium/creatinine ratios (UNa/Cr) and urinary sodium/potassium ratios (UNa/K) were correlated with UCa/Cr (r=0.41, P<0.0001 and r=0.24, P<0.0001, respectively). Urinary potassium/creatinine ratios (UK/Cr) were not (r=0.05, P>0.1)). Children with high UCa/Cr ratios also had higher UNa/Cr and UNa/K (5.6±7.1 vs. 2.6±1.5, P<0.001 and 5.4±2.3 vs. 2.5±0.23, P<0.05, respectively) The study established reference values for random, non-fasting UCa/Cr for healthy Thai children and indicated that urinalysis is not a good indicator of hypercalciuria. Received: 30 April 1999 / Revised: 19 August 1999 / Accepted: 19 August 1999     

Effect of potential renal acid load of foods on urinary citrate excretion in calcium renal stone formers

The aim of this study was to investigate the influence of the potential renal acid load (PRAL) of the diet on the urinary risk factors for renal stone formation. The present series comprises 187 consecutive renal calcium stone patients (114 males, 73 females) who were studied in our stone clinic. Each patient was subjected to an investigation including a 24-h dietary record and 24-h urine sample taken over the same period. Nutrients and calories were calculated by means of food composition tables using a computerized procedure. Daily PRAL was calculated considering the mineral and protein composition of foods, the mean intestinal absorption rate for each nutrient and the metabolism of sulfur-containing amino acids. Sodium, potassium, calcium, magnesium, phosphate, oxalate, urate, citrate, and creatinine levels were measured in the urine. The mean daily PRAL was higher in male than in female patients (24.1±24.0 vs 16.1±20.1 mEq/day, P=0.000). A significantly (P=0.01) negative correlation (R=−0.18) was found between daily PRAL and daily urinary citrate, but no correlation between PRAL and urinary calcium, oxalate, and urate was shown. Daily urinary calcium (R=0.186, P=0.011) and uric acid (R=0.157, P=0.033) were significantly related to the dietary intake of protein. Daily urinary citrate was significantly related to the intakes of copper (R=0.178, P=0.015), riboflavin (R=0.20, P=0.006), piridoxine (R=0.169, P=0.021) and biotin (R=0.196, P=0.007). The regression analysis by stepwise selection confirmed the significant negative correlation between PRAL and urinary citrate (P=0.002) and the significant positive correlation between riboflavin and urinary citrate (P=0.000). Urinary citrate excretion of renal stone formers (RSFs) is highly dependant from dietary acid load. The computation of the renal acid load is advisable to investigate the role of diet in the pathogenesis of calcium stone disease and it is also a useful tool to evaluate the lithogenic potential of the diet of the individual patient.     

Renal physiology in elderly persons with severe immobility syndrome

Objective  The immobility syndrome (IS) is a common condition in the elderly and consists of a reduction in the capacity to perform daily activities because of motor function deterioration. This syndrome leads to characteristic structural and physiological changes in the body, but renal physiology studies have not been conducted on this population. For this reason, we decided to study prospectively changes in renal function in these individuals. Material and methods  We enrolled into this study 17 volunteers over 64 years of age, all of whom lived in the same nursing home. The patients were divided into two groups: nine healthy mobile persons and eight others who suffered from severe IS. Exclusion criteria were the presence of any disease or use of any drug that could induce water and electrolytes alteration. Blood and urine samples were drawn to measure sodium, potassium, creatinine, urea, calcium, phosphorus, magnesium, and uric acid in order to obtain their fractional excretion. Plasma osmolality and vasopressin were also measured. Total body water and lean body mass were obtained by bioelectrical impedance analysis. Statistical analysis was performed applying Student’s t-test (P = 0.01) and Pearson’s correlation test. Results  A significant difference in body water composition was found between the groups. Thus in the IS group plasma sodium level was slightly lower and total water content was significantly higher than in the mobile subjects: 140 ± 5 vs. 143 ± 1 mmol/l (P = 0.01); 61 ± 8% vs. 50 ± 10% (P < 0.001), respectively. Despite these differences, plasma osmolality and vasopressin values were within the normal range in both groups. However, there was a good positive correlation between these two variables in the mobile group only: R 0.9 (mobile) vs. R −0.2 (immobile). We found no significant difference in plasma creatinine or fractional excretion of sodium, potassium, calcium, phosphorus, magnesium, urea, and uric acid between the groups. Conclusion  Total body water content was significantly higher in the elderly who suffered from severe immobility syndrome than in healthy mobile elderly. In contrast with the mobile group, for which there was a good positive correlation between plasma osmolality and plasma vasopressin, for individuals with IS there was no correlation between plasma osmolality and plasma vasopressin.