The Role of Inhibitors and other Factors in the Pathogenesis of Recurrent Calcium-Containing Renal Stones

1977 ◽  
Vol 53 (2) ◽  
pp. 141-148 ◽  
Author(s):  
J. M. Baumann ◽  
S. Bisaz ◽  
R. Felix ◽  
H. Fleisch ◽  
U. Ganz ◽  
...  
Keyword(s):  
Inhibitory Activity ◽  
Stone Formation ◽  
Renal Stones ◽  
Urinary Calcium ◽  
Stone Disease ◽  
Calcium Excretion ◽  
Crystal Formation ◽  
Inorganic Pyrophosphate ◽  
Control Subjects ◽  
Stone Formers

1. In order to assess the relative importance of possible pathogenetic factors in the formation of calcium-containing renal stones, a group of 18 patients (12 men, six women) with active, recurrent stone disease were compared with 16 age-matched control subjects (10 men, six women) given an identical diet. 2. Fifteen (83%) of the patients showed at least one, eight (44%) showed two, and one (6%) patient showed three abnormalities that might predispose to stone formation. 3. Increased urinary calcium excretion was the most common abnormality (11 patients, 61%), particularly in the women (83%). 4. A diminished excretion of inhibitors of crystal formation of calcium phosphate was the next most common abnormality, which occurred in eight patients (44%), all of whom were men. It was largely attributable to a diminished excretion of inorganic pyrophosphate (PPi). The PPi/orthophosphate ratios were also lower in the stone-formers. Significant differences in residual inhibitory activity after enzymatic removal of PPi between control subjects and stone-formers could not be found in 24 h urine samples but were present during certain times of the day. Pyrophosphate showed a higher inhibitory activity in urine than in control solutions, this enhancement being absent in stone-formers. 5. Nine (50%) of the patients, but only one of the control subjects, produced crystal aggregates greater than 50 μm in diameter after an oral load of oxalate.

Renal Stones and Intravenous Fielding

PEDIATRICS ◽  
1980 ◽  
Vol 65 (4) ◽  
pp. 861-861
Author(s):  
Jose F. Pascual
Keyword(s):  
Calcium Phosphate ◽  
Renal Stone ◽  
Potent Inhibitor ◽  
Stone Formation ◽  
Renal Stones ◽  
Urinary Calcium ◽  
Etiologic Factor ◽  
Calcium Excretion ◽  
Crystal Formation ◽  
Calcium Infusion

Adelman et al1 report nephrolithiasis as another complication that may be seen associated with total parenteral nutrition (TPN). The authors implicate parenteral calcium infusion as the cause of calcium phosphate calculi in their patient. Another possible etiologic factor in renal stone formation is that of hypophosphatemia. Urinary excretion of pyrophosphate, a potent inhibitor of calcium crystal formation, is decreased in the presence of hypophosphatemia, thus favoring calculi formation. It has also been shown that a decrease in cellular phosphate in the renal cortex2 may stimulate increased formation of 1,25(OH)2D3, which in turn will cause an increase in urinary calcium excretion.3

scholarly journals CALCIUM

2010 ◽  
Vol 17 (04) ◽  
pp. 698-701
Author(s):  
MUHAMMAD ISHAQ ◽  
ISRAR AHMED AKHUND ◽  
MOULA BUX LAGHARI ◽  
Muhammad Sabir
Keyword(s):  
Urinary Tract ◽  
Serum Calcium ◽  
Upper Urinary Tract ◽  
Urinary Calcium ◽  
Stone Disease ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Stone Formers ◽  
Study Results ◽  
Urinary Tract Stone

Aims & Objectives: To evaluate the effects of Serum Calcium and Urinary Calcium excretion on upper urinary tract stone diseases in the Peshawar (a high stone incidence belt). Subjects & Methods: One hundred patients (age 20-60years) who were suffering severely from upper urinary tract stone disease were selected from LRH and Hayatabad Medical Complex Hospitals of Peshawar, same numbers of healthy controls from the same region were also selected for the study. Results: When results were summed up and testParameters were compared, it was seen that mean Serum Calcium in stone formers was greater than that of non-stone formers (P<0.001). Same pattern was also observed (P< 0.001) in both groups regarding mean urinary calcium excretion. Conclusions: We concluded that calcium is a definitive risk factor in upper urinary tract stone disease. However we suggest further work and research on wide scale population inorder to evaluate this relation. 

scholarly journals The Variability and Dietary Dependence of Urinary Oxalate Excretion in Recurrent Calcium Stone Formers

1987 ◽  
Vol 24 (4) ◽  
pp. 385-390 ◽  
Author(s):  
J M Brown ◽  
G Stratmann ◽  
D M Cowley ◽  
B M Mottram ◽  
A H Chalmers
Keyword(s):  
Calcium Intake ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Stone Disease ◽  
Calcium Excretion ◽  
Urinary Oxalate ◽  
Calcium Stone ◽  
Oxalate Excretion ◽  
Stone Formers ◽  
Urinary Oxalate Excretion

Twenty-two recurrent calcium stone formers had 24-h urinary oxalate excretions on their home diets which were significantly greater than those of 30 normal subjects (0·48±0·23 mmol/d; mean±SD compared with 0·31±0·11; P<0·01). The stone formers also demonstrated marked day to day variability in oxalate excretion indicating that a single normal urinary oxalate measurement did not exclude significant hyperoxaluria at other times. On a hospital diet containing 1000 mg calcium per day, urinary oxalate excretion fell significantly from 0·48±0·23 mmol/d to 0·32±0·12; P<0·01. As the urinary calcium excretion in and out of hospital was similar, it seems unlikely that low calcium intake at home was responsible for the hyperoxaluria. All patients had recurrent symptomatic stone disease and had been advised to avoid foods rich in oxalate. Whilst poor compliance is a possible explanation for the variability in oxalate excretion, we believe it is more likely that there is an inadvertent intake of oxalogenic precursors in their diet. As normal subjects do not demonstrate hyperoxaluria on similar home diets, stone formers may have a metabolic defect in the handling of these precursors.

Hyperoxaluria in Idiopathic Calcium Stone Disease: Further Evidence of Intestinal Hyperabsorption of Oxalate

1982 ◽  
Vol 63 (4) ◽  
pp. 381-385 ◽  
Author(s):  
M. Marangella ◽  
B. Fruttero ◽  
M. Bruno ◽  
F. Linari
Keyword(s):  
Intestinal Absorption ◽  
Direct Relationship ◽  
Urinary Calcium ◽  
Stone Disease ◽  
Calcium Excretion ◽  
Calcium Stone ◽  
Oxalate Excretion ◽  
Oxalate Absorption ◽  
Stone Formers ◽  
Kinetics Of

1. Seventeen healthy controls and 63 patients with idiopathic calcium stone disease of the urinary tract were investigated for urinary calcium and oxalate excretion and for [14C]oxalate intestinal absorption. 2. Under comparable controlled dietary intake a significant increase in calcium excretion was found in patients with stone disease. Oxalate excretion and [14C]oxalate intestinal absorption were mildly but not significantly increased. When patients with stone disease were subdivided into normocalciuric and hypercalciuric subjects, oxalate excretion and [14C]oxalate absorption were significantly increased in the latter. There was a significant direct relationship between calcium excretion and both oxalate excretion and [14C]oxalate absorption. 3. [14C]Oxalate absorption increased significantly in 22 stone-formers when dietary calcium was changed from normal to low. 4. The kinetics of [14C]oxalate intestinal absorption showed that the main difference between normocalciuric and hypercalciuric subjects occurred within the first 6 h after the oxalate-labelled meal. 5. These results confirm that mild hyperoxaluria is a frequent feature of idiopathic calcium stone disease even when patients and controls are studied under controlled dietary conditions. Our data are consistent with the hypothesis that hyperoxaluria is secondary to calcium hyperabsorption and is upper intestinal in origin.

scholarly journals Urinary phosphorus rather than urinary calcium possibly increases renal stone formation in a sample of Asian Indian, male stone-formers

2007 ◽  
Vol 98 (6) ◽  
pp. 1224-1228 ◽  
Author(s):  
Shoma Berkemeyer ◽  
Anupam Bhargava ◽  
Usha Bhargava
Keyword(s):  
Renal Stone ◽  
Stone Formation ◽  
Renal Stones ◽  
Urinary Calcium ◽  
Healthy Controls ◽  
Dietary Intakes ◽  
Stone Formers ◽  
Dietary Record ◽  
Biochemical Analyses ◽  
Serum And Urine

The contribution of dietary Ca and P in renal stone formation is debated. Thus, the main objective was to investigate if there were any differences in the dietary, serum and urine values of Ca and P in stone formers (SF) compared with healthy controls (HC). The secondary aim was to analyse if dietary, serum and urine Ca and P correlated. The study enrolled ten patients with renal stones admitted for stone removal and ten healthy controls. Their dietary macronutrients, Ca and P intakes were calculated from 2-d dietary records. On the second day of dietary record 24-h urine was collected and on the third day morning a 5 ml blood sample was collected. Biochemical analyses were conducted for serum and urine Ca, P and uric acid with qualitative renal stone analysis. All the dietary intakes and urine P were significantly higher (P < 0·05) in SF than in HC. Correlation results showed that in SF dietary Ca correlated to serum and urine Ca. No such correlations were seen for P. Additionally, in SF urine Ca correlated to dietary proteins and fats but not to carbohydrates. None of the biochemical values lay outside the normal range of values. The study suggests urine P rather than urine Ca to be probably at work in the formation of renal stones. Limitation of protein intake with normal Ca intakes could provide a suitable measure to avoid renal stone formation.

Calcium Oxalate Crystalluria and Urine Saturation in Recurrent Renal Stone-Formers

1971 ◽  
Vol 40 (5) ◽  
pp. 365-374 ◽  
Author(s):  
W. G. Robertson ◽  
M. Peacock ◽  
B. E. C. Nordin
Keyword(s):  
Calcium Oxalate ◽  
Stone Formation ◽  
Basal Diet ◽  
Renal Stones ◽  
Degree Of Saturation ◽  
Sodium Oxalate ◽  
Spontaneous Crystallization ◽  
Control Series ◽  
Control Subjects ◽  
Stone Formers

1. The degree of saturation with calcium oxalate has been determined in fresh urine samples from six patients with recurrent calcium oxalate-containing renal stones and six normal control subjects who were studied under the same conditions of diet and fluid intake. 2. The degree of saturation of urine with calcium oxalate was significantly higher in the group of stone-formers than in the control series and more often exceeded the amount needed for spontaneous crystallization of calcium oxalate (formation product). This was accounted for by the higher concentration of calcium and oxalate in the urine of the stone-formers. 3. Crystals of calcium oxalate were observed in all freshly examined urines in which the formation product of calcium oxalate was exceeded. Since the formation product of calcium oxalate was exceeded more often in the urines of stone-formers than in the urines of the control subjects, this accounted for the greater calcium oxalate crystalluria of the stone-formers. 4. Addition of a small quantity of sodium oxalate to the basal diets of the two groups resulted in a greater increase in the urine saturation and calcium oxalate crystalluria of the stone-formers, thus accentuating the difference observed between the two groups when they were given the basal diet. 5. Calcium oxalate crystalluria was related quantitatively to the degree of over-saturation of urine with calcium oxalate, although uric acid solubility may play a small role at low pH values. 6. The results are consistent with a ‘hyperexcretion—crystallization’ mechanism of stone formation.

scholarly journals Calcium and Vitamin D Supplementation and Their Association with Kidney Stone Disease: A Narrative Review

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4363
Author(s):  
Matteo Bargagli ◽  
Pietro Manuel Ferraro ◽  
Matteo Vittori ◽  
Gianmarco Lombardi ◽  
Giovanni Gambaro ◽  
...  
Keyword(s):  
Vitamin D ◽  
Kidney Stone ◽  
Stone Formation ◽  
Vitamin D Supplementation ◽  
Stone Disease ◽  
Normal Body Mass Index ◽  
Calcium Excretion ◽  
Kidney Stone Disease ◽  
Low Calcium Diet ◽  
Stone Formers

Kidney stone disease is a multifactorial condition influenced by both genetic predisposition and environmental factors such as lifestyle and dietary habits. Although different monogenic polymorphisms have been proposed as playing a causal role for calcium nephrolithiasis, the prevalence of these mutations in the general population and their complete pathogenetic pathway is yet to be determined. General dietary advice for kidney stone formers includes elevated fluid intake, dietary restriction of sodium and animal proteins, avoidance of a low calcium diet, maintenance of a normal body mass index, and elevated intake of vegetables and fibers. Thus, balanced calcium consumption protects against the risk for kidney stones by reducing intestinal oxalate availability and its urinary excretion. However, calcium supplementation given between meals might increase urinary calcium excretion without the beneficial effect on oxalate. In kidney stone formers, circulating active vitamin D has been found to be increased, whereas higher plasma 25-hydroxycholecalciferol seems to be present only in hypercalciuric patients. The association between nutritional vitamin D supplements and the risk for stone formation is currently not completely understood. However, taken together, available evidence might suggest that vitamin D administration worsens the risk for stone formation in patients predisposed to hypercalciuria. In this review, we analyzed and discussed available literature on the effect of calcium and vitamin D supplementation on the risk for kidney stone formation.

MO113CALCULATED URINARY CALCIUM-OXALATE SATURATION (ßCAOX) IS NOT SPECIFICALLY ELEVATED IN PATIENTS WITH PRIMARY HYPEROXALURIA

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Bernd Hoppe ◽  
Wolfgang Böhm ◽  
Cristina Martin Higueras
Keyword(s):  
Calcium Oxalate ◽  
Primary Hyperoxaluria ◽  
Urinary Calcium ◽  
Stone Disease ◽  
Urinary Calcium Excretion ◽  
Urine Specimen ◽  
Calcium Excretion ◽  
Stone Formers ◽  
Enzyme Defects ◽  
Urinary Oxalate Excretion

Abstract Background and Aims In the primary hyperoxalurias (PH; types 1-3) recurrent urolithiasis (UL) and/or progressive nephrocalcinosis (NC) are the clinical hallmarks. Three different enzyme defects lead to endogenous oxalate overproduction and to extremely elevated urinary oxalate excretion (UOx). Thus, it seems logical that urine is supersaturated for calcium-oxalate (CaOx). It was, hence, speculated that urinary CaOx saturation (ßCaOx), calculated by computed programs, is significantly higher as compared to that of patients with idiopathic CaOx stones. We now aimed to evaluate and calculate urinary ßCaOx in PH patients according to type, as well as in non-PH patients with UL or NC. Method The computed equilibrium program EQUIL2 was used for the calculation of ßCaOx. For this, 24 h urine specimen of 70 patients with non-PH NC (46 male, 24 female, median age 6.06 (range 0.3-31.4 years)), of 149 idiopathic CaOx UL (90/59 m/f, age 8.5 (0.1-68.6)), of 51 PH 1 patients (31/21, age 12.33 (0.8-63.8)), of 5 PH 2 patients (3/2, age 5.41 (4.3-12.9)) and of 14 PH 3 patients (8/6, age 8.5 (2.9-29.3)) were analyzed for all necessary components. All patients were in stable kidney function (eGFR &gt; 45 ml/min). Results Uox was higher in the PH patients as compared to the non-PH UL or NC patients (p &lt; 0.05). However, there was no statistical difference between the Uox in PH 1 vs PH 2 or PH 3 patients, although, a clear effect of B6 medication was visible in PH1 patients. Urinary calcium excretion was lower (not significant) in PH patients as compared to NC/UL. There was no difference in ßCaOx when PH were compared to non-PH patients and it mostly remained in the normal range. Conclusion Urine ßCaOx is similar in PH and non-PH stone formers. Therefore, calculation of ßCaOx using computed programs is not a reliable parameter to define the definitively extreme CaOx supersaturation of urine from PH patients. This miscalculation is related to a rather lowish urinary calcium excretion in PH as compared to other UL/NC patients. Therefore, we recommend not to use such programs to express the risk of recurrent stone disease or nephrocalcinosis in PH.

scholarly journals Recurrent urolithiasis following parathyroidectomy for primary hyperparathyroidism

2013 ◽  
Vol 95 (7) ◽  
pp. 523-528 ◽  
Author(s):  
C Rowlands ◽  
A Zyada ◽  
S Zouwail ◽  
H Joshi ◽  
MJ Stechman ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Recurrence Rate ◽  
Stone Formation ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Stone Formers ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Introduction The effect of parathyroidectomy on the incidence of recurrent stone formation is uncertain. We aimed to compare the biochemistry and recurrence rate of urolithiasis in patients with primary hyperparathyroidism (pHPT) and stone formation (SF) and non-stone formation (NSF) with idiopathic stone formers (ISF). Methods Patients with pHPT and SF (Group 1) were identified from a prospective database. pHPT patients and NSF (Group 2) and ISFs (Group 3) were randomly selected from respective databases to form three equal groups. Preoperative and postoperative biochemical data were analysed and recurrent urolithiasis diagnosed if present on follow-up radiology. Out-of-area patients were asked about recurrence via telephone. Results From July 2002 to October 2011, 640 patients had parathyroidectomy for pHPT. Of these, 66 (10.3%) had a history of renal colic; one was lost to follow-up. Patient demographics were similar across all three groups. Three months post-parathyroidectomy, Groups 1 and 2 had significantly reduced serum calcium concentrations (p<0.01). Group 1 had lower urinary calcium excretion after parathyroidectomy (p<0.01), but estimated glomerular filtration rate did not change following surgery. During median follow-up of 4.33 years (0.25–9 years) in Groups 1 and 2 and 5.08 years (0.810–8 years) in Group 3, one patient (1.5%) in Group 1 and 16 patients (25%) in Group 3 had recurrent urolithiasis (p<0.01). No Group 2 patients developed stones. Conclusion Curative parathyroidectomy confers a low recurrence rate for urolithiasis, but does not prevent recurrence in all patients. Further research should aim to identify the risk factors for continued SF in these patients.

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