View clinical trials related to Hypercalciuria.
Filter by:The goal of this National Registry is to is to collect information from patients with rare kidney diseases, so that it that can be used for research. The purpose of this research is to: - Develop Clinical Guidelines for specific rare kidney diseases. These are written recommendations on how to diagnose and treat a medical condition. - Audit treatments and outcomes. An audit makes checks to see if what should be done is being done and asks if it could be done better. - Further the development of future treatments. Participants will be invited to participate on clinical trials and other studies. The registry has the capacity to feedback relevant information to patients and in conjunction with Patient Knows Best (Home - Patients Know Best), allows patients to provide information themselves, including their own reported quality of life and outcome measures.
In industrialized countries, it is estimated that around 10% of the population suffers from nephrolithiasis (NL). Numerous recent epidemiological studies report that the prevalence and incidence of NL continue to increase, with a prevalence that has nearly doubled over the past two decades. A patient who presented with a first episode of renal lithiasis has an estimated recurrence rate of nearly 50% at 5 years in adults. It is therefore wiser to consider NL as a chronic pathology and not as a simple isolated attack of painful crisis. NL therefore represents a real public health problem with a significant impact on the quality of life of patients, with considerable socio-economic repercussions. In clinical practice, calcium lithiasis is the most common and occurs in 90% of cases.The stones mainly consist of calcium oxalate (whewellite, weddellite) but also calcium phosphate (carbapatite, brushite). One of the risk factors for calcium lithiasis is the over-saturation of urine with calcium, which can lead to crystal formation. The most common metabolic abnormality found in patients with NL is hypercalciuria.It is defined as an increased excretion of urinary calcium.We can first distinguish hypercalciuria secondary to another pathology such as primary hyperparathyroidism, sarcoidosis, distal tubular acidosis, hypervitaminosis D, immobilization... from idiopathic hypercalciuria (HI), at the origin of so-called primary calcium lithiasis.HI is estimated to affect 30-60% of adults with NL. Idiopathic hypercalciuria is associated with low bone mineral density. Patients with NL have significantly lower T-score values in the vertebrae, hips, and femoral necks.Patients with NL have an increased risk of fractures and are 4 times more likely to develop osteoporosis. It is currently proposed that idiopathic hypercalciuria may be the cause of the decrease in bone mineral density in lithiasis patients.This bone demineralization appears to be associated with an increase in vascular calcifications.These, like NL, are believed to be linked to extra-osia calcium deposits.There is an inverse relationship between bone mineral density and arterial wall thickness (partly due to vascular calcifications) suggesting a relationship between arteriosclerosis and osteoporosis. This relationship would be much more pronounced in lithiasis women. In addition, several observations report an increase in cardiovascular morbidity in people with NL. NL should therefore be seen as a systemic disease and is also associated with several pathologies such as: metabolic syndrome, arterial hypertension, diabetes and cardiovascular diseases. To the knowledge of the investigators, no statistical data concerning the prevalence of vascular calcifications and bone demineralization in the population of lithiasis patients in Belgium has been published to date. In this context, the aim of this study is to assess the prevalence of vascular calcifications (early state of arteriosclerosis) as well as the bone mineral density in the lithiasis population followed at the Brugmann University Hospital and with idiopathic hypercalciuria.
Hypercalciuria is one of the most frequent metabolic disorders associated with nephrolithiasis and/or nephrocalcinosis leading to Chronic Kidney Disease (CKD) and bone complications in adults. Hypercalciuria can be secondary to increased intestinal absorption and/or increased renal distal tubular reabsorption of calcium due to increased active vitamin D, i.e. 1,25(OH)2D, levels. The management of hypercalciuria is challenging. Classic management based on hyperhydration and dietary advice has low impact on calciuria and therefore on CKD progression. Other strategies such as hydrochlorothiazide can be proposed, however with an uncertain medical benefit in view of side effects (hypokalemia, asthenia, potential cutaneous long-term side effects). Azoles are known to inhibit the 1α-hydroxylase and therefore decrease 1,25(OH)2D levels. These antifungal drugs are commonly used in neonates, infants and adults; pharmacokinetic data are well described. Recently, to improve azoles tolerance, fluconazole has been successfully reported to reduce calciuria in patients with CYP24A1 mutation (1 adult) or NPTIIc mutations (1 child), while maintaining a stable renal function. Based on these observations, the investigators hypothesize that fluconazole is effective to decrease and normalize calciuria in patients with hypercalciuria and increased 1,25(OH)2D levels. The primary objective is to demonstrate that fluconazole normalizes or decreases calciuria after 18 weeks of treatment in patients with hypercalciuria and increased 1,25(OH)2D levels. The secondary objectives aim to describe: - the effects of fluconazole on the evolution over time of the calcium/phosphate metabolism, - the evolution of renal function, - the cohort at Baseline and after 4 months of treatment period, - the safety of fluconazole, - the onset of potential mycological resistances, - and the treatment compliance. This is a prospective, interventional, national, randomized in 2 parallel groups (1:1), controlled versus placebo, double blind trial. This study will involve patients between 10 and 60 years of age suffering from nephrolithiasis and/or nephrocalcinosis with hypercalciuria (> 0.1 mmol/kg/d) and increased 1,25 (OH)2D levels (≥ 150 pmol/l) and 25-OH-D levels (≥50 nmol/L). FLUCOLITH study is a unique opportunity to develop a new indication of a well-known and not expensive drug (e.g. fluconazole) in rare renal diseases, the ultimate objective being the secondary prevention of CKD worsening in these patients. If the results of this proof-of-concept randomized controlled trial are positive, the investigators will propose an extension phase to evaluate the long term efficacy and safety of fluconazole on renal and bone parameters.
The investigator's objective is to compare and evaluate the impact of nutritional treatment vs. pharmacological treatment (hydrochlorothiazide) in bone mineral density in children with idiopathic hypercalciuria. A randomized, open-label, one-year follow-up study will be conducted in children aged 5 to 21 years with a confirmed diagnosis of idiopathic hypercalciuria or lithiasis, excluding those patients with secondary hypercalciuria (primary hyperoxaluria, treatment with vitamin D, Bartter syndrome, primary hyperparathyroidism), previous kidney transplantation. The impact of diet (hyposodic, calcium intake according to DIR for age, normal protein intake and high water intake) will be evaluated vs. the pharmacological treatment (hydrochlorothiazide) on bone mineral density.
Determine the association between duration and dose of chronic conventional therapy with Pi and renal (nephrocalcinosis/nephrolithiasis), vascular (endothelial function), and cardiovascular function (echo- cardiography) in patients with hereditary hypophosphatemic rickets with hypercalciuria (HHRH) and patients with X-linked hypophosphatemia (XLH).
This open-label study will determine if chlorthalidone is safe and effective for the use of reducing urinary calcium excretion over 4 weeks in subjects with type 1 diabetes
This study evaluates the efficacy of rifampin in the treatment of hypercalcemia and/or hypercalciuria in participants with at least one inactivating mutation of the CYP24A1 gene. Eligible subjects will receive rifampin for a total of 16 weeks during this study.
Recommendations for vitamin D supplementation for subjets between 2 and 18 years offer strong sequential doses of vitamin D: 2 times 100 000 units in spaced winter period of 3 months. Data from the literature show a further increase in the incidence of oxalo-calcium stones in children and adolescents associated with hypercalciuria with training Randall plates, essential step lithogenesis calcium oxalate. Knowing the links between vitamin D and urinary calcium excretion, these data lead to the question of increased sensitivity in some children with vitamin D, sensitivity could explain these situations with hypercalciuria increase the gallstone risk. This increased sensitivity to vitamin D may unmask particularly if inputs of high doses of vitamin responsible then a transient hypercalciuria with development of microcrystals.
The aim of this study is to know the difference between protein profiles (multi-analyte profile) of PH1 patients, idiopathic hypercalciuria (IH) patients and PH1 patients 'siblings. Idiopathic hypercalciuria is a less severe kidney disease that PH1, which also leads to the formation of kidney stones. The aim is to identify patterns of discriminating markers associated with primary hyperoxaluria type 1 (PH1) that will significantly improve clinical diagnosis and prognosis.
Hypoparathyroidism is a rare condition in which the parathyroid glands fail to produce sufficient amount of parathyroid hormone or the parathyroid hormone produced lacks biologic activity. The most common cause of hypoparathyroidism is damage to or removal of the parathyroid glands due to neck surgery for another condition. Occurrence of hypercalciuria under treatment is a frequent concern in primary hypoparathyroidism, limiting correction of hypocalcemia. Hypoparathyroidism can also be caused by an autoimmune process. In rare cases, hypoparathyroidism may occur as a genetic disorder inherited as an autosomal recessive, autosomal dominant or X-linked recessive trait. The autosomal dominant hypocalcemia (ADH) is mainly caused by heterozygous activating mutations in the CASR gene encoding CaSR). As other severe presentation of primary hypothyroidism, ADH is characterized by the increased risk to develop hypercalciuria and nephrolithiasis. The purpose of the study is to compare two therapeutic approaches in severe hypoparathyroidism in order to limit the risk of nephrocalcinosis and renal failure when attempting to correct hypocalcemia: rhPTH(1-34) vs association of active vitamin D and hydrochlorothiazide. The European Society of Endocrinology Clinical has indeed recently published guidelines for the treatment of chronic hypoparathyroidism in adults. These guidelines suggest considering treatment with a thiazide diuretic In a patient with hypercalciuria and replacement therapy with PTH in patients who do not stably and safely maintain their serum and urinary calcium in the target range.