ReviewCureus2025
Idiopathic Hypercalciuria: A Comprehensive Review of Clinical Insights and Management Strategies.
Review in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Predictive value of family history of kidney stones for metabolic abnormalities and stone composition.World journal of urology · 2026Article
- Importance of Recognizing Renal Tubular Disorders as a Cause of Bone Hypomineralization and Fractures in Adults.Diagnostics (Basel, Switzerland) · 2026Review
- Article
- Urolithiasis in Children-Clinical Picture, Pathogenesis, and Diagnostic Approach.Biomolecules · 2026Review
- Endocrine-related osteoporosis: the state of the art.Frontiers in endocrinology · 2026Review
- Pregnancy and Lactation Associated Bone Fragility.Journal of the Endocrine Society · 2025Review
- Diagnosis and Emerging Biomarkers of Cystic Fibrosis-Related Kidney Disease (CFKD).Journal of clinical medicine · 2025Review
- Investigating the association between calcium-phosphorus balance and osteoarthritis: Evidence from NHANES 2007-2016.Medicine · 2025Observational
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic hypercalciuria (IH) is a metabolic condition characterized by excessive calcium excretion in urine without identifiable secondary causes, such as hyperparathyroidism or malignancy. It is a significant clinical entity due to its association with kidney stones, nephrocalcinosis, and osteoporosis, leading to reduced quality of life and long-term complications. This comprehensive review discusses the pathophysiology, clinical manifestations, diagnostic strategies, and management approaches for IH. The disorder arises from a multifaceted interplay of renal, intestinal, and skeletal factors. Impaired renal tubular calcium reabsorption, heightened intestinal calcium absorption, and increased bone resorption are key contributors to its pathogenesis. Genetic predispositions, including mutations in calcium-regulating receptors and transporters, further complicate its etiology. Patients often present with kidney stones, bone pain, or reduced bone mineral density, although asymptomatic cases are not uncommon. Diagnosing IH requires a thorough evaluation to exclude secondary causes, with 24-hour urinary calcium excretion serving as a crucial diagnostic marker. Management focuses on mitigating complications and improving quality of life through hydration, dietary modifications, and pharmacological therapy. Thiazide diuretics are the cornerstone of treatment, effectively reducing urinary calcium levels and preventing stone formation. Adjunctive measures include citrate supplementation and lifestyle interventions such as weight management and adequate physical activity. For patients with severe nephrolithiasis or nephrocalcinosis, surgical intervention may be necessary. Despite significant advancements, IH remains a diagnostic and therapeutic challenge due to its diverse clinical presentations and underlying mechanisms. A multidisciplinary approach, incorporating tailored medical and dietary strategies, is essential for optimal management. Future research into its genetic and molecular basis holds promise for developing more targeted interventions and improving patient outcomes. This review aims to provide a practical, up-to-date guide for clinicians managing this complex yet common metabolic disorder.
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Registered trials
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