The molecular basis of kidney stones

Craig B. Langman*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

13 Scopus citations


Purpose of review: To emphasize an exploration of mechanisms of kidney stone disease based on a molecular understanding of excess urinary excretions of calcium, oxalate, cystine, and uric acid. Recent findings: Hypercalciuria is discussed relative to mutations in the renal chloride genes CLCN5 and CLCNKB, WNK kinases, ATPB61, and NPT2. Hyperoxaluria is discussed relative to mutations in AGXT and GRHPR. Cystinuria is discussed relative to mutations in SLC3A1 and SLC7A9. Hyperuricosuria is discussed with novel gene findings, and hyperxanthinuria with new findings in XDH. Summary: An enhanced understanding of the diagnosis, course, and prognosis for genetic causes of kidney stone diseases has been made available to the clinician caring for patients with kidney stones and to the scientist interested in their cause, as a result of molecular breakthroughs in the kidney handling of normal urinary constituents. We look forward to a new era of the therapeutics of kidney stones based on such advances.

Original languageEnglish (US)
Pages (from-to)188-193
Number of pages6
JournalCurrent opinion in pediatrics
Issue number2
StatePublished - Apr 1 2004


  • Cystinuria
  • Genetic diseases
  • Idiopathic hypercalciuria
  • Primary hyperoxaluria
  • Uric acid

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health


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