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Tamm-Horsfall glycoprotein and calcium nephrolithiasis
1Policlinic of Medicine, University Hospital, Berne, Switzerland.
Mineral and Electrolyte Metabolism
|January 1, 1994
Summary
Tamm-Horsfall glycoprotein (THP) influences calcium oxalate crystal aggregation. THP can inhibit or promote aggregation based on solution conditions and its own aggregation state, impacting kidney stone formation.
Area of Science:
- Biochemistry
- Nephrology
- Crystallography
Background:
- Tamm-Horsfall glycoprotein (THP) is a major urinary protein.
- Conflicting data exist regarding THP's role in calcium oxalate crystallization.
- Calcium oxalate crystals are the primary component of kidney stones.
Purpose of the Study:
- To review the dual role of THP in calcium oxalate crystal aggregation.
- To elucidate the mechanisms underlying THP's pro-aggregatory and anti-aggregatory effects.
- To investigate the implications of abnormal THP variants in recurrent kidney stone disease.
Main Methods:
- Literature review focusing on calcium oxalate crystal aggregation.
- Analysis of THP's behavior under varying solution conditions (pH, ionic strength, ion concentrations).
- Examination of THP self-aggregation and its impact on inhibitory activity.
Main Results:
- THP acts as an inhibitor of calcium oxalate crystal aggregation in low pH, high ionic strength, and high ion concentration conditions.
- THP self-aggregation reduces its inhibitory capacity.
- Abnormal THP variants promote aggregation in recurrent stone formers, especially at high calcium concentrations.
- Citrate chelates calcium ions, reducing THP self-aggregation and converting promoting THPs into inhibitors.
Conclusions:
- THP's effect on calcium oxalate crystal aggregation is context-dependent.
- Abnormal THP self-aggregation contributes to kidney stone formation.
- Citrate may mitigate kidney stone risk by modulating THP activity.