Tamm-Horsfall Protein is a Critical Renal Defense Factor Protecting Against Calcium Oxalate Crystal Formation

Mo, Lan; Huang, Hongying; Zhu, Xinhua; Shapiro, Ellen; Hasty, David L.; Wu, Xianwei

doi:10.1016/s0022-5347(05)00093-5

Cited by 21 publications

(28 citation statements)

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“…Uromodulin deficiency in humans may be a risk factor for nephrolithiasis. UMOD knock-out mice models have shown a propensity for increased calcium crystal formation in the urinary tract and a reduced ability to inhibit the adhesion of calcium oxalate monohydrate crystals to renal epithelial cells [17,18].…”

Section: Functions Of Uromodulinmentioning

confidence: 99%

Uromodulin: old friend with new roles in health and disease

Iorember

Vehaskari

2013

Pediatr Nephrol

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Section: Functions Of Uromodulinmentioning

confidence: 99%

Uromodulin: old friend with new roles in health and disease

Iorember

Vehaskari

2013

Pediatr Nephrol

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“…[16] In another study, in a mice lacking Uromodulin, it was observed that in addition to increased concentration of urine phosphorus and calcium phosphate super saturation, there was interstitial deposits of calcium phosphate within the renal papillae. [17] Thus, in addition to decreased renal function due to TAL damage, patients with severely attenuated Uromodulin may become more susceptible to pathophysiology associated with elevated calciumphosphorus product.…”

Section: Discussionmentioning

confidence: 96%

Uromodulin Levels in Chronic Kidney Disease

Shalia

Halankar

2016

Int J of Biomed & Adv Res

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Objectives: Uromodulin is a protein exclusively produced by Kidney in tubular cells lining thick ascending limb (TAL) of the loop of Henle. It has been linked to water electrolyte balance, protective role against urinary tract infections and renal stone formation. To analyse its trend in Chronic Kidney Disease (CKD), its levels were analysed in serum and urine of patients at different stages of CKD. Methods: CKD stage-1 and stage-2 (N=14), Stage-3 (N=24), Stage-4 (N=9), Stage-5 (N= 19) and controls (N=16) were recruited as per the National Kidney Foundation -Kidney Disease Outcome Quality Initiative guidelines. Uromodulin levels were analysed by enzyme linked immunsorbent assay (ELISA). Results: Uromodulin levels both in serum and urine decreased with decreasing kidney function. Bivariate analysis within CKD group showed significant (p=0.001) positive correlation of urinary Uromodulin (spearman correlation [rs]=0.664) and serum Uromodulin (rs=0.855) levels with eGFR and significant (p=0.001) negative correlation of urinary Uromodulin (rs= ̶ 0.872) and serum Uromodulin (rs= ̶ 0.859) with serum creatinine levels. Serum Uromodulin levels in addition showed significant (p=0.001) negative correlation with phosphorus (rs = ̶ 0.523) and corrected calcium phosphorus product (rs= ̶ 0.484). Conclusion: Serum and urine levels of Uromodulin decreased with increasing severity of CKD. Apart from its other protecting role, its reduction may accelerate pathophysiology associated with elevated calcium-phosphorus product in CKD.

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“…These studies demonstrated that after a hyperoxaluric load was given, there was a compensatory increased expression of the remaining (OPN or THP) macromolecule [56,57]. While this response was not enough to prevent crystallization, it suggested a potential synergistic relationship.…”

Section: Hyperoxaluriamentioning

confidence: 98%

“…By performing selective knockout (KO) of osteopontin (OPN) and Tamm-Horsfall protein (THP), investigators have established the critical role of these macromolecules as inhibitors of stone formation. For a summary of the mice models of nephrocalcinosis please refer to [57].…”

Section: Hyperoxaluriamentioning

confidence: 99%

Animal models of urinary stone disease

Tzou

Taguchi

Chi

et al. 2016

International Journal of Surgery

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h i g h l i g h t sMultiple methods induce animal hyperoxaluria and calcium oxalate crystal formation. Knockout mice models have been shown to produce hypercalciuria and cystinuria. Drosophila melanogaster represents a powerful genetic model for stone disease. a r t i c l e i n f o a b s t r a c tThe etiology of stone disease remains unknown despite the major technological advances in the treatment of urinary calculi. Clinically, urologists have relied on 24-h urine collections for the last 30e40 years to help direct medical therapy in hopes of reducing stone recurrence; yet little progress has been made in preventing stone disease. As such, there is an urgent need to develop reliable animal models to study the pathogenesis of stone formation and to assess novel interventions. A variety of vertebrate and invertebrate models have been used to help understand stone pathogenesis. Genetic knockout and exogenous induction models are described. Surrogates for an endpoint of stone formation have been urinary crystals on histologic examination and/or urinalyses. Other models are able to actually develop true stones. It is through these animal models that real breakthroughs in the management of urinary stone disease will become a reality.

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Tamm-Horsfall Protein is a Critical Renal Defense Factor Protecting Against Calcium Oxalate Crystal Formation

Cited by 21 publications

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Uromodulin: old friend with new roles in health and disease

Uromodulin: old friend with new roles in health and disease

Uromodulin Levels in Chronic Kidney Disease

Animal models of urinary stone disease

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