Renal calcium stones: insights from the control of bone mineralization

Moochhala, Shabbir H.; Sayer, John A.; Carr, Georgina; Simmons, Nicholas L.

doi:10.1113/expphysiol.2007.040790

Cited by 56 publications

(45 citation statements)

References 47 publications

(71 reference statements)

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“…Surprisingly, despite the flurry of interest in the pyrophosphate trans porter ANK, which is expressed in the joints and kidney, no renal calcifications have been found in mice with aberrant ANK function. 113 The renal handling of phosphate and calcium has been reviewed by Berndt and Kumar, 114 Huang and Miller, 115 and Sayer et al 116 …”

Section: Potential Roles Of Oxalate In Nephrolithiasismentioning

confidence: 98%

Oxalate in renal stone disease: the terminal metabolite that just won't go away

Marengo

Romani

2008

Nat Rev Nephrol

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The incidence of calcium oxalate nephrolithiasis in the US has been increasing throughout the past three decades. Biopsy studies show that both calcium oxalate nephrolithiasis and nephrocalcinosis probably occur by different mechanisms in different subsets of patients. Before more-effective medical therapies can be developed for these conditions, we must understand the mechanisms governing the transport and excretion of oxalate and the interactions of the ion in general and renal physiology. Blood oxalate derives from diet, degradation of ascorbate, and production by the liver and erythrocytes. In mammals, oxalate is a terminal metabolite that must be excreted or sequestered. The kidneys are the primary route of excretion and the site of oxalate's only known function. Oxalate stimulates the uptake of chloride, water, and sodium by the proximal tubule through the exchange of oxalate for sulfate or chloride via the solute carrier SLC26A6. Fecal excretion of oxalate is stimulated by hyperoxalemia in rodents, but no similar phenomenon has been observed in humans. Studies in which rats were treated with (14)C-oxalate have shown that less than 2% of a chronic oxalate load accumulates in the internal organs, plasma, and skeleton. These studies have also demonstrated that there is interindividual variability in the accumulation of oxalate, especially by the kidney. This Review summarizes the transport and function of oxalate in mammalian physiology and the ion's potential roles in nephrolithiasis and nephrocalcinosis.

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Section: Potential Roles Of Oxalate In Nephrolithiasismentioning

confidence: 98%

Oxalate in renal stone disease: the terminal metabolite that just won't go away

Marengo

Romani

2008

Nat Rev Nephrol

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“…PPi is a metabolic product from cellular metabolism and also plays roles in calcium sequestration, modification of enzyme function and modulation of mineralisation [2]. Recently, a molecular candidate for a pyrophosphate transporter, 596 ANKH (alias ANK) has been identified [3,4].…”

Section: Introductionmentioning

confidence: 99%

The Pyrophosphate Transporter ANKH is Expressed in Kidney and Bone Cells and Colocalises to the Primary Cilium/Basal Body Complex

Carr

Moochhala²,

Eley³

et al. 2009

Cell Physiol Biochem

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Background/Aims: ANKH encodes a putative pyrophosphate transporter named ANKH, which regulates tissue calcification. ANKH is a transmembrane protein with at least 8 predicted transmembrane domains. Sequence analysis reveals a possible cilial localisation motif immediately after the last transmembrane segment. Here we aim to determine the subcellular localisation of ANKH in ciliated epithelial cells and murine tissue and identify colocalisation using ciliary/basal body markers. Methods: Using murine kidney, renal epithelial cells and osteoblast cells we investigated the expression and localisation of ANKH using RT-PCR, Western blotting and immunocytochemistry. Results: Here we confirm endogenous expression of ANKH mRNA and protein in whole mouse kidney as well as mouse renal epithelial cell lines M1 and mpkCCDcl4 and the osteoblast cell line MC3T3-E1. Using antibodies directed towards ANKH, we confirm cilial and basal body localisation in renal tissues and renal epithelial cells, in addition to a centrosomal localisation in dividing mpkCCDcl4 cells. We also establish that the osteoblast cell line MC3T3-E1 forms an epithelioid cell layer, with junctional complex formation and primary cilia expression. ANKH is also seen within cilial and basal body structures of MC3T3-E1 cells. An ANKH-3XFLAG construct expressed in mpkCCDcl4 cells also localises to the primary cilium/basal body complex confirming this localisation. Conclusion: We conclude that the transmembrane protein ANKH is expressed in cilia and basal body structures, and postulate a sensory role at this location.

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“…Literature survey suggests that various acidic metabolites such as hippuric acid, oxalic acid, formic acid, and benzoic acids are formed on EG metabolism causing metabolic acidosis. Renal tubular acidosis eventually promotes renal calcium leakage which along with increased resorption of calcium from bones and increased intestinal absorption of calcium leads to hypercalciuria and hypercalcemia [26][27][28].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of magnesium lactate gluconate and Garcinia cambogia fruit extract in experimentally induced renal calculi in rats

Kyada¹,

Mansuri²,

Patel³

2017

J Intercult Ethnopharmacol

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Aim: Antiurolithiatic activity of magnesium lactate gluconate (MLG) and aqueous extract of Garcinia cambogia (GC) fruit was studied. Materials and Methods: The study was performed during December 2016 to April 2017. Urolithiasis was induced in male Wistar rats by administration of 0.75% v/v ethylene glycol for 21 days. From 8 th day onward, intervention with MLG (200 and 400 mg/kg b.w.) and GC (100 and 200 mg/kg b.w.) was started. At the end of the treatment period, biochemical parameters affecting renal stone formation were estimated in the serum, urine, kidney homogenate, and histopathology of harvested kidneys was performed. Results: From in vivo evaluation, it was observed that MLG 400 mg/kg b.w., GC 100 mg/kg b.w., and GC 200 mg/kg b.w. significantly reduced nitrogenous waste products in serum (blood urea nitrogen, creatinine, and uric acid) as well as calculogenic promoters in urine (phosphate and oxalate) and kidney homogenate (calcium, phosphate, and oxalate) when compared to disease control animals. The MLG 200 and MLG 400 were ineffective in restoring superoxide dismutase (SOD) and catalase (CAT) enzyme activity, whereas GC 100, GC 200, and Cystone ® 400 mg/kg b.w. significantly elevated SOD and CAT enzymes in urolithiatic rat kidney. Conclusions: MLG and GC extracts are capable of preventing calcium oxalate (CaOx) crystal formation and subsequent deposition in renal tubules. The principle mechanism underlying nephroprotective effect of test drugs might be attributed to their calcium ion chelating ability and CaOx crystallization inhibitory activity. It is further asserted that GC was more potent than MLG in overall kidney protection by virtue of its antioxidant potential.

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Renal calcium stones: insights from the control of bone mineralization

Cited by 56 publications

References 47 publications

Oxalate in renal stone disease: the terminal metabolite that just won't go away

Oxalate in renal stone disease: the terminal metabolite that just won't go away

The Pyrophosphate Transporter ANKH is Expressed in Kidney and Bone Cells and Colocalises to the Primary Cilium/Basal Body Complex

Protective effect of magnesium lactate gluconate and Garcinia cambogia fruit extract in experimentally induced renal calculi in rats

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