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array:25 [ "pii" => "S2013251417300196" "issn" => "20132514" "doi" => "10.1016/j.nefroe.2017.01.016" "estado" => "S300" "fechaPublicacion" => "2017-01-01" "aid" => "213" "copyright" => "Sociedad Española de Nefrología" "copyrightAnyo" => "2016" "documento" => "article" "crossmark" => 0 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "ssu" "cita" => "Nefrologia (English Version). 2017;37:5-8" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 3589 "formatos" => array:3 [ "EPUB" => 358 "HTML" => 2596 "PDF" => 635 ] ] "Traduccion" => array:1 [ "es" => array:20 [ "pii" => "S0211699516300595" "issn" => "02116995" "doi" => "10.1016/j.nefro.2016.04.008" "estado" => "S300" "fechaPublicacion" => "2017-01-01" "aid" => "213" "copyright" => "Sociedad Española de Nefrología" "documento" => "article" "crossmark" => 0 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "ssu" "cita" => "Nefrologia. 2017;37:5-8" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 8810 "formatos" => array:3 [ "EPUB" => 405 "HTML" => 7349 "PDF" => 1056 ] ] "es" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Revisión</span>" "titulo" => "¿Es el sistema calicreína/quinina renal un factor modulador de la calciuria?" "tienePdf" => "es" "tieneTextoCompleto" => "es" "tieneResumen" => array:2 [ 0 => "es" 1 => "en" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "5" "paginaFinal" => "8" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Is the renal kallikrein-kinin system a factor that modulates calciuria?" ] ] "contieneResumen" => array:2 [ "es" => true "en" => true ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figura 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1707 "Ancho" => 1534 "Tamanyo" => 109728 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Modelo esquemático que muestra como la calicreína tisular participa de la regulación del canal epitelial de calcio TRPV5 en el túbulo contorneado distal tardío.</p> <p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">La calicreína tisular producida por el túbulo conector es liberada dentro del fluido urinario. Alli actua sobre el quininogeno (QN) filtrado o segregado localmente y produce finalmente bradiquinina (BK). La BK actúa sobre su receptor B2 (BKRB<span class="elsevierStyleInf">2</span>) activando la vía de fosfolipasa C/diacilglicerol/proteincinasa C (PLC/DAG/PKC) induciendo la localización del canal de calcio TRPV5 a nivel de la membrana apical y favorece la reabsorción de calcio tubular. La BK es degradada por la endopeptidasa neutra (NEP) y la quininasa CYP renal.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Armando Luis Negri" "autores" => array:1 [ 0 => array:2 [ "nombre" => "Armando Luis" "apellidos" => "Negri" ] ] ] ] ] "idiomaDefecto" => "es" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2013251417300196" "doi" => "10.1016/j.nefroe.2017.01.016" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2013251417300196?idApp=UINPBA000064" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0211699516300595?idApp=UINPBA000064" "url" => "/02116995/0000003700000001/v3_201702240054/S0211699516300595/v3_201702240054/es/main.assets" ] ] "itemSiguiente" => array:20 [ "pii" => "S2013251417300202" "issn" => "20132514" "doi" => "10.1016/j.nefroe.2017.01.017" "estado" => "S300" "fechaPublicacion" => "2017-01-01" "aid" => "221" "copyright" => "Sociedad Española de Nefrología" "documento" => "article" "crossmark" => 0 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "ssu" "cita" => "Nefrologia (English Version). 2017;37:9-19" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 8011 "formatos" => array:3 [ "EPUB" => 344 "HTML" => 5972 "PDF" => 1695 ] ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Review</span>" "titulo" => "Gut microbiota in chronic kidney disease" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "9" "paginaFinal" => "19" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Microbiota intestinal en la enfermedad renal crónica" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Secundino Cigarran Guldris, Emilio González Parra, Aleix Cases Amenós" "autores" => array:3 [ 0 => array:2 [ "nombre" => "Secundino Cigarran" "apellidos" => "Guldris" ] 1 => array:2 [ "nombre" => "Emilio González" "apellidos" => "Parra" ] 2 => array:2 [ "nombre" => "Aleix Cases" "apellidos" => "Amenós" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0211699516300728" "doi" => "10.1016/j.nefro.2016.05.008" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0211699516300728?idApp=UINPBA000064" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2013251417300202?idApp=UINPBA000064" "url" => "/20132514/0000003700000001/v1_201703230033/S2013251417300202/v1_201703230033/en/main.assets" ] "itemAnterior" => array:20 [ "pii" => "S2013251417300172" "issn" => "20132514" "doi" => "10.1016/j.nefroe.2017.01.014" "estado" => "S300" "fechaPublicacion" => "2017-01-01" "aid" => "249" "copyright" => "Sociedad Española de Nefrología" "documento" => "article" "crossmark" => 0 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "sco" "cita" => "Nefrologia (English Version). 2017;37:1-4" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 4818 "formatos" => array:3 [ "EPUB" => 351 "HTML" => 3569 "PDF" => 898 ] ] "en" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial</span>" "titulo" => "Incremental hemodialysis schedule at the start of renal replacement therapy" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "1" "paginaFinal" => "4" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Hemodiálisis incremental como forma de inicio del tratamiento sustitutivo renal" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1359 "Ancho" => 1643 "Tamanyo" => 96963 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Incidence and prevalence of patients treated with 2 haemodialysis sessions a week.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Milagros Fernández Lucas, José Luis Teruel" "autores" => array:2 [ 0 => array:2 [ "nombre" => "Milagros" "apellidos" => "Fernández Lucas" ] 1 => array:2 [ "nombre" => "José Luis" "apellidos" => "Teruel" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S021169951630114X" "doi" => "10.1016/j.nefro.2016.08.002" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S021169951630114X?idApp=UINPBA000064" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2013251417300172?idApp=UINPBA000064" "url" => "/20132514/0000003700000001/v1_201703230033/S2013251417300172/v1_201703230033/en/main.assets" ] "en" => array:20 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Review</span>" "titulo" => "Is the renal kallikrein-kinin system a factor that modulates hypercalciuria?" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "5" "paginaFinal" => "8" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "Armando Luis Negri" "autores" => array:1 [ 0 => array:3 [ "nombre" => "Armando Luis" "apellidos" => "Negri" "email" => array:1 [ 0 => "armando.negri@gmail.com" ] ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Cátedra de Fisiología y Biofísica, Universidad del Salvador, Buenos Aires, Argentina" "identificador" => "aff0005" ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "¿Es el sistema calicreína/quinina renal un factor modulador de la calciuria?" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1707 "Ancho" => 1502 "Tamanyo" => 105045 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Schematic model showing how tissue kallikrein participates in the regulation of the TRPV5 calcium epithelial channel in the late distal convoluted tubule. The tissue kallikrein produced by the connecting tubule is released into the urinary fluid. It is there that it acts on the filtered or locally secreted kininogen (KN) and finally produces bradykinin (BK). BK acts on its B2 receptor (BKRB<span class="elsevierStyleInf">2</span>), activating the phospholipase C/diacylglycerol/protein kinase C (PLC/DAG/PKC) pathway by inducing the TRPV5 calcium channel localisation at the apical membrane level and favours the reabsorption of tubular calcium. BK is degraded by neutral endopeptidase (NEP) and renal CYP kinase.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Tubular reabsorption of calcium is one of the main factors that determine serum calcium concentration and its urinary excretion. Most of the filtered calcium (60–70%) is reabsorbed in the proximal tubule, primarily by a paracellular mechanism that is not significantly sensitive to calcium regulatory hormones. Another 20–25% of the filtered calcium is reabsorbed in the thick ascending limb of Henle's loop, primarily by paracellular pathway, and involves claudins 16, 19 and 14. The distal convoluted and collective tubule is where fine regulation of hypercalciuria occurs, and where a significant fraction (10–15%) of the filtered calcium load is reabsorbed. In this tubular segment, calcium is reabsorbed by a transcellular mechanism, and enters through calcium channels present in the apical membrane. Under normal conditions, the tubular reabsorption of calcium is tightly regulated. Non-hormonal factors such as ECF volume, acid/base status and plasma concentrations of magnesium and calcium exert an influence on the management of calcium in the renal tubule.<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">1–3</span></a> Extrarenal hormonal factors, such as parathyroid hormone and 1,25-dihydroxyvitamin D, also regulate the tubular reabsorption of calcium.<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">4</span></a> In contrast, relatively little is known about the possible contribution of intrarenal factors in the regulation of the renal tubular transport of calcium.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Calcium epithelial channel TRPV5 and its regulation by tubular factors</span><p id="par0010" class="elsevierStylePara elsevierViewall">The molecular basis of active transcellular transport of calcium in the distal nephron has recently been discovered. This process involves the apical influx of calcium through the calcium epithelial channel (TRPV5), which is the limiting step in the transcellular transport of calcium.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">5</span></a> Consistent with this is the lack of TRPV5 channel resulting in a decrease in the distal tubular reabsorption of calcium and the production of renal hypercalciuria.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">6</span></a> Several calciotropic hormones that are known to alter renal reabsorption of calcium affect the expression of TRPV5; others stimulate TRPV5 channel traffic to the plasma membrane, while a number of ions and associated proteins control the activity of the channel at the plasma membrane level.<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">7</span></a> The dynamic presence of the TRPV5 channel on the surface of the tubular cell is mediated by an endosomal recycling process that allows the internalisation of the channel to make it reappear again at the level of the plasma membrane. One of the proteins synthesised by the distal tubule is the klotho anti-ageing hormone. Klotho is a single-pass transmembrane protein, expressed primarily in the kidneys and choroid plexus. Membrane klotho functions as a bound coreceptor of fibroblast growth factor 23 (FGF-23) in the kidney and parathyroid gland. The extracellular domain of klotho is composed of 2 internal repetitions, KL1 and KL2, which can be cleaved and released into the blood and into the tubular lumen and act as hormones. Klotho upregulates TRPV5 both from within and outside the tubular cell. The intracellular action of klotho is likely mediated by an increase in protein trafficking of the channel to the apical membrane, while its extracellular action would be due to inhibition of the endocytosis of the caveolae where the calcium channels are found. Both effects compromise klotho sialidase activity by modifying the glycosylation status of the calcium channel and, therefore, trapping the channel at the cell surface level.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">8</span></a> Consistent with the positive influence of klotho on TRPV5-mediated calcium reabsorption is that the mice without <span class="elsevierStyleItalic">klotho</span> expression have urinary loss of calcium, hyperparathyroidism, and hypervitaminosis D.<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">9</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Another of the proteins that are synthesised in the distal tubule and secreted in the tubular fluid is tissue kallikrein (TK).<a class="elsevierStyleCrossRefs" href="#bib0155"><span class="elsevierStyleSup">10–12</span></a> TK is a serine protease involved in the generation of kinins in many organs, including the kidney.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">13</span></a> The kinins generated in the collecting tubule through TK inhibit the reabsorption of sodium chloride, through the activation of the bradykinin B2 receptors located along the epithelial cells of the collecting tubule. These kinins are immediately inactivated by 2 kidney-specific enzymes (kininases), the carboxypeptidase Y-like (CPY) exopeptidase, and the neutral endopeptidase (NEP)<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">14</span></a> (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). In addition, TK, through its catalytic activity, acts directly on the epithelial sodium channel (ENac) to modulate its activity, without being critical for the renal regulation of sodium homeostasis. TK-deficient mice exhibit a net transepithelial absorption of K<span class="elsevierStyleSup">+</span> in the cortical collecting tubule due to an abnormal activation of colonic-type H<span class="elsevierStyleSup">+</span>, K<span class="elsevierStyleSup">+</span>-ATPase in intercalated cells and reduced secretion of K<span class="elsevierStyleSup">+</span> by the principal cells secondary to a decrease in ENac activity. Therefore, TK is a kaliuretic factor that, independent from aldosterone, provides rapid protection against hyperkalemia after dietary K load.<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">15</span></a> Partial deficiency of TK in humans precludes proper adaptation to a load of potassium.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">16</span></a> TK-deficient mice have recently been shown to exhibit hypercalciuria of renal origin<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">17</span></a> comparable to the <span class="elsevierStyleItalic">leak</span> of calcium observed in <span class="elsevierStyleItalic">knockout</span> mice for TRPV5. TK distribution mainly overlaps that of the TRPV5 channel in the distal nephron, and the expression of the kallikrein gene is increased in low calcium diets. Recently, TK has been shown to stimulate active reabsorption of calcium via the type 2 bradykinin receptor that compromises the activation of TRPV5 via protein kinase C.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">18</span></a> This indicates that kallikrein could be a physiological modulator of the tubular reabsorption of calcium.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Pharmacological manipulations of the renal kallikrein-kinin system</span><p id="par0020" class="elsevierStylePara elsevierViewall">Secretion of renal kallikreins by collecting tubule cells may be increased by ATP-dependent potassium (KATP) channel blockers. Thus, oral administration of glibenclamide (a KATP channel blocker) or U18177, a kidney-selective KATP channel blocker, induces natriuresis and an increase in secretion of kallikreins that suppress the elevation of systolic blood pressure in Sprague Dawley rats who received 8% sodium chloride in their diet. These effects are counteracted by coadministration of a bradykinin B2 receptor antagonist (B2RA), FR17365. This indicates that KATP channel blocking induces diuresis and natriuresis through the release of renal kallikreins.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">14</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Ebelactone B and poststatin are inhibitors of CPY renal kininase. Administration of these drugs to a DOCA-salt-induced hypertension rat model prevents the development of salt-dependent hypertension.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">14</span></a> A neutral endopeptidase enzyme inhibitor, BP102, also suppresses systolic blood pressure elevation, but its effect is weaker than ebelactone B. Interestingly, young, genetically hypertensive SHR rats exhibiting hypercalciuria have an attenuated ability to secrete renal kallikreins as compared to normotensive WKY rats.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">19</span></a> To date, there are no studies in which the renal kallikrein-kinin system is manipulated with the above drugs to see if hypercalciuria is modified in these animals.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Tissue kallikrein deficiency in humans and its effect on hypercalciuria</span><p id="par0030" class="elsevierStylePara elsevierViewall">There is a polymorphism with loss of function of the human TK gene called R53H (H allele) that produces a significant decrease in enzymatic activity. In a crossover study in young white males, 30 of the subjects were homozygous for R53H and 10 were heterozygous for the same gene. They were randomised to 7-day periods with a low calcium diet (10<span class="elsevierStyleHsp" style=""></span>mmol/day) associated with a low Na/high K diet or a high Na/low K diet to modulate the synthesis of TK.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">20</span></a> On the seventh day of each diet, participants were studied before and during a 2-hour infusion of furosemide, which functionally excludes the thick ascending limb of Henle's loop and increases the supply of calcium to the distal tubular segments. Urinary kallikrein activity was 50–60% lower in participants with R53H than in those without R53R. The adaptation of urinary calcium excretion to the contrasting Na/K diets was not affected in the participants who were carriers of R53H. In contrast, after the infusion of furosemide, R53H participants had significantly lower serum ionised calcium concentrations than R53R participants (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.0001) and a non-significant tendency to greater calcium urinary excretion than R53R participants. These effects were more marked with low-Na/high-K diets.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Another recent study analysed TK polymorphisms in Japanese volunteers and examined the association between the H allele in the promoter region, which is shown to produce a decrease in promoter activity, and urine kallikrein activity.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">21</span></a> Ninety and 73 volunteers were analysed for the promoter and coding regions of the tissue kallikrein gene, respectively. The presence of the H allele in the Japanese population was common, a 24%. One synonymous and three non-synonymous polymorphisms were found in the coding regions. They studied the physiological parameters in subjects treated with an ad libitum diet. Urinary kallikrein activity was not significantly decreased in subjects with the H allele as compared with individuals without the H allele, although it was low in 2 homozygotes for the H allele. However, urinary excretion of calcium and sodium were higher in subjects with the H allele than in those without that allele.</p><p id="par0040" class="elsevierStylePara elsevierViewall">From these studies, it follows that the polymorphism with loss of function of the human TK gene (H allele) is relatively frequent. These individuals have a tendency to a high urinary excretion of calcium and sodium and this defect is more evident during the infusion of furosemide, exaggerating the defects of reabsorption in the distal tubule.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">End-note</span><p id="par0045" class="elsevierStylePara elsevierViewall">In the future, it will be necessary to study whether the renal kallikrein-kinin system is altered in animals with hypercalciuria and in humans with idiopathic hypercalciuria. This system could be modified by kidney-selective KATP channel blockers that increase the secretion of renal tissue kallikrein or through the increase of urinary kinin by renal CPY kininase inhibitors, such as ebelactone B and poststatin. Thus, it is conceivable that recurrent renal lithiasis caused by idiopathic hypercalciuria could be treated with drugs other than thiazide diuretics.</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Conflicts of interest</span><p id="par0050" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:11 [ 0 => array:3 [ "identificador" => "xres818632" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec815682" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres818633" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec815681" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Calcium epithelial channel TRPV5 and its regulation by tubular factors" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Pharmacological manipulations of the renal kallikrein-kinin system" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Tissue kallikrein deficiency in humans and its effect on hypercalciuria" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "End-note" ] 9 => array:2 [ "identificador" => "sec0030" "titulo" => "Conflicts of interest" ] 10 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2016-01-20" "fechaAceptado" => "2016-04-28" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec815682" "palabras" => array:3 [ 0 => "Tissue kallikrein" 1 => "Calciuria" 2 => "Regulation" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec815681" "palabras" => array:3 [ 0 => "Calicreína tisular" 1 => "Calciuria" 2 => "Regulación" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Renal tubular calcium reabsorption is one of the principal factors that determine serum calcium concentration and calcium excretion. Calcium excretion is regulated by the distal convoluted tubule and connecting tubule, where the epithelial calcium channel TRPV5 can be found, which limits the rate of transcellular calcium transport. The dynamic presence of the TRPV5 channel on the surface of the tubular cell is mediated by an endosomal recycling process. Different intrarenal factors are involved in calcium channel fixation in the apical membrane, including the anti-ageing hormone klotho and tissue kallikrein (TK). Both proteins are synthesised in the distal tubule and secreted in the tubular fluid. TK stimulates active calcium reabsorption through the bradykinin receptor B2 that compromises TRPV5 activation through the protein kinase C pathway. TK-deficient mice show hypercalciuria of renal origin comparable to that seen in TRPV5 knockout mice. There is a polymorphism with loss of function of the human TK gene R53H (allele H) that causes a marked decrease in enzymatic activity. The presence of the allele H seems to be common at least in the Japanese population (24%). These individuals have a tendency to greater calcium and sodium excretion in urine that is more evident during furosemide infusion. Future studies should analyse if manipulating the renal kallikrein-kinin system can correct idiopathic hypercalciuria with drugs other than thiazide diuretics.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La reabsorción tubular de calcio es uno de los principales factores que determinan la concentración sérica de calcio y su excreción urinaria. El túbulo contorneado distal y conector es donde se produce la regulación fina de la calciuria. A ese nivel se encuentra el canal epitelial de Ca (TRPV5), que es el paso limitante en el transporte transcelular de Ca. La presencia dinámica del canal TRPV5 en la superficie de la célula tubular está mediada por un proceso de reciclado endosómico. Distintos factores intrarrenales intervienen en la fijación del canal de calcio en la membrana aplical, entre ellos la hormona antienvejecimiento klotho y la calicreína tisular (CT). Ambas proteínas son sintetizadas en el túbulo distal y secretadas en el fluido tubular. La calicreína tisular estimula la reabsorción activa de calcio por vía del receptor de bradiquinina tipo 2 que compromete la activación del of TRPV5 por vía de la protein cinasa C. Los ratones deficientes en CT muestran hipercalciuria de origen renal comparable a la pérdida de calcio que se observa en los ratones <span class="elsevierStyleItalic">knockout</span> para el TRPV5. Existe un polimorfismo con pérdida de función del gen de la CT humana denominado R53H (alelo H) que produce una gran disminución de la actividad enzimática. La presencia del alelo H, por lo menos en la población japonesa, parece ser frecuente (24%). Estos individuos tiene una tendencia a excreción más alta de calcio y sodio en orina que se manifiesta más durante la infusión de furosemida. En el futuro habrá que estudiar si la manipulación del sistema calicreína-quinina renal permite corregir la hipercalciuria idiopática con fármacos diferentes a los diuréticos tiazídicos.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Luis A. ¿Es el sistema calicreína/quinina renal un factor modulador de la calciuria? Nefrologia. 2017;37:5–8.</p>" ] ] "multimedia" => array:1 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1707 "Ancho" => 1502 "Tamanyo" => 105045 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Schematic model showing how tissue kallikrein participates in the regulation of the TRPV5 calcium epithelial channel in the late distal convoluted tubule. The tissue kallikrein produced by the connecting tubule is released into the urinary fluid. It is there that it acts on the filtered or locally secreted kininogen (KN) and finally produces bradykinin (BK). BK acts on its B2 receptor (BKRB<span class="elsevierStyleInf">2</span>), activating the phospholipase C/diacylglycerol/protein kinase C (PLC/DAG/PKC) pathway by inducing the TRPV5 calcium channel localisation at the apical membrane level and favours the reabsorption of tubular calcium. BK is degraded by neutral endopeptidase (NEP) and renal CYP kinase.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:21 [ 0 => array:3 [ "identificador" => "bib0110" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Calciuric response to an acute acid load in healthy subjects and hypercalciuric calcium stone formers" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "P. Houillier" 1 => "M. Normand" 2 => "M. Froissart" 3 => "A. Blanchard" 4 => "P. Jungers" 5 => "M. 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Year/Month | Html | Total | |
---|---|---|---|
2024 November | 5 | 2 | 7 |
2024 October | 49 | 40 | 89 |
2024 September | 72 | 23 | 95 |
2024 August | 83 | 50 | 133 |
2024 July | 52 | 27 | 79 |
2024 June | 71 | 42 | 113 |
2024 May | 69 | 26 | 95 |
2024 April | 52 | 36 | 88 |
2024 March | 51 | 21 | 72 |
2024 February | 41 | 38 | 79 |
2024 January | 39 | 21 | 60 |
2023 December | 35 | 33 | 68 |
2023 November | 67 | 39 | 106 |
2023 October | 74 | 39 | 113 |
2023 September | 62 | 22 | 84 |
2023 August | 71 | 23 | 94 |
2023 July | 45 | 23 | 68 |
2023 June | 50 | 28 | 78 |
2023 May | 70 | 26 | 96 |
2023 April | 38 | 17 | 55 |
2023 March | 79 | 18 | 97 |
2023 February | 56 | 18 | 74 |
2023 January | 32 | 18 | 50 |
2022 December | 82 | 34 | 116 |
2022 November | 60 | 38 | 98 |
2022 October | 67 | 41 | 108 |
2022 September | 70 | 32 | 102 |
2022 August | 69 | 57 | 126 |
2022 July | 35 | 38 | 73 |
2022 June | 41 | 46 | 87 |
2022 May | 54 | 22 | 76 |
2022 April | 43 | 43 | 86 |
2022 March | 46 | 43 | 89 |
2022 February | 104 | 53 | 157 |
2022 January | 57 | 36 | 93 |
2021 December | 53 | 46 | 99 |
2021 November | 292 | 41 | 333 |
2021 October | 53 | 57 | 110 |
2021 September | 61 | 33 | 94 |
2021 August | 52 | 51 | 103 |
2021 July | 64 | 37 | 101 |
2021 June | 41 | 39 | 80 |
2021 May | 55 | 59 | 114 |
2021 April | 138 | 89 | 227 |
2021 March | 63 | 43 | 106 |
2021 February | 78 | 43 | 121 |
2021 January | 66 | 26 | 92 |
2020 December | 38 | 13 | 51 |
2020 November | 59 | 20 | 79 |
2020 October | 30 | 17 | 47 |
2020 September | 35 | 18 | 53 |
2020 August | 97 | 14 | 111 |
2020 July | 80 | 15 | 95 |
2020 June | 118 | 25 | 143 |
2020 May | 58 | 14 | 72 |
2020 April | 42 | 20 | 62 |
2020 March | 38 | 15 | 53 |
2020 February | 54 | 22 | 76 |
2020 January | 67 | 29 | 96 |
2019 December | 51 | 33 | 84 |
2019 November | 61 | 30 | 91 |
2019 October | 61 | 26 | 87 |
2019 September | 79 | 25 | 104 |
2019 August | 50 | 16 | 66 |
2019 July | 47 | 13 | 60 |
2019 June | 49 | 27 | 76 |
2019 May | 57 | 18 | 75 |
2019 April | 98 | 27 | 125 |
2019 March | 64 | 33 | 97 |
2019 February | 47 | 16 | 63 |
2019 January | 41 | 28 | 69 |
2018 December | 166 | 46 | 212 |
2018 November | 281 | 22 | 303 |
2018 October | 207 | 18 | 225 |
2018 September | 88 | 21 | 109 |
2018 August | 49 | 19 | 68 |
2018 July | 45 | 18 | 63 |
2018 June | 50 | 11 | 61 |
2018 May | 52 | 16 | 68 |
2018 April | 73 | 9 | 82 |
2018 March | 59 | 11 | 70 |
2018 February | 44 | 9 | 53 |
2018 January | 58 | 11 | 69 |
2017 December | 44 | 4 | 48 |
2017 November | 62 | 13 | 75 |
2017 October | 36 | 7 | 43 |
2017 September | 56 | 8 | 64 |
2017 August | 100 | 11 | 111 |
2017 July | 69 | 6 | 75 |
2017 June | 72 | 8 | 80 |
2017 May | 81 | 15 | 96 |
2017 April | 46 | 7 | 53 |
2017 March | 52 | 6 | 58 |
2017 February | 5 | 1 | 6 |