Sejoong Kim, N. Heo, J. Jung, M. Son, H. Jang, Jay-Wook Lee, Y. Oh, K. Na, K. Joo, J. Han
{"title":"Contents Index Vol. 115, 2010","authors":"Sejoong Kim, N. Heo, J. Jung, M. Son, H. Jang, Jay-Wook Lee, Y. Oh, K. Na, K. Joo, J. Han","doi":"10.1159/000319721","DOIUrl":"https://doi.org/10.1159/000319721","url":null,"abstract":"","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"97 1","pages":"I - VI"},"PeriodicalIF":0.0,"publicationDate":"2010-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64458978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Brandoni, G. D. Giusto, R. Franca, S. Passamonti, A. Torres
{"title":"Subject Index Vol. 114, 2010","authors":"A. Brandoni, G. D. Giusto, R. Franca, S. Passamonti, A. Torres","doi":"10.1159/000313557","DOIUrl":"https://doi.org/10.1159/000313557","url":null,"abstract":"","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"114 1","pages":"p42 - p42"},"PeriodicalIF":0.0,"publicationDate":"2010-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000313557","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64396996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Brandoni, G. D. Giusto, R. Franca, S. Passamonti, A. Torres
{"title":"Contents Vol. 114, 2010","authors":"A. Brandoni, G. D. Giusto, R. Franca, S. Passamonti, A. Torres","doi":"10.1159/000313558","DOIUrl":"https://doi.org/10.1159/000313558","url":null,"abstract":"","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"114 1","pages":"pI - pVI"},"PeriodicalIF":0.0,"publicationDate":"2010-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64396576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background/aims: The plasma concentration of catecholamines and their metabolites generated by catechol-O-methyl transferase (COMT) were measured and their correlation with the progress of renal dysfunction was investigated in two distinctive animal models: a 5/6 nephrectomized Sprague-Dawley rat model and a 1/2 nephrectomized diabetic fatty Zucker rat model.
Methods: A highly sensitive, high-performance liquid chromatography-peroxyoxalate chemiluminescence reaction detection was employed to obtain values for the ratio [NMN]/([NE] + [NMN]), where [NE] represents the plasma concentration of norepinephrine and [NMN] represents the plasma concentration of normetanephrine.
Results: The [NMN]/([NE] + [NMN]) ratio correlated with both the increase in blood urea nitrogen concentration and the decrease in creatinine clearance.
Conclusion: The [NMN]/([NE] + [NMN]) ratio represents a quantitative indicator of the progress of renal dysfunction in the animal models. Regulation of COMT activity seemed to relate with the progress of renal dysfunction.
{"title":"Quantification of norepinephrine and its metabolites in the plasma of renal failure models.","authors":"Hiroshi Iijima, Yuji Okada, Makoto Tsunoda, Tomoko Takamiya, Kazuhiro Imai","doi":"10.1159/000318177","DOIUrl":"https://doi.org/10.1159/000318177","url":null,"abstract":"<p><strong>Background/aims: </strong>The plasma concentration of catecholamines and their metabolites generated by catechol-O-methyl transferase (COMT) were measured and their correlation with the progress of renal dysfunction was investigated in two distinctive animal models: a 5/6 nephrectomized Sprague-Dawley rat model and a 1/2 nephrectomized diabetic fatty Zucker rat model.</p><p><strong>Methods: </strong>A highly sensitive, high-performance liquid chromatography-peroxyoxalate chemiluminescence reaction detection was employed to obtain values for the ratio [NMN]/([NE] + [NMN]), where [NE] represents the plasma concentration of norepinephrine and [NMN] represents the plasma concentration of normetanephrine.</p><p><strong>Results: </strong>The [NMN]/([NE] + [NMN]) ratio correlated with both the increase in blood urea nitrogen concentration and the decrease in creatinine clearance.</p><p><strong>Conclusion: </strong>The [NMN]/([NE] + [NMN]) ratio represents a quantitative indicator of the progress of renal dysfunction in the animal models. Regulation of COMT activity seemed to relate with the progress of renal dysfunction.</p>","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"116 2","pages":"p9-p16"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000318177","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29111509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-01-01Epub Date: 2010-05-12DOI: 10.1159/000314542
Sejoong Kim, Nam Ju Heo, Ji Yong Jung, Min-Jeong Son, Hye Ryoun Jang, Jay Wook Lee, Yun Kyu Oh, Ki Young Na, Kwon Wook Joo, Jin Suk Han
Background: In chronic renal failure (CRF), residual nephrons can increase their excretion of sodium (Na) and potassium (K). However, the mechanisms of renal Na and K regulation in late-stage CRF have not been clearly investigated.
Methods: We examined altered expression of major renal Na and K transporters in Sprague-Dawley rats at 4 and 12 weeks after a 5/6 nephrectomy.
Results: CRF rats were azotemic and had gradually increased levels of urinary Na and K excretion over time. At 4 weeks, the abundance of Na-K-2Cl cotransporter (NKCC2), and Na-Cl cotransporter (NCC) in CRF rats increased significantly (477 and 222% of the control, respectively). In contrast, expression of NKCC2 and NCC decreased markedly at 12 weeks (55.4 and 30.8%, respectively). Expression of epithelial Na channel-alpha increased throughout the whole period. The abundance of renal outer medullary K-channel (ROMK) and Na-K-ATPase did not decrease at 4 weeks, but it was reduced at 12 weeks.
Conclusion: We suggest that increased urinary Na excretion in late-stage CRF may be associated with decreased expression of renal Na transporters except ENaC compared to early-stage CRF, and that increased urinary K excretion in the late stage of CRF may not be related to expression of ROMK.
背景:在慢性肾功能衰竭(CRF)中，残留的肾单位可以增加钠(Na)和钾(K)的排泄，然而，晚期CRF中肾脏Na和K的调节机制尚未明确研究。方法:在5/6肾切除术后4周和12周，我们检测了Sprague-Dawley大鼠肾脏主要Na和K转运蛋白的表达变化。结果:CRF大鼠呈氮化，随着时间的推移，尿钠和钾排泄水平逐渐升高。4周时，CRF大鼠Na-K-2Cl共转运体(NKCC2)和Na-Cl共转运体(NCC)的丰度显著增加(分别为对照组的477%和222%)。相比之下，NKCC2和NCC的表达在12周时明显下降(分别为55.4和30.8%)。上皮Na通道α的表达在整个时期均有所增加。肾外髓k通道(ROMK)和na - k - atp酶的丰度在4周时没有减少，但在12周时有所减少。结论:我们认为，与早期CRF相比，晚期CRF尿Na排泄增加可能与肾中除ENaC外的Na转运蛋白表达降低有关，而晚期CRF尿K排泄增加可能与ROMK表达无关。
{"title":"Changes in the sodium and potassium transporters in the course of chronic renal failure.","authors":"Sejoong Kim, Nam Ju Heo, Ji Yong Jung, Min-Jeong Son, Hye Ryoun Jang, Jay Wook Lee, Yun Kyu Oh, Ki Young Na, Kwon Wook Joo, Jin Suk Han","doi":"10.1159/000314542","DOIUrl":"https://doi.org/10.1159/000314542","url":null,"abstract":"<p><strong>Background: </strong>In chronic renal failure (CRF), residual nephrons can increase their excretion of sodium (Na) and potassium (K). However, the mechanisms of renal Na and K regulation in late-stage CRF have not been clearly investigated.</p><p><strong>Methods: </strong>We examined altered expression of major renal Na and K transporters in Sprague-Dawley rats at 4 and 12 weeks after a 5/6 nephrectomy.</p><p><strong>Results: </strong>CRF rats were azotemic and had gradually increased levels of urinary Na and K excretion over time. At 4 weeks, the abundance of Na-K-2Cl cotransporter (NKCC2), and Na-Cl cotransporter (NCC) in CRF rats increased significantly (477 and 222% of the control, respectively). In contrast, expression of NKCC2 and NCC decreased markedly at 12 weeks (55.4 and 30.8%, respectively). Expression of epithelial Na channel-alpha increased throughout the whole period. The abundance of renal outer medullary K-channel (ROMK) and Na-K-ATPase did not decrease at 4 weeks, but it was reduced at 12 weeks.</p><p><strong>Conclusion: </strong>We suggest that increased urinary Na excretion in late-stage CRF may be associated with decreased expression of renal Na transporters except ENaC compared to early-stage CRF, and that increased urinary K excretion in the late stage of CRF may not be related to expression of ROMK.</p>","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"115 4","pages":"p31-41"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000314542","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28978644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-01-01Epub Date: 2010-01-08DOI: 10.1159/000274484
Francisco E Anacleto, Lesley J Bruce, Peter Clayton, Shivram Hegde, Lourdes P Resontoc, Oliver Wrong
Aim: To describe the clinical features and genetic basis of distal renal tubular acidosis (dRTA) in Filipino children.
Methods: Clinical description and gene analysis of affected members of 7 families.
Results: In all affected children, the disease was associated with mutations of the SLC4A1 gene that codes for the bicarbonate/chloride anion-exchanger 1 (AE1, band 3) protein situated in the red cell membrane and the alpha-intercalated (proton-secreting) cell of the renal collecting duct. In 2 families, affected children were homozygous for a substitution of aspartic acid for glycine in residue 701 of the AE1 protein (G701D); in the other 5 families, affected children were compound heterozygotes of this mutation with the AE1 mutation (Delta400-408) that causes Southeast Asian ovalocytosis (SAO). All affected children had morphological red cell changes that closely resembled SAO, including the children who were homozygous for G701D and did not have the SAO mutation. Homozygous G701D thus produces morphological red cell changes that are not readily distinguishable from SAO. The parents of all 7 families were originally domiciled in the islands of the Visayas group in the central part of the Philippine archipelago.
Conclusion: Recessive renal tubular acidosis in Filipinos is usually caused by SLC4A1 mutations, commonly G701D.
{"title":"Distal renal tubular acidosis in Filipino children, caused by mutations of the anion-exchanger SLC4A1 (AE1, Band 3) gene.","authors":"Francisco E Anacleto, Lesley J Bruce, Peter Clayton, Shivram Hegde, Lourdes P Resontoc, Oliver Wrong","doi":"10.1159/000274484","DOIUrl":"https://doi.org/10.1159/000274484","url":null,"abstract":"<p><strong>Aim: </strong>To describe the clinical features and genetic basis of distal renal tubular acidosis (dRTA) in Filipino children.</p><p><strong>Methods: </strong>Clinical description and gene analysis of affected members of 7 families.</p><p><strong>Results: </strong>In all affected children, the disease was associated with mutations of the SLC4A1 gene that codes for the bicarbonate/chloride anion-exchanger 1 (AE1, band 3) protein situated in the red cell membrane and the alpha-intercalated (proton-secreting) cell of the renal collecting duct. In 2 families, affected children were homozygous for a substitution of aspartic acid for glycine in residue 701 of the AE1 protein (G701D); in the other 5 families, affected children were compound heterozygotes of this mutation with the AE1 mutation (Delta400-408) that causes Southeast Asian ovalocytosis (SAO). All affected children had morphological red cell changes that closely resembled SAO, including the children who were homozygous for G701D and did not have the SAO mutation. Homozygous G701D thus produces morphological red cell changes that are not readily distinguishable from SAO. The parents of all 7 families were originally domiciled in the islands of the Visayas group in the central part of the Philippine archipelago.</p><p><strong>Conclusion: </strong>Recessive renal tubular acidosis in Filipinos is usually caused by SLC4A1 mutations, commonly G701D.</p>","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"114 2","pages":"p19-24"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000274484","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28642641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-01-01Epub Date: 2010-01-27DOI: 10.1159/000277633
Mitchell L Halperin, Man S Oh, Kamel S Kamel
In physiologic terms, water diuresis has two components, the ability to excrete a large volume of water and the need to ‘desalinate’ this urine. The basic concept is that nephron segments that lack aquaporins do not reabsorb an appreciable volume of water even though there is an extremely large transtubular osmolar driving force ( table 1 ). After a large and rapid intake of water, the concentration of sodium (Na + ) in arterial plasma (P Na ) falls and the volume of cells in the brain increases [2] . The function of water diuresis is to minimize this fall in the P Na and thereby, prevent the development of a dangerous degree of brain cell swelling [3] . On the other hand, control mechanisms are needed to permit the retention of a small and safe volume of ingested water ( 1 liter in an adult), which can be used at a later time for heat dissipation by evaporation of water in sweat [4] . This explains why the arterial P Na can fall to 136 mmol/l without inhibiting the release of vasopressin sufficiently to initiate a water diuresis providing that water is not ingested quickly. If water is ingested rapidly, the arterial (but not necessarily the brachial venous) P Na falls sufficiently to provide the signal to inhibit the release of vasopressin [2] . To add a quantitative perspective to the renal control system for water homeostasis, consider a 70-kg adult huIn this issue of Nephron , Bockenhauer et al. [1] describe a family with 6 members who had mutations in the gene encoding the V 2 receptor for vasopressin that should cause congenital nephrogenic diabetes insipidus. They gathered clinical data on these patients including their response to the administration of desaminoD -arginine vasopressin (dDAVP). They performed in vitro studies of V 2 receptor cell surface expression, the affinity of vasopressin to bind to its V 2 receptor and produce cyclic AMP, as well as on the effects of the chaperone SR121463 on these parameters. Thus this is an impressive state-ofthe-art investigation, which employs a breadth of techniques. Our goal is to provide a critique of the clinical parameters that are used to determine whether a sufficient number of aquaporin-2 water channels (AQP2) are inserted in the luminal membranes of the late distal nephron in patients with nephrogenic diabetes insipidus in response to certain interventions. If this occurred, the rate of excretion of electrolyte-free water in the urine must decrease appreciably, but other causes for this fall in urine output must first be ruled out. As a background, we begin with a succinct synopsis of the physiology of this process and this is followed by an examination of the three clinical tools commonly employed in this assessment – urine flow rate, osmole excretion rate, and urine osmolality (U Osm ). Published online: January 27, 2010
{"title":"Integrating effects of aquaporins, vasopressin, distal delivery of filtrate and residual water permeability on the magnitude of water diuresis.","authors":"Mitchell L Halperin, Man S Oh, Kamel S Kamel","doi":"10.1159/000277633","DOIUrl":"https://doi.org/10.1159/000277633","url":null,"abstract":"In physiologic terms, water diuresis has two components, the ability to excrete a large volume of water and the need to ‘desalinate’ this urine. The basic concept is that nephron segments that lack aquaporins do not reabsorb an appreciable volume of water even though there is an extremely large transtubular osmolar driving force ( table 1 ). After a large and rapid intake of water, the concentration of sodium (Na + ) in arterial plasma (P Na ) falls and the volume of cells in the brain increases [2] . The function of water diuresis is to minimize this fall in the P Na and thereby, prevent the development of a dangerous degree of brain cell swelling [3] . On the other hand, control mechanisms are needed to permit the retention of a small and safe volume of ingested water ( 1 liter in an adult), which can be used at a later time for heat dissipation by evaporation of water in sweat [4] . This explains why the arterial P Na can fall to 136 mmol/l without inhibiting the release of vasopressin sufficiently to initiate a water diuresis providing that water is not ingested quickly. If water is ingested rapidly, the arterial (but not necessarily the brachial venous) P Na falls sufficiently to provide the signal to inhibit the release of vasopressin [2] . To add a quantitative perspective to the renal control system for water homeostasis, consider a 70-kg adult huIn this issue of Nephron , Bockenhauer et al. [1] describe a family with 6 members who had mutations in the gene encoding the V 2 receptor for vasopressin that should cause congenital nephrogenic diabetes insipidus. They gathered clinical data on these patients including their response to the administration of desaminoD -arginine vasopressin (dDAVP). They performed in vitro studies of V 2 receptor cell surface expression, the affinity of vasopressin to bind to its V 2 receptor and produce cyclic AMP, as well as on the effects of the chaperone SR121463 on these parameters. Thus this is an impressive state-ofthe-art investigation, which employs a breadth of techniques. Our goal is to provide a critique of the clinical parameters that are used to determine whether a sufficient number of aquaporin-2 water channels (AQP2) are inserted in the luminal membranes of the late distal nephron in patients with nephrogenic diabetes insipidus in response to certain interventions. If this occurred, the rate of excretion of electrolyte-free water in the urine must decrease appreciably, but other causes for this fall in urine output must first be ruled out. As a background, we begin with a succinct synopsis of the physiology of this process and this is followed by an examination of the three clinical tools commonly employed in this assessment – urine flow rate, osmole excretion rate, and urine osmolality (U Osm ). Published online: January 27, 2010","PeriodicalId":18996,"journal":{"name":"Nephron Physiology","volume":"114 1","pages":"p11-7"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000277633","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28676942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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