Patients with gastrointestinal bleeding often require large volume blood transfusion. Among the various side effects of blood transfusion, the increase of potassium levels is a serious one which is often overlooked. We report a case of severe hyperkalemia in a patient with gastric bleeding after large volume transfusion of packed red blood cells. The patient had hyperkalemia at baseline associated with his receiving medication as well as acute renal failure following hypovolemia. The baseline hyperkalemia was further aggravated after massive transfusions of packed red blood cells in a short period of time. The associated pathogenetic mechanisms resulting in the increase of potassium levels are presented. A number of risk factors which increase the risk of hyperkalemia after blood transfusion are discussed. Moreover, appropriate management strategies for the prevention of blood transfusion associated hyperkalemia are also presented. Physicians should always keep in mind the possibility of hyperkalemia in cases of blood transfusion.
{"title":"Severe hyperkalemia following blood transfusions: Is there a link?","authors":"C. Rizos, H. Milionis, M. Elisaf","doi":"10.5527/wjn.v6.i1.53","DOIUrl":"https://doi.org/10.5527/wjn.v6.i1.53","url":null,"abstract":"Patients with gastrointestinal bleeding often require large volume blood transfusion. Among the various side effects of blood transfusion, the increase of potassium levels is a serious one which is often overlooked. We report a case of severe hyperkalemia in a patient with gastric bleeding after large volume transfusion of packed red blood cells. The patient had hyperkalemia at baseline associated with his receiving medication as well as acute renal failure following hypovolemia. The baseline hyperkalemia was further aggravated after massive transfusions of packed red blood cells in a short period of time. The associated pathogenetic mechanisms resulting in the increase of potassium levels are presented. A number of risk factors which increase the risk of hyperkalemia after blood transfusion are discussed. Moreover, appropriate management strategies for the prevention of blood transfusion associated hyperkalemia are also presented. Physicians should always keep in mind the possibility of hyperkalemia in cases of blood transfusion.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"6 1","pages":"53 - 56"},"PeriodicalIF":0.0,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81632457","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}
G. Tsoulfas, P. Agorastou, D. Ko, M. Hertl, N. Elias, A. Cosimi, T. Kawai
AIM To compare laparoscopic and open living donor nephrectomy, based on the results from a single center during a decade. METHODS This is a retrospective review of all living donor nephrectomies performed at the Massachusetts General Hospital, Harvard Medical School, Boston, between 1/1998 - 12/2009. Overall there were 490 living donors, with 279 undergoing laparoscopic living donor nephrectomy (LLDN) and 211 undergoing open donor nephrectomy (OLDN). Demographic data, operating room time, the effect of the learning curve, the number of conversions from laparoscopic to open surgery, donor preoperative glomerular filtration rate and creatinine (Cr), donor and recipient postoperative Cr, delayed graft function and donor complications were analyzed. Statistical analysis was performed. RESULTS Overall there was no statistically significant difference between the LLDN and the OLDN groups regarding operating time, donor preoperative renal function, donor and recipient postoperative kidney function, delayed graft function or the incidence of major complications. When the last 100 laparoscopic cases were analyzed, there was a statistically significant difference regarding operating time in favor of the LLDN, pointing out the importance of the learning curve. Furthermore, another significant difference between the two groups was the decreased length of stay for the LLDN (2.87 d for LLDN vs 3.6 d for OLDN). CONCLUSION Recognizing the importance of the learning curve, this paper provides evidence that LLDN has a safety profile comparable to OLDN and decreased length of stay for the donor.
{"title":"Laparoscopic vs open donor nephrectomy: Lessons learnt from single academic center experience","authors":"G. Tsoulfas, P. Agorastou, D. Ko, M. Hertl, N. Elias, A. Cosimi, T. Kawai","doi":"10.5527/wjn.v6.i1.45","DOIUrl":"https://doi.org/10.5527/wjn.v6.i1.45","url":null,"abstract":"AIM To compare laparoscopic and open living donor nephrectomy, based on the results from a single center during a decade. METHODS This is a retrospective review of all living donor nephrectomies performed at the Massachusetts General Hospital, Harvard Medical School, Boston, between 1/1998 - 12/2009. Overall there were 490 living donors, with 279 undergoing laparoscopic living donor nephrectomy (LLDN) and 211 undergoing open donor nephrectomy (OLDN). Demographic data, operating room time, the effect of the learning curve, the number of conversions from laparoscopic to open surgery, donor preoperative glomerular filtration rate and creatinine (Cr), donor and recipient postoperative Cr, delayed graft function and donor complications were analyzed. Statistical analysis was performed. RESULTS Overall there was no statistically significant difference between the LLDN and the OLDN groups regarding operating time, donor preoperative renal function, donor and recipient postoperative kidney function, delayed graft function or the incidence of major complications. When the last 100 laparoscopic cases were analyzed, there was a statistically significant difference regarding operating time in favor of the LLDN, pointing out the importance of the learning curve. Furthermore, another significant difference between the two groups was the decreased length of stay for the LLDN (2.87 d for LLDN vs 3.6 d for OLDN). CONCLUSION Recognizing the importance of the learning curve, this paper provides evidence that LLDN has a safety profile comparable to OLDN and decreased length of stay for the donor.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"8 1","pages":"45 - 52"},"PeriodicalIF":0.0,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79310706","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}
H. Rondon-Berrios, C. Argyropoulos, T. Ing, D. Raj, D. Malhotra, E. Agaba, M. Rohrscheib, Z. Khitan, G. Murata, J. Shapiro, A. Tzamaloukas
Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level.
{"title":"Hypertonicity: Clinical entities, manifestations and treatment","authors":"H. Rondon-Berrios, C. Argyropoulos, T. Ing, D. Raj, D. Malhotra, E. Agaba, M. Rohrscheib, Z. Khitan, G. Murata, J. Shapiro, A. Tzamaloukas","doi":"10.5527/wjn.v6.i1.1","DOIUrl":"https://doi.org/10.5527/wjn.v6.i1.1","url":null,"abstract":"Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"45 1","pages":"1 - 13"},"PeriodicalIF":0.0,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88439688","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}
D. Mukherjee, R. Sinha, Md. Shakil Akhtar, Agnisekhar Saha
AIM To ascertain the frequency of hyponatremic hypertensive syndrome (HHS) in a cohort of children with hypertensive emergency in a tertiary pediatric hospital. METHODS A retrospective review was undertaken among children with hypertensive emergency admitted in our tertiary children hospital between June 2014 and December 2015 with an aim to identify any children with HHS. Three children with HHS were identified during this period. RESULTS The 3 patients with HHS presented with hypertensive emergency. They were initially managed with Labetalol infusion and thereafter switched to oral anti-hypertensives (combination of Nifedipine sustained release, Hydralazine and Beta Blocker). All 3 were diagnosed to have unilateral renal artery stenosis. One child was lost to follow up, whereas the other 2 underwent renal angioplasty which was followed with normalization of blood pressure. CONCLUSION Despite activation of renin angiotensin axis secondary to renal artery stenosis, these groups of children have significant hyponatremia. Renal re-vascularisation produces excellent results in most of them.
{"title":"Hyponatremic hypertensive syndrome - a retrospective cohort study","authors":"D. Mukherjee, R. Sinha, Md. Shakil Akhtar, Agnisekhar Saha","doi":"10.5527/wjn.v6.i1.41","DOIUrl":"https://doi.org/10.5527/wjn.v6.i1.41","url":null,"abstract":"AIM To ascertain the frequency of hyponatremic hypertensive syndrome (HHS) in a cohort of children with hypertensive emergency in a tertiary pediatric hospital. METHODS A retrospective review was undertaken among children with hypertensive emergency admitted in our tertiary children hospital between June 2014 and December 2015 with an aim to identify any children with HHS. Three children with HHS were identified during this period. RESULTS The 3 patients with HHS presented with hypertensive emergency. They were initially managed with Labetalol infusion and thereafter switched to oral anti-hypertensives (combination of Nifedipine sustained release, Hydralazine and Beta Blocker). All 3 were diagnosed to have unilateral renal artery stenosis. One child was lost to follow up, whereas the other 2 underwent renal angioplasty which was followed with normalization of blood pressure. CONCLUSION Despite activation of renin angiotensin axis secondary to renal artery stenosis, these groups of children have significant hyponatremia. Renal re-vascularisation produces excellent results in most of them.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"132 1","pages":"41 - 44"},"PeriodicalIF":0.0,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90882593","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}
AIM To evaluate the effects of the non-selective, non-steroidal anti-inflammatory drug (NSAID) acetylsalicylic acid (ASA), on ex vivo embryonic kidney growth and development. METHODS Pairs of fetal mouse kidneys at embryonic day 12.5 were cultured ex vivo in increasing concentrations of ASA (0.04-0.4 mg/mL) for up to 7 d. One organ from each pair was grown in control media and was used as the internal control for the experimental contralateral organ. In some experiments, organs were treated with ASA for 48 h and then transferred either to control media alone or control media containing 10 μmol/L prostaglandin E2 (PGE2) for a further 5 d. Fetal kidneys were additionally obtained from prostaglandin synthase 2 homozygous null or heterozygous (PTGS2-/- and PTGS2-/+) embryos and grown in culture. Kidney cross-sectional area was used to determine treatment effects on kidney growth. Whole-mount labelling to fluorescently detect laminin enabled crude determination of epithelial branching using confocal microscopy. RESULTS Increasing ASA concentration (0.1, 0.2 and 0.4 mg/mL) significantly inhibited metanephric growth (P < 0.05). After 7 d of culture, exposure to 0.2 mg/mL and 0.4 mg/mL reduced organ size to 53% and 23% of control organ size respectively (P < 0.01). Addition of 10 μmol/L PGE2 to culture media after exposure to 0.2 mg/mL ASA for 48 h resulted in a return of growth area to control levels. Application of control media alone after cessation of ASA exposure showed no benefit on kidney growth. Despite the apparent recovery of growth area with 10 μmol/L PGE2, no obvious renal tubular structures were formed. The number of epithelial tips generated after 48 h exposure to ASA was reduced by 40% (0.2 mg/mL; P < 0.05) and 47% (0.4 mg/mL; P < 0.01). Finally, growth of PTGS2-/- and PTGS2+/- kidneys in organ culture showed no differences, indicating that PTGS2 derived PGE2 may at best have a minor role. CONCLUSION ASA reduces early renal growth and development but the role of prostaglandins in this may be minor.
{"title":"Acetylsalicylic acid interferes with embryonic kidney growth and development by a prostaglandin-independent mechanism","authors":"S. Welham, A. Sparrow, D. Gardner, M. Elmes","doi":"10.5527/wjn.v6.i1.21","DOIUrl":"https://doi.org/10.5527/wjn.v6.i1.21","url":null,"abstract":"AIM To evaluate the effects of the non-selective, non-steroidal anti-inflammatory drug (NSAID) acetylsalicylic acid (ASA), on ex vivo embryonic kidney growth and development. METHODS Pairs of fetal mouse kidneys at embryonic day 12.5 were cultured ex vivo in increasing concentrations of ASA (0.04-0.4 mg/mL) for up to 7 d. One organ from each pair was grown in control media and was used as the internal control for the experimental contralateral organ. In some experiments, organs were treated with ASA for 48 h and then transferred either to control media alone or control media containing 10 μmol/L prostaglandin E2 (PGE2) for a further 5 d. Fetal kidneys were additionally obtained from prostaglandin synthase 2 homozygous null or heterozygous (PTGS2-/- and PTGS2-/+) embryos and grown in culture. Kidney cross-sectional area was used to determine treatment effects on kidney growth. Whole-mount labelling to fluorescently detect laminin enabled crude determination of epithelial branching using confocal microscopy. RESULTS Increasing ASA concentration (0.1, 0.2 and 0.4 mg/mL) significantly inhibited metanephric growth (P < 0.05). After 7 d of culture, exposure to 0.2 mg/mL and 0.4 mg/mL reduced organ size to 53% and 23% of control organ size respectively (P < 0.01). Addition of 10 μmol/L PGE2 to culture media after exposure to 0.2 mg/mL ASA for 48 h resulted in a return of growth area to control levels. Application of control media alone after cessation of ASA exposure showed no benefit on kidney growth. Despite the apparent recovery of growth area with 10 μmol/L PGE2, no obvious renal tubular structures were formed. The number of epithelial tips generated after 48 h exposure to ASA was reduced by 40% (0.2 mg/mL; P < 0.05) and 47% (0.4 mg/mL; P < 0.01). Finally, growth of PTGS2-/- and PTGS2+/- kidneys in organ culture showed no differences, indicating that PTGS2 derived PGE2 may at best have a minor role. CONCLUSION ASA reduces early renal growth and development but the role of prostaglandins in this may be minor.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"32 1","pages":"21 - 28"},"PeriodicalIF":0.0,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89986940","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}
Systemic inflammation is a recognized feature in chronic kidney disease (CKD). The role of systemic inflammation in the pathogenesis of vascular calcification was recently settled. FGF23 was recently accused as a direct stimulus of systemic inflammation. This finding explains the strong association of FGF23 to vascular calcification and increased mortality among CKD.
{"title":"FGF23 and inflammation","authors":"Usama A A Sharaf El Din, M. Salem, D. Abdulazim","doi":"10.5527/wjn.v6.i1.57","DOIUrl":"https://doi.org/10.5527/wjn.v6.i1.57","url":null,"abstract":"Systemic inflammation is a recognized feature in chronic kidney disease (CKD). The role of systemic inflammation in the pathogenesis of vascular calcification was recently settled. FGF23 was recently accused as a direct stimulus of systemic inflammation. This finding explains the strong association of FGF23 to vascular calcification and increased mortality among CKD.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"23 1","pages":"57 - 58"},"PeriodicalIF":0.0,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90585324","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}
N. Satoh, Masashi Suzuki, M. Nakamura, A. Suzuki, S. Horita, G. Seki, K. Moriya
Dent’s disease is an X-linked renal tubulopathy characterized by low molecular weight proteinuria, hypercalciuria and progressive renal failure. Disease aetiology is associated with mutations in the CLCN5 gene coding for the electrogenic 2Cl-/H+ antiporter chloride channel 5 (CLC-5), which is expressed in the apical endosomes of renal proximal tubules with the vacuolar type H+-ATPase (V-ATPase). Initially identified as a member of the CLC family of Cl- channels, CLC-5 was presumed to provide Cl- shunt into the endosomal lumen to dissipate H+ accumulation by V-ATPase, thereby facilitating efficient endosomal acidification. However, recent findings showing that CLC-5 is in fact not a Cl- channel but a 2Cl-/H+ antiporter challenged this classical shunt model, leading to a renewed and intense debate on its physiological roles. Cl- accumulation via CLC-5 is predicted to play a critical role in endocytosis, as illustrated in mice carrying an artificial Cl- channel mutation E211A that developed defective endocytosis but normal endosomal acidification. Conversely, a recent functional analysis of a newly identified disease-causing Cl- channel mutation E211Q in a patient with typical Dent’s disease confirmed the functional coupling between V-ATPase and CLC-5 in endosomal acidification, lending support to the classical shunt model. In this editorial, we will address the current recognition of the physiological role of CLC-5 with a specific focus on the functional coupling of V-ATPase and CLC-5.
{"title":"Functional coupling of V-ATPase and CLC-5","authors":"N. Satoh, Masashi Suzuki, M. Nakamura, A. Suzuki, S. Horita, G. Seki, K. Moriya","doi":"10.5527/wjn.v6.i1.14","DOIUrl":"https://doi.org/10.5527/wjn.v6.i1.14","url":null,"abstract":"Dent’s disease is an X-linked renal tubulopathy characterized by low molecular weight proteinuria, hypercalciuria and progressive renal failure. Disease aetiology is associated with mutations in the CLCN5 gene coding for the electrogenic 2Cl-/H+ antiporter chloride channel 5 (CLC-5), which is expressed in the apical endosomes of renal proximal tubules with the vacuolar type H+-ATPase (V-ATPase). Initially identified as a member of the CLC family of Cl- channels, CLC-5 was presumed to provide Cl- shunt into the endosomal lumen to dissipate H+ accumulation by V-ATPase, thereby facilitating efficient endosomal acidification. However, recent findings showing that CLC-5 is in fact not a Cl- channel but a 2Cl-/H+ antiporter challenged this classical shunt model, leading to a renewed and intense debate on its physiological roles. Cl- accumulation via CLC-5 is predicted to play a critical role in endocytosis, as illustrated in mice carrying an artificial Cl- channel mutation E211A that developed defective endocytosis but normal endosomal acidification. Conversely, a recent functional analysis of a newly identified disease-causing Cl- channel mutation E211Q in a patient with typical Dent’s disease confirmed the functional coupling between V-ATPase and CLC-5 in endosomal acidification, lending support to the classical shunt model. In this editorial, we will address the current recognition of the physiological role of CLC-5 with a specific focus on the functional coupling of V-ATPase and CLC-5.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"36 1","pages":"14 - 20"},"PeriodicalIF":0.0,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90095503","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}
G. Cao, S. D. Della Penna, N. Kouyoumdzian, M. Choi, S. Gorzalczany, B. Fernández, J. Toblli, M. Rosón
AIM To determine the effect of tempol in normal rats fed high salt on arterial pressure and the balance between antagonist components of the renal renin-angiotensin system. METHODS Sprague-Dawley rats were fed with 8% NaCl high-salt (HS) or 0.4% NaCl (normal-salt, NS) diet for 3 wk, with or without tempol (T) (1 mmol/L, administered in drinking water). Mean arterial pressure (MAP), glomerular filtration rate (GFR), and urinary sodium excretion (UVNa) were measured. We evaluated angiotensin II (Ang II), angiotensin 1-7 (Ang 1-7), angiotensin converting enzyme 2 (ACE2), mas receptor (MasR), angiotensin type 1 receptor (AT1R) and angiotensin type 2 receptor (AT2R) in renal tissues by immunohistochemistry. RESULTS The intake of high sodium produced a slight but significant increase in MAP and differentially regulated components of the renal renin-angiotensin system (RAS). This included an increase in Ang II and AT1R, and decrease in ACE-2 staining intensity using immunohistochemistry. Antioxidant supplementation with tempol increased natriuresis and GFR, prevented changes in blood pressure and reversed the imbalance of renal RAS components. This includes a decrease in Ang II and AT1R, as increase in AT2, ACE2, Ang (1-7) and MasR staining intensity using immunohistochemistry. In addition, the natriuretic effects of tempol were observed in NS-T group, which showed an increased staining intensity of AT2, ACE2, Ang (1-7) and MasR. CONCLUSION These findings suggest that a high salt diet leads to changes in the homeostasis and balance between opposing components of the renal RAS in hypertension to favour an increase in Ang II. Chronic antioxidant supplementation can modulate the balance between the natriuretic and antinatriuretic components of the renal RAS.
{"title":"Immunohistochemical expression of intrarenal renin angiotensin system components in response to tempol in rats fed a high salt diet","authors":"G. Cao, S. D. Della Penna, N. Kouyoumdzian, M. Choi, S. Gorzalczany, B. Fernández, J. Toblli, M. Rosón","doi":"10.5527/wjn.v6.i1.29","DOIUrl":"https://doi.org/10.5527/wjn.v6.i1.29","url":null,"abstract":"AIM To determine the effect of tempol in normal rats fed high salt on arterial pressure and the balance between antagonist components of the renal renin-angiotensin system. METHODS Sprague-Dawley rats were fed with 8% NaCl high-salt (HS) or 0.4% NaCl (normal-salt, NS) diet for 3 wk, with or without tempol (T) (1 mmol/L, administered in drinking water). Mean arterial pressure (MAP), glomerular filtration rate (GFR), and urinary sodium excretion (UVNa) were measured. We evaluated angiotensin II (Ang II), angiotensin 1-7 (Ang 1-7), angiotensin converting enzyme 2 (ACE2), mas receptor (MasR), angiotensin type 1 receptor (AT1R) and angiotensin type 2 receptor (AT2R) in renal tissues by immunohistochemistry. RESULTS The intake of high sodium produced a slight but significant increase in MAP and differentially regulated components of the renal renin-angiotensin system (RAS). This included an increase in Ang II and AT1R, and decrease in ACE-2 staining intensity using immunohistochemistry. Antioxidant supplementation with tempol increased natriuresis and GFR, prevented changes in blood pressure and reversed the imbalance of renal RAS components. This includes a decrease in Ang II and AT1R, as increase in AT2, ACE2, Ang (1-7) and MasR staining intensity using immunohistochemistry. In addition, the natriuretic effects of tempol were observed in NS-T group, which showed an increased staining intensity of AT2, ACE2, Ang (1-7) and MasR. CONCLUSION These findings suggest that a high salt diet leads to changes in the homeostasis and balance between opposing components of the renal RAS in hypertension to favour an increase in Ang II. Chronic antioxidant supplementation can modulate the balance between the natriuretic and antinatriuretic components of the renal RAS.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"1 1","pages":"29 - 40"},"PeriodicalIF":0.0,"publicationDate":"2017-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89673966","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}
T. Grillone, M. Menniti, Francesco Bombardiere, M. Vismara, Stefania Belviso, F. Fabiani, N. Perrotti, R. Iuliano, E. Colao
Gitelman’s syndrome (GS) is a salt-losing tubulopathy with an autosomal recessive inheritance caused by mutations of SLC12A3, which encodes for the thiazide-sensitive NaCl cotransporter. In this study we report a new mutation of SLC12A3 found in two brothers affected by GS. Hypokalemia, hypocalciuria and hyper-reninemia were present in both patients while hypomagnesemia was detected only in one. Both patients are compound heterozygotes carrying one well known GS associated mutation (c.2581 C > T) and a new one (c.283delC) in SLC12A3 gene. The new mutation results in a possible frame-shift with a premature stop-codon (pGln95ArgfsX19). The parents of the patients, heterozygous carriers of the mutations found in SLC12A3, have no disease associated phenotype. Therefore, the new mutation is causative of GS.
{"title":"New SLC12A3 disease causative mutation of Gitelman’s syndrome","authors":"T. Grillone, M. Menniti, Francesco Bombardiere, M. Vismara, Stefania Belviso, F. Fabiani, N. Perrotti, R. Iuliano, E. Colao","doi":"10.5527/wjn.v5.i6.551","DOIUrl":"https://doi.org/10.5527/wjn.v5.i6.551","url":null,"abstract":"Gitelman’s syndrome (GS) is a salt-losing tubulopathy with an autosomal recessive inheritance caused by mutations of SLC12A3, which encodes for the thiazide-sensitive NaCl cotransporter. In this study we report a new mutation of SLC12A3 found in two brothers affected by GS. Hypokalemia, hypocalciuria and hyper-reninemia were present in both patients while hypomagnesemia was detected only in one. Both patients are compound heterozygotes carrying one well known GS associated mutation (c.2581 C > T) and a new one (c.283delC) in SLC12A3 gene. The new mutation results in a possible frame-shift with a premature stop-codon (pGln95ArgfsX19). The parents of the patients, heterozygous carriers of the mutations found in SLC12A3, have no disease associated phenotype. Therefore, the new mutation is causative of GS.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"22 1","pages":"551 - 555"},"PeriodicalIF":0.0,"publicationDate":"2016-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79330275","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. C. da Silva, Marcelo de Sousa Tavares, M. Penido
AIM To investigate the prevalence of nutritional parameters of risk for cardiovascular disease (CVD) and kidney diseases in healthy preschool children. METHODS This is an observational cross-sectional study with 60 healthy children, of both genders, aged two to six years old and 56 mothers, in Belo Horizonte, Minas Gerais, Brazil. Preschool children and their families with regular activities at public schools were invited to paticipate in the study. The following characteristics were assessed: Socio-demographic condictions, clinical health, anthropometric, biochemical, lifestyle and data on food consumption. The 56 healthy children were divided into two groups, overweight (C1) and non-overweight (C2), as well as their mothers, respectively, in overweight (M1) and non-overweight (M2). Nutritional status was defined according to results obtained through the Anthro® Software for nutritional analysis. RESULTS Thirty-five children were male, with mean age of 4.44 ± 1.0 years old. Eighty-nine percent of them were eutrophic, 86.7% were sedentary and they had five meals a day. Body mass index (BMI) for age and total cholesterol (TC) was higher on C1 (P = 0.0001) and high density lipoprotein cholesterol (HDL-c) was higher on C2. Mothers were 32.5 ± 7.1 years old, mostly married and employed. Eighty-six percent of them were sedentary and 62.5% were overweight with BMI = 26.38 ± 5.07 kg/m2. Eighteen percent of the overweight mothers had isolated total hypercholesterolemia (TC levels elevated) and 12.5% had low HDL-c levels. The present study showed an association between overweight and obesity during the preschool years and the correspondent mothers’ nutritional status of overweight and obesity (OR = 4.96; 95%CI: 0.558-44.17). There was a positive correlation between the food risk associated with CVD by children and mothers when their consumption was 4 times/wk (P = 0.049; r = 0.516) or daily (P = 0.000008; r = 0.892). CONCLUSION Analyzed children showed high rates of physical inactivity, high serum cholesterol levels and high consumption of food associated with risk for CVD and renal disease. Changes in habits should be encouraged early in kindergarten.
{"title":"Prevalence of risk factors for cardiovascular and kidney disease in Brazilian healthy preschool children","authors":"A. C. da Silva, Marcelo de Sousa Tavares, M. Penido","doi":"10.5527/wjn.v5.i6.507","DOIUrl":"https://doi.org/10.5527/wjn.v5.i6.507","url":null,"abstract":"AIM To investigate the prevalence of nutritional parameters of risk for cardiovascular disease (CVD) and kidney diseases in healthy preschool children. METHODS This is an observational cross-sectional study with 60 healthy children, of both genders, aged two to six years old and 56 mothers, in Belo Horizonte, Minas Gerais, Brazil. Preschool children and their families with regular activities at public schools were invited to paticipate in the study. The following characteristics were assessed: Socio-demographic condictions, clinical health, anthropometric, biochemical, lifestyle and data on food consumption. The 56 healthy children were divided into two groups, overweight (C1) and non-overweight (C2), as well as their mothers, respectively, in overweight (M1) and non-overweight (M2). Nutritional status was defined according to results obtained through the Anthro® Software for nutritional analysis. RESULTS Thirty-five children were male, with mean age of 4.44 ± 1.0 years old. Eighty-nine percent of them were eutrophic, 86.7% were sedentary and they had five meals a day. Body mass index (BMI) for age and total cholesterol (TC) was higher on C1 (P = 0.0001) and high density lipoprotein cholesterol (HDL-c) was higher on C2. Mothers were 32.5 ± 7.1 years old, mostly married and employed. Eighty-six percent of them were sedentary and 62.5% were overweight with BMI = 26.38 ± 5.07 kg/m2. Eighteen percent of the overweight mothers had isolated total hypercholesterolemia (TC levels elevated) and 12.5% had low HDL-c levels. The present study showed an association between overweight and obesity during the preschool years and the correspondent mothers’ nutritional status of overweight and obesity (OR = 4.96; 95%CI: 0.558-44.17). There was a positive correlation between the food risk associated with CVD by children and mothers when their consumption was 4 times/wk (P = 0.049; r = 0.516) or daily (P = 0.000008; r = 0.892). CONCLUSION Analyzed children showed high rates of physical inactivity, high serum cholesterol levels and high consumption of food associated with risk for CVD and renal disease. Changes in habits should be encouraged early in kindergarten.","PeriodicalId":23745,"journal":{"name":"World Journal of Nephrology","volume":"15 1","pages":"507 - 516"},"PeriodicalIF":0.0,"publicationDate":"2016-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81664747","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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