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Article ; Online: The Old West analogy for acid-base buffering.

Bobulescu, Ion Alexandru

2020 Volume 44, Issue 2, Page(s) 210–211

MeSH term(s)	Acid-Base Equilibrium/physiology ; Buffers ; Humans ; Hydrogen-Ion Concentration ; Medical Illustration/education ; Physiology/education ; Students
Chemical Substances	Buffers
Language	English
Publishing date	2020-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	1024917-5
ISSN	1522-1229 ; 1043-4046
ISSN (online)	1522-1229
ISSN	1043-4046
DOI	10.1152/advan.00033.2020
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Article ; Online: Dopamine reduces cell surface Na

Hu, Ming Chang / Bobulescu, I Alexandru / Quiñones, Henry / Gisler, Serge M / Moe, Orson W

American journal of physiology. Renal physiology

2017 Volume 313, Issue 4, Page(s) F1018–F1025

Abstract: The intrarenal autocrine-paracrine dopamine (DA) system mediates a significant fraction of the natriuresis in response to a salt load. DA inhibits a number of ... ...

Abstract	The intrarenal autocrine-paracrine dopamine (DA) system mediates a significant fraction of the natriuresis in response to a salt load. DA inhibits a number of Na
MeSH term(s)	Animals ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Cells, Cultured ; Didelphis ; Dopamine/pharmacology ; Dose-Response Relationship, Drug ; Down-Regulation ; Exocytosis/drug effects ; Kidney/drug effects ; Kidney/metabolism ; Natriuresis/drug effects ; Protein Transport ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/metabolism ; Time Factors
Chemical Substances	Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2017-08-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00251.2017
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Article ; Online: Luminal Na(+)/H (+) exchange in the proximal tubule.

Bobulescu, I Alexandru / Moe, Orson W

Pflugers Archiv : European journal of physiology

2008 Volume 458, Issue 1, Page(s) 5–21

Abstract: The proximal tubule is critical for whole-organism volume and acid-base homeostasis by reabsorbing filtered water, NaCl, bicarbonate, and citrate, as well as by excreting acid in the form of hydrogen and ammonium ions and producing new bicarbonate in the ...

Abstract	The proximal tubule is critical for whole-organism volume and acid-base homeostasis by reabsorbing filtered water, NaCl, bicarbonate, and citrate, as well as by excreting acid in the form of hydrogen and ammonium ions and producing new bicarbonate in the process. Filtered organic solutes such as amino acids, oligopeptides, and proteins are also retrieved by the proximal tubule. Luminal membrane Na(+)/H(+) exchangers either directly mediate or indirectly contribute to each of these processes. Na(+)/H(+) exchangers are a family of secondary active transporters with diverse tissue and subcellular distributions. Two isoforms, NHE3 and NHE8, are expressed at the luminal membrane of the proximal tubule. NHE3 is the prevalent isoform in adults, is the most extensively studied, and is tightly regulated by a large number of agonists and physiological conditions acting via partially defined molecular mechanisms. Comparatively little is known about NHE8, which is highly expressed at the lumen of the neonatal proximal tubule and is mostly intracellular in adults. This article discusses the physiology of proximal Na(+)/H(+) exchange, the multiple mechanisms of NHE3 regulation, and the reciprocal relationship between NHE3 and NHE8 at the lumen of the proximal tubule.
MeSH term(s)	Acid-Base Equilibrium/physiology ; Adult ; Gene Expression Regulation ; Humans ; Infant, Newborn ; Kidney Tubules, Proximal/metabolism ; Protein Isoforms/metabolism ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/agonists ; Sodium-Hydrogen Exchangers/physiology
Chemical Substances	Protein Isoforms ; SLC9A3 protein, human ; SLC9A8 protein, human ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers
Language	English
Publishing date	2008-10-14
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-008-0595-1
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Article: Na+/H+ exchangers in renal regulation of acid-base balance.

Bobulescu, I Alexandru / Moe, Orson W

Seminars in nephrology

2006 Volume 26, Issue 5, Page(s) 334–344

Abstract: The kidney plays key roles in extracellular fluid pH homeostasis by reclaiming bicarbonate (HCO(3)(-)) filtered at the glomerulus and generating the consumed HCO(3)(-) by secreting protons (H(+)) into the urine (renal acidification). Sodium-proton ... ...

Abstract	The kidney plays key roles in extracellular fluid pH homeostasis by reclaiming bicarbonate (HCO(3)(-)) filtered at the glomerulus and generating the consumed HCO(3)(-) by secreting protons (H(+)) into the urine (renal acidification). Sodium-proton exchangers (NHEs) are ubiquitous transmembrane proteins mediating the countertransport of Na(+) and H(+) across lipid bilayers. In mammals, NHEs participate in the regulation of cell pH, volume, and intracellular sodium concentration, as well as in transepithelial ion transport. Five of the 10 isoforms (NHE1-4 and NHE8) are expressed at the plasma membrane of renal epithelial cells. The best-studied isoform for acid-base homeostasis is NHE3, which mediates both HCO(3)(-) absorption and H(+) excretion in the renal tubule. This article reviews some important aspects of NHEs in the kidney, with special emphasis on the role of renal NHE3 in the maintenance of acid-base balance.
MeSH term(s)	Acid-Base Equilibrium/physiology ; Acidosis/physiopathology ; Adaptation, Physiological ; Animals ; Humans ; Nephrons/physiology ; Sodium-Hydrogen Exchangers/physiology
Chemical Substances	Sodium-Hydrogen Exchangers
Language	English
Publishing date	2006-11-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2006.07.001
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Article ; Online: Renal lipid metabolism and lipotoxicity.

Bobulescu, Ion Alexandru

Current opinion in nephrology and hypertension

2010 Volume 19, Issue 4, Page(s) 393–402

Abstract: Purpose of review: Lipid accumulation in nonadipose tissues is increasingly recognized to contribute to organ injury through a process termed lipotoxicity, but whether this process occurs in the kidney is still uncertain. This article briefly summarizes ...

Abstract	Purpose of review: Lipid accumulation in nonadipose tissues is increasingly recognized to contribute to organ injury through a process termed lipotoxicity, but whether this process occurs in the kidney is still uncertain. This article briefly summarizes the normal role of lipids in renal physiology and the current evidence linking excess lipids and lipotoxicity to renal dysfunction. Recent findings: Evidence suggesting that renal lipid accumulation and lipotoxicity may lead to kidney dysfunction has mounted significantly over recent years. Abnormal renal lipid content has been described in a number of animal models and has been successfully manipulated using pharmacologic or genetic strategies. There is some heterogeneity among studies with regard to the mechanisms, consequences, and localization of lipid accumulation in the kidney, explainable at least in part by inherent differences between animal models. The relevance of these findings for human pathophysiology remains to be established. Summary: Current knowledge on renal lipid physiology and pathophysiology is insufficient, but provides a strong foundation and incentive for further exploration. The future holds significant challenges in this area, especially with regard to applicability of research findings to the human kidney in vivo, but also the opportunity to transform our understanding of an array of kidney disorders.
MeSH term(s)	Albumins/metabolism ; Animals ; Dyslipidemias ; Humans ; Kidney/metabolism ; Kidney/physiology ; Kidney/physiopathology ; Kidney Diseases/physiopathology ; Lipid Metabolism/physiology ; Lipids/physiology ; Triglycerides/metabolism
Chemical Substances	Albumins ; Lipids ; Triglycerides
Language	English
Publishing date	2010-05-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0b013e32833aa4ac
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Zs.A 3686: Show issues

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Article ; Online: Net Acid Excretion and Urinary Organic Anions in Idiopathic Uric Acid Nephrolithiasis.

Bobulescu, I Alexandru / Park, Sun K / Xu, L H Richie / Blanco, Francisco / Poindexter, John / Adams-Huet, Beverley / Davidson, Taylor L / Sakhaee, Khashayar / Maalouf, Naim M / Moe, Orson W

Clinical journal of the American Society of Nephrology : CJASN

2019 Volume 14, Issue 3, Page(s) 411–420

Abstract: Background and objectives: Idiopathic uric acid nephrolithiasis, which is closely associated with obesity and the metabolic syndrome, is increasing in prevalence. Unduly acidic urine pH, the quintessential pathophysiologic feature of this disease, is in ...

Abstract	Background and objectives: Idiopathic uric acid nephrolithiasis, which is closely associated with obesity and the metabolic syndrome, is increasing in prevalence. Unduly acidic urine pH, the quintessential pathophysiologic feature of this disease, is in part explained by inadequate excretion of the principal urinary buffer ammonium. The role of net acid excretion in the pathogenesis of uric acid nephrolithiasis is incompletely understood. Design, setting, participants, & measurements: We compared acid-base parameters of patients with idiopathic uric acid nephrolithiasis with matched control subjects under controlled diets in an inpatient metabolic unit. Measurements included fasting blood and 24-hour urine chemistries and 24-hour urine metabolomic analysis. Comparisons between groups included analysis of covariance models controlling for urine pH or body mass index. Results: Subjects with idiopathic uric acid nephrolithiasis had lower urine pH (5.5 versus 5.9; Conclusions: Higher acid load to the kidney, resulting in higher urinary net acid excretion, is an important factor in the pathogenesis of idiopathic uric acid nephrolithiasis.
MeSH term(s)	Acid-Base Equilibrium ; Biomarkers/urine ; Body Mass Index ; Case-Control Studies ; Diet/adverse effects ; Female ; Humans ; Hydrogen-Ion Concentration ; Kidney/physiopathology ; Male ; Middle Aged ; Nephrolithiasis/diagnosis ; Nephrolithiasis/etiology ; Nephrolithiasis/physiopathology ; Nephrolithiasis/urine ; Pilot Projects ; Renal Elimination ; Risk Factors ; Uric Acid/urine
Chemical Substances	Biomarkers ; Uric Acid (268B43MJ25)
Language	English
Publishing date	2019-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.10420818
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Article ; Online: Quantification of renal steatosis in type II diabetes mellitus using dixon-based MRI.

Yokoo, Takeshi / Clark, Haley R / Pedrosa, Ivan / Yuan, Qing / Dimitrov, Ivan / Zhang, Yue / Lingvay, Ildiko / Beg, Muhammad S / Bobulescu, I Alexandru

Journal of magnetic resonance imaging : JMRI

2016 Volume 44, Issue 5, Page(s) 1312–1319

Abstract: Purpose: To evaluate renal lipid content in subjects with and without type II diabetes mellitus (DM2) using Dixon-based magnetic resonance imaging (MRI).: Materials and methods: This retrospective study was approved by the Institutional Review Board ... ...

Abstract	Purpose: To evaluate renal lipid content in subjects with and without type II diabetes mellitus (DM2) using Dixon-based magnetic resonance imaging (MRI). Materials and methods: This retrospective study was approved by the Institutional Review Board and compliant with the Health Insurance Portability and Accountability Act. Sixty-nine adults with or without DM2 (n = 29, n = 40) underwent 3T MRI of the abdomen using 3D multiecho Dixon gradient-echo acquisition and proton-density fat fraction (FF) reconstruction. FF values were recorded within segmented regions of interest in the kidneys and liver. The FF measurement error was estimated from the within-subject difference between the right and left kidneys using Bland-Altman analysis. Correlation between renal FF, hepatic FF, and body mass index (BMI) was evaluated. The association between renal FF and DM2 was evaluated by Wilcoxon rank sum test as well as by multivariate regression to correct for potential confounding effects of age, sex, BMI, creatinine, and hepatic FF. P < 0.05 was considered statistically significant. Results: Per-subject 95% limits of agreement of the renal FF measurement were [-3.26%, +3.22%]. BMI was significantly correlated with renal FF (r = 0.266, P = 0.027) and with liver FF (r = 0.344, P = 0.006). Correlation between renal and hepatic FF did not reach statistical significance (r = 0.215, P = 0.090). Median renal FF (±interquartile range) was 2.18% (±2.52%) in the DM2 cohort, significantly higher than 0.80% (±2.63%) in the non-DM2 cohort (P < 0.001). After correcting for potential confounders, the relationship between DM2 and renal FF remained statistically significant (P = 0.005). Conclusion: Renal lipid content can be measured noninvasively using Dixon-based MRI and may be increased in subjects with DM2 compared to those without DM2. J. Magn. Reson. Imaging 2016;44:1312-1319.
MeSH term(s)	Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/diagnostic imaging ; Diabetes Mellitus, Type 2/metabolism ; Diabetic Nephropathies/diagnostic imaging ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/metabolism ; Female ; Humans ; Image Enhancement/methods ; Image Interpretation, Computer-Assisted/methods ; Lipid Metabolism ; Magnetic Resonance Imaging/methods ; Male ; Middle Aged ; Molecular Imaging/methods ; Reproducibility of Results ; Sensitivity and Specificity
Language	English
Publishing date	2016-03-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1146614-5
ISSN	1522-2586 ; 1053-1807
ISSN (online)	1522-2586
ISSN	1053-1807
DOI	10.1002/jmri.25252
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Article ; Online: Renal lipid accumulation, oxidative stress and uric acid handling in a rodent model of obesity and metabolic syndrome.

Rosenthal, Tara R / Park, Sun K / Kairamkonda, Subash / Khatoon, Sabiha / Pop, Laurentiu M / Bobulescu, Ion Alexandru

Journal of investigative medicine : the official publication of the American Federation for Clinical Research

2020

Abstract: Hyperuricemia is more prevalent among people with obesity and metabolic syndrome, and is associated with adverse clinical outcomes. We hypothesized that increased renal reabsorption of uric acid (UA) in obesity and metabolic syndrome may be an adaptive ... ...

Abstract	Hyperuricemia is more prevalent among people with obesity and metabolic syndrome, and is associated with adverse clinical outcomes. We hypothesized that increased renal reabsorption of uric acid (UA) in obesity and metabolic syndrome may be an adaptive response of the kidney when faced with fatty acid-induced oxidative stress. To test this hypothesis, we examined lipid accumulation, markers of oxidative stress, and renal UA handling in Zucker diabetic fatty (ZDF) rats, and in matched lean control animals. Rats were randomized to either normal rodent chow or a diet supplemented with antioxidants (α-tocopheryl acetate, sodium selenite, zinc sulfate, and ascorbic acid), and were followed up for either 4 or 20 weeks after randomization. Dietary antioxidant supplementation had no significant effects in lean control rats but led to partial improvement in markers of elevated oxidative stress in the kidney of ZDF rats. Renal UA handling was not affected by antioxidant supplementation. We observed robust correlations between renal lipid content and oxidative stress markers in the pooled experimental groups, particularly in older animals after 20 weeks on the study diets. Dietary antioxidant supplementation did not prevent the gradual decline in renal function observed in older ZDF rats. These findings suggest that hyperuricemia in the ZDF rat model of obesity and the metabolic syndrome is not caused by renal oxidative stress, that there may be a pathophysiological link between lipid accumulation and oxidative stress in the kidney, and that antioxidant supplementation does not prevent age-related decline in renal function in ZDF rats.
Language	English
Publishing date	2020-12-15
Publishing country	England
Document type	Journal Article
ZDB-ID	1217870-6
ISSN	1708-8267 ; 0009-9279 ; 1081-5589
ISSN (online)	1708-8267
ISSN	0009-9279 ; 1081-5589
DOI	10.1136/jim-2020-001608
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Article: Renal Lipid Metabolism Abnormalities in Obesity and Clear Cell Renal Cell Carcinoma.

Bobulescu, Ion Alexandru / Pop, Laurentiu M / Mani, Chinnadurai / Turner, Kala / Rivera, Christian / Khatoon, Sabiha / Kairamkonda, Subash / Hannan, Raquibul / Palle, Komaraiah

Metabolites

2021 Volume 11, Issue 9

Abstract: Clear cell renal cell carcinoma is the most common and deadly type of cancer affecting the kidney, and is characterized histologically by large intracellular lipid deposits. These deposits are thought to result from lipid metabolic reprogramming ... ...

Abstract	Clear cell renal cell carcinoma is the most common and deadly type of cancer affecting the kidney, and is characterized histologically by large intracellular lipid deposits. These deposits are thought to result from lipid metabolic reprogramming occurring in tumor cells, but the exact mechanisms and implications of these metabolic alterations are incompletely understood. Obesity is an independent risk factor for clear cell renal cell carcinoma, and is also associated with lipid accumulation in noncancerous epithelial cells of the proximal tubule, where clear cell renal cell carcinoma originates. This article explores the potential link between obesity-associated renal lipid metabolic disturbances and lipid metabolic reprogramming in clear cell renal cell carcinoma, and discusses potential implications for future research.
Language	English
Publishing date	2021-09-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo11090608
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Article ; Online: Adiponectin alters renal calcium and phosphate excretion through regulation of klotho expression.

Rutkowski, Joseph M / Pastor, Johanne / Sun, Kai / Park, Sun K / Bobulescu, I Alexandru / Chen, Christopher T / Moe, Orson W / Scherer, Philipp E

Kidney international

2016 Volume 91, Issue 2, Page(s) 324–337

Abstract: The kidney controls systemic calcium and phosphate levels and disturbances of its control mechanisms can lead to a variety of diseases. The insulin-sensitizing adipokine adiponectin is renoprotective and accelerates functional recovery following renal ... ...

Abstract	The kidney controls systemic calcium and phosphate levels and disturbances of its control mechanisms can lead to a variety of diseases. The insulin-sensitizing adipokine adiponectin is renoprotective and accelerates functional recovery following renal injury. However, unlike other adipokines, adiponectin is reduced in obesity. High adiponectin levels are also correlated with bone loss, suggestive of an additional action in mineral metabolism. Using knockout, wild-type, and adiponectin-overexpressing transgenic mice, we sought to identify the mechanistic basis for adiponectin's ability to regulate calcium and phosphate balance at the level of the kidney. Adiponectin knockout mice exhibited lower serum calcium, lower urinary calcium excretion, and markedly lower serum fibroblast growth factor 23 (FGF23) levels, although circulating klotho concentrations were significantly higher than in wild-type littermates. The transgenic mice exhibited lower bone mass and strength, particularly compared to adiponectin knockout mice. The transgenic mice were hyper-responsive to a 2% phosphate-enriched diet, exhibiting 2-fold higher serum FGF23 and concomitantly higher fractional phosphate excretion. These mice also excreted more calcium with calcium-enriched diet and had less renal klotho protein expression. In contrast, the knockout mice exhibited a smaller increase in FGF23 and maintained elevated klotho levels on both mineral challenges. Kidney-specific adiponectin expression in doxycycline-inducible adiponectin mice and adiponectin addition in vitro confirmed adiponectin's ability to reduce tubular epithelial cell klotho secretion. Thus, adiponectin alters calcium and phosphate balance and renal mineral excretion, in part, through klotho. This work highlights the profound effects of adipose tissue on renal function and has identified a new mechanism by which adiponectin may regulate bone mass.
MeSH term(s)	Adiponectin/deficiency ; Adiponectin/genetics ; Adiponectin/metabolism ; Animals ; Biomechanical Phenomena ; Calcium, Dietary/blood ; Calcium, Dietary/metabolism ; Calcium, Dietary/urine ; Collagen/metabolism ; Dogs ; Femur/metabolism ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/blood ; Fibrosis ; Genotype ; Glucuronidase/blood ; Glucuronidase/genetics ; Homeostasis ; Hormones/blood ; Kidney/metabolism ; Kidney/pathology ; Kidney Tubules/metabolism ; Klotho Proteins ; Madin Darby Canine Kidney Cells ; Male ; Mice, Knockout ; Osteogenesis ; Phenotype ; Phosphates/blood ; Phosphates/metabolism ; Phosphates/urine ; Phosphorus, Dietary/blood ; Phosphorus, Dietary/metabolism ; Phosphorus, Dietary/urine ; Renal Elimination ; Spine/metabolism ; Transfection
Chemical Substances	Adiponectin ; Adipoq protein, mouse ; Calcium, Dietary ; Fgf23 protein, mouse ; Hormones ; Phosphates ; Phosphorus, Dietary ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Collagen (9007-34-5) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2016-11-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2016.09.016
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