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Article ; Online: The Role of the Endocrine System in the Regulation of Acid-Base Balance by the Kidney and the Progression of Chronic Kidney Disease.

Nagami, Glenn T / Kraut, Jeffrey A

International journal of molecular sciences

2024 Volume 25, Issue 4

Abstract: Systemic acid-base status is primarily determined by the interplay of net acid production (NEAP) arising from metabolism of ingested food stuffs, buffering of NEAP in tissues, generation of bicarbonate by the kidney, and capture of any bicarbonate ... ...

Abstract	Systemic acid-base status is primarily determined by the interplay of net acid production (NEAP) arising from metabolism of ingested food stuffs, buffering of NEAP in tissues, generation of bicarbonate by the kidney, and capture of any bicarbonate filtered by the kidney. In chronic kidney disease (CKD), acid retention may occur when dietary acid production is not balanced by bicarbonate generation by the diseased kidney. Hormones including aldosterone, angiotensin II, endothelin, PTH, glucocorticoids, insulin, thyroid hormone, and growth hormone can affect acid-base balance in different ways. The levels of some hormones such as aldosterone, angiotensin II and endothelin are increased with acid accumulation and contribute to an adaptive increase in renal acid excretion and bicarbonate generation. However, the persistent elevated levels of these hormones can damage the kidney and accelerate progression of CKD. Measures to slow the progression of CKD have included administration of medications which inhibit the production or action of deleterious hormones. However, since metabolic acidosis accompanying CKD stimulates the secretion of several of these hormones, treatment of CKD should also include administration of base to correct the metabolic acidosis.
MeSH term(s)	Humans ; Acid-Base Equilibrium/physiology ; Bicarbonates/metabolism ; Aldosterone/metabolism ; Angiotensin II/metabolism ; Kidney/metabolism ; Renal Insufficiency, Chronic/metabolism ; Acidosis/metabolism ; Endothelins/metabolism ; Endocrine System/metabolism
Chemical Substances	Bicarbonates ; Aldosterone (4964P6T9RB) ; Angiotensin II (11128-99-7) ; Endothelins
Language	English
Publishing date	2024-02-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25042420
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Article ; Online: Regulation of Acid-Base Balance in Patients With Chronic Kidney Disease.

Nagami, Glenn T / Kraut, Jeffrey A

Advances in chronic kidney disease

2022 Volume 29, Issue 4, Page(s) 337–342

Abstract: Normallly the kidneys handle the daily acid load arising from net endogenous acid production from the metabolism of ingested animal protein (acid) and vegetables (base). With chronic kidney disease, reduced acid excretion by the kidneys is primarily due ... ...

Abstract	Normallly the kidneys handle the daily acid load arising from net endogenous acid production from the metabolism of ingested animal protein (acid) and vegetables (base). With chronic kidney disease, reduced acid excretion by the kidneys is primarily due to reduced ammonium excretion such that when acid excertion falls below acid porduction, acid accumulation occurs. With even mild reductions in glomerular filtration rate (60 to 90 ml/min), net acid excretion may fall below net acid production resulting in acid retention which may be initially sequestered in interstitial compartments in the kidneys, bones, and muscles resulting in no fall in measured systemic bicarbonate levels (eubicarbonatemic metabolic acidosis). With greater reductions in kidney function, the greater quantities of acid retained spillover systemically resulting in low pH (overt metabolic acidosis). The evaluation of acid-base balance in patients with CKD is complicated by the heterogeneity of clinical acid-base disorders and by the eubicarbonatemic nature of the early phase of acid retention. If supported by more extensive studies, blood gas analyses to confirm the acid-base disorder and newer ways for assessing the presence of acidosis such as urinary citrate measurements may become routine tools to evaluate and treat acid-base disorders in individuals with CKD.
MeSH term(s)	Acid-Base Equilibrium ; Acid-Base Imbalance/etiology ; Animals ; Bicarbonates ; Citrates ; Humans ; Renal Insufficiency, Chronic
Chemical Substances	Bicarbonates ; Citrates
Language	English
Publishing date	2022-09-26
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	1548-5609 ; 1548-5595
ISSN (online)	1548-5609
ISSN	1548-5595
DOI	10.1053/j.ackd.2022.05.004
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Article ; Online: Hyperchloremia - Why and how.

Nagami, Glenn T

Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia

2016 Volume 36, Issue 4, Page(s) 347–353

Abstract: Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the ... ...

Abstract	Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance.
Language	Spanish
Publishing date	2016-07
Publishing country	Spain
Document type	Journal Article
ZDB-ID	632512-9
ISSN	1989-2284 ; 0211-6995
ISSN (online)	1989-2284
ISSN	0211-6995
DOI	10.1016/j.nefro.2016.04.001
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Article ; Online: Non-Anion Gap Metabolic Acidosis: A Clinical Approach to Evaluation.

Rastegar, Mandana / Nagami, Glenn T

American journal of kidney diseases : the official journal of the National Kidney Foundation

2017 Volume 69, Issue 2, Page(s) 296–301

Abstract: Acid-base disturbances can result from kidney or nonkidney disorders. We present a case of high-volume ileostomy output causing large bicarbonate losses and resulting in a non-anion gap metabolic acidosis. Non-anion gap metabolic acidosis can present as ... ...

Abstract	Acid-base disturbances can result from kidney or nonkidney disorders. We present a case of high-volume ileostomy output causing large bicarbonate losses and resulting in a non-anion gap metabolic acidosis. Non-anion gap metabolic acidosis can present as a form of either acute or chronic metabolic acidosis. A complete clinical history and physical examination are critical initial steps to begin the evaluation process, followed by measuring serum electrolytes with a focus on potassium level, blood gas, urine pH, and either direct or indirect urine ammonium concentration. The present case was selected to highlight the differential diagnosis of a non-anion gap metabolic acidosis and illustrate a systematic approach to this problem.
MeSH term(s)	Acid-Base Equilibrium ; Acidosis/diagnosis ; Aged ; Humans ; Male
Language	English
Publishing date	2017-02
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	604539-x
ISSN	1523-6838 ; 0272-6386
ISSN (online)	1523-6838
ISSN	0272-6386
DOI	10.1053/j.ajkd.2016.09.013
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Zs.MO 468: Show issues

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Article ; Online: Regulation of Acid-Base Balance in Chronic Kidney Disease.

Nagami, Glenn T / Hamm, L Lee

Advances in chronic kidney disease

2017 Volume 24, Issue 5, Page(s) 274–279

Abstract: The kidneys play a major role in the regulation of acid-base balance by reabsorbing bicarbonate filtered by the glomeruli and excreting titratable acids and ammonia into the urine. In CKD, with declining kidney function, acid retention and metabolic ... ...

Abstract	The kidneys play a major role in the regulation of acid-base balance by reabsorbing bicarbonate filtered by the glomeruli and excreting titratable acids and ammonia into the urine. In CKD, with declining kidney function, acid retention and metabolic acidosis occur, but the extent of acid retention depends not only on the degree of kidney impairment but also on the dietary acid load. Acid retention can occur even when the serum bicarbonate level is apparently normal. With reduced kidney function, acid transport processes in the surviving nephrons are augmented but as disease progresses ammonia excretion and, in some individuals, the ability to reabsorb bicarbonate falls, whereas titratable acid excretion is preserved until kidney function is severely impaired. Urinary ammonia levels are used to gauge the renal response to acid loads and are best assessed by direct measurement of urinary ammonia levels rather than by indirect assessments. In individuals with acidosis from CKD, an inappropriately low degree of ammonia excretion points to the pathogenic role of impaired urinary acid excretion. The presence of a normal bicarbonate level in CKD complicates the interpretation of the urinary ammonia excretion as such individuals could be in acid-base balance or could be retaining acid without manifesting a low bicarbonate level. At this time, the decision to give bicarbonate supplementation in CKD is reserved for those with a bicarbonate level of 22 mEq/L, but because of potential harm of overtreatment, supplementation should be adjusted to maintain a bicarbonate level of <26 mEq/L.
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	1548-5609 ; 1548-5595
ISSN (online)	1548-5609
ISSN	1548-5595
DOI	10.1053/j.ackd.2017.07.004
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Article ; Online: Proteomic analysis of murine kidney proximal tubule sub-segment derived cell lines reveals preferences in mitochondrial pathway activity.

Ferreira, Ricardo Melo / de Almeida, Rita / Culp, Clayton / Witzmann, Frank / Wang, Mu / Kher, Rajesh / Nagami, Glenn T / Mohallem, Rodrigo / Andolino, Chaylen Jade / Aryal, Uma K / Eadon, Michael T / Bacallao, Robert L

Journal of proteomics

2023 Volume 289, Page(s) 104998

Abstract: The proximal tubule (PT) is a nephron segment that is responsible for the majority of solute and water reabsorption in the kidney. Each of its sub-segments have specialized functions; however, little is known about the genes and proteins that determine ... ...

Abstract	The proximal tubule (PT) is a nephron segment that is responsible for the majority of solute and water reabsorption in the kidney. Each of its sub-segments have specialized functions; however, little is known about the genes and proteins that determine the oxidative phosphorylation capacity of the PT sub-segments. This information is critical to understanding kidney function and will provide a comprehensive landscape of renal cell adaptations to injury, physiologic stressors, and development. This study analyzed three immortalized murine renal cell lines (PT S1, S2, and S3 segments) for protein content and compared them to a murine fibroblast cell line. All three proximal tubule cell lines generate ATP predominantly by oxidative phosphorylation while the fibroblast cell line is glycolytic. The proteomic data demonstrates that the most significant difference in proteomic signatures between the cell lines are proteins known to be localized in the nucleus followed by mitochondrial proteins. Mitochondrial metabolic substrate utilization assays were performed using the proximal tubule cell lines to determine substrate utilization kinetics thereby providing a physiologic context to the proteomic dataset. This data will allow researchers to study differences in nephron-specific cell lines, between epithelial and fibroblast cells, and between actively respiring cells and glycolytic cells. SIGNIFICANCE: Proteomic analysis of proteins expressed in immortalized murine renal proximal tubule cells was compared to a murine fibroblast cell line proteome. The proximal tubule segment specific cell lines: S1, S2 and S3 are all grown under conditions whereby the cells generate ATP by oxidative phosphorylation while the fibroblast cell line utilizes anaerobic glycolysis for ATP generation. The proteomic studies allow for the following queries: 1) comparisons between the proximal tubule segment specific cell lines, 2) comparisons between polarized epithelia and fibroblasts, 3) comparison between cells employing oxidative phosphorylation versus anaerobic glycolysis and 4) comparisons between cells grown on clear versus opaque membrane supports. The data finds major differences in nuclear protein expression and mitochondrial proteins. This proteomic data set will be an important baseline dataset for investigators who need immortalized renal proximal tubule epithelial cells for their research.
MeSH term(s)	Mice ; Animals ; Proteomics ; Kidney ; Kidney Tubules, Proximal/metabolism ; Cell Line ; Mitochondrial Proteins/metabolism ; Adenosine Triphosphate/metabolism
Chemical Substances	Mitochondrial Proteins ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2023-08-30
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2400835-7
ISSN	1876-7737 ; 1874-3919
ISSN (online)	1876-7737
ISSN	1874-3919
DOI	10.1016/j.jprot.2023.104998
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Article ; Online: The use and interpretation of serum bicarbonate concentration in dialysis patients.

Kraut, Jeffrey A / Nagami, Glenn T

Seminars in dialysis

2014 Volume 27, Issue 6, Page(s) 577–579

MeSH term(s)	Acidosis/diagnosis ; Acidosis/etiology ; Acidosis/therapy ; Bicarbonates/blood ; Humans ; Kidney Failure, Chronic/complications ; Kidney Failure, Chronic/metabolism ; Kidney Failure, Chronic/therapy ; Renal Dialysis
Chemical Substances	Bicarbonates
Language	English
Publishing date	2014-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1028193-9
ISSN	1525-139X ; 0894-0959
ISSN (online)	1525-139X
ISSN	0894-0959
DOI	10.1111/sdi.12269
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Article: Role of angiotensin II in the enhancement of ammonia production and secretion by the proximal tubule in metabolic acidosis.

Nagami, Glenn T

American journal of physiology. Renal physiology

2008 Volume 294, Issue 4, Page(s) F874–80

Abstract: Acidosis and angiotensin II stimulate ammonia production and transport by the proximal tubule. We examined the modulatory effect of the type 1 angiotensin II receptor blocker losartan on the ability of metabolic acidosis to stimulate ammonia production ... ...

Abstract	Acidosis and angiotensin II stimulate ammonia production and transport by the proximal tubule. We examined the modulatory effect of the type 1 angiotensin II receptor blocker losartan on the ability of metabolic acidosis to stimulate ammonia production and secretion by mouse S2 proximal tubule segments. Mice given NH(4)Cl for 7 days developed metabolic acidosis (low serum bicarbonate concentration) and increased urinary excretion of ammonia. S2 tubule segments from acidotic mice displayed higher rates of ammonia production and secretion compared with those from control mice. However, when losartan was coadministered in vivo with NH(4)Cl, both the acidosis-induced increase in urinary ammonia excretion and the adaptive increase in ammonia production and secretion of microperfused S2 segments were largely blocked. In renal cortical tissue, losartan blocked the acid-induced increase in brush-border membrane NHE3 expression but had no effect on the acid-induced upregulation of phosphate-dependent glutaminase or phosphoenolpyruvate carboxykinase 1 in cortical homogenates. Addition of angiotensin II to the microperfusion solution enhanced ammonia secretion and production rates in tubules from NH(4)Cl-treated and control mice in a losartan-inhibitable manner. These results demonstrate that a 7-day acid challenge induces an adaptive increase in ammonia production and secretion by the proximal tubule and suggest that during metabolic acidosis, angiotensin II signaling is necessary for adaptive enhancements of ammonia excretion by the kidney and ammonia production and secretion by S2 proximal tubule segments, as mediated, in part, by angiotensin receptor-dependent enhancement of NHE3 expression.
MeSH term(s)	Acidosis/physiopathology ; Ammonia/metabolism ; Ammonium Chloride/pharmacology ; Angiotensin II/physiology ; Animals ; Disease Models, Animal ; Kidney Cortex/drug effects ; Kidney Cortex/physiopathology ; Kidney Tubules, Proximal/secretion ; Losartan/pharmacology ; Male ; Mice ; Perfusion
Chemical Substances	Ammonium Chloride (01Q9PC255D) ; Angiotensin II (11128-99-7) ; Ammonia (7664-41-7) ; Losartan (JMS50MPO89)
Language	English
Publishing date	2008-04
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603837-2
ISSN	1522-1466 ; 1931-857X ; 0363-6127
ISSN (online)	1522-1466
ISSN	1931-857X ; 0363-6127
DOI	10.1152/ajprenal.00286.2007
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Article ; Online: The serum anion gap in the evaluation of acid-base disorders: what are its limitations and can its effectiveness be improved?

Kraut, Jeffrey A / Nagami, Glenn T

Clinical journal of the American Society of Nephrology : CJASN

2013 Volume 8, Issue 11, Page(s) 2018–2024

Abstract: The serum anion gap has been utilized to identify errors in the measurement of electrolytes, to detect paraproteins, and, most relevant to the nephrologist, to evaluate patients with suspected acid-base disorders. In regard to the latter purpose, ... ...

Abstract	The serum anion gap has been utilized to identify errors in the measurement of electrolytes, to detect paraproteins, and, most relevant to the nephrologist, to evaluate patients with suspected acid-base disorders. In regard to the latter purpose, traditionally an increased anion gap is identified when it exceeds the upper limit of normal for a particular clinical laboratory measurement. However, because there is a wide range of normal values (often 8-10 mEq/L), an increase in anion concentration can be present in the absence of an increased anion gap. In addition, the type of retained anion can affect the magnitude of the increase in anion gap relative to change in serum [HCO3(-)] being greater with lactic acidosis compared with ketoacidosis. This review examines the methods of calculation of the serum anion gap in textbooks and published literature, the effect of perturbations other than changes in acid-base balance, and its effectiveness in identifying mild and more severe disturbances in acid-base balance. Limitations of the present methods of determining the normal anion gap and change in the anion gap are highlighted. The possibility of identifying the baseline value for individuals to optimize the use of the calculation in the detection of metabolic acidosis is suggested.
MeSH term(s)	Acid-Base Equilibrium ; Acid-Base Imbalance/blood ; Acid-Base Imbalance/diagnosis ; Acid-Base Imbalance/physiopathology ; Acid-Base Imbalance/therapy ; Animals ; Biomarkers/blood ; Humans ; Models, Biological ; Predictive Value of Tests ; Prognosis ; Reference Values
Chemical Substances	Biomarkers
Language	English
Publishing date	2013-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.04040413
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Article: Ammonia production and secretion by S3 proximal tubule segments from acidotic mice: role of ANG II.

Nagami, Glenn T

American journal of physiology. Renal physiology

2004 Volume 287, Issue 4, Page(s) F707–12

Abstract: ANG II has potent effects on ammonia production and secretion rates by the proximal tubule and is found in substantial concentrations in the lumen of the proximal tubule in vivo. Because our previous studies demonstrated that acid loading enhanced the ... ...

Abstract	ANG II has potent effects on ammonia production and secretion rates by the proximal tubule and is found in substantial concentrations in the lumen of the proximal tubule in vivo. Because our previous studies demonstrated that acid loading enhanced the stimulatory effects of ANG II on ammonia production and secretion by S2 proximal tubule segments, we examined the effect of ANG II on ammonia production and secretion by isolated, perfused S3 segments from nonacidotic control mice and acidotic mice given NH4Cl for 7 days. In the absence of ANG II, ammonia production and secretion rates were no different in S3 segments from acidotic and control mice. By contrast, when ANG II was present in the luminal perfusion solution, ammonia production and secretion rates were stimulated, in a losartan-inhibitable manner, to a greater extent in S3 segments from acidotic mice. Ammonia secretion rates in S3 segments were largely inhibited by perfusion with a low-sodium solution containing amiloride in the presence or absence of ANG II. These results demonstrated that isolated, perfused mouse S3 proximal tubule segments produce and secrete ammonia, that NH4Cl-induced acidosis does not affect the basal rates of ammonia production and secretion, and that ANG II, added to the luminal fluid, stimulates ammonia production and secretion to a greater extent in S3 segments from acidotic mice. These findings suggest that S3 segments, in the presence of ANG II, can contribute to the enhanced renal excretion that occurs with acid loading.
MeSH term(s)	Acid-Base Equilibrium/physiology ; Acidosis/metabolism ; Amiloride/pharmacology ; Ammonia/urine ; Ammonium Chloride/pharmacology ; Angiotensin II/pharmacology ; Animals ; Buffers ; Carbon Dioxide/blood ; Diuretics/pharmacology ; Kidney Tubules, Proximal/drug effects ; Kidney Tubules, Proximal/metabolism ; Kidney Tubules, Proximal/secretion ; Male ; Mice ; Sodium/pharmacology ; Vasoconstrictor Agents/pharmacology
Chemical Substances	Buffers ; Diuretics ; Vasoconstrictor Agents ; Ammonium Chloride (01Q9PC255D) ; Angiotensin II (11128-99-7) ; Carbon Dioxide (142M471B3J) ; Ammonia (7664-41-7) ; Amiloride (7DZO8EB0Z3) ; Sodium (9NEZ333N27)
Language	English
Publishing date	2004-10
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603837-2
ISSN	1522-1466 ; 1931-857X ; 0363-6127
ISSN (online)	1522-1466
ISSN	1931-857X ; 0363-6127
DOI	10.1152/ajprenal.00189.2003
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