Aldosterone is classically associated with the regulation of salt and potassium homeostasis but has also profound effects on acid-base balance. During acidosis, circulating aldosterone levels are increased and the hormone acts in concert with angiotensin II and other factors to stimulate renal acid excretion. Pharmacological blockade of aldosterone action as well as inherited or acquired syndromes of impaired aldosterone release or action impair the renal response to acid loading and cause hyperkalemic renal tubular acidosis. The mineralocorticoid receptor (MR) mediating the genomic effects of aldosterone is expressed in all cells of the distal nephron including all subtypes of intercalated cells. In acid-secretory type A intercalated cells, aldosterone stimulates proton secretion into urine, whereas in non-type A intercalated cells, aldosterone increases the activity of the luminal anion exchanger pendrin stimulating bicarbonate secretion and chloride reabsorption. Aldosterone has also stimulatory effects on proton secretion that may be mediated by a non-genomic pathway. In addition, aldosterone indirectly stimulates renal acid excretion by enhancing sodium reabsorption through the epithelial sodium channel ENaC. Increased sodium reabsorption enhances the lumen-negative transepithelial voltage that facilitates proton secretion by neighboring intercalated cells. This indirect coupling of sodium reabsorption and proton secretion is thought to underlie the fludrocortisone-furosemide test for maximal urinary acidification in patients with suspected distal renal tubular acidosis. In patients with CKD, acidosis-induced aldosterone may contribute to progression of kidney disease. In summary, aldosterone is a powerful regulator of renal acid excretion required for normal acid-base balance.

Keywords:
Mineralocorticoids, Acid-base balance, Aldosterone, Acidosis
1.
Hamm LL, Alpern RJ, Preisig PA: Cellular mechanisms of renal tubular acidification; in Alpern RJ, Hebert SC (eds): Seldin and Giebisch's The Kidney Physiology and Pathophysiology. New York, Academic Press, 2008, pp 1539-1585.
2.
Curthoys NP: Renal ammonium ion production and excretion; in Alpern RJ, Hebert SC (eds): Seldin and Giebisch's The Kidney Physiology and Pathophysiology. Philadelphia, Elsevier, 2008, pp 1601-1619.
3.
Christensen EI, Wagner CA, Kaissling B: Uriniferous tubule: structural and functional organization. Compr Physiol 2012;2:805-861.
4.
Wagner CA, Devuyst O, Bourgeois S, Mohebbi N: Regulated acid-base transport in the collecting duct. Pflugers Arch 2009;458:137-156.
5.
Ackermann D, Gresko N, Carrel M, Loffing-Cueni D, Habermehl D, Gomez-Sanchez C, Rossier BC, Loffing J: In vivo nuclear translocation of mineralocorticoid and glucocorticoid receptors in rat kidney: differential effect of corticosteroids along the distal tubule. Am J Physiol Renal Physiol 2010;299:F1473-F1485.
6.
Biner HL, Arpin-Bott MP, Loffing J, Wang X, Knepper M, Hebert SC, Kaissling B: Human cortical distal nephron: distribution of electrolyte and water transport pathways. J Am Soc Nephrol 2002;13:836-847.
7.
Loffing J, Loffing-Cueni D, Valderrabano V, Klausli L, Hebert SC, Rossier BC, Hoenderop JG, Bindels RJ, Kaissling B: Distribution of transcellular calcium and sodium transport pathways along mouse distal nephron. Am J Physiol Renal Physiol 2001;281:F1021-F1027.
8.
Lang F, Quehenberger P, Greger R, Silbernagl S, Stockinger P: Evidence for a bicarbonate leak in the proximal tubule of the rat kidney. Pflugers Arch 1980;386:239-244.
9.
Orlowski J, Grinstein S: Diversity of the mammalian sodium/proton exchanger SLC9 gene family. Pflugers Arch 2004;447:549-565.
10.
Romero MF, Fulton CM, Boron WF: The SLC4 family of HCO3- transporters. Pflugers Arch 2004;447:495-509.
11.
Capasso G, Unwin R, Rizzo M, Pica A, Giebisch G: Bicarbonate transport along the loop of Henle: molecular mechanisms and regulation. J Nephrol 2002(suppl 5):S88-S96.
12.
Jakobsen JK, Odgaard E, Wang W, Elkjaer ML, Nielsen S, Aalkjaer C, Leipziger J: Functional up-regulation of basolateral Na+-dependent HCO3- transporter NBCn1 in medullary thick ascending limb of K+-depleted rats. Pflugers Arch 2004;448:571-578.
13.
Moret C, Dave MH, Schulz N, Jiang JX, Verrey F, Wagner CA: Regulation of renal amino acid transporters during metabolic acidosis. Am J Physiol Renal Physiol 2007;292:F555-F566.
14.
Broer S: The SLC38 family of sodium-amino acid co-transporters. Pflugers Arch 2014;466:155-172.
15.
Wagner CA, Devuyst O, Belge H, Bourgeois S, Houillier P: The rhesus protein RhCG: a new perspective in ammonium transport and distal urinary acidification. Kidney Int 2011;79:154-161.
16.
Stettner P, Bourgeois S, Marsching C, Traykova-Brauch M, Porubsky S, Nordstrom V, Hopf C, Koesters R, Sandhoff R, Wiegandt H, Wagner CA, Grone HJ, Jennemann R: Sulfatides are required for renal adaptation to chronic metabolic acidosis. Proc Natl Acad Sci USA 2013;110:9998-10003.
17.
Wagner CA, Finberg KE, Breton S, Marshansky V, Brown D, Geibel JP: Renal vacuolar H+-ATPase. Physiol Rev 2004;84:1263-1314.
18.
Weiner ID, Hamm LL: Molecular mechanisms of renal ammonia transport. Annu Rev Physiol 2007;69:317-340.
19.
Biver S, Belge H, Bourgeois S, Van Vooren P, Nowik M, Scohy S, Houillier P, Szpirer J, Szpirer C, Wagner CA, Devuyst O, Marini AM: A role for rhesus factor Rhcg in renal ammonium excretion and male fertility. Nature 2008;456:339-343.
20.
Bourgeois S, Bounoure L, Christensen EI, Ramakrishnan SK, Houillier P, Devuyst O, Wagner CA: Haploinsufficiency of the ammonia transporter Rhcg predisposes to chronic acidosis: Rhcg is critical for apical and basolateral ammonia transport in the mouse collecting duct. J Biol Chem 2013;288:5518-5529.
21.
Bounoure L, Ruffoni D, Muller R, Kuhn GA, Bourgeois S, Devuyst O, Wagner CA: The role of the renal ammonia transporter Rhcg in metabolic responses to dietary protein. J Am Soc Nephrol 2014;25:2040-2052.
22.
Hamm LL, Simon EE: Roles and mechanisms of urinary buffer excretion. Am J Physiol 1987;253:F595-F605.
23.
Nowik M, Picard N, Stange G, Capuano P, Tenenhouse HS, Biber J, Murer H, Wagner CA: Renal phosphaturia during metabolic acidosis revisited: molecular mechanisms for decreased renal phosphate reabsorption. Pflugers Arch 2008;457:539-549.
24.
Aruga S, Wehrli S, Kaissling B, Moe OW, Preisig PA, Pajor AM, Alpern RJ: Chronic metabolic acidosis increases NaDC-1 mRNA and protein abundance in rat kidney. Kidney Int 2000;58:206-215.
25.
Wagner CA, Hernando N, Forster IC, Biber J: The SLC34 family of sodium-dependent phosphate transporters. Pflugers Arch 2014;466:139-153.
26.
Royaux IE, Wall SM, Karniski LP, Everett LA, Suzuki K, Knepper MA, Green ED: Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion. Proc Natl Acad Sci USA 2001;98:4221-4226.
27.
Wagner CA, Mohebbi N, Capasso G, Geibel JP: The anion exchanger pendrin (SLC26A4) and renal acid-base homeostasis. Cell Physiol Biochem 2011;28:497-504.
28.
Gueutin V, Vallet M, Jayat M, Peti-Peterdi J, Corniere N, Leviel F, Sohet F, Wagner CA, Eladari D, Chambrey R: Renal β-intercalated cells maintain body fluid and electrolyte balance. J Clin Invest 2013;123:4219-4231.
29.
Jacques T, Picard N, Miller RL, Riemondy KA, Houillier P, Sohet F, Ramakrishnan SK, Busst CJ, Jayat M, Corniere N, Hassan H, Aronson PS, Hennings JC, Hubner CA, Nelson RD, Chambrey R, Eladari D: Overexpression of pendrin in intercalated cells produces chloride-sensitive hypertension. J Am Soc Nephrol 2013;24:1104-1113.
30.
Wesson DE, Simoni J, Green DF: Reduced extracellular pH increases endothelin-1 secretion by human renal microvascular endothelial cells. J Clin Invest 1998;101:578-583.
31.
Khanna A, Simoni J, Hacker C, Duran MJ, Wesson DE: Increased endothelin activity mediates augmented distal nephron acidification induced by dietary protein. J Am Soc Nephrol 2004;15:2266-2275.
32.
Khanna A, Simoni J, Wesson DE: Endothelin-induced increased aldosterone activity mediates augmented distal nephron acidification as a result of dietary protein. J Am Soc Nephrol 2005;16:1929-1935.
33.
Eiam-Ong S, Hilden SA, King AJ, Johns CA, Madias NE: Endothelin-1 stimulates the Na+/H+ and Na+/HCO3- transporters in rabbit renal cortex. Kidney Int 1992;42:18-24.
34.
Laghmani K, Preisig PA, Moe OW, Yanagisawa M, Alpern RJ: Endothelin-1/endothelin-B receptor-mediated increases in NHE3 activity in chronic metabolic acidosis. J Clin Invest 2001;107:1563-1569.
35.
Pallini A, Hulter HN, Muser J, Krapf R: Role of endothelin-1 in renal regulation of acid-base equilibrium in acidotic humans. Am J Physiol Renal Physiol 2012;303:F991-F999.
36.
Kalhoff H, Rascher W, Diekmann L, Stock GJ, Manz F: Urinary excretion of aldosterone, arginine vasopressin and cortisol in premature infants with maximum renal acid stimulation. Acta Paediatr 1995;84:490-494.
37.
Perez GO, Oster JR, Vaamonde CA, Katz FH: Effect of NH4Cl on plasma aldosterone, cortisol and renin activity in supine man. J Clin Endocrinol Metab 1977;45:762-767.
38.
Yamauchi T, Harada T, Kurono M, Matsui N: Effect of exercise-induced acidosis on aldosterone secretion in men. Eur J Appl Physiol Occup Physiol 1998;77:409-412.
39.
Gyorke ZS, Sulyok E, Guignard JP: Ammonium chloride metabolic acidosis and the activity of renin-angiotensin-aldosterone system in children. Eur J Pediatr 1991;150:547-549.
40.
Nowik M, Kampik NB, Mihailova M, Eladari D, Wagner CA: Induction of metabolic acidosis with ammonium chloride (NH4Cl) in mice and rats - species differences and technical considerations. Cell Physiol Biochem 2010;26:1059-1072.
41.
Schambelan M, Sebastian A, Katuna BA, Arteaga E: Adrenocortical hormone secretory response to chronic NH4Cl-induced metabolic acidosis. Am J Physiol 1987;252:E454-E460.
42.
Henger A, Tutt P, Riesen WF, Hulter HN, Krapf R: Acid-base and endocrine effects of aldosterone and angiotensin II inhibition in metabolic acidosis in human patients. J Lab Clin Med 2000;136:379-389.
43.
Augustinsson O, Johansson K: Ammonium chloride induced acidosis and aldosterone secretion in the goat. Acta Physiol Scand 1986;128:535-540.
44.
Jones GV, Wall BM, Williams HH, Presley DN, Sapir DG, Cooke CR: Modulation of plasma aldosterone by physiological changes in hydrogen ion concentration. Am J Physiol 1992;262:R269-R275.
45.
Guagliardo NA, Yao J, Bayliss DA, Barrett PQ: TASK channels are not required to mount an aldosterone secretory response to metabolic acidosis in mice. Mol Cell Endocrinol 2011;336:47-52.
46.
Raff H, Jankowski B: Effect of CO2/pH on the aldosterone response to hypoxia in bovine adrenal cells in vitro. Am J Physiol 1993;265:R820-R825.
47.
Rothenberger F, Velic A, Stehberger PA, Kovacikova J, Wagner CA: Angiotensin II stimulates vacuolar H+-ATPase activity in renal acid-secretory intercalated cells from the outer medullary collecting duct. J Am Soc Nephrol 2007;18:2085-2093.
48.
Geibel J, Giebisch G, Boron WF: Angiotensin II stimulates both Na+-H+ exchange and Na+/HCO3- cotransport in the rabbit proximal tubule. Proc Natl Acad Sci USA 1990;87:7917-7920.
49.
Nagami GT: Enhanced ammonia secretion by proximal tubules from mice receiving NH4Cl: role of angiotensin II. Am J Physiol Renal Physiol 2002;282:F472-F477.
50.
Wagner CA, Giebisch G, Lang F, Geibel JP: Angiotensin II stimulates vesicular H+-ATPase in rat proximal tubular cells. Proc Natl Acad Sci USA 1998;95:9665-9668.
51.
Wagner CA, Mohebbi N, Uhlig U, Giebisch GH, Breton S, Brown D, Geibel JP: Angiotensin II stimulates H-ATPase activity in intercalated cells from isolated mouse connecting tubules and cortical collecting ducts. Cell Physiol Biochem 2011;28:513-520.
52.
Levine DZ, Iacovitti M, Buckman S, Harrison V: In vivo modulation of rat distal tubule net HCO3 flux by VIP, isoproterenol, angiotensin II, and ADH. Am J Physiol 1994;266:F878-F883.
53.
Levine DZ, Iacovitti M, Buckman S, Burns KD: Role of angiotensin II in dietary modulation of rat late distal tubule bicarbonate flux in vivo. J Clin Invest 1996;97:120-125.
54.
Liu FY, Cogan MG: Angiotensin II: a potent regulator of acidification in the rat early proximal convoluted tubule. J Clin Invest 1987;80:272-275.
55.
Nagami GT: Role of angiotensin II in the enhancement of ammonia production and secretion by the proximal tubule in metabolic acidosis. Am J Physiol Renal Physiol 2008;294:F874-F880.
56.
Wagner CA, Geibel JP: Acid-base transport in the collecting duct. J Nephrol 2002;15(suppl 5):S112-S127.
57.
Schlatter E, Haxelmans S, Ankorina I, Kleta R: Regulation of Na+/H+ exchange by diadenosine polyphosphates, angiotensin II, and vasopressin in rat cortical collecting duct. J Am Soc Nephrol 1995;6:1223-1229.
58.
Karet FE: Mechanisms in hyperkalemic renal tubular acidosis. J Am Soc Nephrol 2009;20:251-254.
59.
Reyes AJ, Leary WP, Crippa G, Maranhao MF, Hernandez-Hernandez R: The aldosterone antagonist and facultative diuretic eplerenone: a critical review. Eur J Intern Med 2005;16:3-11.
60.
Sebastian A, Sutton JM, Hulter HN, Schambelan M, Poler SM: Effect of mineralocorticoid replacement therapy on renal acid-base homeostasis in adrenalectomized patients. Kidney Int 1980;18:762-773.
61.
Mitsuuchi Y, Kawamoto T, Naiki Y, Miyahara K, Toda K, Kuribayashi I, Orii T, Yasuda K, Miura K, Nakao K, et al: Congenitally defective aldosterone biosynthesis in humans: the involvement of point mutations of the P-450C18 gene (CYP11B2) in CMO II deficient patients. Biochem Biophys Res Commun 1992;182:974-979.
62.
Geller DS, Rodriguez-Soriano J, Vallo Boado A, Schifter S, Bayer M, Chang SS, Lifton RP: Mutations in the mineralocorticoid receptor gene cause autosomal dominant pseudohypoaldosteronism type I. Nat Genet 1998;19:279-281.
63.
Eiam-Ong S, Kurtzman NA, Sabatini S: Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium. J Clin Invest 1993;91:2385-2392.
64.
Boyden LM, Choi M, Choate KA, Nelson-Williams CJ, Farhi A, Toka HR, Tikhonova IR, Bjornson R, Mane SM, Colussi G, Lebel M, Gordon RD, Semmekrot BA, Poujol A, Valimaki MJ, De Ferrari ME, Sanjad SA, Gutkin M, Karet FE, Tucci JR, Stockigt JR, Keppler-Noreuil KM, Porter CC, Anand SK, Whiteford ML, Davis ID, Dewar SB, Bettinelli A, Fadrowski JJ, Belsha CW, Hunley TE, Nelson RD, Trachtman H, Cole TR, Pinsk M, Bockenhauer D, Shenoy M, Vaidyanathan P, Foreman JW, Rasoulpour M, Thameem F, Al-Shahrouri HZ, Radhakrishnan J, Gharavi AG, Goilav B, Lifton RP: Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities. Nature 2012;482:98-102.
65.
Wilson FH, Disse-Nicodeme S, Choate KA, Ishikawa K, Nelson-Williams C, Desitter I, Gunel M, Milford DV, Lipkin GW, Achard JM, Feely MP, Dussol B, Berland Y, Unwin RJ, Mayan H, Simon DB, Farfel Z, Jeunemaitre X, Lifton RP: Human hypertension caused by mutations in WNK kinases. Science 2001;293:1107-1112.
66.
Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM: A chimaeric 11β-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature 1992;355:262-265.
67.
Lifton RP, Dluhy RG, Powers M, Rich GM, Gutkin M, Fallo F, Gill JR Jr, Feld L, Ganguly A, Laidlaw JC, Murnaghan DJ, Kaufman C, Stockigt JR, Ulick S, Lalouel JM: Hereditary hypertension caused by chimaeric gene duplications and ectopic expression of aldosterone synthase. Nat Genet 1992;2:66-74.
68.
Beuschlein F, Boulkroun S, Osswald A, Wieland T, Nielsen HN, Lichtenauer UD, Penton D, Schack VR, Amar L, Fischer E, Walther A, Tauber P, Schwarzmayr T, Diener S, Graf E, Allolio B, Samson-Couterie B, Benecke A, Quinkler M, Fallo F, Plouin PF, Mantero F, Meitinger T, Mulatero P, Jeunemaitre X, Warth R, Vilsen B, Zennaro MC, Strom TM, Reincke M: Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension. Nat Genet 2013;45:440-444, 444e1-2.
69.
Tauber P, Penton D, Stindl J, Humberg E, Tegtmeier I, Sterner C, Beuschlein F, Reincke M, Barhanin J, Bandulik S, Warth R: Pharmacology and pathophysiology of mutated KCNJ5 found in adrenal aldosterone producing adenomas. Endocrinology 2014;155:1353-1362.
70.
Luke RG, Galla JH: It is chloride depletion alkalosis, not contraction alkalosis. J Am Soc Nephrol 2012;23:204-207.
71.
Shibata S, Rinehart J, Zhang J, Moeckel G, Castaneda-Bueno M, Stiegler AL, Boggon TJ, Gamba G, Lifton RP: Mineralocorticoid receptor phosphorylation regulates ligand binding and renal response to volume depletion and hyperkalemia. Cell Metab 2013;18:660-671.
72.
Thompson A, Bailey MA, Michael AE, Unwin RJ: Effects of changes in dietary intake of sodium and potassium and of metabolic acidosis on 11β-hydroxysteroid dehydrogenase activities in rat kidney. Exp Nephrol 2000;8:44-51.
73.
Gros R, Ding Q, Sklar LA, Prossnitz EE, Arterburn JB, Chorazyczewski J, Feldman RD: GPR30 expression is required for the mineralocorticoid receptor-independent rapid vascular effects of aldosterone. Hypertension 2011;57:442-451.
74.
DuBose TD Jr, Caflisch CR: Effect of selective aldosterone deficiency on acidification in nephron segments of the rat inner medulla. J Clin Invest 1988;82:1624-1632.
75.
Winter C, Schulz N, Giebisch G, Geibel JP, Wagner CA: Nongenomic stimulation of vacuolar H+-ATPases in intercalated renal tubule cells by aldosterone. Proc Natl Acad Sci USA 2004;101:2636-2641.
76.
Winter C, Kampik NB, Vedovelli L, Rothenberger F, Paunescu TG, Stehberger PA, Brown D, John H, Wagner CA: Aldosterone stimulates vacuolar H+-ATPase activity in renal acid-secretory intercalated cells mainly via a protein kinase C-dependent pathway. Am J Physiol Cell Physiol 2011;301:C1251-C1261.
77.
Stone DK, Seldin DW, Kokko JP, Jacobson HR: Mineralocorticoid modulation of rabbit medullary collecting duct acidification. A sodium-independent effect. J Clin Invest 1983;72:77-83.
78.
Hulter HN, Ilnicki LP, Harbottle JA, Sebastian A: Impaired renal H+ secretion and NH3 production in mineralocorticoid-deficient glucocorticoid-replete dogs. Am J Physiol 1977;232:F136-F146.
79.
Hays SR: Mineralocorticoid modulation of apical and basolateral membrane H+/OH-/HCO3- transport processes in the rabbit inner stripe of outer medullary collecting duct. J Clin Invest 1992;90:180-187.
80.
Mohebbi N, Perna A, van der Wijst J, Becker HM, Capasso G, Wagner CA: Regulation of two renal chloride transporters, AE1 and pendrin, by electrolytes and aldosterone. PLoS One 2013;8:e55286.
81.
Verlander JW, Hassell KA, Royaux IE, Glapion DM, Wang ME, Everett LA, Green ED, Wall SM: Deoxycorticosterone upregulates PDS (Slc26a4) in mouse kidney: role of pendrin in mineralocorticoid-induced hypertension. Hypertension 2003;42:356-362.
82.
Wall SM, Kim YH, Stanley L, Glapion DM, Everett LA, Green ED, Verlander JW: NaCl restriction upregulates renal Slc26a4 through subcellular redistribution: role in Cl- conservation. Hypertension 2004;44:982-987.
83.
Pelzl L, Pakladok T, Pathare G, Fakhri H, Michael D, Wagner CA, Paulmichl M, Lang F: DOCA-sensitive pendrin expression in kidney, heart, lung and thyroid tissues. Cell Physiol Biochem 2012;30:1491-1501.
84.
Adler L, Efrati E, Zelikovic I: Molecular mechanisms of epithelial cell-specific expression and regulation of the human anion exchanger (pendrin) gene. Am J Physiol Cell Physiol 2008;294:C1261-C1276.
85.
Pech V, Kim YH, Weinstein AM, Everett LA, Pham TD, Wall SM: Angiotensin II increases chloride absorption in the cortical collecting duct in mice through a pendrin-dependent mechanism. Am J Physiol Renal Physiol 2007;292:F914-F920.
86.
Grossmann C, Gekle M: Interaction between mineralocorticoid receptor and epidermal growth factor receptor signaling. Mol Cell Endocrinol 2012;350:235-241.
87.
Paunescu TG, Ljubojevic M, Russo LM, Winter C, McLaughlin MM, Wagner CA, Breton S, Brown D: cAMP stimulates apical V-ATPase accumulation, microvillar elongation, and proton extrusion in kidney collecting duct A-intercalated cells. Am J Physiol Renal Physiol 2010;298:F643-F654.
88.
Loffing J, Zecevic M, Feraille E, Kaissling B, Asher C, Rossier BC, Firestone GL, Pearce D, Verrey F: Aldosterone induces rapid apical translocation of ENaC in early portion of renal collecting system: possible role of SGK. Am J Physiol Renal Physiol 2001;280:F675-F682.
89.
Rossier BC, Pradervand S, Schild L, Hummler E: Epithelial sodium channel and the control of sodium balance: interaction between genetic and environmental factors. Annu Rev Physiol 2002;64:877-897.
90.
Kovacikova J, Winter C, Loffing-Cueni D, Loffing J, Finberg KE, Lifton RP, Hummler E, Rossier B, Wagner CA: The connecting tubule is the main site of the furosemide-induced urinary acidification by the vacuolar H+-ATPase. Kidney Int 2006;70:1706-1716.
91.
Walsh SB, Shirley DG, Wrong OM, Unwin RJ: Urinary acidification assessed by simultaneous furosemide and fludrocortisone treatment: an alternative to ammonium chloride. Kidney Int 2007;71:1310-1316.
92.
Batlle DC: Segmental characterization of defects in collecting tubule acidification. Kidney Int 1986;30:546-554.
93.
Sebastian A, McSherry E, Morris RC Jr: Impaired renal conservation of sodium and chloride during sustained correction of systemic acidosis in patients with type 1, classic renal tubular acidosis. J Clin Invest 1976;58:454-469.
94.
Sebastian A, McSherry E, Morris RC Jr: Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis. J Clin Invest 1971;50:667-678.
95.
Muto S, Asano Y, Okazaki H, Kano S: Renal potassium wasting in distal renal tubular acidosis: role of aldosterone. Intern Med 1992;31:1047-1051.
96.
Wesson DE, Nathan T, Rose T, Simoni J, Tran RM: Dietary protein induces endothelin-mediated kidney injury through enhanced intrinsic acid production. Kidney Int 2007;71:210-217.
97.
Wesson DE, Simoni J: Acid retention during kidney failure induces endothelin and aldosterone production which lead to progressive GFR decline, a situation ameliorated by alkali diet. Kidney Int 2010;78:1128-1135.
98.
Wesson DE, Simoni J, Broglio K, Sheather S: Acid retention accompanies reduced GFR in humans and increases plasma levels of endothelin and aldosterone. Am J Physiol Renal Physiol 2011;300:F830-F837.
99.
De Brito-Ashurst I, Varagunam M, Raftery MJ, Yaqoob MM: Bicarbonate supplementation slows progression of CKD and improves nutritional status. J Am Soc Nephrol 2009;20:2075-2084.
100.
Wesson DE, Jo CH, Simoni J: Angiotensin II receptors mediate increased distal nephron acidification caused by acid retention. Kidney Int 2012;82:1184-1194.
101.
Thomas W, Harvey BJ: Mechanisms underlying rapid aldosterone effects in the kidney. Annu Rev Physiol 2011;73:335-357.
102.
Dooley R, Harvey BJ, Thomas W: Non-genomic actions of aldosterone: from receptors and signals to membrane targets. Mol Cell Endocrinol 2012;350:223-234.
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