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Erschienen in:

15.03.2024 | Originalien

Aldosteron und Niere – eine komplexe Interaktion

verfasst von: Dr. Christoph Schwarz, Prof. PD Dr. Gregor Lindner

Erschienen in: Journal für Endokrinologie, Diabetologie und Stoffwechsel | Ausgabe 2/2024

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Zusammenfassung

Aldosteron ist ein Hormon mit dualer Wirkung auf die Niere. Es ist einerseits Teil eines Regulationssystems zur Aufrechterhaltung des Natrium(= Volumen‑)Haushalts, andererseits ist es für die Stabilität des Kaliumhaushalts und des Säure-Basenhaushalts mitverantwortlich. Störungen des Aldosteronsystems kennzeichnen sich deshalb durch verminderten oder erhöhten S‑Kaliumspiegel bzw. Hypo- oder Hypertonie. Aldosteron wirkt am sogenannten Aldosteron-sensitiven Abschnitt des distalen Tubulus des Nephrons, wo es verschiedene Ionentransporter aktiviert, welche die Natriumresorption und die Kaliumsekretion fördern. Schwieriger zu verstehen ist, dass eine erhöhte Aldosteronaktivität nicht immer zu einer Hypokaliämie führt (Aldosteronparadoxon) und dass Störungen von (Aldosteron-abhängigen) Ionentransportern im distalen Tubulus der Niere zu scheinbar paradoxen Situationen führen, in denen das Ausmaß der Aldosteronsekretion in der Nebenniere nicht mit der zu erwartenden Aldosteronwirkung übereinstimmt (Pseudo-Hypo‑/Hyperaldosteronismus). Dahinter können sich seltene monogenetische Erkrankungen, aber auch erworbene Ursachen verbergen. Anhand von drei Fallbeispielen werden die wesentlichen Interaktionen zwischen Aldosteron und dem distalen Tubulusabschnitt der Niere erklärt.
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Literatur
1.
Zurück zum Zitat Buffolo F, Tetti M, Mulatero P, Monticone S (2022) Aldosterone as a mediator of cardiovascular damage. Hypertens 79:1899–1911 Buffolo F, Tetti M, Mulatero P, Monticone S (2022) Aldosterone as a mediator of cardiovascular damage. Hypertens 79:1899–1911
2.
Zurück zum Zitat Rossier BC, Baker ME, Studer RA (2015) Epithelial sodium transport and its control by aldosterone: the story of our internal environment revisited. Physiol Rev 95:297–340PubMed Rossier BC, Baker ME, Studer RA (2015) Epithelial sodium transport and its control by aldosterone: the story of our internal environment revisited. Physiol Rev 95:297–340PubMed
3.
Zurück zum Zitat Oliver WJ, Cohen EL, Neel JV (1975) Blood pressure, sodium intake, and sodium related hormones in the Yanomamo Indians, a ‘no-salt’ culture. Circulation 52:146–151PubMed Oliver WJ, Cohen EL, Neel JV (1975) Blood pressure, sodium intake, and sodium related hormones in the Yanomamo Indians, a ‘no-salt’ culture. Circulation 52:146–151PubMed
4.
Zurück zum Zitat Escoubet B et al (2013) Cardiovascular effects of aldosterone: insight from adult carriers of mineralocorticoid receptor mutations. Circ Cardiovasc Genet 6:381–390PubMed Escoubet B et al (2013) Cardiovascular effects of aldosterone: insight from adult carriers of mineralocorticoid receptor mutations. Circ Cardiovasc Genet 6:381–390PubMed
6.
Zurück zum Zitat Ayuzawa N, Fujita T (2021) The mineralocorticoid receptor in salt-sensitive hypertension and renal injury. J Am Soc Nephrol 32:279–289PubMedPubMedCentral Ayuzawa N, Fujita T (2021) The mineralocorticoid receptor in salt-sensitive hypertension and renal injury. J Am Soc Nephrol 32:279–289PubMedPubMedCentral
7.
Zurück zum Zitat Nishimoto M et al (2019) Mineralocorticoid receptor blockade suppresses dietary salt-induced ACEI/ARB-resistant albuminuria in non-diabetic hypertension: a sub-analysis of evaluate study. Hypertens Res 42:514–521PubMed Nishimoto M et al (2019) Mineralocorticoid receptor blockade suppresses dietary salt-induced ACEI/ARB-resistant albuminuria in non-diabetic hypertension: a sub-analysis of evaluate study. Hypertens Res 42:514–521PubMed
8.
Zurück zum Zitat Nogueira EF, Xing Y, Morris CAV, Rainey WE (2009) Role of angiotensin II-induced rapid response genes in the regulation of enzymes needed for aldosterone synthesis. J Mol Endocrinol 42:319–330PubMedPubMedCentral Nogueira EF, Xing Y, Morris CAV, Rainey WE (2009) Role of angiotensin II-induced rapid response genes in the regulation of enzymes needed for aldosterone synthesis. J Mol Endocrinol 42:319–330PubMedPubMedCentral
9.
Zurück zum Zitat Bandulik S, Tauber P, Lalli E, Barhanin J, Warth R (2015) Two-pore domain potassium channels in the adrenal cortex. Pflugers Arch 467:1027–1042PubMed Bandulik S, Tauber P, Lalli E, Barhanin J, Warth R (2015) Two-pore domain potassium channels in the adrenal cortex. Pflugers Arch 467:1027–1042PubMed
10.
Zurück zum Zitat Epstein M, Kovesdy CP, Clase CM, Sood MM, Pecoits-Filho R (2022) Aldosterone, mineralocorticoid receptor activation, and CKD: a review of evolving treatment paradigms. Am J Kidney Dis 80:658–666PubMed Epstein M, Kovesdy CP, Clase CM, Sood MM, Pecoits-Filho R (2022) Aldosterone, mineralocorticoid receptor activation, and CKD: a review of evolving treatment paradigms. Am J Kidney Dis 80:658–666PubMed
11.
Zurück zum Zitat Palmer BF, Clegg DJ (2022) Extrarenal effects of aldosterone on potassium homeostasis. Kidney360 3:561–568PubMedPubMedCentral Palmer BF, Clegg DJ (2022) Extrarenal effects of aldosterone on potassium homeostasis. Kidney360 3:561–568PubMedPubMedCentral
12.
Zurück zum Zitat Funder JW, Pearce PT, Smith R, Smith AI (1988) Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated. Science 242:583–585PubMed Funder JW, Pearce PT, Smith R, Smith AI (1988) Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated. Science 242:583–585PubMed
13.
Zurück zum Zitat Shibata S et al (2013) Mineralocorticoid receptor phosphorylation regulates ligand binding and renal response to volume depletion and hyperkalemia. Cell Metab 18:660–671PubMedPubMedCentral Shibata S et al (2013) Mineralocorticoid receptor phosphorylation regulates ligand binding and renal response to volume depletion and hyperkalemia. Cell Metab 18:660–671PubMedPubMedCentral
14.
Zurück zum Zitat Gallafassi EA, Bezerra MB, Rebouças NA (2023) Control of sodium and potassium homeostasis by renal distal convoluted tubules. Braz J Med Biol Res 56:e12392PubMedPubMedCentral Gallafassi EA, Bezerra MB, Rebouças NA (2023) Control of sodium and potassium homeostasis by renal distal convoluted tubules. Braz J Med Biol Res 56:e12392PubMedPubMedCentral
15.
Zurück zum Zitat Funder JW (2013) Angiotensin retains sodium by dephosphorylating mineralocorticoid receptors in renal intercalated cells. Cell Metab 18:609–610PubMed Funder JW (2013) Angiotensin retains sodium by dephosphorylating mineralocorticoid receptors in renal intercalated cells. Cell Metab 18:609–610PubMed
16.
Zurück zum Zitat Pech V et al (2015) Pendrin gene ablation alters ENaC subcellular distribution and open probability. Am J Physiol Renal Physiol 309:F154–F163PubMedPubMedCentral Pech V et al (2015) Pendrin gene ablation alters ENaC subcellular distribution and open probability. Am J Physiol Renal Physiol 309:F154–F163PubMedPubMedCentral
17.
Zurück zum Zitat Winter C et al (2011) 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 301:C1251–C1261PubMedPubMedCentral Winter C et al (2011) 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 301:C1251–C1261PubMedPubMedCentral
18.
Zurück zum Zitat Kristensen M, Fenton RA, Poulsen SB (2022) Dissecting the effects of Aldosterone and hypokalemia on the epithelial na+ channel and the nacl cotransporter. Front Physiol 13:800055PubMedPubMedCentral Kristensen M, Fenton RA, Poulsen SB (2022) Dissecting the effects of Aldosterone and hypokalemia on the epithelial na+ channel and the nacl cotransporter. Front Physiol 13:800055PubMedPubMedCentral
19.
Zurück zum Zitat Cheng L et al (2019) Rapid Aldosterone-mediated signaling in the DCT increases activity of the Thiazide-sensitive NaCl cotransporter. J Am Soc Nephrol 30:1454–1470PubMedPubMedCentral Cheng L et al (2019) Rapid Aldosterone-mediated signaling in the DCT increases activity of the Thiazide-sensitive NaCl cotransporter. J Am Soc Nephrol 30:1454–1470PubMedPubMedCentral
20.
Zurück zum Zitat Arroyo JP, Ronzaud C, Lagnaz D, Staub O, Gamba G (2011) Aldosterone paradox: differential regulation of ion transport in distal nephron. Physiology 26:115–123PubMed Arroyo JP, Ronzaud C, Lagnaz D, Staub O, Gamba G (2011) Aldosterone paradox: differential regulation of ion transport in distal nephron. Physiology 26:115–123PubMed
21.
Zurück zum Zitat Hoorn EJ, Gritter M, Cuevas CA, Fenton RA (2020) Regulation of the Renal NaCl cotransporter and Its role in potassium homeostasis. Physiol Rev 100:321–356PubMed Hoorn EJ, Gritter M, Cuevas CA, Fenton RA (2020) Regulation of the Renal NaCl cotransporter and Its role in potassium homeostasis. Physiol Rev 100:321–356PubMed
22.
Zurück zum Zitat McDonough AA, Fenton RA (2022) Potassium homeostasis: sensors, mediators, and targets. Pflugers Arch 474:853–867PubMedPubMedCentral McDonough AA, Fenton RA (2022) Potassium homeostasis: sensors, mediators, and targets. Pflugers Arch 474:853–867PubMedPubMedCentral
23.
Zurück zum Zitat Pearce D, Manis AD, Nesterov V, Korbmacher C (2022) Regulation of distal tubule sodium transport: mechanisms and roles in homeostasis and pathophysiology. Pflugers Arch 474:869–884PubMedPubMedCentral Pearce D, Manis AD, Nesterov V, Korbmacher C (2022) Regulation of distal tubule sodium transport: mechanisms and roles in homeostasis and pathophysiology. Pflugers Arch 474:869–884PubMedPubMedCentral
24.
Zurück zum Zitat Thomson SC, Blantz RC (2008) Glomerulotubular balance, tubuloglomerular feedback, and salt homeostasis. J Am Soc Nephrol 19:2272–2275PubMed Thomson SC, Blantz RC (2008) Glomerulotubular balance, tubuloglomerular feedback, and salt homeostasis. J Am Soc Nephrol 19:2272–2275PubMed
25.
Zurück zum Zitat Bassett MH, White PC, Rainey WE (2004) The regulation of aldosterone synthase expression. Mol Cell Endocrinol 217:67–74PubMed Bassett MH, White PC, Rainey WE (2004) The regulation of aldosterone synthase expression. Mol Cell Endocrinol 217:67–74PubMed
26.
Zurück zum Zitat Gonzalez-Villalobos RA et al (2013) The absence of intrarenal ACE protects against hypertension. J Clin Invest 123:2011–2023PubMedPubMedCentral Gonzalez-Villalobos RA et al (2013) The absence of intrarenal ACE protects against hypertension. J Clin Invest 123:2011–2023PubMedPubMedCentral
27.
Zurück zum Zitat Saccomani G, Mitchell KD, Navar LG (1990) Angiotensin II stimulation of Na(+)-H+ exchange in proximal tubule cells. Am J Physiol 258:F1188–F1195PubMed Saccomani G, Mitchell KD, Navar LG (1990) Angiotensin II stimulation of Na(+)-H+ exchange in proximal tubule cells. Am J Physiol 258:F1188–F1195PubMed
28.
Zurück zum Zitat Castañeda-Bueno M et al (2017) Phosphorylation by PKC and PKA regulate the kinase activity and downstream signaling of WNK4. Proc Natl Acad Sci U S A 114:E879–E886PubMedPubMedCentral Castañeda-Bueno M et al (2017) Phosphorylation by PKC and PKA regulate the kinase activity and downstream signaling of WNK4. Proc Natl Acad Sci U S A 114:E879–E886PubMedPubMedCentral
29.
Zurück zum Zitat van der Lubbe N et al (2011) Angiotensin II induces phosphorylation of the thiazide-sensitive sodium chloride cotransporter independent of aldosterone. Kidney Int 79:66–76PubMed van der Lubbe N et al (2011) Angiotensin II induces phosphorylation of the thiazide-sensitive sodium chloride cotransporter independent of aldosterone. Kidney Int 79:66–76PubMed
30.
Zurück zum Zitat Hirohama D et al (2018) Aldosterone is essential for Angiotensin II-induced upregulation of Pendrin. J Am Soc Nephrol 29:57–68PubMed Hirohama D et al (2018) Aldosterone is essential for Angiotensin II-induced upregulation of Pendrin. J Am Soc Nephrol 29:57–68PubMed
31.
Zurück zum Zitat Nesterov V et al (2021) Critical role of the mineralocorticoid receptor in aldosterone-dependent and aldosterone-independent regulation of ENaC in the distal nephron. Am J Physiol Renal Physiol 321:F257–F268PubMedPubMedCentral Nesterov V et al (2021) Critical role of the mineralocorticoid receptor in aldosterone-dependent and aldosterone-independent regulation of ENaC in the distal nephron. Am J Physiol Renal Physiol 321:F257–F268PubMedPubMedCentral
32.
Zurück zum Zitat Maeoka Y et al (2022) Mineralocorticoid receptor antagonists cause natriuresis in the absence of Aldosterone. Hypertens 79:1423–1434 Maeoka Y et al (2022) Mineralocorticoid receptor antagonists cause natriuresis in the absence of Aldosterone. Hypertens 79:1423–1434
33.
Zurück zum Zitat Wu P et al (2020) Effect of Angiotensin II on ENaC in the distal convoluted tubule and in the cortical collecting duct of mineralocorticoid receptor deficient mice. J Am Heart Assoc 9:e14996PubMedPubMedCentral Wu P et al (2020) Effect of Angiotensin II on ENaC in the distal convoluted tubule and in the cortical collecting duct of mineralocorticoid receptor deficient mice. J Am Heart Assoc 9:e14996PubMedPubMedCentral
34.
Zurück zum Zitat Yue P et al (2011) Angiotensin II diminishes the effect of SGK1 on the WNK4-mediated inhibition of ROMK1 channels. Kidney Int 79:423–431PubMed Yue P et al (2011) Angiotensin II diminishes the effect of SGK1 on the WNK4-mediated inhibition of ROMK1 channels. Kidney Int 79:423–431PubMed
35.
Zurück zum Zitat Gong Y, Hou J (2017) Claudins in barrier and transport function—the kidney. Pflugers Arch 469:105–113PubMed Gong Y, Hou J (2017) Claudins in barrier and transport function—the kidney. Pflugers Arch 469:105–113PubMed
36.
Zurück zum Zitat Le Moellic C et al (2005) Aldosterone and tight junctions: modulation of claudin‑4 phosphorylation in renal collecting duct cells. Am J Physiol, Cell Physiol 289:C1513–C1521PubMed Le Moellic C et al (2005) Aldosterone and tight junctions: modulation of claudin‑4 phosphorylation in renal collecting duct cells. Am J Physiol, Cell Physiol 289:C1513–C1521PubMed
37.
Zurück zum Zitat Sassi A et al (2020) Interaction between epithelial sodium channel γ‑subunit and Claudin‑8 modulates paracellular sodium permeability in renal collecting duct. J Am Soc Nephrol Jasn 31:1009–1023PubMed Sassi A et al (2020) Interaction between epithelial sodium channel γ‑subunit and Claudin‑8 modulates paracellular sodium permeability in renal collecting duct. J Am Soc Nephrol Jasn 31:1009–1023PubMed
38.
Zurück zum Zitat Shibata S (2019) Role of Pendrin in the pathophysiology of Aldosterone-induced hypertension. Am J Hypertens 32:607–613PubMed Shibata S (2019) Role of Pendrin in the pathophysiology of Aldosterone-induced hypertension. Am J Hypertens 32:607–613PubMed
39.
Zurück zum Zitat Leviel F et al (2010) The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. J Clin Invest 120:1627–1635PubMedPubMedCentral Leviel F et al (2010) The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. J Clin Invest 120:1627–1635PubMedPubMedCentral
40.
Zurück zum Zitat Ganong WF, Mulrow PJ (1958) Rate of change in sodium and potassium excretion after injection of aldosterone into the aorta and renal artery of the dog. Am J Physiol 195:337–342PubMed Ganong WF, Mulrow PJ (1958) Rate of change in sodium and potassium excretion after injection of aldosterone into the aorta and renal artery of the dog. Am J Physiol 195:337–342PubMed
41.
Zurück zum Zitat Velarde-Miranda C, Gomez-Sanchez EP, Gomez-Sanchez CE (2013) Regulation of aldosterone biosynthesis by the Kir3.4 (KCNJ5) potassium channel. Clin Exp Pharmacol Physiol 40:895–901PubMed Velarde-Miranda C, Gomez-Sanchez EP, Gomez-Sanchez CE (2013) Regulation of aldosterone biosynthesis by the Kir3.4 (KCNJ5) potassium channel. Clin Exp Pharmacol Physiol 40:895–901PubMed
42.
Zurück zum Zitat Guagliardo NA et al (2019) Adrenal tissue-specific deletion of TASK channels causes Aldosterone-driven Angiotensin II-independent hypertension. Hypertens 73:407–414 Guagliardo NA et al (2019) Adrenal tissue-specific deletion of TASK channels causes Aldosterone-driven Angiotensin II-independent hypertension. Hypertens 73:407–414
43.
Zurück zum Zitat Rengarajan S et al (2014) Increasing plasma [K+] by intravenous potassium infusion reduces NCC phosphorylation and drives kaliuresis and natriuresis. Am J Physiol Renal Physiol 306:F1059–F1068PubMedPubMedCentral Rengarajan S et al (2014) Increasing plasma [K+] by intravenous potassium infusion reduces NCC phosphorylation and drives kaliuresis and natriuresis. Am J Physiol Renal Physiol 306:F1059–F1068PubMedPubMedCentral
44.
Zurück zum Zitat Sorensen MV et al (2013) Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice. Kidney Int 83:811–824PubMed Sorensen MV et al (2013) Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice. Kidney Int 83:811–824PubMed
45.
Zurück zum Zitat Bazúa-Valenti S et al (2015) The effect of WNK4 on the na+-cl− cotransporter is modulated by intracellular chloride. J Am Soc Nephrol 26:1781–1786PubMed Bazúa-Valenti S et al (2015) The effect of WNK4 on the na+-cl− cotransporter is modulated by intracellular chloride. J Am Soc Nephrol 26:1781–1786PubMed
46.
Zurück zum Zitat Pleinis JM et al (2021) WNKs are potassium-sensitive kinases. Am J Physiol, Cell Physiol 320:C703–C721PubMed Pleinis JM et al (2021) WNKs are potassium-sensitive kinases. Am J Physiol, Cell Physiol 320:C703–C721PubMed
47.
Zurück zum Zitat Grimm PR et al (2023) Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure. J Clin Invest 133:e158498PubMedPubMedCentral Grimm PR et al (2023) Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure. J Clin Invest 133:e158498PubMedPubMedCentral
48.
Zurück zum Zitat Nesterov V, Bertog M, Korbmacher C (2022) High baseline ROMK activity in the mouse late distal convoluted and early connecting tubule probably contributes to aldosterone-independent K+ secretion. Am J Physiol Renal Physiol 322:F42–F54PubMed Nesterov V, Bertog M, Korbmacher C (2022) High baseline ROMK activity in the mouse late distal convoluted and early connecting tubule probably contributes to aldosterone-independent K+ secretion. Am J Physiol Renal Physiol 322:F42–F54PubMed
49.
Zurück zum Zitat Todkar A et al (2015) Mechanisms of renal control of potassium homeostasis in complete aldosterone deficiency. J Am Soc Nephrol 26:425–438PubMed Todkar A et al (2015) Mechanisms of renal control of potassium homeostasis in complete aldosterone deficiency. J Am Soc Nephrol 26:425–438PubMed
50.
Zurück zum Zitat Wade JB et al (2011) Differential regulation of ROMK (Kir1.1) in distal nephron segments by dietary potassium. Am J Physiol Ren Physiol 300:F1385–F1393 Wade JB et al (2011) Differential regulation of ROMK (Kir1.1) in distal nephron segments by dietary potassium. Am J Physiol Ren Physiol 300:F1385–F1393
51.
Zurück zum Zitat Saha B et al (2023) Potassium activates mTORC2-dependent SGK1 phosphorylation to stimulate epithelial sodium channel: role in rapid renal responses to dietary potassium. J Am Soc Nephrol 34:1019–1038PubMedPubMedCentral Saha B et al (2023) Potassium activates mTORC2-dependent SGK1 phosphorylation to stimulate epithelial sodium channel: role in rapid renal responses to dietary potassium. J Am Soc Nephrol 34:1019–1038PubMedPubMedCentral
52.
Zurück zum Zitat Yang L et al (2021) ENaC and ROMK channels in the connecting tubule regulate renal K+ secretion. J Gen Physiol 153:e202112902PubMedPubMedCentral Yang L et al (2021) ENaC and ROMK channels in the connecting tubule regulate renal K+ secretion. J Gen Physiol 153:e202112902PubMedPubMedCentral
53.
Zurück zum Zitat Wald H, Garty H, Palmer LG, Popovtzer MM (1998) Differential regulation of ROMK expression in kidney cortex and medulla by aldosterone and potassium. Am J Physiol 275:F239–F245PubMed Wald H, Garty H, Palmer LG, Popovtzer MM (1998) Differential regulation of ROMK expression in kidney cortex and medulla by aldosterone and potassium. Am J Physiol 275:F239–F245PubMed
54.
Zurück zum Zitat Cornelius RJ et al (2015) Low Na, high K diet and the role of aldosterone in BK-mediated K excretion. PLoS ONE 10:e115515PubMedPubMedCentral Cornelius RJ et al (2015) Low Na, high K diet and the role of aldosterone in BK-mediated K excretion. PLoS ONE 10:e115515PubMedPubMedCentral
55.
Zurück zum Zitat Mamenko MV et al (2017) The renal TRPV4 channel is essential for adaptation to increased dietary potassium. Kidney Int 91:1398–1409PubMedPubMedCentral Mamenko MV et al (2017) The renal TRPV4 channel is essential for adaptation to increased dietary potassium. Kidney Int 91:1398–1409PubMedPubMedCentral
56.
Zurück zum Zitat Stavniichuk A et al (2023) TRPV4 expression in the renal tubule is necessary for maintaining whole body K+ homeostasis. Am J Physiol Renal Physiol 324:F603–F616PubMedPubMedCentral Stavniichuk A et al (2023) TRPV4 expression in the renal tubule is necessary for maintaining whole body K+ homeostasis. Am J Physiol Renal Physiol 324:F603–F616PubMedPubMedCentral
57.
Zurück zum Zitat van Buren M, Rabelink AJ, Bijlsma JA, Koomans HA (1993) Natriuretic and kaliuretic response to potassium load: modulation by sodium intake. Nephrol Dial Transplant 8:495–500PubMed van Buren M, Rabelink AJ, Bijlsma JA, Koomans HA (1993) Natriuretic and kaliuretic response to potassium load: modulation by sodium intake. Nephrol Dial Transplant 8:495–500PubMed
58.
Zurück zum Zitat Kamel KS, Schreiber M, Halperin ML (2018) Renal potassium physiology: integration of the renal response to dietary potassium depletion. Kidney Int 93:41–53PubMed Kamel KS, Schreiber M, Halperin ML (2018) Renal potassium physiology: integration of the renal response to dietary potassium depletion. Kidney Int 93:41–53PubMed
59.
Zurück zum Zitat Young DB, Paulsen AW (1983) Interrelated effects of aldosterone and plasma potassium on potassium excretion. Am J Physiol 244:F28–F34PubMed Young DB, Paulsen AW (1983) Interrelated effects of aldosterone and plasma potassium on potassium excretion. Am J Physiol 244:F28–F34PubMed
60.
Zurück zum Zitat Thomson MN et al (2020) WNK bodies cluster WNK4 and SPAK/OSR1 to promote NCC activation in hypokalemia. Am J Physiol Renal Physiol 318:F216–F228PubMed Thomson MN et al (2020) WNK bodies cluster WNK4 and SPAK/OSR1 to promote NCC activation in hypokalemia. Am J Physiol Renal Physiol 318:F216–F228PubMed
61.
Zurück zum Zitat Wang M‑X et al (2018) Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel. Kidney Int 93:893–902PubMedPubMedCentral Wang M‑X et al (2018) Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel. Kidney Int 93:893–902PubMedPubMedCentral
62.
Zurück zum Zitat Murillo-de-Ozores AR et al (2022) Multiple molecular mechanisms are involved in the activation of the kidney sodium-chloride cotransporter by hypokalemia. Kidney Int 102:1030–1041PubMedPubMedCentral Murillo-de-Ozores AR et al (2022) Multiple molecular mechanisms are involved in the activation of the kidney sodium-chloride cotransporter by hypokalemia. Kidney Int 102:1030–1041PubMedPubMedCentral
63.
Zurück zum Zitat Al-Qusairi L et al (2023) Dietary anions control potassium excretion: it is more than a poorly absorbable anion effect. Am J Physiol Renal Physiol 325:F377–F393PubMed Al-Qusairi L et al (2023) Dietary anions control potassium excretion: it is more than a poorly absorbable anion effect. Am J Physiol Renal Physiol 325:F377–F393PubMed
64.
Zurück zum Zitat Wei Y, Zavilowitz B, Satlin LM, Wang WH (2007) Angiotensin II inhibits the ROMK-like small conductance K channel in renal cortical collecting duct during dietary potassium restriction. J Biol Chem 282:6455–6462PubMed Wei Y, Zavilowitz B, Satlin LM, Wang WH (2007) Angiotensin II inhibits the ROMK-like small conductance K channel in renal cortical collecting duct during dietary potassium restriction. J Biol Chem 282:6455–6462PubMed
65.
Zurück zum Zitat Elabida B et al (2011) Chronic potassium depletion increases adrenal progesterone production that is necessary for efficient renal retention of potassium. Kidney Int 80:256–262PubMed Elabida B et al (2011) Chronic potassium depletion increases adrenal progesterone production that is necessary for efficient renal retention of potassium. Kidney Int 80:256–262PubMed
66.
Zurück zum Zitat Blanchard A et al (2020) Adrenal adaptation in potassium-depleted men: role of progesterone? Nephrol Dial Transplant 35:1901–1908PubMed Blanchard A et al (2020) Adrenal adaptation in potassium-depleted men: role of progesterone? Nephrol Dial Transplant 35:1901–1908PubMed
67.
Zurück zum Zitat Gumz ML, Lynch IJ, Greenlee MM, Cain BD, Wingo CS (2010) The renal H+-K+-ATPases: physiology, regulation, and structure. Am J Physiol Renal Physiol 298:F12–F21PubMed Gumz ML, Lynch IJ, Greenlee MM, Cain BD, Wingo CS (2010) The renal H+-K+-ATPases: physiology, regulation, and structure. Am J Physiol Renal Physiol 298:F12–F21PubMed
68.
Zurück zum Zitat Lasaad S et al (2023) GDF15 mediates renal cell plasticity in response to potassium depletion in mice. Acta Physiol 239:e14046 Lasaad S et al (2023) GDF15 mediates renal cell plasticity in response to potassium depletion in mice. Acta Physiol 239:e14046
69.
Zurück zum Zitat Pham TD et al (2022) Pendrin-null mice develop severe hypokalemia following dietary Na+ and K+ restriction: role of ENaC. Am J Physiol Renal Physiol 322:F486–F497PubMedPubMedCentral Pham TD et al (2022) Pendrin-null mice develop severe hypokalemia following dietary Na+ and K+ restriction: role of ENaC. Am J Physiol Renal Physiol 322:F486–F497PubMedPubMedCentral
70.
Zurück zum Zitat Terker AS et al (2015) Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride. Cell Metab 21:39–50PubMedPubMedCentral Terker AS et al (2015) Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride. Cell Metab 21:39–50PubMedPubMedCentral
71.
Zurück zum Zitat Wu A et al (2023) Randomized trial on the effect of oral potassium chloride supplementation on the thiazide-sensitive sodium chloride cotransporter in healthy adults. Kidney Int Rep 8:1201–1212PubMedPubMedCentral Wu A et al (2023) Randomized trial on the effect of oral potassium chloride supplementation on the thiazide-sensitive sodium chloride cotransporter in healthy adults. Kidney Int Rep 8:1201–1212PubMedPubMedCentral
72.
Zurück zum Zitat Xu N et al (2017) Hypokalemia and pendrin induction by aldosterone. Hypertens 69:855–862 Xu N et al (2017) Hypokalemia and pendrin induction by aldosterone. Hypertens 69:855–862
73.
Zurück zum Zitat Pham TD et al (2020) Aldosterone regulates pendrin and epithelial sodium channel activity through intercalated cell mineralocorticoid receptor-dependent and -independent mechanisms over a wide range in serum potassium. J Am Soc Nephrol 31:483–499PubMedPubMedCentral Pham TD et al (2020) Aldosterone regulates pendrin and epithelial sodium channel activity through intercalated cell mineralocorticoid receptor-dependent and -independent mechanisms over a wide range in serum potassium. J Am Soc Nephrol 31:483–499PubMedPubMedCentral
74.
Zurück zum Zitat Terker AS et al (2016) Direct and indirect mineralocorticoid effects determine distal salt transport. J Am Soc Nephrol 27:2436–2445PubMed Terker AS et al (2016) Direct and indirect mineralocorticoid effects determine distal salt transport. J Am Soc Nephrol 27:2436–2445PubMed
75.
Zurück zum Zitat Ayuzawa N et al (2020) Two mineralocorticoid receptor-mediated mechanisms of pendrin activation in distal nephrons. J Am Soc Nephrol 31:748–764PubMedPubMedCentral Ayuzawa N et al (2020) Two mineralocorticoid receptor-mediated mechanisms of pendrin activation in distal nephrons. J Am Soc Nephrol 31:748–764PubMedPubMedCentral
76.
Zurück zum Zitat Ozbaki-Yagan N, Liu X, Bodnar AJ, Ho J, Butterworth MB (2020) Aldosterone-induced microRNAs act as feedback regulators of mineralocorticoid receptor signaling in kidney epithelia. FASEB J 34:11714–11728PubMed Ozbaki-Yagan N, Liu X, Bodnar AJ, Ho J, Butterworth MB (2020) Aldosterone-induced microRNAs act as feedback regulators of mineralocorticoid receptor signaling in kidney epithelia. FASEB J 34:11714–11728PubMed
77.
Zurück zum Zitat Schrier RW (2010) Aldosterone ‘escape’ vs ‘breakthrough. Nat Rev Nephrol 6:61PubMed Schrier RW (2010) Aldosterone ‘escape’ vs ‘breakthrough. Nat Rev Nephrol 6:61PubMed
78.
Zurück zum Zitat Khandelwal P, Deinum J (2022) Monogenic forms of low-renin hypertension: clinical and molecular insights. Pediatr Nephrol 37:1495–1509PubMed Khandelwal P, Deinum J (2022) Monogenic forms of low-renin hypertension: clinical and molecular insights. Pediatr Nephrol 37:1495–1509PubMed
79.
Zurück zum Zitat Nanba K, Rainey WE (2022) Pathophysiology of bilateral hyperaldosteronism. Curr Opin Endocrinol Diabetes Obes 29:233–242PubMedPubMedCentral Nanba K, Rainey WE (2022) Pathophysiology of bilateral hyperaldosteronism. Curr Opin Endocrinol Diabetes Obes 29:233–242PubMedPubMedCentral
80.
Zurück zum Zitat Meyer LS, Gong S, Reincke M, Williams TA (2020) Angiotensin II type 1 receptor autoantibodies in primary aldosteronism. Horm Metab Res 52:379–385PubMedPubMedCentral Meyer LS, Gong S, Reincke M, Williams TA (2020) Angiotensin II type 1 receptor autoantibodies in primary aldosteronism. Horm Metab Res 52:379–385PubMedPubMedCentral
82.
Zurück zum Zitat Boyle RA, Baker JE, Charu V, Rainey WE, Bhalla V (2021) Masking by hypokalemia-primary aldosteronism with undetectable aldosterone. Clin Kidney J 14:1269–1271PubMed Boyle RA, Baker JE, Charu V, Rainey WE, Bhalla V (2021) Masking by hypokalemia-primary aldosteronism with undetectable aldosterone. Clin Kidney J 14:1269–1271PubMed
83.
Zurück zum Zitat Freeman MW et al (2023) Phase 2 trial of Baxdrostat for treatment-resistant hypertension. N Engl J Med 388:395–405PubMed Freeman MW et al (2023) Phase 2 trial of Baxdrostat for treatment-resistant hypertension. N Engl J Med 388:395–405PubMed
84.
Zurück zum Zitat Grimm PR, Coleman R, Delpire E, Welling PA (2017) Constitutively active SPAK causes hyperkalemia by activating NCC and remodeling distal tubules. J Am Soc Nephrol Jasn 28:2597–2606PubMed Grimm PR, Coleman R, Delpire E, Welling PA (2017) Constitutively active SPAK causes hyperkalemia by activating NCC and remodeling distal tubules. J Am Soc Nephrol Jasn 28:2597–2606PubMed
85.
Zurück zum Zitat Favre GA et al (2012) Localization of tubular adaptation to renal sodium loss in Gitelman syndrome. Clin J Am Soc Nephrol 7:472–478PubMedPubMedCentral Favre GA et al (2012) Localization of tubular adaptation to renal sodium loss in Gitelman syndrome. Clin J Am Soc Nephrol 7:472–478PubMedPubMedCentral
86.
Zurück zum Zitat Geller DS et al (1998) Mutations in the mineralocorticoid receptor gene cause autosomal dominant pseudohypoaldosteronism type I. Nat Genet 19:279–281PubMed Geller DS et al (1998) Mutations in the mineralocorticoid receptor gene cause autosomal dominant pseudohypoaldosteronism type I. Nat Genet 19:279–281PubMed
87.
Zurück zum Zitat Geller DS et al (2006) Autosomal dominant pseudohypoaldosteronism type 1: mechanisms, evidence for neonatal lethality, and phenotypic expression in adults. J Am Soc Nephrol 17:1429–1436PubMed Geller DS et al (2006) Autosomal dominant pseudohypoaldosteronism type 1: mechanisms, evidence for neonatal lethality, and phenotypic expression in adults. J Am Soc Nephrol 17:1429–1436PubMed
88.
Zurück zum Zitat Riepe FG (2009) Clinical and molecular features of type 1 pseudohypoaldosteronism. Horm Res 72:1–9PubMed Riepe FG (2009) Clinical and molecular features of type 1 pseudohypoaldosteronism. Horm Res 72:1–9PubMed
89.
Zurück zum Zitat Bandhakavi M et al (2021) Clinical characteristics and treatment requirements of children with autosomal recessive pseudohypoaldosteronism. Eur J Endocrinol 184:K15–K20PubMed Bandhakavi M et al (2021) Clinical characteristics and treatment requirements of children with autosomal recessive pseudohypoaldosteronism. Eur J Endocrinol 184:K15–K20PubMed
90.
Zurück zum Zitat Rubera I et al (2003) Collecting duct-specific gene inactivation of alphaENaC in the mouse kidney does not impair sodium and potassium balance. J Clin Invest 112:554–565PubMedPubMedCentral Rubera I et al (2003) Collecting duct-specific gene inactivation of alphaENaC in the mouse kidney does not impair sodium and potassium balance. J Clin Invest 112:554–565PubMedPubMedCentral
91.
Zurück zum Zitat Boscardin E et al (2018) Plasma potassium determines NCC abundance in adult kidney-specific γENaC knockout. J Am Soc Nephrol 29:977–990PubMedPubMedCentral Boscardin E et al (2018) Plasma potassium determines NCC abundance in adult kidney-specific γENaC knockout. J Am Soc Nephrol 29:977–990PubMedPubMedCentral
92.
Zurück zum Zitat Boscardin E et al (2017) Severe hyperkalemia is rescued by low-potassium diet in renal βENaC-deficient mice. Pflugers Arch 469:1387–1399PubMed Boscardin E et al (2017) Severe hyperkalemia is rescued by low-potassium diet in renal βENaC-deficient mice. Pflugers Arch 469:1387–1399PubMed
93.
Zurück zum Zitat Perrier R et al (2016) Severe salt-losing syndrome and Hyperkalemia induced by adult nephron-specific knockout of the epithelial sodium channel α‑subunit. J Am Soc Nephrol 27:2309–2318PubMed Perrier R et al (2016) Severe salt-losing syndrome and Hyperkalemia induced by adult nephron-specific knockout of the epithelial sodium channel α‑subunit. J Am Soc Nephrol 27:2309–2318PubMed
94.
Zurück zum Zitat Kerem E et al (1999) Pulmonary epithelial sodium-channel dysfunction and excess airway liquid in pseudohypoaldosteronism. N Engl J Med 341:156–162PubMed Kerem E et al (1999) Pulmonary epithelial sodium-channel dysfunction and excess airway liquid in pseudohypoaldosteronism. N Engl J Med 341:156–162PubMed
95.
Zurück zum Zitat Delforge X et al (2019) Transient pseudohypoaldosteronism: a potentially severe condition affecting infants with urinary tract malformation. J Pediatr Urol 15:265.e1–265.e7PubMed Delforge X et al (2019) Transient pseudohypoaldosteronism: a potentially severe condition affecting infants with urinary tract malformation. J Pediatr Urol 15:265.e1–265.e7PubMed
96.
Zurück zum Zitat Batlle DC, Arruda JA, Kurtzman NA (1981) Hyperkalemic distal renal tubular acidosis associated with obstructive uropathy. N Engl J Med 304:373–380PubMed Batlle DC, Arruda JA, Kurtzman NA (1981) Hyperkalemic distal renal tubular acidosis associated with obstructive uropathy. N Engl J Med 304:373–380PubMed
97.
Zurück zum Zitat Zietse R, Zoutendijk R, Hoorn EJ (2009) Fluid, electrolyte and acid-base disorders associated with antibiotic therapy. Nat Rev Nephrol 5:193–202PubMed Zietse R, Zoutendijk R, Hoorn EJ (2009) Fluid, electrolyte and acid-base disorders associated with antibiotic therapy. Nat Rev Nephrol 5:193–202PubMed
98.
Zurück zum Zitat Schaedel C et al (1999) Lung symptoms in pseudohypoaldosteronism type 1 are associated with deficiency of the alpha-subunit of the epithelial sodium channel. J Pediatr 135:739–745PubMed Schaedel C et al (1999) Lung symptoms in pseudohypoaldosteronism type 1 are associated with deficiency of the alpha-subunit of the epithelial sodium channel. J Pediatr 135:739–745PubMed
99.
Zurück zum Zitat Ellison DH, Terker AS, Gamba G (2016) Potassium and its discontents: new insight, new treatments. J Am Soc Nephrol 27:981–989PubMed Ellison DH, Terker AS, Gamba G (2016) Potassium and its discontents: new insight, new treatments. J Am Soc Nephrol 27:981–989PubMed
100.
Zurück zum Zitat O’Shaughnessy KM (2015) Gordon Syndrome: a continuing story. Pediatr Nephrol 30:1903–1908PubMed O’Shaughnessy KM (2015) Gordon Syndrome: a continuing story. Pediatr Nephrol 30:1903–1908PubMed
101.
Zurück zum Zitat Arroyo JP et al (2011) Nedd4‑2 modulates renal Na+- Cl− cotransporter via the aldosterone-SGK1-Nedd4‑2 pathway. J Am Soc Nephrol Jasn 22:1707–1719PubMed Arroyo JP et al (2011) Nedd4‑2 modulates renal Na+- Cl− cotransporter via the aldosterone-SGK1-Nedd4‑2 pathway. J Am Soc Nephrol Jasn 22:1707–1719PubMed
102.
Zurück zum Zitat Faresse N et al (2012) Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype. Am J Physiol Renal Physiol 302:F977–F985PubMed Faresse N et al (2012) Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype. Am J Physiol Renal Physiol 302:F977–F985PubMed
103.
Zurück zum Zitat Picard N et al (2014) Protein phosphatase 1 inhibitor‑1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension. J Am Soc Nephrol 25:511–522PubMed Picard N et al (2014) Protein phosphatase 1 inhibitor‑1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension. J Am Soc Nephrol 25:511–522PubMed
104.
Zurück zum Zitat Adachi M et al (2023) Classification of pseudohypoaldosteronism type II as type IV renal tubular acidosis: results of a literature review. Endocr J 70:723–729PubMed Adachi M et al (2023) Classification of pseudohypoaldosteronism type II as type IV renal tubular acidosis: results of a literature review. Endocr J 70:723–729PubMed
105.
Zurück zum Zitat López-Cayuqueo KI et al (2018) A mouse model of pseudohypoaldosteronism type II reveals a novel mechanism of renal tubular acidosis. Kidney Int 94:514–523PubMed López-Cayuqueo KI et al (2018) A mouse model of pseudohypoaldosteronism type II reveals a novel mechanism of renal tubular acidosis. Kidney Int 94:514–523PubMed
106.
Zurück zum Zitat Yamauchi K et al (2004) Disease-causing mutant WNK4 increases paracellular chloride permeability and phosphorylates claudins. Proc Natl Acad Sci U S A 101:4690–4694PubMedPubMedCentral Yamauchi K et al (2004) Disease-causing mutant WNK4 increases paracellular chloride permeability and phosphorylates claudins. Proc Natl Acad Sci U S A 101:4690–4694PubMedPubMedCentral
107.
Zurück zum Zitat Healy JK (2014) Pseudohypoaldosteronism Type II. Hypertension 63:648–654PubMed Healy JK (2014) Pseudohypoaldosteronism Type II. Hypertension 63:648–654PubMed
108.
Zurück zum Zitat Hoorn EJ et al (2011) The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nat Med 17:1304–1309PubMedPubMedCentral Hoorn EJ et al (2011) The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nat Med 17:1304–1309PubMedPubMedCentral
109.
Zurück zum Zitat Gao Z‑X et al (2023) Activation of Kir4.1/Kir5.1 contributes to the cyclosporin A‑induced stimulation of the renal NaCl cotransporter and hyperkalemic hypertension. Acta Physiol 238:e13948 Gao Z‑X et al (2023) Activation of Kir4.1/Kir5.1 contributes to the cyclosporin A‑induced stimulation of the renal NaCl cotransporter and hyperkalemic hypertension. Acta Physiol 238:e13948
110.
Zurück zum Zitat Ishizawa K et al (2019) Calcineurin dephosphorylates Kelch-like 3, reversing phosphorylation by angiotensin II and regulating renal electrolyte handling. Proc Natl Acad Sci U S A 116:3155–3160PubMedPubMedCentral Ishizawa K et al (2019) Calcineurin dephosphorylates Kelch-like 3, reversing phosphorylation by angiotensin II and regulating renal electrolyte handling. Proc Natl Acad Sci U S A 116:3155–3160PubMedPubMedCentral
111.
Zurück zum Zitat Shoda W et al (2017) Calcineurin inhibitors block sodium-chloride cotransporter dephosphorylation in response to high potassium intake. Kidney Int 91:402–411PubMed Shoda W et al (2017) Calcineurin inhibitors block sodium-chloride cotransporter dephosphorylation in response to high potassium intake. Kidney Int 91:402–411PubMed
112.
Zurück zum Zitat An C, Liang J, Zhang K, Su X (2016) Polymorphisms in the SLC12A3 gene encoding sodium-chloride cotransporter are associated with hypertension: a family-based study in the Mongolian population. Kidney Blood Press Res 41:18–28PubMed An C, Liang J, Zhang K, Su X (2016) Polymorphisms in the SLC12A3 gene encoding sodium-chloride cotransporter are associated with hypertension: a family-based study in the Mongolian population. Kidney Blood Press Res 41:18–28PubMed
113.
Zurück zum Zitat Erger F (2018) Monogene Formen der arteriellen Hypertonie. Med Genet 30:391–399 Erger F (2018) Monogene Formen der arteriellen Hypertonie. Med Genet 30:391–399
114.
Zurück zum Zitat Rizzolo K, Beck NM, Ambruso SL (2022) Syndromes of pseudo-hyperaldosteronism. Clin J Am Soc Nephrol 17:581–584PubMedPubMedCentral Rizzolo K, Beck NM, Ambruso SL (2022) Syndromes of pseudo-hyperaldosteronism. Clin J Am Soc Nephrol 17:581–584PubMedPubMedCentral
115.
Zurück zum Zitat Shimkets RA et al (1994) Liddle’s syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel. Cell 79:407–414PubMed Shimkets RA et al (1994) Liddle’s syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel. Cell 79:407–414PubMed
116.
Zurück zum Zitat Hansson JH et al (1995) Hypertension caused by a truncated epithelial sodium channel gamma subunit: genetic heterogeneity of Liddle syndrome. Nat Genet 11:76–82PubMed Hansson JH et al (1995) Hypertension caused by a truncated epithelial sodium channel gamma subunit: genetic heterogeneity of Liddle syndrome. Nat Genet 11:76–82PubMed
117.
Zurück zum Zitat Rossier BC, Schild L (2008) Epithelial sodium channel: mendelian versus essential hypertension. Hypertens 52:595–600 Rossier BC, Schild L (2008) Epithelial sodium channel: mendelian versus essential hypertension. Hypertens 52:595–600
118.
Zurück zum Zitat Salih M et al (2017) A missense mutation in the extracellular domain of αENaC causes Liddle syndrome. J Am Soc Nephrol 28:3291–3299PubMedPubMedCentral Salih M et al (2017) A missense mutation in the extracellular domain of αENaC causes Liddle syndrome. J Am Soc Nephrol 28:3291–3299PubMedPubMedCentral
119.
Zurück zum Zitat Ronzaud C et al (2013) Renal tubular NEDD4‑2 deficiency causes NCC-mediated salt-dependent hypertension. J Clin Invest 123:657–665PubMedPubMedCentral Ronzaud C et al (2013) Renal tubular NEDD4‑2 deficiency causes NCC-mediated salt-dependent hypertension. J Clin Invest 123:657–665PubMedPubMedCentral
120.
Zurück zum Zitat Warnock DG (2001) Liddle syndrome: genetics and mechanisms of Na+ channel defects. Am J Med Sci 322:302–307PubMed Warnock DG (2001) Liddle syndrome: genetics and mechanisms of Na+ channel defects. Am J Med Sci 322:302–307PubMed
121.
Zurück zum Zitat Bohnert BN et al (2021) Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na+ channel in the mouse kidney. Am J Physiol Ren Physiol 321:F480–F493 Bohnert BN et al (2021) Experimental nephrotic syndrome leads to proteolytic activation of the epithelial Na+ channel in the mouse kidney. Am J Physiol Ren Physiol 321:F480–F493
122.
Zurück zum Zitat Essigke D et al (2022) Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity. Pflugers Arch 474:613–624PubMedPubMedCentral Essigke D et al (2022) Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity. Pflugers Arch 474:613–624PubMedPubMedCentral
123.
Zurück zum Zitat Artunc F et al (2022) Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice. Pflugers Arch 474:217–229PubMed Artunc F et al (2022) Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice. Pflugers Arch 474:217–229PubMed
124.
Zurück zum Zitat Geller DS et al (2000) Activating mineralocorticoid receptor mutation in hypertension exacerbated by pregnancy. Science 289:119–123PubMed Geller DS et al (2000) Activating mineralocorticoid receptor mutation in hypertension exacerbated by pregnancy. Science 289:119–123PubMed
125.
Zurück zum Zitat Hindosh N, Hindosh R, Dada B, Bal S (2022) Geller syndrome: a rare cause of persistent hypokalemia during pregnancy. Cureus 14:e26272PubMedPubMedCentral Hindosh N, Hindosh R, Dada B, Bal S (2022) Geller syndrome: a rare cause of persistent hypokalemia during pregnancy. Cureus 14:e26272PubMedPubMedCentral
126.
Zurück zum Zitat Zennaro M‑C, Fernandes-Rosa F (2017) 30 years of the mineralocorticoid receptor: mineralocorticoid receptor mutations. J Endocrinol 234:T93–T106PubMed Zennaro M‑C, Fernandes-Rosa F (2017) 30 years of the mineralocorticoid receptor: mineralocorticoid receptor mutations. J Endocrinol 234:T93–T106PubMed
127.
Zurück zum Zitat Hunter RW et al (2015) Hypertrophy in the distal convoluted tubule of an 11β-Hydroxysteroid dehydrogenase type 2 knockout model. J Am Soc Nephrol 26:1537–1548PubMed Hunter RW et al (2015) Hypertrophy in the distal convoluted tubule of an 11β-Hydroxysteroid dehydrogenase type 2 knockout model. J Am Soc Nephrol 26:1537–1548PubMed
128.
Zurück zum Zitat Yau M et al (2017) Clinical, genetic, and structural basis of apparent mineralocorticoid excess due to 11β-hydroxysteroid dehydrogenase type 2 deficiency. Proc Natl Acad Sci U S A 114:E11248–E11256PubMedPubMedCentral Yau M et al (2017) Clinical, genetic, and structural basis of apparent mineralocorticoid excess due to 11β-hydroxysteroid dehydrogenase type 2 deficiency. Proc Natl Acad Sci U S A 114:E11248–E11256PubMedPubMedCentral
129.
Zurück zum Zitat Ueda K et al (2017) Renal dysfunction induced by kidney-specific gene deletion of Hsd11b2 as a primary cause of salt-dependent hypertension. Hypertens 70:111–118 Ueda K et al (2017) Renal dysfunction induced by kidney-specific gene deletion of Hsd11b2 as a primary cause of salt-dependent hypertension. Hypertens 70:111–118
130.
131.
Zurück zum Zitat Kuriakose K, Nesbitt WJ, Greene M, Harris B (2018) Posaconazole-induced pseudohyperaldosteronism. Antimicrob Agents Chemother 62:e2130–17PubMedPubMedCentral Kuriakose K, Nesbitt WJ, Greene M, Harris B (2018) Posaconazole-induced pseudohyperaldosteronism. Antimicrob Agents Chemother 62:e2130–17PubMedPubMedCentral
132.
Zurück zum Zitat Brandi SL, Feltoft CL, Serup J, Eldrup E (2021) Pseudohyperaldosteroism during itraconazole treatment: a hitherto neglected clinically significant side effect. BMJ Case Rep 14:e243191PubMedPubMedCentral Brandi SL, Feltoft CL, Serup J, Eldrup E (2021) Pseudohyperaldosteroism during itraconazole treatment: a hitherto neglected clinically significant side effect. BMJ Case Rep 14:e243191PubMedPubMedCentral
133.
Zurück zum Zitat Dötsch J, Dörr HG, Stalla GK, Sippell WG (2001) Effect of glucocorticoid excess on the cortisol/cortisone ratio. Steroids 66:817–820PubMed Dötsch J, Dörr HG, Stalla GK, Sippell WG (2001) Effect of glucocorticoid excess on the cortisol/cortisone ratio. Steroids 66:817–820PubMed
134.
Zurück zum Zitat Vitellius G, Lombes M (2020) Genetics in endocrinology: glucocorticoid resistance syndrome. Eur J Endocrinol 182:R15–R27PubMed Vitellius G, Lombes M (2020) Genetics in endocrinology: glucocorticoid resistance syndrome. Eur J Endocrinol 182:R15–R27PubMed
135.
Zurück zum Zitat Claahsen-van der Grinten HL et al (2022) Congenital adrenal hyperplasia-current insights in pathophysiology, diagnostics, and management. Endocr Rev 43:91–159PubMed Claahsen-van der Grinten HL et al (2022) Congenital adrenal hyperplasia-current insights in pathophysiology, diagnostics, and management. Endocr Rev 43:91–159PubMed
136.
Zurück zum Zitat Bulsari K, Falhammar H (2017) Clinical perspectives in congenital adrenal hyperplasia due to 11β-hydroxylase deficiency. Endocrine 55:19–36PubMed Bulsari K, Falhammar H (2017) Clinical perspectives in congenital adrenal hyperplasia due to 11β-hydroxylase deficiency. Endocrine 55:19–36PubMed
138.
Zurück zum Zitat Sun M et al (2021) The broad phenotypic spectrum of 17α-hydroxylase/17,20-lyase (CYP17A1) deficiency: a case series. Eur J Endocrinol 185:729–741PubMedPubMedCentral Sun M et al (2021) The broad phenotypic spectrum of 17α-hydroxylase/17,20-lyase (CYP17A1) deficiency: a case series. Eur J Endocrinol 185:729–741PubMedPubMedCentral
139.
Zurück zum Zitat Zhou Y, Xue X, Shi P, Lu Q, Lv S (2021) Multidisciplinary team management of 46,XY 17α-hydroxylase deficiency: a case report and literature review. J Int Med Res 49:300060521993965PubMed Zhou Y, Xue X, Shi P, Lu Q, Lv S (2021) Multidisciplinary team management of 46,XY 17α-hydroxylase deficiency: a case report and literature review. J Int Med Res 49:300060521993965PubMed
140.
Zurück zum Zitat Schwab KO, Moisan A‑M, Homoki J, Peter M, Simard J (2005) 17alpha-hydroxylase/17,20-Lyase deficiency due to novel compound heterozygote mutations: treatment for tall stature in a female with male pseudohermaphroditism and spontaneous puberty in her affected sister. J Pediatr Endocrinol Metab 18:403–411PubMed Schwab KO, Moisan A‑M, Homoki J, Peter M, Simard J (2005) 17alpha-hydroxylase/17,20-Lyase deficiency due to novel compound heterozygote mutations: treatment for tall stature in a female with male pseudohermaphroditism and spontaneous puberty in her affected sister. J Pediatr Endocrinol Metab 18:403–411PubMed
141.
Zurück zum Zitat Bockenhauer D, Kleta R (2021) Tubulopathy meets Sherlock Holmes: biochemical fingerprinting of disorders of altered kidney tubular salt handling. Pediatr Nephrol 36:2553–2561PubMedPubMedCentral Bockenhauer D, Kleta R (2021) Tubulopathy meets Sherlock Holmes: biochemical fingerprinting of disorders of altered kidney tubular salt handling. Pediatr Nephrol 36:2553–2561PubMedPubMedCentral
142.
Zurück zum Zitat Reichold M et al (2010) KCNJ10 gene mutations causing EAST syndrome (epilepsy, ataxia, sensorineural deafness, and tubulopathy) disrupt channel function. Proc Natl Acad Sci U S A 107:14490–14495PubMedPubMedCentral Reichold M et al (2010) KCNJ10 gene mutations causing EAST syndrome (epilepsy, ataxia, sensorineural deafness, and tubulopathy) disrupt channel function. Proc Natl Acad Sci U S A 107:14490–14495PubMedPubMedCentral
143.
Zurück zum Zitat Scholl UI et al (2009) Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME syndrome) caused by mutations in KCNJ10. Proc Natl Acad Sci U S A 106:5842–5847PubMedPubMedCentral Scholl UI et al (2009) Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME syndrome) caused by mutations in KCNJ10. Proc Natl Acad Sci U S A 106:5842–5847PubMedPubMedCentral
144.
Zurück zum Zitat Schlingmann KP et al (2021) Defects in KCNJ16 cause a novel tubulopathy with hypokalemia, salt wasting, disturbed acid-base homeostasis, and sensorineural deafness. J Am Soc Nephrol 32:1498–1512PubMedPubMedCentral Schlingmann KP et al (2021) Defects in KCNJ16 cause a novel tubulopathy with hypokalemia, salt wasting, disturbed acid-base homeostasis, and sensorineural deafness. J Am Soc Nephrol 32:1498–1512PubMedPubMedCentral
145.
Zurück zum Zitat Wang W‑H, Lin D‑H (2022) Inwardly rectifying K+ channels 4.1 and 5.1 (Kir4.1/Kir5.1) in the renal distal nephron. Am J Physiol Cell Physiol 323:C277–C288PubMedPubMedCentral Wang W‑H, Lin D‑H (2022) Inwardly rectifying K+ channels 4.1 and 5.1 (Kir4.1/Kir5.1) in the renal distal nephron. Am J Physiol Cell Physiol 323:C277–C288PubMedPubMedCentral
146.
Zurück zum Zitat Lo J, Forst A‑L, Warth R, Zdebik AA (2022) EAST/SeSAME syndrome and beyond: the spectrum of Kir4.1- and Kir5.1-associated channelopathies. Front Physiol 13:852674PubMedPubMedCentral Lo J, Forst A‑L, Warth R, Zdebik AA (2022) EAST/SeSAME syndrome and beyond: the spectrum of Kir4.1- and Kir5.1-associated channelopathies. Front Physiol 13:852674PubMedPubMedCentral
147.
Zurück zum Zitat Seys E et al (2017) Clinical and genetic spectrum of Bartter syndrome type 3. J Am Soc Nephrol 28:2540–2552PubMedPubMedCentral Seys E et al (2017) Clinical and genetic spectrum of Bartter syndrome type 3. J Am Soc Nephrol 28:2540–2552PubMedPubMedCentral
148.
Zurück zum Zitat Schlingmann KP, de Baaij JHF (2022) The genetic spectrum of Gitelman(-like) syndromes. Curr Opin Nephrol Hypertens 31:508–515PubMedPubMedCentral Schlingmann KP, de Baaij JHF (2022) The genetic spectrum of Gitelman(-like) syndromes. Curr Opin Nephrol Hypertens 31:508–515PubMedPubMedCentral
149.
Zurück zum Zitat Loffing J et al (2004) Altered renal distal tubule structure and renal Na(+) and Ca(2+) handling in a mouse model for Gitelman’s syndrome. J Am Soc Nephrol Jasn 15:2276–2288PubMed Loffing J et al (2004) Altered renal distal tubule structure and renal Na(+) and Ca(2+) handling in a mouse model for Gitelman’s syndrome. J Am Soc Nephrol Jasn 15:2276–2288PubMed
150.
Zurück zum Zitat Eder M et al (2020) Markers of potassium homeostasis in salt losing tubulopathies-associations with hyperaldosteronism and hypomagnesemia. BMC Nephrol 21:256PubMedPubMedCentral Eder M et al (2020) Markers of potassium homeostasis in salt losing tubulopathies-associations with hyperaldosteronism and hypomagnesemia. BMC Nephrol 21:256PubMedPubMedCentral
151.
Zurück zum Zitat Patel-Chamberlin M et al (2016) The role of epithelial sodium channel ENaC and the apical cl−/HCO3−exchanger pendrin in compensatory salt reabsorption in the setting of na-cl Cotransporter (NCC) inactivation. PLoS ONE 11:e150918PubMedPubMedCentral Patel-Chamberlin M et al (2016) The role of epithelial sodium channel ENaC and the apical cl−/HCO3−exchanger pendrin in compensatory salt reabsorption in the setting of na-cl Cotransporter (NCC) inactivation. PLoS ONE 11:e150918PubMedPubMedCentral
152.
Zurück zum Zitat Soleimani M et al (2012) Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure. Proc Natl Acad Sci U S A 109:13368–13373PubMedPubMedCentral Soleimani M et al (2012) Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure. Proc Natl Acad Sci U S A 109:13368–13373PubMedPubMedCentral
153.
Zurück zum Zitat Seyberth HW (2008) An improved terminology and classification of Bartter-like syndromes. Nat Clin Pract Nephrol 4:560–567PubMed Seyberth HW (2008) An improved terminology and classification of Bartter-like syndromes. Nat Clin Pract Nephrol 4:560–567PubMed
154.
Zurück zum Zitat Dimke H et al (2013) Activation of the Ca(2+)-sensing receptor increases renal claudin-14 expression and urinary Ca(2+) excretion. Am J Physiol Renal Physiol 304:F761–F769PubMed Dimke H et al (2013) Activation of the Ca(2+)-sensing receptor increases renal claudin-14 expression and urinary Ca(2+) excretion. Am J Physiol Renal Physiol 304:F761–F769PubMed
155.
Zurück zum Zitat Vargas-Poussou R et al (2002) Functional characterization of a calcium-sensing receptor mutation in severe autosomal dominant hypocalcemia with a Bartter-like syndrome. J Am Soc Nephrol 13:2259–2266PubMed Vargas-Poussou R et al (2002) Functional characterization of a calcium-sensing receptor mutation in severe autosomal dominant hypocalcemia with a Bartter-like syndrome. J Am Soc Nephrol 13:2259–2266PubMed
156.
Metadaten
Titel
Aldosteron und Niere – eine komplexe Interaktion
verfasst von
Dr. Christoph Schwarz
Prof. PD Dr. Gregor Lindner
Publikationsdatum
15.03.2024
Verlag
Springer Vienna
Erschienen in
Journal für Endokrinologie, Diabetologie und Stoffwechsel / Ausgabe 2/2024
Print ISSN: 3004-8915
Elektronische ISSN: 3004-8923
DOI
https://doi.org/10.1007/s41969-024-00224-8