Secondary hyperaldosteronism differential diagnosis: Difference between revisions

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Latest revision as of 20:36, 14 September 2017

Secondary hyperaldosteronism should be differentiated from other diseases causing hypertension and hypokalemia.^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]^[9]^[10]^[11]^[12]^[13]^[14]^[15]

	Cause	Laboratory
	Cause	Renin activity	Aldosterone levels	urinary free cortisone
Renin-producing tumors		↑	↑	↓
Apparent mineralocorticoid excess		↓	↓	↓↓
Licorice ingestion		↓	↓	Moderate ↑
Ectopic ACTH production		↓	↑	Markedly ↑↑
Primary hyperaldosteronism		↓	↑	↓
Familial hyperaldosteronism		↓	↑	↓
Cushing syndrome		↓	↑	Markedly ↑↑
Renal artery stenosis		↑	↑	↓
Liddle's syndrome		↓	↓	↓
Diuretic use		Nl		↓
17 alpha hydroxylase deficiency		↓	↓	↓
11 beta hydroxylase deficiency		↓	↓	↓
Coarctation of aorta				↓

Pseudohyperaldosteronism causes:

Pseudohyperaldosteronism causes	Disease	Cause		Labratory
Pseudohyperaldosteronism causes	Disease	Cause		Elevated mineralocorticoid	Renin	Aldosterone	Treatment
Endogenous causes	Deﬁciency of 17a-hydroxylase			Deoxycorticosterone (DOC)	↓	↓
	11b-hydroxylase			Deoxycorticosterone (DOC)	↓	↓
	Apparent mineralocorticoid excess syndrome (AME)	Genetic or acquired defect of 11-HSD			↓	↓	dexamethasone and/or MR-blockers
	Liddle’s syndrome	Mutation of the epithelial sodium channels (ENaC) gene in the distal renal tubules			↓	↓	amiloride or triamterene can reverse the clinical picture reactivating the renin aldosterone
	Cushing’s syndrome	The main pathogenetic mechanism is linked to the excess of cortisol which saturates 11-HSD2 activity, allowing cortisol to bind MR. A similar picture is also related to over secretion of cortisol by adrenocortical carcinomas. In some cases the disease is associated with secondary hyperaldosteronism due to a direct activation of the renin angiotensin system by glucocorticoids.
	Insensitivity to glucocorticoids (Chrousos syndrome)	mutations in glucocorticoid receptor (GR) gene		Deoxycorticosterone (DOC)	↓	↓	dexamethasone
	Aldosterone-secreting adrenocortical carcinoma
	Geller’s syndrome	mutation of MR that alters its speciﬁcity and allows progesterone to bind MR	severe hypertension particularly during pregnancy		↓	↓
	Gordon’s syndrome or pseudohypoaldosteronism type 2	due to different mutations correlated to different phenotypes. Mutations of at least four genes have been identiﬁed, including WNK1 and WNK4	hypertension, characterized by hyperkalemia, normal renal function		↓	↓	thiazide diuretics and/or dietary sodium restriction
Exogenous causes	Corticosteroids with mineralocorticoid activity
	Hypersodic diets
	Water intossications
	Licorice
	grapefruit
	Contraceptives
	Some progestins
Particular causes of hypertension	Sclerosis of juxtaglomerular apparatus (diabetic microangiopathy and/or of the elderly)
	FANS
	B-Adrenergic agonists
	Aging
	Low-renin essential hypertension
	Autonomic dysfunction
	Partial/total nephrectomy or removal of renal tissue

S

Hypertension and Hypokalemia

Plasma renin activity

Normal or High (Plasma Renin/Aldosterone ratio <10

Suppressed (Plasma Renin/Aldosterone ratio >20

*Renin-secreting tumors
*Diuretic use
*Renovascular hypertension
*Coarctation of aorta
*Malignant phase hypertension

Urinary aldosterone

Elevated

Normal

Low

Conn's syndrome (Primary aldosteronism)

Profound K+ depletion

• 17 alpha hydroxylase deficiency
• 11 beta hydroxylase deficiency
• Liddle's syndrome
• Licorice ingestion
• Deoxycortisone producing tumor

Add Mineralocrticoid antagonist for 8 weeks

BP response

No BP response

• Deoxycorticosterone excess( Tumor, 17 alpha hydroxylase and 11 beta hydroxylase deficiency)
• Licorice ingestion
•Glucocorticoid resistance

Liddle's syndrome)

References

↑ Wada N, Jin S, Hui SP, Yanagisawa K, Kurosawa T, Chiba H (2014). "[Differential diagnosis of primary aldosteronism by measurement of hybrid steroids using mass spectrometry]". Rinsho Byori (in Japanese). 62 (3): 276–82. PMID 24800505.
↑ Nielsen ML, Pareek M, Andersen I (2012). "[Liquorice-induced hypertension and hypokalaemia]". Ugeskr. Laeg. (in Danish). 174 (15): 1024–5. PMID 22487411.
↑ Chow KM, Ma RC, Szeto CC, Li PK (2012). "Polycystic kidney disease presenting with hypertension and hypokalemia". Am. J. Kidney Dis. 59 (2): 270–2. doi:10.1053/j.ajkd.2011.08.020. PMID 21962616.
↑ Sarafidis PA, Georgianos PI, Germanidis G, Giavroglou C, Nikolaidis P, Lasaridis AN, Madias NE (2012). "Hypertension and symptomatic hypokalemia in a patient with simultaneous unilateral stenoses of intrarenal arteries and mesangioproliferative glomerulonephritis". Am. J. Kidney Dis. 59 (3): 434–8. doi:10.1053/j.ajkd.2011.11.001. PMID 22154539.
↑ Khosla N, Hogan D (2006). "Mineralocorticoid hypertension and hypokalemia". Semin. Nephrol. 26 (6): 434–40. doi:10.1016/j.semnephrol.2006.10.004. PMID 17275580.
↑ Weiner ID (2013). "Endocrine and hypertensive disorders of potassium regulation: primary aldosteronism". Semin. Nephrol. 33 (3): 265–76. doi:10.1016/j.semnephrol.2013.04.007. PMC 3748390. PMID 23953804.
↑ Martell-Claros N, Abad-Cardiel M, Alvarez-Alvarez B, García-Donaire JA, Pérez CF (2015). "Primary aldosteronism and its various clinical scenarios". J. Hypertens. 33 (6): 1226–32. doi:10.1097/HJH.0000000000000546. PMID 25715092.
↑ Franse LV, Pahor M, Di Bari M, Somes GW, Cushman WC, Applegate WB (2000). "Hypokalemia associated with diuretic use and cardiovascular events in the Systolic Hypertension in the Elderly Program". Hypertension. 35 (5): 1025–30. PMID 10818057.
↑ Rossi E, Farnetti E, Nicoli D, Sazzini M, Perazzoli F, Regolisti G, Grasselli C, Santi R, Negro A, Mazzeo V, Mantero F, Luiselli D, Casali B (2011). "A clinical phenotype mimicking essential hypertension in a newly discovered family with Liddle's syndrome". Am. J. Hypertens. 24 (8): 930–5. doi:10.1038/ajh.2011.76. PMID 21525970.
↑ Ruecker B, Lang-Muritano M, Spanaus K, Welzel M, l'Allemand D, Phan-Hug F, Katschnig C, Konrad D, Holterhus PM, Schoenle EJ (2015). "The Aldosterone/Renin Ratio as a Diagnostic Tool for the Diagnosis of Primary Hypoaldosteronism in Newborns and Infants". Horm Res Paediatr. 84 (1): 43–8. doi:10.1159/000381852. PMID 25968592.
↑ Ardhanari S, Kannuswamy R, Chaudhary K, Lockette W, Whaley-Connell A (2015). "Mineralocorticoid and apparent mineralocorticoid syndromes of secondary hypertension". Adv Chronic Kidney Dis. 22 (3): 185–95. doi:10.1053/j.ackd.2015.03.002. PMID 25908467.
↑ Iglesias P, Tajada P, Martínez I, Díez JJ (2009). "[Salt-wasting congenital adrenal hyperplasia associated to hyperreninemic hyperaldosteronism]". Med Clin (Barc) (in Spanish; Castilian). 132 (2): 80–1. doi:10.1016/j.medcli.2008.09.002. PMID 19174076.
↑ Kikuta Y, Sanjo K, Nakajima K, Ashizawa I, Ojima M (1988). "Primary aldosteronism in childhood due to primary adrenal hyperplasia". Tohoku J. Exp. Med. 155 (1): 57–70. PMID 3413779.
↑ Hassan-Smith Z, Stewart PM (2011). "Inherited forms of mineralocorticoid hypertension". Curr Opin Endocrinol Diabetes Obes. 18 (3): 177–85. doi:10.1097/MED.0b013e3283469444. PMID 21494136.
↑ Bartter FC, Henkin RI, Bryan GT (1968). "Aldosterone hypersecretion in "non-salt-losing" congenital adrenal hyperplasia". J. Clin. Invest. 47 (8): 1742–52. doi:10.1172/JCI105864. PMC 297334. PMID 4299011.

[pmid24800505-1] Wada N, Jin S, Hui SP, Yanagisawa K, Kurosawa T, Chiba H (2014). "[Differential diagnosis of primary aldosteronism by measurement of hybrid steroids using mass spectrometry]". Rinsho Byori (in Japanese). 62 (3): 276–82. PMID 24800505.

[pmid22487411-2] Nielsen ML, Pareek M, Andersen I (2012). "[Liquorice-induced hypertension and hypokalaemia]". Ugeskr. Laeg. (in Danish). 174 (15): 1024–5. PMID 22487411.

[pmid21962616-3] Chow KM, Ma RC, Szeto CC, Li PK (2012). "Polycystic kidney disease presenting with hypertension and hypokalemia". Am. J. Kidney Dis. 59 (2): 270–2. doi:10.1053/j.ajkd.2011.08.020. PMID 21962616.

[pmid22154539-4] Sarafidis PA, Georgianos PI, Germanidis G, Giavroglou C, Nikolaidis P, Lasaridis AN, Madias NE (2012). "Hypertension and symptomatic hypokalemia in a patient with simultaneous unilateral stenoses of intrarenal arteries and mesangioproliferative glomerulonephritis". Am. J. Kidney Dis. 59 (3): 434–8. doi:10.1053/j.ajkd.2011.11.001. PMID 22154539.

[pmid17275580-5] Khosla N, Hogan D (2006). "Mineralocorticoid hypertension and hypokalemia". Semin. Nephrol. 26 (6): 434–40. doi:10.1016/j.semnephrol.2006.10.004. PMID 17275580.

[pmid23953804-6] Weiner ID (2013). "Endocrine and hypertensive disorders of potassium regulation: primary aldosteronism". Semin. Nephrol. 33 (3): 265–76. doi:10.1016/j.semnephrol.2013.04.007. PMC 3748390. PMID 23953804.

[pmid25715092-7] Martell-Claros N, Abad-Cardiel M, Alvarez-Alvarez B, García-Donaire JA, Pérez CF (2015). "Primary aldosteronism and its various clinical scenarios". J. Hypertens. 33 (6): 1226–32. doi:10.1097/HJH.0000000000000546. PMID 25715092.

[pmid10818057-8] Franse LV, Pahor M, Di Bari M, Somes GW, Cushman WC, Applegate WB (2000). "Hypokalemia associated with diuretic use and cardiovascular events in the Systolic Hypertension in the Elderly Program". Hypertension. 35 (5): 1025–30. PMID 10818057.

[pmid21525970-9] Rossi E, Farnetti E, Nicoli D, Sazzini M, Perazzoli F, Regolisti G, Grasselli C, Santi R, Negro A, Mazzeo V, Mantero F, Luiselli D, Casali B (2011). "A clinical phenotype mimicking essential hypertension in a newly discovered family with Liddle's syndrome". Am. J. Hypertens. 24 (8): 930–5. doi:10.1038/ajh.2011.76. PMID 21525970.

[pmid25968592-10] Ruecker B, Lang-Muritano M, Spanaus K, Welzel M, l'Allemand D, Phan-Hug F, Katschnig C, Konrad D, Holterhus PM, Schoenle EJ (2015). "The Aldosterone/Renin Ratio as a Diagnostic Tool for the Diagnosis of Primary Hypoaldosteronism in Newborns and Infants". Horm Res Paediatr. 84 (1): 43–8. doi:10.1159/000381852. PMID 25968592.

[pmid25908467-11] Ardhanari S, Kannuswamy R, Chaudhary K, Lockette W, Whaley-Connell A (2015). "Mineralocorticoid and apparent mineralocorticoid syndromes of secondary hypertension". Adv Chronic Kidney Dis. 22 (3): 185–95. doi:10.1053/j.ackd.2015.03.002. PMID 25908467.

[pmid19174076-12] Iglesias P, Tajada P, Martínez I, Díez JJ (2009). "[Salt-wasting congenital adrenal hyperplasia associated to hyperreninemic hyperaldosteronism]". Med Clin (Barc) (in Spanish; Castilian). 132 (2): 80–1. doi:10.1016/j.medcli.2008.09.002. PMID 19174076.

[pmid3413779-13] Kikuta Y, Sanjo K, Nakajima K, Ashizawa I, Ojima M (1988). "Primary aldosteronism in childhood due to primary adrenal hyperplasia". Tohoku J. Exp. Med. 155 (1): 57–70. PMID 3413779.

[pmid21494136-14] Hassan-Smith Z, Stewart PM (2011). "Inherited forms of mineralocorticoid hypertension". Curr Opin Endocrinol Diabetes Obes. 18 (3): 177–85. doi:10.1097/MED.0b013e3283469444. PMID 21494136.

[pmid4299011-15] Bartter FC, Henkin RI, Bryan GT (1968). "Aldosterone hypersecretion in "non-salt-losing" congenital adrenal hyperplasia". J. Clin. Invest. 47 (8): 1742–52. doi:10.1172/JCI105864. PMC 297334. PMID 4299011.

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@@ Line 1: / Line 1: @@
 __NOTOC__
 {{Secondary hyperaldosteronism }}
+Secondary hyperaldosteronism should be differentiated from other diseases causing '''[[hypertension]]''' and '''[[hypokalemia]]'''.<ref name="pmid24800505">{{cite journal |vauthors=Wada N, Jin S, Hui SP, Yanagisawa K, Kurosawa T, Chiba H |title=[Differential diagnosis of primary aldosteronism by measurement of hybrid steroids using mass spectrometry] |language=Japanese |journal=Rinsho Byori |volume=62 |issue=3 |pages=276–82 |year=2014 |pmid=24800505 |doi= |url=}}</ref><ref name="pmid22487411">{{cite journal |vauthors=Nielsen ML, Pareek M, Andersen I |title=[Liquorice-induced hypertension and hypokalaemia] |language=Danish |journal=Ugeskr. Laeg. |volume=174 |issue=15 |pages=1024–5 |year=2012 |pmid=22487411 |doi= |url=}}</ref><ref name="pmid21962616">{{cite journal |vauthors=Chow KM, Ma RC, Szeto CC, Li PK |title=Polycystic kidney disease presenting with hypertension and hypokalemia |journal=Am. J. Kidney Dis. |volume=59 |issue=2 |pages=270–2 |year=2012 |pmid=21962616 |doi=10.1053/j.ajkd.2011.08.020 |url=}}</ref><ref name="pmid22154539">{{cite journal |vauthors=Sarafidis PA, Georgianos PI, Germanidis G, Giavroglou C, Nikolaidis P, Lasaridis AN, Madias NE |title=Hypertension and symptomatic hypokalemia in a patient with simultaneous unilateral stenoses of intrarenal arteries and mesangioproliferative glomerulonephritis |journal=Am. J. Kidney Dis. |volume=59 |issue=3 |pages=434–8 |year=2012 |pmid=22154539 |doi=10.1053/j.ajkd.2011.11.001 |url=}}</ref><ref name="pmid17275580">{{cite journal |vauthors=Khosla N, Hogan D |title=Mineralocorticoid hypertension and hypokalemia |journal=Semin. Nephrol. |volume=26 |issue=6 |pages=434–40 |year=2006 |pmid=17275580 |doi=10.1016/j.semnephrol.2006.10.004 |url=}}</ref><ref name="pmid23953804">{{cite journal |vauthors=Weiner ID |title=Endocrine and hypertensive disorders of potassium regulation: primary aldosteronism |journal=Semin. Nephrol. |volume=33 |issue=3 |pages=265–76 |year=2013 |pmid=23953804 |pmc=3748390 |doi=10.1016/j.semnephrol.2013.04.007 |url=}}</ref><ref name="pmid25715092">{{cite journal |vauthors=Martell-Claros N, Abad-Cardiel M, Alvarez-Alvarez B, García-Donaire JA, Pérez CF |title=Primary aldosteronism and its various clinical scenarios |journal=J. Hypertens. |volume=33 |issue=6 |pages=1226–32 |year=2015 |pmid=25715092 |doi=10.1097/HJH.0000000000000546 |url=}}</ref><ref name="pmid10818057">{{cite journal |vauthors=Franse LV, Pahor M, Di Bari M, Somes GW, Cushman WC, Applegate WB |title=Hypokalemia associated with diuretic use and cardiovascular events in the Systolic Hypertension in the Elderly Program |journal=Hypertension |volume=35 |issue=5 |pages=1025–30 |year=2000 |pmid=10818057 |doi= |url=}}</ref><ref name="pmid21525970">{{cite journal |vauthors=Rossi E, Farnetti E, Nicoli D, Sazzini M, Perazzoli F, Regolisti G, Grasselli C, Santi R, Negro A, Mazzeo V, Mantero F, Luiselli D, Casali B |title=A clinical phenotype mimicking essential hypertension in a newly discovered family with Liddle's syndrome |journal=Am. J. Hypertens. |volume=24 |issue=8 |pages=930–5 |year=2011 |pmid=21525970 |doi=10.1038/ajh.2011.76 |url=}}</ref><ref name="pmid25968592">{{cite journal |vauthors=Ruecker B, Lang-Muritano M, Spanaus K, Welzel M, l'Allemand D, Phan-Hug F, Katschnig C, Konrad D, Holterhus PM, Schoenle EJ |title=The Aldosterone/Renin Ratio as a Diagnostic Tool for the Diagnosis of Primary Hypoaldosteronism in Newborns and Infants |journal=Horm Res Paediatr |volume=84 |issue=1 |pages=43–8 |year=2015 |pmid=25968592 |doi=10.1159/000381852 |url=}}</ref><ref name="pmid25908467">{{cite journal |vauthors=Ardhanari S, Kannuswamy R, Chaudhary K, Lockette W, Whaley-Connell A |title=Mineralocorticoid and apparent mineralocorticoid syndromes of secondary hypertension |journal=Adv Chronic Kidney Dis |volume=22 |issue=3 |pages=185–95 |year=2015 |pmid=25908467 |doi=10.1053/j.ackd.2015.03.002 |url=}}</ref><ref name="pmid19174076">{{cite journal |vauthors=Iglesias P, Tajada P, Martínez I, Díez JJ |title=[Salt-wasting congenital adrenal hyperplasia associated to hyperreninemic hyperaldosteronism] |language=Spanish; Castilian |journal=Med Clin (Barc) |volume=132 |issue=2 |pages=80–1 |year=2009 |pmid=19174076 |doi=10.1016/j.medcli.2008.09.002 |url=}}</ref><ref name="pmid3413779">{{cite journal |vauthors=Kikuta Y, Sanjo K, Nakajima K, Ashizawa I, Ojima M |title=Primary aldosteronism in childhood due to primary adrenal hyperplasia |journal=Tohoku J. Exp. Med. |volume=155 |issue=1 |pages=57–70 |year=1988 |pmid=3413779 |doi= |url=}}</ref><ref name="pmid21494136">{{cite journal |vauthors=Hassan-Smith Z, Stewart PM |title=Inherited forms of mineralocorticoid hypertension |journal=Curr Opin Endocrinol Diabetes Obes |volume=18 |issue=3 |pages=177–85 |year=2011 |pmid=21494136 |doi=10.1097/MED.0b013e3283469444 |url=}}</ref><ref name="pmid4299011">{{cite journal |vauthors=Bartter FC, Henkin RI, Bryan GT |title=Aldosterone hypersecretion in "non-salt-losing" congenital adrenal hyperplasia |journal=J. Clin. Invest. |volume=47 |issue=8 |pages=1742–52 |year=1968 |pmid=4299011 |pmc=297334 |doi=10.1172/JCI105864 |url=}}</ref>
 {| class="wikitable"
+! rowspan="2" |
+! rowspan="2" |Cause
+! colspan="4" |Laboratory
+|-
+!Renin activity
+!Aldosterone levels
+!urinary free cortisone
 !
-!Cause
+|-
+|[[Renin-producing tumors]]
+|
+|↑
+|↑
+|↓
+|
+|-
+|[[Apparent mineralocorticoid excess]]
+|
+|↓
+|↓
+|↓↓
+|
+|-
+|[[Licorice]] ingestion
+|
+|↓
+|↓
+|Moderate ↑
+|
+|-
+|Ectopic ACTH production
+|
+|↓
+|↑
+|Markedly ↑↑
+|
+|-
+|Primary hyperaldosteronism
+|
+|↓
+|↑
+|↓
+|
+|-
+|Familial hyperaldosteronism
+|
+|↓
+|↑
+|↓
+|
+|-
+|Cushing syndrome
+|
+|↓
+|↑
+|Markedly ↑↑
+|
+|-
+|Renal artery stenosis
+|
+|↑
+|↑
+|↓
+|
+|-
+|[[Liddle's syndrome]]
+|
+|↓
+|↓
+|↓
+|
+|-
+|[[Diuretic]] use
+|
+|Nl
+|
+|↓
+|
+|-
+|[[17 alpha-hydroxylase deficiency|17 alpha hydroxylase deficiency]]
+|
+|↓
+|↓
+|↓
+|
+|-
+|[[11β-hydroxylase deficiency|11 beta hydroxylase deficiency]]
+|
+|↓
+|↓
+|↓
+|
+|-
+|Coarctation of aorta
+|
+|
+|
+|↓
+|
+|}
+Pseudohyperaldosteronism causes:
+{| class="wikitable"
+! rowspan="2" |Pseudohyperaldosteronism causes
+! rowspan="2" |Disease
+! rowspan="2" |Cause
 !
+! colspan="3" |Labratory
 !
 |-
-|Renin secreting tumors
+!
+!Elevated mineralocorticoid
+!Renin
+!Aldosterone
+!Treatment
+|-
+| rowspan="9" |Endogenous causes
+|Deﬁciency of 17a-hydroxylase
+|
+|
+| rowspan="2" |Deoxycorticosterone (DOC)
+| rowspan="2" |↓
+| rowspan="2" |↓
+| rowspan="2" |
+|-
+|11b-hydroxylase
+|
+|
+|-
+|Apparent mineralocorticoid excess syndrome (AME)
+|Genetic or acquired defect of 11-HSD
+|
+|
+|↓
+|↓
+|dexamethasone and/or MR-blockers
+|-
+|Liddle’s syndrome
+|Mutation of the epithelial sodium channels (ENaC) gene in the distal renal tubules
+|
+|
+|↓
+|↓
+|amiloride or triamterene can reverse the clinical picture reactivating the renin aldosterone
+|-
+|Cushing’s syndrome
+|The main pathogenetic mechanism is linked to the excess
+of cortisol which saturates 11-HSD2 activity, allowing cortisol to bind MR. A similar picture is also related to over secretion of cortisol by adrenocortical carcinomas. In some cases the disease is associated with secondary hyperaldosteronism due to a direct activation of the renin angiotensin system by glucocorticoids.
+|
+|
 |
 |
 |
 |-
-|Apparent mineralocorticoid excess
+|Insensitivity to glucocorticoids (Chrousos syndrome)
+|mutations in glucocorticoid receptor (GR) gene
+|
+|Deoxycorticosterone (DOC)
+|↓
+|↓
+|dexamethasone
+|-
+|Aldosterone-secreting adrenocortical carcinoma
+|
+|
+|
 |
 |
 |
 |-
-|Licorice ingestion
+|Geller’s syndrome
+|mutation of MR that alters its speciﬁcity and allows progesterone to bind MR
+|severe hypertension particularly during pregnancy
 |
+|↓
+|↓
 |
+|-
+|Gordon’s syndrome or pseudohypoaldosteronism type 2
+|due to different mutations correlated to different phenotypes. Mutations of at least four genes have been identiﬁed, including WNK1 and WNK4
+|hypertension, characterized by hyperkalemia, normal renal function
 |
+|↓
+|↓
+|thiazide diuretics and/or dietary sodium restriction
 |-
-|Ectopic ACTH production
+| rowspan="7" |Exogenous causes
+|Corticosteroids with mineralocorticoid activity
+|
+|
+|
+|
+|
+|
+|-
+|Hypersodic diets
+|
+|
+|
+|
+|
+|
+|-
+|Water intossications
+|
+|
+|
+|
+|
+|
+|-
+|Licorice
+|
+|
+|
+|
+|
+|
+|-
+|grapefruit
+|
+|
+|
+|
+|
+|
+|-
+|Contraceptives
+|
+|
+|
+|
+|
+|
+|-
+|Some progestins
+|
+|
+|
+|
+|
+|
+|-
+| rowspan="7" |Particular causes of hypertension
+|Sclerosis of juxtaglomerular apparatus (diabetic microangiopathy and/or of the elderly)
+|
+|
+|
+|
+|
+|
+|-
+|FANS
+|
+|
+|
+|
+|
+|
+|-
+|B-Adrenergic agonists
+|
+|
+|
 |
 |
 |
 |-
-|Primary hyperaldosteronism
+|Aging
+|
+|
+|
 |
 |
 |
 |-
-|Familial hypoaldosteronism
+|Low-renin essential hypertension
+|
+|
+|
 |
 |
 |
 |-
-|Cushing syndrome
+|Autonomic dysfunction
+|
+|
+|
 |
 |
 |
 |-
-|Renal artery stenosis
+|Partial/total nephrectomy or removal of renal tissue
+|
+|
+|
 |
 |
 |
 |}
+S{{familytree/start}}{{familytree | | | | | | | | | A01 | | | | | |A01=Hypertension and Hypokalemia}}
+{{familytree | | | | | | | | | |!| | | | | | | | }}
+{{familytree | | | | | | | | | B01 | | | | | |B01=Plasma renin activity}}
+{{familytree | | |,|-|-|-|-|-|-|^|-|-|-|-|-|-|.| }}
+{{familytree | | C01 | | | | | | | | | | | |C02|C01=Normal or High (Plasma Renin/Aldosterone ratio <10|C02=Suppressed (Plasma Renin/Aldosterone ratio >20}}
+{{familytree | | |!| | | | | | | | | | | | | |!| }}
+{{familytree | | D01 | | | | | | | | | | | |D02|D01=*Renin-secreting tumors<br>*Diuretic use<br>*Renovascular hypertension<br>*Coarctation of aorta<br>*Malignant phase hypertension|D02=Urinary aldosterone}}
+{{familytree | | | | | | | | | | | | |,|-|-|-|+|-|-|-|-|.|}}
+{{familytree | | | | | | | | | | | | E01 | | E02 | | | E03 |E01=Elevated|E02=Normal|E03=Low|}}
+{{familytree | | | | | | | | | | | | |!| | | |!| | | | |!| | }}
+{{familytree | | | | | | | | | | | | F01 | | F02 | | | F03 |F01=Conn's syndrome (Primary aldosteronism)|F02=Profound K+ depletion|F03=• 17 alpha hydroxylase deficiency<br>• 11 beta hydroxylase deficiency<br>• Liddle's syndrome<br>• Licorice ingestion<br>• Deoxycortisone producing tumor|}}
+{{familytree | | | | | | | | | | | | | | | | | | | | | |!| | | | }}
+{{familytree | | | | | | | | | | | | | | | | | | | | |G01|G01=Add Mineralocrticoid antagonist for 8 weeks}}
+{{familytree | | | | | | |,|-|-|-|-|-|-|-|-|-|-|-|-|-|-|^|-|-|-|-|-|-|-|-|-|-|-|-|-|-|.}}
+{{familytree | | | | | |H01| | | | | | | | | | | | | | | | | | | | | | | | | | | |H02|H01=BP response|H02=No BP response}}
+{{familytree | | | | | | |!| | | | | | | | | | | | | | | | | | | | | | | | | | | | | |!| }}
+{{familytree | | | | | |I01| | | | | | | | | | | | | | | | | | | | | | | | | | | |I02|I01=• Deoxycorticosterone excess( Tumor, 17 alpha hydroxylase and 11 beta hydroxylase deficiency)<br>• Licorice ingestion<br>•Glucocorticoid resistance|I02=Liddle's syndrome)|}}
+{{familytree/end}}
+==References==
+{{Reflist|2}}

Secondary hyperaldosteronism differential diagnosis: Difference between revisions

Latest revision as of 20:36, 14 September 2017

References

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