. 2016 Dec 14;102(4):1182–1192. doi: 10.1210/jc.2016-2986

Table 1.

Summary of Clinicopathological Characteristics of 25 Cases

No.	Age	Sex	Laterality	Post B2 Histological Dx		PAC (ng/dL)	PRA	ARR	Captopril Challenge ARR^a	Lateralization Index in AVS Before Cosyntropin Loading	Lateralization Index in AVS After Cosyntropin Loading	Serum K	Preoperation Status			Postoperation Status			Spironolactone Body		Paradoxical Hyperplasia
No.	Age	Sex	Laterality	Left	Right	PAC (ng/dL)	PRA	ARR	Captopril Challenge ARR^a	Lateralization Index in AVS Before Cosyntropin Loading	Lateralization Index in AVS After Cosyntropin Loading	Serum K	SBP	DBP	No. of Antihypertensive Drugs	SBP	DBP	No. of Antihypertensive Drugs	Nodule	ZG	Paradoxical Hyperplasia
1	25	M	Bilateral	DH	DH	11.4	0.8	14.3	2.1	2.77	1.21	4.4	122	62	7	117	71	1	-	-
2	27	F	Bilateral	DH	DH	44.6	2.7	16.5	5.1	1.5	1.92	4.3	112	68	1	120	82	0	-	-
3	32	F	Bilateral	DH	DH	13.9	0.6	23.2	1.8	2.19	1.06	3.4	113	67	3	115	87	0	-	-
4	43	F	Bilateral	DH	DH	38.2	1.8	21.2	4.3	1.51	1.35	4	120	82	5	111	73	1	+	+
5	44	M	Bilateral	DH	DH	14.8	0.4	37	18.2	7.38	1.23	4.7	119	74	4	120	69	0	+	+
6	44	F	Bilateral	DH	DH	19.9	2.3	8.7	5.2	1.33	1.03	3.4	119	64	3	118	82	1	-	-
7	44	F	Bilateral	DH	DH	19.7	0.4	49.3	10.7	1.71	1.49	4.7	111	76	2	127	82	0	-	-
8	42	M	Unilateral	Not resected	DH	17.4	0.7	24.9	9.1	1.41	2.71	4.8	120	70	8	117	84	0	-	-
9	49	M	Unilateral	Not resected	DH	47	0.1	470	171	9.73	18.7	3.1	118	88	4	110	74	0	-	+
10	51	M	Bilateral	Not resected	DH	15.6	0.7	22.3	6	2.22	1.67	3.5	122	84	3	103	70	0	+	-
11	61	M	Bilateral	Not resected	DH	13	0.5	26	46.5	6.49	2.47	4.3	119	69	2	118	74	0	+	-
12	47	F	Bilateral	DH	Not resected	16.9	0.6	28.2	46.3	3.77^a	1.52^a	3.5	99	66	3	98	81	0	-	-
13	32	M	Bilateral	MN	MN	7.2	0.3	24	5.2	2.18	1.22	4.1	121	86	5	119	78	1	-	-	Weak/weak
14	36	F	Bilateral	MN	MN	17.4	0.5	34.8	25.7	1.54	2.03	4.8	120	86	2	129	88	1	-	-	^+/+
15	37	F	Bilateral	MN	MN	11.3	0.4	28.3	39.5	1.26	1.33	4.4	115	59	4	119	76	1	+	-	^+/+
16	40	M	Bilateral	MN	MN	13.8	0.1	138	35.7	1.63	1.51	3.9	126	81	6	126	86	1	+	-	^−/−
17	47	F	Bilateral	MN	MN	11	0.2	55	48.5	2.47	1.61	3.5	126	88	4	100	73	1	-	-	^+/+
18	30	M	Bilateral	Not resected	MN	14.4	1.6	9	4.6	4.87	1.43	3.7	143	88	6	139	84	3	+	-	Weak
19	43	F	Unilateral	Not resected	MN	15.5	0.8	19.4	(1.3/47.7) 36.7^b	3.04	7.95	3.3	125	97	1	123	98	0	-	-	+
20	49	F	Bilateral	Not resected	MN	18.4	0.7	26.3	N/A	2.67	1.71	3.3	136	84	1	133	89	0	-	-	Weak
21	61	F	Unilateral	Not resected	MN	10.3	0.4	25.8	(0.9/52.8) 58.6^b	5.27	46.8	4.2	164	103	1	146	83	0	-	-	+
22	61	F	Unilateral	Not resected	MN	36.2	0.3	120.7	(0.3/36.2) 120.7^b	3.41	10.5	3.9	158	98	1	156	90	0	-	-	+
23	69	M	Bilateral	Not resected	MN	9.9	0.4	24.8	12.3	2.53	1.63	3.9	123	84	4	144	87	2	+	-	+
24	69	F	Unilateral	Not resected	MN	23.5	0.2	117.5	28.7	11.1	4.91	4.5	124	66	2	116	63	0	-	-	+
25	36	M	Unilateral	MN	Not resected	20.2	0.4	50.5	15.2	3.19	4.6	4	116	70	5	133	95	0	-	-	+

Twenty-five consecutive cases with available resected adrenals from 2005 to 2015 that met the following criteria were retrospectively selected from 2 institutions: clinical hypertension associated with aldosterone hypersecretion, improvement of hypertensive status according to blood pressure, and the number of antihypertensive drugs before and after surgery. Twenty-one cases were from Tohoku University Hospital (from 2005 to 2015), and 4 cases from Asahikawa Red Cross Hospital (from 2014 to 2015). Biological PA confirmation was determined by the captopril loading test (Tohoku University), and the flosemide loading test followed by walking (Asahikawa Red Cross Hospital). All cases were negative according to cross-sectional imaging. No cases had microAPAs (as assessed by histology and CYP11B2 IHC). All patients underwent unilateral or bilateral adrenal resection for persistent hypertension resistant to multiple antihypertensive medications, cardiovascular complications, juvenile hypertension, or some adrenal gland surface irregularities according to cross-sectional imaging. Lateralization of all cases was clinically categorized by AVS, using the cutoff value of 2.6 of lateralization index after adrenocorticotropic hormone loading (17). Twenty-five cases were classified as ZG hyperplasia, similar to that seen adjacent to APAs. As in APA cases, ZGs are morphologically hyperplastic but negative for CYP11B2, suggesting the inability to produce aldosterone. In addition, ZG paradoxical hyperplasia was generally less pronounced in MN than APA. Adjacent ZGs in some MN cases demonstrated even atrophic changes. Spironolactone bodies were detected both in nodular and nonnodular cortical cells in DH, but only in cortical cells of micronodules in MN, and these cells harboring spironolactone bodies were positive for CYP11B2.

Abbreviations: ARR, aldosterone renin ratio; DBP, diatolic blood pressure; Dx, diagnosis; F, female; M, male; N/A, not available; PAC, plasma aldosterone concentration; PRA, plasma renin activity; SBP, systolic blood pressure.

^{^a}

Canulation failure.

^{^b}

PRA/PAC (ARR) value 2 hours after flosemide loading followed by walk.