International Journal of Clinical Medicine, 2011, 2, 206-211
doi:10.4236/ijcm.2011.23034 Published Online July 2011 (http://www.SciRP.org/journal/ijcm)
Coexistence of the Hypersecretion of
Catecholamine, Adrenal Cortical Nodular
Hyperplasia, and Nephrotic-Range Proteinuria of
Focal Segmental Scleronephrosis: Is It
Fat-Induced Hypertension?
Khanh vinh quốc Lương1, Lan Thị Hòang Nguyễn1, Sĩ văn Nguyễn2, Ninh T. Nguyễn3
1Vietnamese American Research Foundation, Westminster, USA; 2Department of Pathology/Garden Grove Medical Center, Garden
Grove, USA; 3Department of Surgery/UCI Medical Center, Orange, USA.
Received January 1st, 2011; revised March 15th, 2011; accepted April 6th, 2011.
ABSTRACT
Two patients had a long history of hypertension and one of them also had a nephrotic-range proteinuria secondary to
focal segmental scleronephrosis which had been diagnosed by kidney biopsy. They presented with uncontrolled hyper-
tension. Laboratory examination suggested hypersecretion of catecholamines by the left adrenal glands in both patients
and primary aldosteronism in one of them. A computed tomography scan revealed small nodules on left adrenal gland
in both patients. Patients underwent laparoscopic left adrenalectomy. After surgery, blood pressure was normalized
and proteinuria was resolved. Most interestingly, prominent adipocytes infiltrated were detected in the adrenal cortex
and were associated with the presence of lymphocytes, which suggested that adipocytes might have a role in the patho-
genesis of these diseases in our patients.
Keywords: Pheochromocytoma, Aldosteronism, Adipocyte, Ne phrotic Syn dro me, Focal Segmental Scleronephrosis,
Adrenal Cortical Hyperplasia
1. Introduction
Obesity is a known risk factor for both cardiovascular
disease and mortality. Adipose tissue is a secretory or-
gan that produces a variety of bio active substances
(adipokines) and is involved in the regulation of various
biological processes. Adipokines may interact with
many organs in the body, such as blood vessels, adrenal
glands, and kidneys. In literature, fatty infiltration has
been noted in adrenal glands. Park et al. [1] reported a
case of Cushing’s syndrome with high basal plasma
catecholamine levels. They found that lymphocytic in-
filtration and fatty metaplasia were prominent histologi-
cal features within the nodules of the cortical adrenal
gland. Boyanton et al. [2] also presented a man with an
adrenal tumor and high catecholamine levels but the
histopathologic examination revealed mature adipocytes
and focal hematopoietic elements with normal com-
pressed adrenal tissue. Finally, Ajmi et al. [3] reported
another patient with an adrenal mass and elevated corti-
sol and androgen levels; however, mixed components of
fat and adrenal tissue were only seen on the pathological
specimen.
In the present cases, we will discuss the possible role
of adipocytes that may involve in the pathogenesis in
our patients with hypersecretion of catecholamines, ad-
renal cortical nodular hyperplasia, and nephrotic-range
proteinuria secondary to focal segmental sclerosis of the
kidneys.
2. Case Presentation
Patient A: A 56-year-old Vietnamese man with a 10-
year history of hypertension was being treated with am-
lodipine 10 mg twice a day and amidarone 200 mg daily.
His weight and height were 159 lbs. and 5 feet, respec-
tively. He complained of more frequently palpitation,

Coexistence of the Hypersecretion of Catecholamine, Adrenal Cortical Nodular Hyperplasia, and 207
Nephrotic-Range Proteinuria of Focal Segmental Scleronephrosis: Is It Fat-Induced Hypertension?
anxiety, fatigue, and his blood pressure (BP) had been
uncontrolled at home. Laboratory examination showed a
serum potassium of 4.3 mmol/L (normal, 3.6 - 5.0), se-
rum sodium of 141 mmol/L (normal, 135 - 145), serum
chloride of 108 mmol/L (normal, 96 - 109), serum total
carbon dioxide of 26.6 mmol/L (normal, 20 - 30), serum
creatinine of 1.5 mg/dl (normal, 0.7 - 1.3), serum blood
urea nitrogen (BUN) of 23 mg/dl (normal, 5 - 26), serum
glucose of 87 mg/dl (normal, 65 - 99), and serum thyroid
stimulating hormone (TSH) of 3.34 uIU/ml (normal, 0.5 -
1.5). Further blood tests revealed plasma renin of 4.9
ng/ml/hr (normal, 1.3 - 4), serum aldosterone of 3.5 ng/dl
(normal, 1 - 15), serum cortisol 11.1 µg (normal, 3.1. -
22.4), 24-hours urine for metanephrine of 213 µg (nor-
mal, 35 - 350), 24-hours urine for vanillylmandelic acid
(VMA) of 6.2 mg (normal, 0 - 6), plasma free nor-
metanephrine of 1.19 nmol/L (normal, <0.9), plasma
norepinephrine of 580 pg/ml (normal, <399), plasma
epinephrine of 206 pg/ml (normal, <99), serum chromo-
granin A of 51/ml (normal, 0 - 50). A computed tomo-
graphy (CT) scan of the adrenal gland showed a nodule
0.9 cm at the left adrenal limb.
He then underwent laparoscopic left adrenalectomy.
The specimen consisted of two pieces of adrenal gland
measuring 6 × 4.5 × 0.7 cm in aggregate. The adrenal is
covered with multilobular adipose tissue. Pathological
examination reported a cortical nodular hyperplasia of
the adrenal gland (Figure 1(a)). Most interestingly, there
were abundant adipocytes in the adrenal cortex in asso-
ciation with the presence of lymphocytic infiltration
(Figures 2(a) and 3(a)).
After surgery, his BP has been stable (110/70), and
subsequent levels of serum catecholamine and urinary
VMA decreased to normal values.
Patient B: A 56-year-old Vietnamese man with a
20-year history of hypertension was being treated with
valsartan 320 mg, amlodipine 10 mg, and benazepril 20
mg daily. His weight and height were 161 lbs. and 5 feet
¼ inches, respectively. He complained of cramping in his
extremities and his BP had been uncontrolled at home.
Laboratory examination showed a serum potassium of
3.1 mmol/L (normal, 3.6 - 5.0), serum sodium of 139
mmol/L (normal, 135 - 145), serum chloride of 99
mmol/L (normal, 96 - 109), serum total carbon dioxide of
25 mmol/L (normal, 20 - 30), serum creatinine of 1.5
mg/dl (normal, 0.7 - 1.3), serum blood urea nitrogen
(BUN) of 25 mg/dl (normal, 5 - 26), serum glucose of
103 mg/dl (normal, 65 - 99), serum thyroxine (T4) of 6.8
µg/dl (normal, 4.5 - 12), serum thyronine uptake of 34%
(normal, 24 - 39), and serum thyroid stimulating hor-
mone (TSH) of 1.6 uIU/ml (normal, 0.5 - 1.5). Further
blood tests revealed plasma renin of <0.1 ng/ml/hr
(a)
(b)
Figure 1. Photomicrograph (10×) showing nodular hyper-
plasia of the adrenal cortex. The nodule in the left field is
composed of mostly large clear cells.
(a)
(b)
Figure 2. Photomicrograph (10×) showing infiltrates of nu-
merous adipocytes () and adjacent lymphocytes () in
the adrenal cortex.

Coexistence of the Hypersecretion of Catecholamine, Adrenal Cortical Nodular Hyperplasia, and
Nephrotic-Range Proteinuria of Focal Segmental Scleronephrosis: Is It Fat-Induced Hypertension?
208
(a) (b)
Figure 3. Photomicrograph (40×) showing infiltrates of adipocytes () and adjacent lymphocytes () in the adrenal cortex.
(normal, 1.3 - 4), serum aldosterone of 17.1 ng/dl (nor-
mal, 1 - 15), serum cortisol 11.8 µg (normal, 3.1 - 22.4),
24-hours urine for metanephrine of 503 µg (normal, 35 -
350), 24-hours urine for vanillylmandelic acid (VMA) of
17 mg (normal, 0 - 6), plasma free normetanephrine of
0.96 nmol/L (normal, <0.9), plasma free metanephrine of
0.35 nmol/L (normal, <0.5), serum chromogranin A of
109/ml (normal, 0 - 50). A computed tomography (CT)
scan of the adrenal gland showed the left adrenal limb at
1.8 × 0.9 cm compared to the right adrenal limb at 1.7 ×
0.2 cm. An adrenal vein sample found plasma free
metanephrine of 24.9 nmol/L in the left adrenal vein and
<0.2 nmol/L in the right adrenal vein. Also, plasma free
normetanephrine was 4.95 nmol/L in the left adrenal vein
and 0.44 nmol/L in the right adrenal vein.
He also has had a history of more than 30 years of pro-
teinuria, ranging from 2000 - 4000 mg/day with mild
chronic renal failure and serum creatinine of 1.4 to 1.7
mg/dl. He had a kidney biopsy, suggestive of focal seg-
mental sclerosis (FSS) of the kidney. Before surgery, his
24-hours urine collection for protein and serum crea-
tinine was 2851.6 mg and 1.9 mg/dl, respectively.
He was started on spironolactone 25 mg twice a day
orally with good blood pressure controlled (120/70). His
serum potassium was 5.2 mmol/dl. Also, valsartan, am-
lodipine, and benazepril were discontinued.
He then underwent laparoscopic left adrenalectomy.
The specimen consisted of fibroadipose tissue measuring
11.5 × 3 × 3 cm with the left adrenal gland measuring 7 ×
1 × 1 cm. The entire specimen weighed 42 g. Pathologi-
cal examination reported a section in a longitudinal ori-
entation but none in transverse section. Unfortunately,
the specimen did not show the medullary portion of the
adrenal gland. However, pheochromocytoma could not
be entirely excluded based on the available sections. Still,
changes in the adrenal cortex were suggestive of nodular
hyperplasia (Figure 1(b)). Most interestingly, there were
abundant adipocytes in the adrenal cortex in association
with the presence of lymphocytic infiltration (Figures
2(b) and 3(b)).
After surgery, spironolactone was discontinued and his
BP has been stable (110/70). The laboratory examination
revealed serum creatinine of 1.53 mg/dl, serum glucose
of 80 mg/dl, serum BUN of 17 mg/dl, serum sodium of
136 mmol/L, serum chloride of 100 mmol/L, serum total
carbon dioxide of 22 mmol/L, and urine protein of 320
mg/24hrs. Subsequent levels of serum catecholamine,
renin, aldosterone, and urinary VMA decreased to nor-
mal values.
3. Discussion
Pheochromocytoma, a catecholamine-secreting tumor,
arises from chromaffin cells of the adrenal medulla that
is rare. The simultaneous occurrence of adrenomedullary
and adrenocortical tumors is extremely rare. There are
only five reported cases in the literature [4]. We have
suggested that a local interaction between the adrenocor-
tical and medullary areas may involved.
To our knowledge, coexistence of the the hypersecre-
tion of the catecholamine, adrenal cortical nodular hy-
perplasia, and nephrotic-range proteinuria secondary to
focal segmental scleronephrosis (FSS) has not been re-
ported in the literature. Most interestingly, a prominent
adipocyte infiltrate in the adrenal cortex was seen in as-
sociation with the presence of lymphocytes, which sug-
gested that adipocyte might have a role in the pathogene-
sis of these concomitant diseases in our patients.
Obesity has been associated with increased macro-
phage infiltration of adipose tissue, and these macro-
phages may be an important component of the chronic
inflammatory response involved in the development of
obesity-associated disease. In obese patients, Weisberg et

Coexistence of the Hypersecretion of Catecholamine, Adrenal Cortical Nodular Hyperplasia, and 209
Nephrotic-Range Proteinuria of Focal Segmental Scleronephrosis: Is It Fat-Induced Hypertension?
al. [5] showed that adipose tissue contains an increased
number of macrophages. Drastic weight loss resulted in
both a significant decrease in macrophage number and
changes in chemoattractant gene expression in adipose
tissue [6]. The mechanism of macrophage recruitment to
adipose tissue presumably involves increased secretion
of chemotactic molecules by adipocytes, such as the C-C
motif chemokine ligand 2 (CCL2 or monocyte chemoat-
tractant protein-1) [7-8].
A link between adipose tissue and the cortical adrenal
gland, particularly via the mineralocorticoid aldosterone,
has already been demonstrated. Gene expression in the
renin-angiotensin-aldosterone system (RAAS) was in-
creased in the adipose tissue from obese animal models
and human subjects [9,10]. There are reports of high lev-
els of circulating angiotensinogen (AGT), rennin and
aldosterone; and high levels of activity of angiotensin-
converting enzyme (ACE) in obese patients [11,12].
Weight loss is also associated with a decrease in serum
aldosterone, plasma renin activity, angiotensinogen and
ACE levels [13,14]. Ehrhart-Bornstein et al. [15] incu-
bated fat cells in a conditioned medium from primary
mammary gland adipocyte cultures―with NCI-H295R
adrenocortical cells for 24 hours. They found that adipo-
cyte secretory products directly stimulate aldosterone
secretion 7-fold in human adrenocortical cells (NCI-
H295R). This effect is independent of adipose angio-
tensin II. Possible molecular mechanisms involved in this
aldosterone secretion include acidity by either an oxi-
dized derivative of linoleic acid [16] or by a potent min-
eralocorticoid-releasing factor [15] contained in a me-
dium conditioned by human adipocytes. Furthermore,
Schinner et al. [17] suggested that the Wnt-signaling
pathway is one of the mechanisms mediating the effects
of fat cells on adrenal steroidogenic acute regulatory
(StAR) transcription as well as cortisol and aldosterone
secretion.
The interaction of the sympatho-adrenomedullary sys-
tem with adipose tissue has been reported in the literature.
Resting plasma norepinephrine was found to be a posi-
tive predictor of changes in body mass index [18]. Leptin
is an adipostatic hormone synthesized and secreted by fat
tissues [19]. Plasma leptin concentrations are elevated in
obese subjects [20]. Glasow et al. [21] investigated a
functional leptin receptor in human adrenal tissue and,
they showed a differential action of leptin on human
adrenocortical and chromaffin cell hormone production.
Leptin directly stimulates catecholamine secretion and
synthesis in cultured porcine adrenal medullary chromaf-
fin cells [22].
The association between obesity and nephrotic-range
proteinuria was first reported in 1974 [23]. Since then,
FSS has been linked to massive obesity [24,25]. Obe-
sity-related FSS is distinctive from idiopathic FSS as it is
associated with lower incidence of nephrotic syndrome
and has a more indolent course [26]. However, drastic
weight reduction is associated with a resolution of this
nephrotic syndrome [27]. Plasma adrenomedullin (AM)
has been isolated from human pheochromocytomas and
adipose tissue [28,29]. High levels of plasma AM have
been reported in obese subjects [30]. Plasma AM de-
creased significantly after weight loss from gastric by-
pass surgery [31]. That plasma AM directly related to the
level of proteinuria [32] and changes in AM levels may
be the result of heavy proteinuria [33].
In summary, our patients presented with hypersecre-
tion of catecholamine, cortical nodular hyperplasia of the
adrenal gland. After surgery, their blood pressures were
normalized. Nephrotic-range proteinuria was resolved in
one patient. Most interestingly, prominent adipocytes
infiltrated were seen in the adrenal cortex in association
with the presence of lymphocytes, which suggested that
adipocytes might have a role in the pathogenesis of these
diseases in our patient. However, a coincidence of these
diseases cannot be excluded.
REFERENCES
[1] Y. K. Park, Y. W. Kim, J. W. Kim, Y. K. Choi, Y. T. Ko,
S. W. Ko and M. H. Yang, “Bilateral Primary Pigmented
Nodular Adrenocortical Disease—A Case Report De-
scribing a Rare Cause of Cushing’s Syndrome,” Journal
of Korean Medical Sciences, Vol. 9, No. 6, 1994, pp.
450-457.
[2] Jr. B. L. Boyanton, O. Hampel and M. L. Ostrowski, “A
55-Year-Old Man with a Rib Fracture,” Archives of Pa-
thology and Laboratory Medicine, Vol. 130, No. 1, 2006,
pp. e13-e14.
[3] T. S. Ajmi, C. M. Chaieb, M. Mokni, R. Braham, K. Ach,
A. Maaroufi and L. Chaieb, “Corticomedullary Mixed
Tumor of the Adrenal Gland,” Annales d’Endocrinologie
(Paris), Vol. 70, No. 6, 2009, pp. 473-476.
doi:10.1016/j.ando.2009.09.003
[4] K. V. Q. Luong and L. T. H. Nguyen, “Coexistence of
Primary Aldosteronism and Pheochromocytoma in a
Vietnamese Patient,” The Endocrinologist, Vol. 6, No. 6,
1996, pp. 490-493.
doi:10.1097/00019616-199611000-00011
[5] S. P. Weisberg, D. McCann, M. Desai, M. Rosebaum, R.
L. Leibel and A. W. Ferrante Jr., “Obesity Is Associated
with Macrophage Accumulation in Adipose Tissue,” The
Journal of Clinical Investigation, Vol. 112, No. 12, 2003,
pp. 1796-1808. doi:10.1172/JCI19246
[6] R. Cancello, C. Henegar, N. Viguerie, S. Taleb, C. Poitu,
C. Rouault, M. Coupaye, V. Pelloux, D. Hugol, J. C.
Bouillot, A. Bouloumié, G. Barbatelli, S. Cinti, P. A.
Svensson, G. S. Barsh, J. D. Zucker, A. Basdevant, D.

Coexistence of the Hypersecretion of Catecholamine, Adrenal Cortical Nodular Hyperplasia, and
210
Nephrotic-Range Proteinuria of Focal Segmental Scleronephrosis: Is It Fat-Induced Hypertension?
Langin and K. Clément, “Reduction of Macrophage Infil-
tration and Chemoattractant Gene Expression Changes in
White Adipose Tissue of Morbidly Obese Subjects after
Surgery-Induced Weight Loss,” Diabetes, Vol. 54, No. 8,
2005, pp. 2277-2286. doi:10.2337/diabetes.54.8.2277
[7] P. Sartipy and D. J. Loskutoff, “Monocyte Chemoattrac-
tant Protein 1 in Obesity and Insulin Resistance,” Pro-
ceedings of the National Academy of Sciences of the
United States of America, Vol. 100, No. 12, 2003, pp.
7265-7270. doi:10.1073/pnas.1133870100
[8] J. M. Bruun, A. S. Lihn, S. B. Pedersen and B. Richelsen,
“Monocyte Chemoattractant Protein-1 Release is Higher
in Visceral than Subcutaneous Human Adipose Tissue
(AT): Implication of Macrophages Resident in the AT,”
The Journal of Clinical Endocrinology and Metabolism,
Vol. 90, No. 4, 2005, pp. 2282-2289.
doi:10.1210/jc.2004-1696
[9] F. Massiéra, M. Bloch-Faure, D. Ceiler, K. Murakami, A.
Fukamizu, J. M. Gasc, A. Quignard-Boulangé, R. Negrel,
G Ailhaud, J. Seydoux, P. Meneton and M. Teboul, “Adi-
pose Angiotensinogen Is Involved in Adipose Tissue
Growth and Blood Regulation,” The FASEB Journal, Vol.
15, No. 14, 2001, pp. 2727-2729.
[10] G. Giacchetti, E. Faloi, B. Mariniello, C. Sardu, C. Gatti,
M. A. Camilloni, M. Guerrieri and F. Mantero, “Overex-
pression of the Renin-Angiotensin System in Human Vis-
ceral Adipose Tissue in Normal and Overweight Sub-
jects,” American Journal of Hypertension, Vol. 15, No. 5,
2002, pp. 381-388. doi:10.1016/S0895-7061(02)02257-4
[11] R. Cooper, N. McFarlane-Andersen, F. I. Bennett, R.
Wilks, A. Puras, D. Tewksburry, R. Ward and T. Forres-
ter, “ACE, Angiotensinogen and Obesity: A Potential
Pathway Leading to Hypertension,” Journal of Human
Hypertension, Vol. 11, No. 2, 1997, pp. 107-111.
doi:10.1038/sj.jhh.1000391
[12] T. L. Goodfriend, B. M. Egan and D. E. Kelley, “Aldos-
terone in Obesity,” Endocrine Research, Vol. 24, No. 3-4,
1998, pp. 789-796. doi:10.3109/07435809809032689
[13] M. L. Tuck, J. Sowers, L. Dornfeld, G. Kledzik and M.
Maxwell, “The Effect of Weight Reduction on Blood
Pressure, Plasma Renin Activity, and Plasma Aldosterone
Levels in Obese Patients,” The New England Journal of
Medicine, Vol. 304, No. 16, 1981, pp. 930-933.
doi:10.1056/NEJM198104163041602
[14] S. Engeli, J. Böhnke, K. Gorzelniak, J. Janke, P. Schling,
M. Bader, F. C. Luft and A. M. Sharma, “Weight Loss
and the Renin-Angiotensin-Aldosterone System,” Hype r-
tension, Vol. 45, No. 3, 2005, pp. 356-362.
doi:10.1161/01.HYP.0000154361.47683.d3
[15] M. Ehrhart-Bornstein, V. Lamounier-Zepter, A. Schraven,
J. Langenbach, H. S. Willenberg, A. Barthel, H. Hauner,
S. M. McCann, W. A. Scherbaum and S. R. Bornstein,
“Human Adipocytes Secrete Mineralocorticoid-Releasing
Factors,” Proceedings of the National Academy of Sci-
ences of the United States of America, Vol. 100, No. 24,
2003, pp. 14211-14216. doi:10.1073/pnas.2336140100
[16] T. L. Goodfriend, D. L. Ball, B. M. Egan, W. B. Camp-
bell and K. Nithipatikom, “Epoxy-Keto Derivative of Li-
noleic Acid Stimulates Aldosterone Secretion,” Hyper-
tension, Vol. 43, No. 2, 2004, pp. 358-363.
doi:10.1161/01.HYP.0000113294.06704.64
[17] S. Schinner, H. S. Willenberg, D. Krause, M. Schott, V.
Lamounier-Zepter, A. W. Krug, M. Ehrhart-Bornstein, M.
Bornstein, S. R. Bornstein and W. A. Scherbaum, “Adi-
pocyte-Derived Products Include the Transcription of the
StAR Promoter and Stimulate Aldosterone and Cortisol
secretion from Adrenocortical Cells through the Wnt-Sig-
naling Pathway,” International Journal of Obesity, Vol.
31, No. 5, 2007, pp. 864-870.
[18] K. Masuo, H. Kawaguchi, H. Mikami, T. Orihara and M.
L. Tuck, “Serum Uric Acid and Plasma Norepinephrine
Concentrations Predict Subsequent Weight Gain and Blood
Pressure Elevation,” Hypertension, Vol. 42, No. 4, 2003,
pp. 474-480. doi:10.1161/01.HYP.0000091371.53502.D3
[19] R. S. Ahima and J. S. Flier, “Leptin,” Annual Reviews of
Physiology, Vol. 62, 2000, pp. 413-437.
doi:10.1146/annurev.physiol.62.1.413
[20] N. Eikelis, G. Lambert, G. Wiesner, D. Kaye, M. Schlaich,
M. Morris, J. Hastings, F. Socratous and M. Esler, “Ex-
tra-Adipocyte Leptin Release in Human Obvesity and Its
Relation to Symphoadrenal Function,” American Journal
of Physiology, Endocrinology and Metabolism, Vol. 286,
No. 5, 2004, pp. E744-E752.
doi:10.1152/ajpendo.00489.2003
[21] A. Glasow, A. Haidan, U. Hilbers, M. Breidert, J. Gilles-
pie, W. A. Scherbaum, G. P. Chrousos, and S. R. Born-
stein, “Expression of Ob Receptor in Normal Human Ad-
renals: Differential Regulation of Adrenocortical and
Adrenomedullary Function by Leptin,” The Journal of
Clinical Endocrinology and Metabolism, Vol. 83, No. 12,
1998, pp. 4459-4466. doi:10.1210/jc.83.12.4459
[22] K. Takekoshi, M. Motooka, K. Isobe, F. Normura, T.
Manmoku, K. Ishii and T. Nakai, “Leptin Directly Stimu-
lates Catecholamin Secretion and Synthesis in Cultured
Porcine Adrenal Medullary Chromaffin Cells,” Bioche-
mical and Biophysical Research Communications, Vol.
261, No. 2, 1999, pp. 426-431.
doi:10.1006/bbrc.1999.1025
[23] J. R. Weisinger, R. L. Kempson, L. Eldridge and R. S.
Swenson, “The Nephrotic Syndrome: A Complication of
Massive Obesity,” Annuals of Internal Medicine, Vol. 81,
No. 4, 1974, pp. 440-447.
[24] R. A. Warnke and R. Kempson, “The Nephrotic Syn-
drome in Massive Obesity, A Study by Light, Immuno-
fluorescence and Electron Microscopy,” Archives Patho-
logy and Laboratory Medicine, Vol. 102, No. 8, 1978, pp.
431-438.
[25] J. C. Jennette, L. Charles and W. Grubb, “Glomerulo-
megaly and Focal Segmental Glomerulosclerosis Associ-
ated with Obesity and Sleep Apnea Syndrome,” American
Journal of Kidney Diseases, Vol. 10, No. 6, 1987, pp.
470-472.
[26] N. Kambham, G. S. Markowitz, A. M. Valeri, J. Lin and V.
D. D’Agati, “Obesity-Related Glomerulopathy: An Emer-

Coexistence of the Hypersecretion of Catecholamine, Adrenal Cortical Nodular Hyperplasia, and
Nephrotic-Range Proteinuria of Focal Segmental Scleronephrosis: Is It Fat-Induced Hypertension?
211
ging Epidemic,” Kidney International, Vol. 59, No. 4,
2001, pp. 1498-1509.
doi:10.1046/j.1523-1755.2001.0590041498.x
[27] Y. Huan, J. E. Tomaszewski and D. L. Cohen, “Resolu-
tion of Nephritic Syndrome after Successful Bariatric
Surgery in Patients with Biopsy-Proven FSGS,” Clinical
Nephrology, Vol. 71, No. 1, 2009, pp. 69-73.
[28] K. Kitamura, K. Kangawa, M. Kawamoto, Y. Ichiki, S.
Nakamura, H. Matsuo and T. Eto, “Adrenomedullin: A
Novel Hypotensive Peptide Isolated from Human Pheo-
chromocytoma,” Biochemical and Biophysical Research
Communications, Vol. 192, No. 2, 1993, pp. 553-560.
doi:10.1006/bbrc.1993.1451
[29] Y. Li, C. C. Jiang, X. Wang, Y. Zhang, S. Shibahara and
K. Takahashi, “Adrenomedullin is a Novel Adipokine: A-
drenomedullin in Adipocytes and Adipose Tissues,” Pep-
tides, Vol. 28, No. 5, 2007, pp. 1129-1143.
doi:10.1016/j.peptides.2007.03.005
[30] I. Nomura, J. Kato, M. Tokashiki and K. Kitamura, “In-
creased Plasma Levels of the Mature and Intermediate
Forms of Adrenomedullin in Obesity,” Regular Peptides,
Vol. 158, No. 1-3, 2009, pp. 127-131.
doi:10.1016/j.regpep.2009.08.003
[31] G. Vila, M. Riedl, C. Maier, J. Struck, N. G. Morgen-
thaler, A. Handisurya, G. Prager, B. Ludvik, M. Clodi and
A. Luger, “Plasma MR-proADM Correlates to BMI and
Decreases in Relation to Leptin after Gastric Bypass Sur-
gery,” Obesity, Vol. 17, No. 6, 2009, pp. 1184-1188.
[32] A. Kubo, H. Kurioka, N. Minamino, H. Sato, T. Nishino,
M. Iwano, H. Shiiki, H. Matsuo and K. Dohi, “Plasma
and Urinary Adrenomedullin in Chronic Glomerulone-
phritis Patients with Proteinuria,” Nephron, Vol. 80, No.
2, 1998, pp. 227-230. doi:10.1007/s004670000440
[33] A. Balat, M. Cekmen, M. Yürekli, H. Gülcan, O. Kutlu,
Y. Türköz and S. Yologlu, “Adrenomedullin and Nitrite
Levels in Children with Minimal Change Nephrotic Syn-
drome,” Pediatric Nephrology, Vol. 15, No. 1-2, 2000, pp.
70-73. doi:10.1159/000045172