Renal infarction due to polyarteritis nodosa in a patient with angioimmunoblastic T-cell lymphoma: a case report and a brief review of the literature
Angioimmunoblastic T-cell lymphoma (AITL) is one of the most common subtypes of peripheral T-cell lymphoma (15-20% of all cases), accounting for approximately 1-2% of all non-Hodgkin lymphomas. It often presents autoimmune phenomena including hemolytic anemia, thrombocytopenia, glomerulonephrities and circulating immune complexes (CIC). Polyarteritis nodosa (PAN) is an autoimmune disease characterized by necrotizing vasculitis of medium vessels, which rarely develops in association with hematological malignant disorders. Herein we report the case of a male patient with AITL who had a renal infarction secondary to PAN, mimicking a neoplastic lesion. A 40-year-old man underwent lymph node biopsy in the suspicious of sarcoidosis. On the basis of histological and immunohistochemical findings, a diagnosis of AITL was performed. The patient was successfully treated with a cytarabine-based regimen for 6 cycles. Three months after the initial diagnosis of AITL, a whole body CT-scan showed a lesion in the lower pole of the left kidney. A renal cell carcinoma was suspected, thus a nephrectomy was carried out. The histological findings were compatible with polyarteritis nodosa. To the best of our knowledge, the association between PAN and AITL has been described only once. This relation may be secondary to the induction of an autoimmune phenomenon by the lymphoma with the formation of circulating immune complexes, leading to vessel walls injury. A careful evaluation is needed in the management of AITL patients with signs of renal failure in order to avoid delay of treatment and organ damage. Key words: renal infarction, polyarteritis nodosa, T-cell lymphoma.
CA S E R E P O R T Open Access
Renal infarction due to polyarteritis nodosa in a
patient with angioimmunoblastic T-cell
lymphoma: a case report and a brief review of
Maria Raffaella Ambrosio
, Bruno Jim Rocca
, Alessandro Ginori
, Monica Onorati
, Alberto Fabbri
, Stefano Lazzi
and Sergio Tripodi
Angioimmunoblastic T-cell lymphoma is one of the most common subtypes of peripheral T-cell lymphoma (15-20%
of all cases), accounting for approximately 1-2% of all non-Hodgkin lymphomas. It often presents autoimmune
phenomena including hemol ytic anemia, thrombocytopenia, glomerulonephrities and circulating immune
complexes. Polyarteritis nodosa is an autoimmune disease characterized by necrotizing vasculitis of medium vessels,
which rarely develops in association with hematological malignant disorders. Herein we report the case of a 40-
year-old man who underwent lymph node biopsy in the suspicious of sarcoidosis. On the basis of histological and
immunohistochemical findings, the diagnosis of angioimmunoblastic T-cell lymphoma was performed. The patient
was successfully treated with cytarabine-based regimen for 6 cycles. Three months after the initial diagnosis of
angioimmunoblastic T-cell lymphoma, a whole body computed tomography showed a lesion in the lower pole of
the left kidney. Renal cell carcinoma was suspected, thus a nephrectomy was carried out. The histological findings
were compatible with polyarteritis nodosa. To the best of our knowledge, the association between polyarteritis
nodosa and angioimmunoblastic T-cell lymphoma has been described only once. This relation may be secondary
to the induction of an autoimmune phenomenon by the lymphoma with the formation of circulating immune
complexes, leading to vessels walls injury. A careful evaluation is needed in the management of
angioimmunoblastic T-cell lymphoma patients with signs of renal failure in order to avoid delay of treatment and
organ dam age.
Keywords: Renal infarction, Polyarteritis nodosa, T-cell lymphoma
The World Health Or ganization (WHO) classification of
tumors of hematopoietic and lymphoid tissues defines
the Angioimmunoblastic T-cell lymphoma (AITL) as
one of the more common specific subtypes of peripheral
T-cell neoplasms, accounting for approximately 15-20%
of all cases, or 1-2% of all non-Hodgkin lymphomas .
It occurs in middle age and elderly, with an equal
incidence in males and fe males and has an aggressive
clinical behavior, often with fever, skin rash, general-
ized lymphadenopathy, hepatosplenomegaly and auto-
immune phenomena including hemolytic anemia,
thrombocytopenia, glomerulonephrities and circulating
immune complexes (CIC ). Histologically, it is charac-
terized by polymorphous infiltrate invol ving lymph
nodes, and prominent proliferation of high endot helial
venules and follicular dendritic cells. During the clin-
ical course of a lymphoma , many lesions (not only
direct invasion by neoplastic cells ) may affect the
kidney as broad phenomenon disorders . This
finding is more commo n in Hodgkin’s disea se rather
than non-Hodgkin’s lymphoma. During the clinical
* Correspondence: firstname.lastname@example.org
Department of Human Pathology and Oncology, Pathological Anatomy
Section, University of Siena, via delle Scotte, Siena, 6 - 53100, Italy
Full list of author information is available at the end of the article
© 2012 Ambrosio et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Ambrosio et al. Diagnostic Pathology 2012, 7:50
course of AITL, proliferative glomerulonephritis ,
minimal-change disease [4,5], A-type amyloidosis ,
acute renal failure , immunoglobulin (Ig)M-λ glomeru-
lar thrombi, and membranoproliferative glomeruloneph-
ritis-like lesions , myeloma-like kidney , direct
invasion by lymphoma cells , interstitial nephritis
[10,11], vasculitis [12,13], nephrocalcinosis , Fanconi
syndrome  and nephrotic syndrome due to membran-
ous nephropathy (MN)  may be rarely observed.To
the best of o ur knowledge, there is only one previous
case of AITL a ssociated with polyarteritis nodosa
(PAN) . Herein, we report a very unusual compli-
cation in AITL, a renal necrotic lesion due to vascu-
litis with the appearance of PAN, clinically misdiagnosed
as renal carcinoma, highlighting the possible pathogenic
A 40 year-old-male patient presented to his general
practitioner with a 3-weeks history of myalgia, arthralgia,
fever (37.5°C) and cough which persisted despite a
broad-spectrum antibiotic therapy. For this, he under-
went a chest X-ray examination which showed bilateral
lung nodules and enlarged mediastinal lymph nodes,
with a clinical picture consistent with sarcoidosis. The
patient was admitted to the Pneumologic Unit of Siena
University Hospital. On admission, physical examination
showed generalized lymphadenopathy, splenomegaly and
skin rash. The laboratory data are summarized in Table 1.
The blood count, liver and renal function, as well as
angiotensin converting enzyme (ACE), were within the
reference range. Eosinophilia and hypergammaglobuline-
mia were not found whereas C-reactive protein, lactate
dehydrogenase, β2-microglobulin and serum immuno-
globulins were increased. Since the clinical picture was
doubtful, the patient underwent biopsy of the axillary
lymph node, the maximum diameter of which was 3 cm.
On the basis of clinical presentation and histological
findings, the diagnosis of angioimmunoblastic T-cell
lymphoma stage IVB was made according to the criteria
of WHO classification . The patient received a com-
bination chemotherapy with pegylated liposomal doxo-
rubicin (30 mg/m
, day 1), cytarabine (2 g/m
and dexamethasone (40 mg day 1–4) every 21 days.
After two cycles, the patient presented a marked im-
provement of the systemic symptoms and no superficial
lymphadenopathies were observed. After 3 months a re-
stage whole body computed tomography (CT)-scan was
performed which showed the disappearance of all previ-
ous pathologic findings, but evidenced a lesion of
45 mm in the lower pole of the left kidney (Figure 1).
Such finding was later confirmed by an ultrasound scan,
that showed, at the color Doppler exam, a vascular
pattern consistent with renal cell carcinoma. The patient
was readmitted to the Hospital in order to perform a
nephrectomy. The final diagnosis was renal infarction
due to PAN, according to Carlson . The patient had
negative rheumatoid factor, HLA-B27, streptolysin O,
anti-nuclear, anti-cardiolipin, anti-DNA, anti-smith,
anti-RNP, anti-SSA, anti-SSB, anti-neutrophil cytoplas-
mic and anti-lupus anticoagulant antibodies. Serologies
and PCR for both HBV and HCV were negative. The
histological diagnosis of PAN was also confirmed by clin-
icians according to American College of Rheumatology
(ACR) criteria . After six days, the patient was dis-
charged from hospital without complications. He com-
pleted the chemotherapy induction program (4 cycles)
and underwent consolidation with high-dose chemother-
apy and autologous stem cells transplantation. He is well
five years after surgery.
Serial sections of both axillary lymph node and left kid-
ney were performed, routinely processed, stained with
haematoxylin and eosin and examin ed by light micros-
copy. Histologically, the lymph node architecture was
Table 1 Summary of laboratory data
Our values Normal range
Hb 12,2 g/dl 14-18 g/dl
RBC 5,3 × 10
4,5-6 × 10
WBC 6,6 × 10
4-8 × 10
Hematocrit 45% 40-52%
MCV 90 μm
MCHC 34 g/dl 32-36 g/dl
Platelet count 225 × 10
150-350 × 10
AST 10 UI/l 0-35 UI/l
ALT 10 UI/l 0-35 UI/l
LDH 552 U/l 120-240 U/l
Total protein 8,6 g/dl 6,5-8,0 g/dl
Albumin 42,3 g/l 35,2-50,4 g/l
-microglobulin 5.2 mg/dL 0,1-0,2 mg/dL
Blood urea nitrogen 32 mg/dl 10-50 mg/dl
Creatinine 0,9 mg/dl 0-1,3 mg/dl
Blood glucose 96 mg/dl 70-110 mg/dl
C-reactive protein 35 mg/l 0-5 mg/l
ACE 15 U/l < 40 U/l
IgA 1150 mg/dl 90-450 mg/dl
IgG 2245 mg/dl 80-1800 mg/dl
IgM 135 mg/dl 60-250 mg/dl
Hb Haemoglobin, RBC red blood cells count, WBC white blood cells count, MCV
mean corpuscular volume, MCHC mean cell haemoglobin concentration, AST
serum aspartate aminotransferase, ALT alanine aminotransferase, LDH lactate
dehydrogenase, ACE angiotensin converting enzyme.
Ambrosio et al. Diagnostic Pathology 2012, 7:50 Page 2 of 7
partially effaced by polymorphic cellular infiltration,
burnt-out follicles (Figure 2A) and proliferation of nu-
merous arborizing high-endothelial venules (Figure 2B).
An expansion of paracortex was observed, which was
diffusely infiltrated by a polymorphous population of
small to medium-sized lymphocytes, with distinct cell
membranes, clear to pale cytoplasm, and mild irregular
nuclei (Figure 2C). The neoplastic population was
admixed with small reactive lymphocytes, eosinophils,
plasma cells, histiocytes and numerous follicular den-
dritic cells. Few large immunoblast-like lymphoid cells
with large distinct nuclei and clear cytoplasm were
Figure 1 TC scan findings. A lesion of 45 mm in the upper pole of the left kidney is shown.
Figure 2 Axillary lymph node morphology. Effacement of lymph node architecture with burnt-out follicles (A) and marked vascular
proliferation (B) was observed. The neoplastic cells show clear-to-pale cytoplasm, distinct cell membrane and minimal atypia (C); they mainly
express CD4 (D). EBV-positive B cells are present (inset, D). [A-C: Haematoxylin–Eosin (H&E); Original Magnification (O.M.): 40x; D: CD4 stain, O.M.:
40x; D, inset: EBER in situ hybridization, O.M.: 40x.
Ambrosio et al. Diagnostic Pathology 2012, 7:50 Page 3 of 7
observed intermingled with lymphocytes. In addition,
scattered Reed-Sternberg (RS)-like cells with irregular
multilobated nuclei and large eosino philic nucleoli were
present in the node. Immunohistochemically, the ne o-
plastic T-cells were positive for CD45Ro, CD3, CD10,
LANA-1 and LMP and expressed mostly the CD4 anti-
gen (Figure 2D), although numerous reactive CD8 posi-
tive T-cells were present. CD20, CD79a, PAX-5, CD56,
MUM-1 and CD30 were negative. The large immuno-
blast-like cells and the scattered RS-like cells showed
immunoreactivity to CD20, CD79a and CD30. The pro-
liferation of follicular dendritic cells highlighted by
CD21 and CD23 was prominent throughout the node,
and entrapped high-endothelial venules. By means of in
situ hybridization RNAs (EBERs), EBER-positive signals
were observed in scattered large B immunoblasts and
RS-like cells (Figure 2D, inset). Molecular stud ies
showed monoclonal rearrangement of T-cell receptor
genes and polyclonal rearrangement of immunoglobulin
heavy chain (IgH) receptor. Macroscopic examination of
the left kidney specimen showed a large pale area at the
lower pole, approximately 4 cm in maximum diameter
with a triangular morphology, centered on the renal cor-
tex and consistent with an infarcted area (Figure 3A).
Coagulative necrosis of renal parenchyma (Figure 3B)
and multiple segmentary inflammatory lesions of small
and middle renal arteries were observed on histological
examination. Masson and Giemsa stains showed rupture
of internal elastic lamina with aneurysmal collapse of the
arterial wall (Figure 3C). Some vascular lumina were
obliterated by fibrous stroma and sometimes recanalized
by thin vascular channels (Figure 3D). There was no in-
filtration by neoplastic T-cells.
AITL is a disease of the middle-aged and elde rly people
but it rarely occurs in the fourth decade, as it has hap-
pened in our patient [20,21]. No standard of care has
been established and the prognosis is poor, with a me-
dian survival of less than three years . Responder
patients seem to benefit from high dose chemotherapy
and autologous stem cell transplantation. AITL was pre-
viously considered an atypical reactive process, named
angioimmunoblastic lymphadenopathy ; currently,
overwhelming evidence deriving from molecular and
cytogenetic studies suggests that AITL rises de novo as a
peripheral T-cell lymphoma . The nearly constant as-
sociation with EBV has suggested a possible role for the
virus in the etiology, possibly through an antigen-driven
process. However, the neoplastic T cells are EBV nega-
tive. They express most pan T-cell antigens such as
CD3, CD2 and CD5 and, in vast majority of the cases,
CD4, although numerous reactive CD8 positive T-cells
are often present. In 60-100% of the cases, the tumour
Figure 3 Renal infarction. Gross morphology shows a large pale lesion of the lower pole (A). Histological examination shows coagulative
necrosis of renal parenchyma (B), aneurysmal distension of the arterial wall (C) and rupture of the internal elastic lamina (C, inset, arrow). Some
vascular lumina are obliterated by fibrous stroma and recanalized by thin vascular channels (D). (B-D: Masson stain; O.M.: 40x; 20x; 40x).
Ambrosio et al. Diagnostic Pathology 2012, 7:50 Page 4 of 7
cells expres s CD10, CXCL13 and PD-1. In our case, not
only histological examination of lymph node demon-
strated morphological features of AITL, but also the
presence of T-cell lineage with aberrant CD4 and CD10
expression strongly supported the diagnosis . More-
over, TCR genes showed clonal rearrangement. Immuno-
blast-like cells and RS-like cells showed polyclonal IgH
rearrangement, thus a concomitant large B cell lymph-
oma (a well-known complication in AITL) was excluded.
A review of the literature has demonstrated that a wide
spectrum of renal lesions (not only direct infiltration by
neoplastic cells) in glomeruli, tubule-interstitium and ves-
sels can develop in patients with AITL and angioimmuno-
blastic lymphadenopathy [23-26]. Clinico-pathological
features of the patients are listed in Table 2. To the best of
our knowledge, only one case of AITL associated with
PAN , has been previously described. It concerned an
elderly (71 years) man, who developed an intraperitoneal
hemorrhage two months after the diagnosis of AITL. PAN
is an autoimmune necrotizing systemic vasculitis that pre-
ferentially involves small and medium-sized arteries, with
signs and symptoms resulting from infarction and scarring
of the affected organ. It often starts with non specific
symptoms and laboratory features . Any age group
may be affected, but it is commonly seen in people be-
tween the ages of 40 and 60, as in our case. The most fre-
quent visceral manifestations involve kidney (93.4%), heart
(72%), and gastrointestinal tract (57.4%) ; moreover,
several reports indicate that the disease may affect also
testis and prostate . Currently, the most widely used
vasculitis classification system is that of the ACR which is
based predominantly on clinical findings. Histological
diagnosis of vasculitis is performed according to the
Chapel Hill Consensus Conference criteria  and to the
more recent scheme suggested by Carlson . The pos-
sible mechanism that may explain the relation between
AITL and PAN is represented by the induction of an auto-
immune phenomenon by the lymphoma. It is well known
that AITL cells produce cytokines such as interleukin 6
 and TNF-α , stimulating polyclonal B-cells and
plasma cells to secrete antibodies forming circulating im-
mune complexes (CIC). CIC complete the complement
cascade, releasing vasoactive substances and chemotactic
factors that cause accumulations of inflammatory cells
and release of lysosomal enzymes by ne utrophils, leading
to injury of vessels walls and thrombosis . In the pa-
tient here presented, only serum IgG value and C-react-
ive protein were elevated whereas platelet count and CIC
Table 2 Clinicopathological features of patients with AITL developing renal involvement
Author Sex Age Type of renal lesion Interval
Treatment Clinical outcome
Wood and Harkins  M 76 Diffuse proliferative
Dead for lymphoma
Wood and Harkins  M 79 Minimal change disease 0 Dialysis Dead for renal failure
Bhat et al  F 77 Acute renal failure with
4 None Dead for sepsis
Platzer et al  M 64 Renal failure 0 Prednisolone CR
Bello et al  M 61 Fanconi syndrome 0 Hydrocortisone CR
Bignon et al  M 70 Dysproteinaemia 0 n.a. n.a.
Yamazaki et al  M 72 Endocapillary proliferative
0 Vincristine, prednisolone Dead for alimentary
Nakamoto et al  M 40 Acute interstitial nephritis 16 Prednisolone,
At 60-month follow-up, no
signs of relapse
Duwaji et al  M 71 Proliferative glomerulonephritis 2 CHOP regimen Dead for sepsis
Lim et al  M 33 Amyloidosis 12 CHOP regimen At 12-month follow-up, no
signs of relapse
Hamidou et al  M 56 Vasculitis 0 CHOP regimen Dead for renal failure
De Samblanx et al  M 67 Proliferative glomerulonephritis 0 CHOP regimen At 12-month follow-up, no
signs of relapse
Goto et al  M 73 Direct invasion by lymphoma 0 CHOP regimen At 20-month follow-up, no
signs of relapse
Miura et al  M 70 IgM-λ glomerular thrombi 2 CHOP regimen At 3-month follow-up, no
signs of relapse
Tagashi et al  M 21 Nephrotic syndrome 0 CHOP regimen At 36-month follow-up, no
signs of relapse
CR complete remission; n.a. not available, CHOP Cyclophosphamide, doxorubicin, vincristine, prednisolone.
Ambrosio et al. Diagnostic Pathology 2012, 7:50 Page 5 of 7
were normal. Throughout the course of the disease,
platelet count decrease and CIC increment was docu-
mented. The main diagnostic difficulty was represented
by the absence of signs and symptoms of vasculitis;
moreover, echo-color-doppler and CT scan findings led
to a misdiagnosis of renal carcinoma. Only histological
examination of the kidney which showed necrosis of par-
enchyma and multiple segmentary vasculitis involving
small and middle renal arteries allowed the correct diag-
nosis of PAN which was later confirmed by clinicians.
A careful evaluation is needed in the management of
AITL patients which may exhibit immunodeficiency and
autoimmunity secondary to the neoplastic process .
Herein we report the first case of PAN presenting at
onset with ren al involvement , sequential to AITL, in a
40 year-old man. PAN has rarely been reported in asso-
ciation with AITL but, although infrequent, clinicians
should keep in mind the possibility of an autoimmune
disorder involving kidney, in case signs of renal failure
develop. Renal biopsy and angiography are necessary in
order to avoid delay of treatment and organ damage.
Written informed consent was obt ained from the patient
for publication of this Case Report and any all accom-
panying images. A copy of the written consent is avail-
able for review by the Editor-in-Chief of this journal.
AITL: Angioimmunoblastic T-cell lymphoma; CT: Computed tomography;
PAN: Polyarteritis nodosa; WHO: World Health Organization; CIC: Circulating
immune complexes; Ig: Immunoglobulins; ACE: Angiotensin converting
enzyme; ACR: American College of Rheumatology; RS: Reed-Sternberg;
EBER: EBV-encoded RNA; EBV: Epstein-Barr virus; AILD: Angioimmunoblastic
lymphadenopathy with dysproteinemia.
The Authors declare that they have no competing interests.
MRA wrote the paper; BJR performed analysis of the histological sections; AG
and MO carried out the immunoassays; AF and MC made contributions to
acquisition of clinical data; SL contributed his expertise in the field and
fruitful discussion; SAT coordinated the work and gave final approval of the
version to be published. All authors read and approved the final manuscript.
Department of Human Pathology and Oncology, Pathological Anatomy
Section, University of Siena, via delle Scotte, Siena, 6 - 53100, Italy.
Hematology and Transplant, University of Siena, Siena, Italy.
Chirurgia dei Trapianti, Azienda Ospedaliera Universitaria Senese, Senese,
Received: 5 March 2012 Accepted: 22 April 2012
Published: 8 May 2012
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Cite this article as: Ambrosio et al.: Renal infarction due to polyarteritis
nodosa in a patient with angioimmunoblastic T-cell lymphoma: a case
report and a brief review of the literature. Diagnostic Pathology 2012 7:50.
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