Transcript International CME on Renal Pathology 14th

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14th - 16th March, 2005
Department of Pathology
Sanjay Gandhi Postgraduate
Institute of Medical Sciences
Lucknow- 226014, INDIA
Coordinator:
R.K. Gupta
Professor & Head
Department of Pathology
SGPGIMS, Lucknow, India
US Coordinator:
Surya V. Seshan
Professor of Pathology
Chief, Renal Pathology
Weill Medical College of
Cornell University
New York, NY
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Slide Seminar - II
Pathology of Renal Transplant
Lorraine Racusen
R.K. Gupta
Prof. of Pathology
Johns Hopkins Medical School
Baltimore, MD
Prof & Head
Department of Pathology
SGPGIMS, Lucknow
India
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Slide Seminar- II
Pathology of Renal Transplant
L Racusen & RK Gupta
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Case 1: 38 years male, 2 yrs post renal transplant biopsy
Case 2: 65 years female, 9 days post renal transplant biopsy
Case 3: 34 years female, 3.2 years post renal transplant with H/O UTI &…
Case 4: 58 yrs male, 6 month post-transplant with colonic perforation
Case 5: 31 Yrs male, 4 yrs post-transplant with duodenojejunal mass
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Slide Seminar- II: Pathology of Renal Transplant - Case 1
Case 1
• 38 year old man status post renal transplant 2-3 years before
biopsy.
• Original disease was Alport’s syndrome, complicated by
hypertension.
• Presented with palpitations, and was found to have a
creatinine of 4.9 mg%. With hydration, his creatinine only fell
to 4.1 mg%.
• He was biopsied to rule out rejection and other processes in
the allograft, and to assess for chronic changes.
• There are a variety of processes in this allograft – please
identify.
• What is the prognosis in the short-term? The long-term?
• What special concern is there in a transplant patient with this
underlying disease?
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Slide Seminar- II: Pathology of Renal Transplant - Case 1
Case 1
? Diagnosis
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Slide Seminar- II: Pathology of Renal Transplant - Case 1
Case 1
Diagnosis
 Acute vascular rejection, Banff Grade
2A, with severe tubulo-interstitial
inflammation with C4d positivity
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Slide Seminar- II: Pathology of Renal Transplant - Case 1
Case 1
• The biopsy reveals acute rejection, with mild intimal arteritis
(v1), Banff type 2A, with a severe tubulointerstitial component
(i3, t3). Focal leukocyte margination is noted in glomeruli and
peritubular capillaries, mononuclear with occasional
neutrophils. Though difficult to assess, chronic changes are
significant (ci2-3, ct2-3).
• Immunofluorescence reveals diffuse though mild linear
capillary staining for C4d – R/O anti-donor antibody.
• The patient had been previously treated with OKT3, and had
developed anti-OKT3 antibodies, so he was treated with
thymoglobulin. There was poor response to therapy, and the
patient returned to dialysis within months with a failed
allograft.
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Slide Seminar- II: Pathology of Renal Transplant - Case 1
Case 1
• In the setting of Banff type 2 rejection, a severe
tubulointerstitial component predicts relative resistance to
treatment short-term; the same study also demonstrated
worse outcome with type 2B than with type 2A rejection,
reinforcing the importance of making this distinction on
allograft biopsy.
• The staining for C4d is diffuse, but only mild, with staining
done on frozen tissue using the monoclonal antibody for C4d;
the requirement for a positive reading using this technique is
for strong staining, so this should be interpreted as below
threshold. However, anti-donor antibody should be sought, to
rule out an antibody-mediated component.
The quite
extensive chronic changes portend a poorer long-term (and in
this case short-term!) outcome.
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Slide Seminar- II: Pathology of Renal Transplant - Case 1
Case 1
References:
1.
2.
3.
4.
Haas M, Kraus ES, Samaniego-Picota M, et al, Acute renal
allograft rejection with intimal arteritis: histologic predictors
of response to therapy and graft survival. Kidney Int
61:1516-26, 2002
Racusen LC, Solez K, Colvin RB, et al, The Banff 97
working classification of renal allograft pathology. Kidney
Int 55:713-723, 1999
Racusen LC, Solez K, Colvin R. Fibrosis and atrophy in the
renal allograft – Interim report and new directions. Am J
Transplant 2:203-6, 2002
Racusen LC, Halloran PF, Solez K. Banff 2003 meeting
report: new diagnostic insights and standards. Am J
Transplant 4:1562-6, 2004
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Slide Seminar- II: Pathology of Renal Transplant - Case 1
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Slide Seminar- II: Pathology of Renal Transplant - Case 2
Case 2
• 65 year old female had a history of chronic interstitial
nephritis and was on dialysis.
• She received a living related renal transplant from her
daughter 9 days prior to biopsy.
• The patient has developed a rise in creatinine after
improving function post-operatively.
• A biopsy is performed to rule out rejection. What is you
diagnosis? Indicate possible underlying etiologies.
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Case 2
? Diagnosis
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Slide Seminar- II: Pathology of Renal Transplant - Case 2
Case 2
Diagnosis
Acute vascular rejection, Banff Grade 2B,
with no tubulo-interstitial inflammation
Extensive tubulo-toxic change
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Slide Seminar- II: Pathology of Renal Transplant - Case 2
Case 2
• The biopsy reveals acute rejection, vascular type, with
moderate-to-severe intimal arteries (v2), Banff type 2B,
with no significant tubulointerstitial component (i0, t0).
• A total of 4 small arteries have intimal arteritis, of varying
severity.
• There is significant and extensive isometric vacuolization
of tubular cells – R/O drug toxicity.
• No chronic changes are seen.
• There is minimal C4d staining in peritubular capillaries.
• She was begun on steroids and thymoglobulin for the
rejection; the dose of thymoglobulin had to be decreased
due to pancytopenia.
• Creatinine fell to 0.9 mg%, then stabilized at 1-1.3 mg%.
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Slide Seminar- II: Pathology of Renal Transplant - Case 2
Case 2
Reference:
1.
Racusen LC, Solez K, Colvin RB, et al, The Banff 97
working classification of renal allograft pathology.
Kidney Int 55:713-723, 1999
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Slide Seminar – I : Pathology of Glomerular Diseases - Case 2
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Slide Seminar- II: Pathology of Renal Transplant - Case 3
Case 3
• 34 year old female S/P deceased donor renal transplant
3.2 years prior to biopsy. The cause of end-stage renal
disease is unknown.
• She now presents with a rise in creatnine from 1.9 to 2.9
mg%. She has multiple leukocytes in the urine, and
history of recent urinary tract infection.
• There is some concern that the patient has been noncompliant with her medications. Indicate your
diagnosis/diagnoses.
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Case 3
? Diagnosis
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Slide Seminar- II: Pathology of Renal Transplant - Case 3
Case 3
Diagnosis
Acute cellular rejection, Type IB, with
focal acute pyelonephritis
Membranous glomerulonephritis
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Slide Seminar- II: Pathology of Renal Transplant - Case 3
Case
3
acute cell-mediated
• The biopsy reveals
rejection, moderate-tosevere tubulointerstitial type, Banff type IB, with focally severe
tubulitis (t3). In addition, there was an area in the cortex with
numerous peritubular and intratubular neutrophils, consistent with
bacterial infection. In addition, glomeruli show mild increase in
mesangial matrix, with very mild glomerulitis (g0-1). While difficult to
assess, there appear to be mild-to-moderate chronic changes (ci1-2,
ct1-2).
• Immunofluorescence studies reveal no C4d staining in peritubular
capillaries. However, there is diffuse granular capillary staining for
IgG (2-3+), IgM (trace-1+), C3 (1+) and kappa and lambda light
chains (2-3+), and C4d (2-3+).
• Electron Microscopy reveals subepithelial dense deposits,
confirming a diagnosis of early membranous glomerulopathy.
Presumably this is a de novo disease, thought the cause of the
patient’s end-stage renal disease is unclear.
• Membranous glomerulopathy in the allograft may impinge on graft
survival, but not invariably.
• Pyelonephritis in grafts is not rare – if occurring within the first 3
months, it impacts on graft survival.
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Slide Seminar- II: Pathology of Renal Transplant - Case 3
References:
1.
2.
3.
4.
5.
Racusen LC, et al, Banff 97 (see above)
Denton MD, Singh AK.
Recurrent and de novo
glomerulonephritis in the renal allograft. Semin Nephrol
20:164-75. 2000
Hariharan S. Long-term kidney transplant survival. Am J
Kidney Dis 38:S44-50, 2001
Seikaly MG. Recurrence of primary disease in children
after renal transplantation. Ped Transplant 8:113, 2004
Giral et al, Acute graft pyelonephrits and long-term kidney
graft outcome. Kidney Int 61:1880, 2002
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Slide Seminar – I : Pathology of Glomerular Diseases - Case 1
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Slide Seminar- II: Pathology of Renal Transplant - Case 4
Case 4
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59 Yrs/ Male
Received live related renal allograft 6 months back
Had H/O cyclosporine toxicity and acute cellular rejection
Presented with facial swelling, raised S. creatinine, UTI and
sinusitis
Cald well luck surgery performed
Post operative patient developed acute abdominal pain,
X-ray abdomen showed gas under diaphragm and a
diagnosis of intestinal perforation was made
Exploratory laprotomy done and colonic perforation repaired
Tissue from maxillary sinus and Colonic resection margins for
histopathology
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Maxillary Sinus
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Maxillary Sinus
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Maxillary Sinus
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Colonic Biopsy
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Colonic Biopsy
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Colonic Biopsy
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Case 4
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Slide Seminar- II: Pathology of Renal Transplant - Case 4
Case 4
Diagnosis:
 Post Renal Transplant Mucormycosis
- Maxillary Sinus and Colon
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Microscopy:
• Many broad aseptate fungal hyphae
• Non-parallel walls
• Angioinavsion
• Surrounded by multinucleated histiocytic giant cells
Follow-up
• Patient died due to septicemia after second surgery
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Slide Seminar- II: Pathology of Renal Transplant - Case 4
Mucor:
Ubiquitous aerobic saprophytic opportunistic fungus
of low virulence, however, initiating aggressive and
fatal infection in immunocompromised individuals.
Classification:
Order:
Mucorales
Class:
Zygomycetes
Genera: Mucor, Rhizopus, Absidia.
Morphology:
Broad, twisted, aseptate ribbon like hyphae,
branching at right angles, size: 5 - 25 micron
Special stains:
PAS, GSM and CSM
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Slide Seminar- II: Pathology of Renal Transplant - Case 4
• Fungal infection is an uncommon complication after renal
transplantation
• Mucormycosis is rare fungal infection in immuno-suppressed
patient (Approx 4% in post renal Tx)
• Common clinical presentations- Cerebral, sino-pulmonary,
GIT, Kidney, disseminated and cutaneous
• Local area necrosis and angioinvasion
• Fatal out come in majority of cases
• A high index of suspicion, leading to early diagnosis and
initiation of antifungal treatment, in addition to early surgery,
are keys to a more favorable outcome.
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Slide Seminar- II: Pathology of Renal Transplant - Case 4
References:
1.
2.
3.
4.
Chkhotua A, Yussim A, Tovar A, etal Mucormycosis of
the renal allograft: case report and review of the
literature. Transpl Int. 2001 Dec;14(6):438-41.
Jha V, Chugh KS. Posttransplant infections in the
tropical countries. Artif. Organs 2002: 26 (9): 770- 7.
Reis MA, Costa RS, Ferraz AS. Causes of death in
renal transplant recipients: a study of 102 autopsies
from 1968 to 1991. J R Soc Med. 1995 Jan;88(1):24-7.
Bakshi NA, Volk EE. Pulmonary mucormycosis
diagnosed by fine needle aspiration cytology. A case
report.Acta Cytol. 2001 May-Jun;45(3):411-4.
End
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
•
•
•
•
31 Yrs/ Male
Received live related renal allograft 4 years back
Presented with gastric outlet obstruction
Upper GI endoscopy revealed narrowing of duodenojejunal junction
• CT scan showed mass in D3 and D4 and proximal
jejunum
• Operative findings - large well encapsulated mass in DJ
region
• Resected loop of jejunum with mass for histopathology
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
Gross:
• A large irregular greyish white fleshy and friable mass
with areas of haemorrhage, measuring 11x8x4cm
involving 9 cm length of the jejunum.
• Mesentric fat showed haemorrhage with whitish areas.
• No lymph nodes were found.
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
? Diagnosis
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
Diagnosis :
Post Transplant Monomorphic Diffuse
Large B- Cell Lymphoma - Jejunum
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
• Ulcerated mucosa with dense diffuse infiltration by
predominantly intermediate sized atypical lymphoid cells
displaying round to irregular nuclear contours with clumped
chromatin, inconspicuous nucleoli and scant to moderate
amount of cytoplasm.
• Tumor was extensively present in the lamina propria
• Tumor was infiltrating transmurally upto the serosa.
• At places large atypical lymphoid cells with bizarre
hyperchromatic nuclei and focal lymphoplasmacytoid cells
were also seen.
• Brisk mitotic activity present
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
CD 20
CD 3
CD 30
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
CD 20
CD 3
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CD 30
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
Post Transplant Lymphoproliferative Disorder (PTLD)
• Heterogenous group of lymphoid proliferations.
• Occuring after solid organ and bone marrow
transplantation.
• Variable clinical and histopathological spectrum.
• Scarce data on live related renal allograft recipients.
Incidence:
• Depends upon the intensity and duration of
immunosuppression.
• 0.5 to 2.55 % in renal transplant recipients.
• 2.2-10 % heart, lung and heart-lung transplant
recipient.
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
Classifications of PTLD
•
•
•
•
•
Frizzerra et al 1981
Shapiro et al 1988
Nalesnik et al 1989
Knowels et al 1995
Society for Haematopathologist workshop
1997
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
Society for Haematopathologist workshop (1997)
Early Lesions
 Reactive plasmacytic hyperplasias
 Infectious mononucleosis - like
PTLD Polymorphic
PTLD Monomorphic
 B-Cell Diffuse large cell lymphomas
centroblastic / immunoblastic
 Burkitts / Burkitts like lymphoma
 T-cell lymphomas : Peripheral T-Cell lymphomas
 Anaplastic large cell lymphomas (T or null)
Others
 Plasmacytoma like, T-cell rich / Hodgkins disease like B cell
PTLD
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
Case 5
Clinicopathological Groups
Minnesota group 1992
Early onset PTLD
Late onset PTLD
young patients
older patients
6 to 12 months
38 to 146 months
Polymorphic
Monomorphic
Polyclonal
Monoclonal
EBV positive
EBV negative
Negative for oncogenes
c-myc, ras, p53
Rx
Chemotherapy
Immunosuppression
Antiviral therapy
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Slide Seminar- II: Pathology of Renal Transplant - Case 5
References:
1. Nalesnik MA, Jaffe R, Starlz TE, Demetris AJ, Porter K, Burnham JA etal. The
pathology of posttransplant lymphoproliferative disorder occurring in the setting of
cyclosporine A- prednisolone immunosuppression. Am J of Pathol 1988; 133(1):
173-92.
2. Harris NL, Jafe ES, Stein H, et al. A revised European-American classification of
lymphoid neoplasms. A proposal from the international lymphoma study group.
Blood 1994; 84: 1361-92.
3. Swerdlow SH. Classification of post transplant lymphoproliferative disorders: from
the past to the present. Semin Diag Pathol 1997; 14(1): 2-7.
4. Bates WD, Gray DW, Dada MA, Chetty R, Gatter KC, Davies DR etal.
Lymphoproliferative disorders in Oxford renal transplant patients. J Clin Pathol
2003; 56(6): 439-46.
5. Opelz G, Dohler B. Lymhpoma after solid organ transplantation: a collaborative
transplant study report. Am J Transplant 2004; 4: 222-30.
6. Maniyur R, Anant K, Aneesh S, Vinita E, Manoj J, Rakesh P. Posttransplant
epididymal lymphoma: an aggressive variant. Transplantation 2003; 75(2): 246-7.
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