27
Kidneys, Adrenals, and Retroperitoneum
Fig. 27.9 Birt-Hogg-Dube syndrome. (A) Fine-needle aspiration showing oncocytic cells (Diff-Quikx MP). (B) Resected kidney showing bisected
homogenous yellow-brown well-circumscribed tumor. (C) Histologic section showing hybrid oncocytic cells that are both vacuolated and granular (H&E x MP).
(D) Focal positive membranous staining for cytokeratin-7.
Awareness of the radiologic appearance of a tumor is vital in
the interpretation of renal FNAs, because most tumors display
characteristic radiographic features.
Previously, RCC was most frequently detected initially by
intravenous urography, on which it is characterized as a mass
with decreased or heterogeneous staining quality, the latter
often being caused by cystic degeneration or necrosis within the
tumor.32 Currently, however, there are new and improved tech-
niques for detection and staging of renal masses, including mag-
netic resonance tomography, CT imaging, and ultrasound.
Approximately 75% of RCCs are hypervascular and display
characteristic arteriographic features that permit the diagnosis
of RCC with a high degree of confidence.32 The 25% of RCCs
that are hypovascular appear thus because they are extensively
cystic or necrotic, arise within a cyst, or demonstrate a predomi-
nantly papillary architecture (PRCC).32 The differential diagno-
sis of a hypovascular renal mass also includes benign renal cysts,
abscesses, oncocytoma, urothelial carcinoma (UC) of the renal
pelvis, CDC of the renal medulla, renal lymphoma, XPN, sarco-
matoid RCC, or metastatic renal neoplasms. Renal oncocytomas
are well-encapsulated hypovascular masses, with a distinctive
arrangement of internal vessels in a pattern like the spokes of
a wheel.32 Angiomyolipomas may be differentiated by CT and
ultrasound on the basis of their fat content; however, they are
generally hypervascular and sharply demarcated from the unin-
volved kidney.
clear cell (conventional) Renal cell carcinoma
Renal cell carcinoma accounts for approximately 2% of all
cancers and 60-65% of all renal epithelial neoplasms. It occurs
more commonly in men than in women, with the peak age at
presentation being in the sixth decade of life. It is predominantly
a disease of adults, with few cases being reported in children or
adolescents younger than 20 years.20 Nonrandom chromosomal
changes on chromosomes 3p and 14q and gain of chromo-
some 5q22-qter and trisomy 7 are strong evidence in favor of
a multistep carcinogenesis model involving tumor suppressor
genes as well as proto-oncogenes in the evolution of RCC.63 The
cytogenetics of hereditary RCC associated with VHL disease was
described earlier (see under
Hereditary Kidney Cancer).
How-
ever, somatic mutations or deletions or hypermethylations can
be found in the VHL gene on chromosome 3p in 75-80% of
sporadic tumors (Fig. 27.8).
821
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