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Renal Cancer
Contemporary Management
John A. Libertino
Jason R. Gee
Editors
Second Edition
123
Renal Cancer
John A. Libertino • Jason R. Gee
Editors
Renal Cancer
Contemporary Management
Second Edition
Editors
John A. Libertino Jason R. Gee
Professor of Urology Associate Professor of Urology
Tufts University School of Medicine Tufts University School of Medicine
Boston, MA Boston, MA
USA USA
This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Dedicated to
Dr. Harris Berman, M.D., Dean of Tufts University
School of Medicine
A great Leader in medical education and healthcare delivery
Contents
vii
viii Contents
xix
xx Contributors
1992 and peaked in 2001, but then started to Another likely explanation for the higher inci-
decline with the sharpest decline in recent years dence of kidney cancer observed in developed
of 32% from 2013 to 2015 [6]. countries is the greater availability and more lib-
In the last decade, 18 countries experienced eral use of abdominal computed tomography
increased incidence rates for both men and women, imaging techniques resulting in more incidental
with sharper increases occurring in Latin America, findings of renal masses [8]. Within the United
Brazil, Thailand, and Bulgaria [4]. Reporting bias, States Medicare population, 43% of patients
advancement in health record systems, and acces- receive a CT of the chest or abdomen over a
sibility to healthcare providers should also be con- 5-year period [9]. Tandem with the detection of
sidered in comparing rates accurately between more incidental renal masses is the increased
regions. Increasing incidence and a decreasing diagnosis of small renal masses <4 cm, which
mortality-to-incidence ratio have been found to be now account for 48–66% of new RCC diagnoses
correlated with increasing human development [7]. Tumor size has extensively been shown to be
index levels and gross domestic product per capita correlated with risk of metastasis with a 25%
[7]. One explanation for the rising incidence in increased odds of metastasis with each cm
developed nations is the higher prevalence of risk increase in tumor diameter [10]. In patients with
factors for RCC (such as smoking, obesity, physi- tumor diameter <3 cm, the risk of metastasis is
cal inactivity, and hypertension) present in devel- remote with several active surveillance cohorts
oped countries. Increased access to care and reporting 0–1.1% metastatic events occurring in
availability of advanced therapeutics have been tumors <3 cm [11]. In addition to improvements
postulated to account for the decreased mortality- made in local and systemic therapies for RCC,
to-incidence ratio [6]. the decreasing mortality rates from RCC can also
1 Epidemiology, Screening, and Clinical Staging 3
partly be attributed to the lead-time bias from population [5]. Despite being diagnosed at a
earlier diagnosis and treatment of small renal younger age with more localized disease, black
masses [6]. In states and developed nations that RCC patients also had a significantly lower sur-
have aimed to curtail advanced radiologic testing, vival rate than all other ethnicities [13]. The dis-
there has been recent data to suggest that the inci- parity in survival rates between black patients
dence of renal cancer has plateaued [12]. and other ethnicities is unknown, but can be par-
tially explained by stressors associated with
socioeconomic status, comorbidities such as
emographic Factors in Renal Cell
D hypertension, and lower likelihood of undergoing
Carcinoma nephrectomy or receiving systemic therapies for
metastatic disease [15, 16].
Renal cancer is twice as common in males as RCC tumor subtype also varies among racial
females, and the rate of incidence has continued to groups. Looking at 18 US population-based reg-
rise twice as rapidly in males compared to females. istries of the SEER program in 2011, a study
A 2008 study looking at retrospective data of found that among 84,255 RCC patients, clear cell
39,434 patients from 1988 to 2004 in the California RCC is more common in white populations than
Cancer Registry determined that overall, females black populations (50% vs. 31%), and the papil-
showed a higher percent of localized cancer than lary subtype presents more often in people of
males which may be responsible for a higher rela- African or Caribbean descent than Caucasian
tive survival rate in females. Potential explana- descent (23% vs. 9%). These authors also found
tions for differences in survival rates also include that compared to whites, blacks were four times
biological differences in the tumor, more exten- more likely to have papillary RCC than clear cell
sive use of healthcare system by females, and a RCC, while Asian or Pacific Islanders were less
higher prevalence of hypertension in males [13]. likely to have papillary or chromophobe RCC
With a median age at RCC diagnosis of than white patients [17]. Other rare and aggres-
64 years old, RCC is primarily a malignancy of sive subtypes of RCC such as collecting duct car-
the elderly. In fact, 53.9% of patients are diag- cinoma and renal medullary carcinoma have been
nosed between the ages of 55 and 74, while less linked to African American heritage, with renal
than 10% are diagnosed at less than 45 years of medullary carcinoma seen almost exclusively
age [5]. As mortality rates continue to decrease in with sickle cell trait [18, 19].
the United States and overall RCC incidence
rises, the incidence of RCC in the elderly will
also likely continue to rise. Of note, adolescents isk Factors in the Development
R
and young adults more commonly present with of RCC
rare histologic subtypes such as translocation
carcinoma or renal medullary carcinoma. Though Risk factors for renal cell carcinoma include male
RCC in younger patients is rare, translocation gender, age, smoking, diet, obesity, hypertension,
carcinomas account for up to 50% of all RCC in renal disease, family history, certain medication
patients under the age of 40. [14] use, and occupational exposures. While some
Along with sex and age, race is an important components such as gender and age have been dis-
factor in the epidemiology of RCC. Within the cussed under demographics, current literature
United States, SEER data shows that black and regarding the remaining factors is described below.
Hispanic patients have a higher incidence rate
than all other ethnicities, while Asian and Pacific
Islander patients have the lowest incidence rates. Smoking
Caucasians had an incidence of 22.2 per 100,000
person-years between 2011 and 2015 in compari- According to the International Agency for
son to 25.3 per 100,000 person-years in the black Research on Cancer (IARC) and the US Surgeon
4 S. N. Siddiqui et al.
General, smoking is a well-established causal this includes beer, wine, and liquor. A dose-
risk factor for RCC. Male smokers are shown to dependent risk reduction was discovered in a
have a 50% increased relative risk (RR) and pooled analysis of 12 prospective studies, show-
female smokers are shown to have a 20% ing a 28% lower risk in those who drank more
increased RR for developing these tumors. A than 15 grams per day. Interestingly, no associa-
2005 meta-analysis of 24 studies shows that the tion was found between total fluid intakes from
overall combined RR for developing RCC in other beverages, such as water, juice, milk, tea,
someone who has ever smoked a cigarette was coffee, or soda, implying that alcohol itself is a
1.38 (95% CI = 1.27–1.5). Furthermore, this data modifying factor [25].
reported a dose-response relationship of increas-
ing RR with more exposure to cigarette smoke. A
promising finding from the study indicated that a Obesity
greater length of abstinence from smoking actu-
ally reduced the RR, but this finding requires fur- Obesity was first shown to be associated with
ther investigation [20]. RCC as early as 1984 when McLaughlin et al.
Compared to non-smokers, current smokers conducted a case-control analyses that suggested
with RCC were shown to be at an increased risk body mass index (BMI) and RCC in women were
for death with an HR of 1.7 (95% CI = 1.2–2.5) related [26]. Since then, much more literature has
[21]. Smokers were seen to have a higher likeli- been published regarding the relationship
hood of increased stage or even metastases at between waist-to-hip ratios, weight gain during
diagnosis. Similarly to chronic obstructive pul- adulthood, and mechanisms of its influence on
monary disease (COPD), the pathogenesis of kidney cancer [27]. The World Cancer Research
cigarette smoking in RCC is linked to carbon Fund reports that since the 1980s, obesity has
monoxide exposure and chronic tissue hypoxia. continued to increase in both resource-rich coun-
Smokers with RCC were also shown to have tries as well as low- and middle-income countries
increased DNA damage and mutations within [28]. Between genders, there is an estimated 24%
peripheral blood lymphocytes due to increased risk in men and 34% increased risk in
N-nitrosamine and benzo[α]pyrene diol exposure women for every 5 kg/m increase in BMI [29].
compared to a control group [22, 23]. Proposed mechanisms for the development of
RCC include insulin resistance, sex hormone
dysregulation, inflammatory responses, and oxi-
Diet dative stress [30]. In light of the significant asso-
ciation between obesity and development of
Many different foods and substances have been RCC, further research is needed to elucidate
researched to look for increased risk of causal mechanisms and preventative strategies.
RCC. Most notably, consumption of fruits and
vegetables is shown to be inversely related to the
development of RCC in a meta-analysis review- Hypertension
ing 13 prospective studies [24]. The role of high
fat and protein consumption is more controver- According to the Centers for Disease Control and
sial because while it has been considered a risk Prevention, about 75 million American adults
factor in the past, a large multicenter European had high blood pressure in 2011. This translates
cohort study revealed that there is no significant into 1 in 3 adults having a chronic condition that
association between the development of RCC increases risk for several diseases, such as heart
and these nutrients [20]. disease, renal failure, and stroke [31]. While
Like fruits and vegetables, alcohol has also chronic hypertension is a leading cause for devel-
been inversely associated with renal cancer risk; opment of chronic kidney disease, several studies
1 Epidemiology, Screening, and Clinical Staging 5
over long periods of time, and calcium channel nitrate, and radon, has not been established as a
blockers inhibiting apoptosis to facilitate division risk factor for RCC but is being explored [1]. The
of malignant cells [41, 42]. most extensively examined substance is trichlo-
Similarly to studies on antihypertensive medi- roethylene (TCE), a degreaser used for metal
cations, individual studies examining analgesic’s cleaning that is also present in adhesives, paint
association with RCC have largely been inconsis- removers, typewriter correction fluids, and spot
tent. Among the most commonly used analgesics, removers [46]. The US Environmental Protection
acetaminophen has been implicated with RCC Agency 2001 draft TCE health risk assessment
risk. A large case-control analysis of the US concluded that epidemiologic studies do show an
Kidney Cancer Study showed a positive trend for increased risk of kidney cancer in association
developing RCC with increasing duration of with TCE [47]. TCE is considered a Group 2A
over-the-counter use of acetaminophen, with a “probably” human carcinogen by the International
twofold risk observed for those who took acet- Agency for Research on Cancer (IARC).
aminophen ≥10 years [43]. However, the effect
size was diluted to an odds ratio of 1.5 when pre-
scription use of acetaminophen was included. A Screening for RCC
meta-analysis of four cohort and nine case-
control studies supported this finding with a sum- Although 30% of patients present with metastatic
marized odds ratio of 1.25 (95% CI = 1.1–1.4) disease, the remainder are diagnosed with local-
[44]. A potential biological explanation for acet- ized RCC and may be candidates for definitive
aminophen’s effects is the depletion of glutathi- treatment [48]. Screening programs for earlier
one at higher doses and the subsequent rise in detection and treatment have the potential to
N-acetyl-p-benzoquinone imine (NAPQI). improve survival outcomes if the ideal screening
NAPQI is able to disrupt homeostasis in both regimen is identified. The Wilson and Jungner
kidney and liver cells by binding covalently to criteria for suitable screening include the follow-
DNA [44]. ing: the condition should be a significant health
Nonsteroidal anti-inflammatory drugs problem, there should be a recognizable latent or
(NSAIDs) have also been examined for poten- early symptomatic stage, and there should be an
tially increasing RCC risk. A large meta-analysis accepted treatment for patients with recognized
identifying 20 studies found increased risk of disease [49]. In regard to RCC, well-established
RCC with non-aspirin NSAID use (RR = 1.25, treatments with minimal risk are available for
95% CI = 1.06–1.46), but no relationship between localized tumors. There is currently no recom-
aspirin use and RCC [45]. Other meta-analytic mendation for screening for RCC, but several
reviews have not shown a positive association techniques and regimens have been explored.
between RCC and NSAID use, including the US Cost-effective techniques that have been
Kidney Cancer Study which looked at NSAID explored for early detection of RCC include urine
use and aspirin use in heart regimens [44]. dipstick and biomarkers. Identifying hematuria
Theories for NSAID-mediated RCC carcinogen- on dipstick has not been reliable for RCC due to
esis reference the inhibition of prostaglandin syn- a stronger association with bladder cancer, low
thesis leading to chronic subacute renal injuries; diagnostic yield, as well as poor sensitivity and
these in turn could cause DNA damage and specificity. When comparing incidence of all
uncontrolled cell proliferation. hematuria in patients with RCC to hematuria in
patients with urothelial carcinoma, the rates are
35% versus 94%, respectively [50]. A Korean
Occupational Exposure study that performed 56,632 dipsticks as part of a
checkup on individuals over the age of 20 found
Exposure to agents classically considered carci- hematuria in 3517 patients, but only three cases
nogenic, including cadmium, uranium, arsenic, of RCC were detected among these patients [51].
1 Epidemiology, Screening, and Clinical Staging 7
This is most likely because microscopic hematu- observational studies that were completed, nine
ria is a common finding and less likely to indicate of which were published before 2004 [53]. Of
cancer in a younger, low-risk population. On the these trials, a 1999 Japanese study screened
other hand, biomarkers such as aquaporin 1 219,640 patients (ages 29–70 years) over 13 years
(AQP1) and perilipin 2 (PLIN2) are soluble uri- and detected 193 cases of RCC. These patients
nary proteins with the potential for high specific- were followed to show a 97.4% cumulative sur-
ity and sensitivity, but they still require larger vival rate after 5 years and 94.6% at 10 years
prospective trials [52]. These biomarkers are spe- [58]. A large-scale randomized controlled screen-
cific to clear cell and papillary histologic sub- ing trial would help determine whether these
types, implying that they would produce results indicate a lead-time bias or truly represent
false-negative results in patients with variant his- improved survival outcome.
tology [53]. Other screening considerations include the
Computed tomography (CT) scanning is cur- psychological impact on patients and over-
rently used to screen for a wide variety of malig- diagnosis of small renal masses that may never
nancies in middle-aged Americans. These become clinically significant. A false-positive
screening practices include but are not limited to screening result may result in a similar degree of
abdominal CTs for detection of aortic aneu- patient harm as a false-negative result. Studies
rysms, CT colonography, CT angiography, and have shown that 15–30% of small renal masses
chest CTs for lung cancer. In an era where many are found to be benign after surgical excision
patients are receiving CT imaging, researchers [59]. As a result, clinicians must contemplate the
have attempted to detect solid abdominal organ psychological and emotional impact of deliver-
malignancies simultaneously. One study ing an incorrect diagnosis and potential harm
screened 4543 healthy patients over 40 years old from more unnecessary testing or invasive
who had received an abdominal CT, but solid procedures.
organ malignancy prevalence was only found to
be 0.1%, and therefore, the method was deemed
ineffective [54]. The US Preventive Services Screening of Targeted Populations
Task Force recognizes that despite the not infre-
quent detection of extracolonic incidental With the establishment of known risk factors and
lesions on CT, only 3% require definitive treat- understanding of inheritable conditions, high-
ment [55]. As a result of the overall low inci- risk populations do exist and screening has been
dence of malignant renal masses detected on evaluated for these patients. In 2005, the
screening CT with increased costs and burdens European Association of Urology guidelines had
to the patient and healthcare system, CT has not recommended annual ultrasounds of native kid-
been found to be a cost-effective screening strat- neys in patients who have received transplants
egy for RCC. due to their higher risk for developing RCC [60].
Compared to CT, ultrasound has the benefit of Examining other risk factors, Starke et al. identi-
using benign sound waves instead of ionizing fied 925 patients as high-risk individuals for
radiation while also being less expensive. A 2018 bladder cancer based on age ≥50, smoking with
cost-benefit analysis for sonographic screening ≥10 pack-year history, and occupational carcino-
shows that at $36 US dollars per ultrasound, the gen exposure of ≥15 years. After following these
opportunity to prevent metastatic RCC is worth patients for 6.5 years, ten of the patients were
considering [56]. However, ultrasound is less diagnosed with RCC, indicating a prevalence of
accurate in detecting renal masses than CT, espe- RCC in these patients that is roughly ten times
cially with less sensitivity in detecting lesions higher than the general population [61]. Since
under 3 cm in size [57]. There also is a lack of then, algorithms for early screening and
randomized trials to support the use of ultrasound management have been proposed for asymptom-
screening for RCC. Rossi et al. identified ten atic high-
risk patients [56]. These targeted
8 S. N. Siddiqui et al.
screening methods may be endorsed in the future, mutation of fumarate hydratase (FH), which is a
even if screening of the general population is not. gene that encodes an enzyme in the TCA cycle.
Incidence of von Hippel-Lindau disease is HLRCC-associated kidney cancer has the poten-
1 in 36,000 live births with a penetrance of over tial to be lethal, and therefore, testing in sus-
90% by the age of 65, making it the most com- pected patients begins as early as 8 years old.
mon hereditary renal cancer syndrome [62]. The Patients who are affected with HLRCC should
von Hippel-Lindau gene, VHL, is a tumor sup- subsequently have annual abdominal MRIs to
pressor gene on the short arm of chromosome 3 screen for kidney tumors [67].
(3p25.3). The gene encodes a protein that is part
of the VCB-CUL2 ubiquitin ligase complex,
which is responsible for degradation of hypoxia- Clinical Staging
inducible factor 1 (HIF-1) and insulin-like growth
factor 1 (ILGF-1). Loss of VHL activity leads to Clinical staging systems are developed to classify
cell growth and angiogenesis due to downstream malignant diseases in a uniform manner with
enhanced expression of factors such as VEGF, prognostic capability. They are used to guide
PDGFB, EPO, and TGF-α. CNS hemangioblas- treatment and planning decisions and manage
tomas, clear cell renal carcinomas, pheochromo- expected outcomes by stratifying the risk of can-
cytomas, and pancreatic tumors have all been cer progression. Ultimately, uniform staging sys-
described as part of the phenotypical classifica- tems allow for the comparison of patient
tions of VHL. As patients with VHL have a 70% outcomes worldwide [68]. Flocks and Kadesky
lifetime risk of developing RCC with a mean age proposed one of the earliest kidney cancer stag-
of clinical diagnosis at age 40, screening with ing systems in 1958, including organ-confined,
annual abdominal MRIs from the age of 16 is locally invasive, locally metastatic, and distant
recommended [63]. MRI is preferred over CT to metastatic disease [69]. The predominant TNM
avoid the substantial cumulative radiation expo- staging system used currently (tumor, nodes,
sure annual CT scans would incur. Pathologic metastases) was developed in 1974 by the
examination of nephrectomy specimens from American Joint Committee on Cancer (AJCC)
patients with VHL has revealed that nearly all and the Union Internationale Contre le Cancer,
complex cysts contain RCC [64]. Even normal- renamed the Union for International Cancer
appearing parenchyma on CT may harbor large Control (UICC) [70]. This TNM staging system
numbers of microscopic tumor foci, explaining has had several major revisions to improve prog-
the high risk of multiple and bilateral RCC in nostic accuracy with the most recent update pub-
VHL [65]. lished in 2017 after a structured review process
Other autosomal dominant disorders that with input from several professional groups
increase a patient’s risk for RCC include heredi- (Tables 1.2 and 1.3) [71].
tary papillary renal carcinoma, Birt-Hogg-Dubé In 1987, T1 and T2 renal lesions were divided
(BHD) syndrome, and hereditary leiomyomato- at 2.5 cm in largest dimension by imaging,
sis and renal cell carcinoma (HLRCC). The which did not differentiate well between surviv-
American Urological Association states that als for these groups [72]. In 1997, T2 disease
genetic counseling should be strongly recom- started at 7 cm for greater differentiation from
mended for patients suspected of having familial T1 [73]. The 2002 AJCC update further subdi-
RCC [66]. These conditions generally require vided T1 disease, T1a ≤4 cm and T1b 4–7 cm
screening in the form of germline mutation test- [74]. Work done by the Cleveland Clinic con-
ing rather than biomarkers. In BHD families or tributed to this development [75]. They described
patients who present with cutaneous fibrofollicu- 485 patients who underwent partial nephrec-
lomas, familial pneumothorax, or oncocytic tomy prior to 1997, finding that 5-year cancer-
RCC pathology, germline FLCN testing should specific survival was better with tumor diameter
begin at age 21. HLRCC involves a germline ≤4 cm compared to 4–7 cm and >7 cm (Fig. 1.1).
Another random document with
no related content on Scribd:
The Holy Virgin’s Descent into Hell. (XII. century.)
In spite of the prohibition of the Church, apocryphal
literature reached Russia from Byzantium by way of Bulgaria,
and not only spread all over Russia as a possession of the
people, but even crept into ecclesiastical literature, serving
frequently the same purpose as the writings of the Church
Fathers. These apocryphal productions, of which there is a
very large number, held sway over the people from the twelfth
to the seventeenth century, and even now form the
background of many popular tales and songs, especially of
those of the “wandering people” and beggars. One of the
most beautiful stories of this kind is The Holy Virgin’s Descent
into Hell, the Russian manuscript of which goes back to the
twelfth century. Similar stories were also current in Italy,
where there were colonies of Bulgarian Manicheans, who
were most active in disseminating them. Dante was, no doubt,
acquainted with them when he wrote his Divine Comedy.
The Holy Virgin wished to see the torments of the souls, and She
spoke to Michael, the archistrategos: “Tell me all things that are upon
earth!” And Michael said to Her: “As you say, Blessed One: I shall tell
you all things.” And the Holy Virgin said to him: “How many torments
are there, that the Christian race is suffering?” And the
archistrategos said to Her: “Uncountable are the torments!” And the
Blessed One spoke to him: “Show me, in heaven and upon earth!”
Then the archistrategos ordered the angels to come from the
south, and Hell was opened. And She saw those that were suffering
in Hell, and there was a great number of men and women, and there
was much weeping. And the Blessed One asked the archistrategos:
“Who are these?” And the archistrategos said: “These are they who
did not believe in the Father and the Son and the Holy Ghost, but
forgot God and believed in things which God has created for our
sakes; they called everything God: the sun and the moon, the earth
and water, beasts and reptiles. They changed Troyán, Khors, Velés,
Perún[100] to gods, and believed in evil spirits. They are even now
held in evil darkness, therefore they suffer such torments.”
And She saw in another place a great darkness. Said the Holy
Lady: “What is this darkness, and who are those who dwell therein?”
Spoke the archistrategos: “Many souls dwell in this place.” Spoke the
Holy Virgin: “Let the darkness be dispersed that I may see the
torment.” And the angels who watched over the torment answered:
“We have been enjoined not to let them see light until the coming of
your blessed Son who is brighter than seven suns.” And the Holy
Virgin was saddened, and She raised Her eyes to the angels and
looked at the invisible throne of Her Father and spoke: “In the name
of the Father and the Son and the Holy Ghost! Let the darkness be
taken off that I may see this torment.”
And the darkness was lifted, and seven heavens were seen, and
there dwelt there a great multitude of men and women, and there
was loud weeping and a mighty noise. When the Holy Virgin saw
them, She spoke to them, weeping tears: “What have you done,
wretched and unworthy people, and what has brought you here?”
There was no voice, nor an answer from them. And the watching
angels spoke: “Wherefore do you not speak?” And the tormented
said: “Blessed One! We have not seen light for a long time, and we
cannot look up.” The Holy Virgin looking at them wept bitterly. And
the tormented, seeing Her, said: “How is it, Holy Virgin, you have
visited us? Your blessed Son came upon earth and did not ask for
us, nor Abraham the patriarch, nor Moses the prophet, nor John the
Baptist, nor Paul the apostle, the Lord’s favourite. But you, Holy
Virgin and intercessor, you are a protection for the Christian
people.”... Then spoke the Holy Virgin to Michael the archistrategos:
“What is their sin?” And Michael said: “These are they who did not
believe in the Father and the Son and the Holy Ghost, nor in you,
Holy Virgin! They did not want to proclaim your name, nor that from
you was born our Lord Jesus Christ who, having come in the flesh,
has sanctified the earth through baptism: it is for this that they are
tormented here.” Weeping again, the Holy Virgin spoke to them:
“Wherefore do you live in error? Do you not know that all creation
honours my name?” When the Holy Virgin said this, darkness fell
again upon them.
The archistrategos spoke to Her: “Whither, Blessed One, do you
want to go now? To the south, or to the north?” The Blessed One
spoke: “Let us go out to the south!” And there came the cherubim
and the seraphim and four hundred angels, and took the Holy Virgin
to the south where there was a river of fire. There was a multitude of
men and women there, and they stood in the river, some to their
waists, some to their shoulders, some to their necks and some
above their heads. Seeing this, the Holy Virgin wept aloud and asked
the archistrategos: “Who are they that are immerged up to their
waists in the fire?” And the archistrategos said to Her: “They are
those who have been cursed by their fathers and mothers,—for this
the cursed ones suffer torment here.” And the Holy Virgin said: “And
those who are in the fiery flame up to their necks, who are they?”
The angel said to Her: “They are those who have eaten human flesh,
—for this they are tormented here.” And the Holy One said: “Those
who are immerged in the fiery flame above their heads, who are
they?” And the archistrategos spoke: “Those are they, Lady, who
holding the cross have sworn falsely.”... The Holy One spoke to the
archistrategos: “I beg you this one thing, let me also enter, that I may
suffer together with the Christians, for they have called themselves
the children of my Son.” And the archistrategos said: “Rest yourself
in paradise!” And the Holy One said: “I beg you, move the hosts of
the seven heavens and all the host of the angels that we may pray
for the sinners, and God may accept our prayer and have mercy
upon them. I beg you, order the angelic host to carry me to the
heavenly height and to take me before the invisible Father!”
The archistrategos so ordered, and there appeared the cherubim
and seraphim and carried the Blessed One to the heavenly height,
and put Her down at the throne of the invisible Father. She raised
Her hands to Her blessed Son and said: “Have mercy, O Master,
upon the sinners, for I have seen them, and I could not endure: let
me be tormented together with the Christians!” And there came a
voice to Her and said: “How can I have mercy upon them? I see the
nails in my Son’s hands.” And She said: “Master! I do not pray for the
infidel Jews, but for the Christians I ask Thy forgiveness!” And a
voice came to Her: “I see how they have had no mercy upon my
children, so I can have no mercy upon them.”
Spoke again the Holy One: “Have mercy, O Master, upon the
sinners,—the creation of Thine own hands, who proclaim Thy name
over the whole earth and even in their torments, and who in all
places say: “Most Holy Lady, Mother of God, aid us!” Then the Lord
spoke to Her: “Hear, Holy Mother of God! There is not a man who
does not praise Thy name. I will not abandon them, neither in
heaven, nor upon earth.” And the Holy Virgin said: “Where is Moses,
the prophet? Where are all the prophets? And you, fathers, who
have never committed a sin? Where is Paul, God’s favourite? Where
is the Sunday, the pride of the Christian? And where is the power of
the worshipful cross through which Adam and Eve were delivered
from their curse?” Then Michael the archistrategos and all the angels
spoke: “Have mercy, O Master, upon the sinners!” And Moses wept
loud and said: “Have mercy upon them, O Lord! For I have given
them Thy Law!” And John wept and said: “Have mercy, O Master! I
preached Thy gospel to them.” And Paul wept and said: “Have
mercy, O Master! For I carried Thine epistles to the churches.”
And those that were in the darkness heard of this, and they all
wept with one voice and said: “Have mercy upon us, Son of God!
Have mercy upon us, King of all eternity!” And the Master said: “Hear
all! I have planted paradise, and created man according to my
image, and made him lord over paradise, and gave him eternal life.
But they have disobeyed me and sinned in their selfishness and
delivered themselves to death.... You became Christians only in
words, and did not keep my commands; for this you find yourselves
now in the fire everlasting, and I ought not to have mercy upon you!
But to-day, through the goodness of my Father who sent me to you,
and through the intercession of my Mother who wept much for you,
and through Michael, the archistrategos of the gospel, and through
the multitude of my martyrs who have laboured much in your behalf,
I give you from Good Thursday to the holy Pentecost, day and night,
for a rest, and you praise the Father and the Son and the Holy
Ghost!” And they all answered: “Glory be to Thy goodness! Glory to
the Father and the Son and the Holy Ghost, now and for ever!”
FOOTNOTES:
[99] The slope of the mountain near Kíev, where to-day is the
suburb of Podól.
[100] Pagan divinities. For Troyán, see note on p. 82; Khors,
the god of the sun (cf. note on p. 93); Velés, the god of
abundance (cf. note on p. 83); Perún, the god of thunder (see p.
70).
Daniel the Prisoner. (XIII. century.)
For some unknown reason Daniel had been imprisoned in
an island in the Lake of Lach, in the Government of Olónetsk.
He seems to have belonged to the druzhína of Yarosláv
Vsévolodovich of Pereyáslavl, who died in 1247 as Grand
Prince of Vladímir. That is all that is known about the life of
this layman, one of the few in the old period whose writing
has come down to our times. The begging letter which he
addressed to the Prince is composed of incorrectly quoted
biblical passages and popular saws and proverbs; many of
these he drew from an ancient collection, The Bee, in which
moral subjects are arranged in chapters. In their turn, Daniel’s
saws have largely entered into the composition of a very
popular collection of the same kind, The Emerald.
A SERMON ON OMENS
THE ZADÓNSHCHINA
Let us go, O brothers, into the midnight country, the lot of Japheth,
[102] the son of Noah, from whom has risen the most glorious Russia;
let us there ascend the Kíev mountains, and look by the smooth
Dnieper over the whole Russian land, and hence to the Eastern land,
the lot of Shem, the son of Noah, from whom were born the Chinese,
[103] the pagan Tartars, the Mussulmans. They had defeated the race
of Japheth on the river Kayála.[104] And ever since, the Russian land
has been unhappy, and from the battle of the Kálka[105] up to
Mamáy’s defeat it has been covered with grief and sorrow, weeping
and lamenting its children. The Prince and the boyárs, and all the
brave men who had left all their homes, and wealth, and wives,
children, and cattle, having received honour and glory of this world,
have laid down their heads for the Russian land and the Christian
faith.
Let us come together, brothers and friends, sons of Russia! Let us
join word to word! Let us make the Russian land merry, and cast
sorrow on the eastern regions that are to the lot of Shem! Let us sing
about the victory over the heathen Mamáy, and an eulogy to the
Grand Prince Dmítri Ivánovich and his brother,[106] Prince Vladímir
Andréevich!... We shall sing as things have happened, and will not
race in thought, but will mention the times of the first years; we will
praise the wise Boyán,[107] the famous musician in Kíev town. That
wise Boyán put his golden fingers on the living strings, sang the
glory of the Russian princes, to the first Prince Rúrik, Ígor Rúrikovich
and Svyatosláv, Yaropólk, Vladímir Svyatoslávich, Yarosláv
Vladímirovich, praising them with songs and melodious musical
words.—But I shall mention Sofóniya of Ryazán, and shall praise in
songs and musical words the Prince Dmítri Ivánovich and his
brother, Prince Vladímir Andréevich, for their bravery and zeal was
for the Russian land and the Christian faith. For this, Grand Prince
Dmítri Ivánovich and his brother, Prince Vladímir Andréevich,
sharpened their hearts in bravery, arose in their strength, and
remembered their ancestor, Prince Vladímir of Kíev, the tsar of
Russia.
O lark, joy of beautiful days! Fly to the blue clouds, look towards
the strong city of Moscow, sing the glory of Grand Prince Dmítri
Andréevich! They have risen like falcons from the Russian land
against the fields of the Pólovtses. The horses neigh at the Moskvá;
the drums are beaten at the Kolómna; the trumpets blare at
Serpukhóv; the glory resounds over the whole Russian land.
Wonderfully the standards stand at the great Don; the embroidered
flags flutter in the wind; the gilded coats of mail glisten. The bells are
tolled in the vyéche[108] of Nóvgorod the Great. The men of
Nóvgorod stand in front of St. Sophia, and speak as follows: “We
shall not get in time to the aid of Grand Prince Dmítri Ivánovich.”
Then they flew together like eagles from the whole midnight country.
They were not eagles that flew together, but posádniks[109] that went
out with 7000 men from Nóvgorod the Great to Grand Prince Dmítri
Ivánovich and to his brother Vladímir Andréevich.
All the Russian princes came to the aid of Grand Prince Dmítri
Ivánovich, and they spoke as follows: “Lord Grand Prince! Already
do the pagan Tartars encroach upon our fields, and take away our
patrimony. They stand between the Don and Dnieper, on the river
Mechá.[110] But we, lord, will go beyond the swift river Don, will gain
glory in all the lands, will be an object of conversation for the old
men, and a memory for the young.”
Thus spoke Grand Prince Dmítri Ivánovich to his brothers, the
Russian princes: “My dear brothers, Russian princes! We are of the
same descent, from Grand Prince Iván Danílovich.[111] So far we
brothers have not been insulted either by falcon, or vulture, or white
gerfalcon, or this dog, pagan Mamáy.”
Nightingale! If you could only sing the glory of these two brothers,
Ólgerd’s sons,[112] Andréy of Pólotsk and Dmítri of Bryansk, for they
were born in Lithuania on a shield of the vanguard, swaddled under
trumpets, raised under helmets, fed at the point of the spear, and
given drink with the sharp sword. Spoke Andréy to his brother Dmítri:
“We are two brothers, sons of Ólgerd, grandchildren of Gedemín,
great-grandchildren of Skoldimér. Let us mount our swift steeds, let
us drink, O brother, with our helmets the water from the swift Don, let
us try our tempered swords.”
And Dmítri spoke to him: “Brother Andréy! We will not spare our
lives for the Russian land and Christian faith, and to avenge the
insult to Grand Prince Dmítri Ivánovich. Already, O brother, there is a
din and thunder in the famous city of Moscow. But, brother, it is not a
din or thunder: it is the noise made by the mighty army of Grand
Prince Dmítri Ivánovich and his brother Prince Vladímir Andréevich;
the brave fellows thunder with their gilded helmets and crimson
shields. Saddle, brother Andréy, your good swift steeds, for mine are
ready, having been saddled before. We will ride out, brother, into the
clear field, and will review our armies, as many brave men of
Lithuania as there are with us, but there are with us of the brave men
of Lithuania seven thousand mailed soldiers.”
Already there have arisen strong winds from the sea; they have
wafted a great cloud to the mouth of the Dnieper, against the
Russian land; bloody clouds have issued from it, and blue lightnings
flash through them. There will be a mighty din and thunder between
the Don and the Dnieper, and bodies of men will fall on the field of
Kulikóvo, and blood will flow on the river Nepryádva, for the carts
have already creaked between the Don and Dnieper, and the pagan
Tartars march against the Russian land. Grey wolves howl: they wish
at the river Mechá to invade the Russian land. Those are not grey
wolves: the infidel Tartars have come; they wish to cross the country
in war, and to conquer the Russian land. The geese have cackled
and the swans have flapped their wings,—pagan Mamáy has come
against the Russian land and has brought his generals....
What is that din and thunder so early before daybreak? Prince
Vladímir Andréevich has reviewed his army and is leading it to the
great Don. And he says to his brother, Grand Prince Dmítri
Ivánovich: “Slacken not, brother, against the pagan Tartars, for the
infidels are already in the Russian land, and are taking away our
patrimony!”...
The falcons and gerfalcons have swiftly flown across the Don, and
have swooped down on the many flocks of swans: the Russian
princes have attacked the Tartar might, and they strike with their
steel lances against the Tartar armour; the tempered swords thunder
against the Tartar helmets on the field of Kulikóvo, on the river
Nepryádva. Black is the earth under the hoofs, but they had sowed
the field with Tartar bones, and the earth was watered with their
blood, and mighty armies passed by and trampled down hills and
fields, and the rivers, springs and lakes were turbid. They uttered
mighty cries in the Russian land ... and they vanquished the Tartar
horde on the field of Kulikóvo, on the river Nepryádva.
On that field mighty clouds encountered, and in them lightnings
frequently flashed, and terrible thunders clapped: it is the Russian
brave warriors who were engaging the pagan Tartars for the great
insult, and their mighty gilded armour glistened, and the Russian
princes thundered with their tempered swords against the Tartar
helmets....
At that time neither soldiers nor shepherds called in the field near
the Don, in the land of Ryazán, but only ravens croaked for the sake
of the bodies of the dead, so that it was a terror and a pity to hear:
for the grass was watered with blood, and the trees were bent to the
ground with sorrow, and the birds sang pitiful songs. All princesses
and wives of the boyárs and generals wept for the slain. Fedósya,
the wife of Mikúla Vasílevich,[113] and Mary, the wife of Dmítri, wept
early in the morning at Moscow, standing on the city wall, and spoke
as follows: “Don, Don, you are a swift river, and have cut through
stone walls, and flow through the land of the Pólovtses! Bring back
my beloved one to me!”...
All over the Russian land there spread joy and merriment: the
Russian glory was borne through the land, but shame and
destruction came on the pagan Tartars, evil Mussulmans.... The
Grand Prince by his own bravery and with his druzhína vanquished
pagan Mamáy for the sake of the Russian land and the Christian
faith. The pagans deposited their own arms under the Russian
swords, and the trumpets were not sounded, their voices were silent.
Mamáy galloped away from his druzhína, howled like a grey wolf,
and ran away to the city of Khafest....[114]
FOOTNOTES:
TRAVEL TO INDIA