American Journal of Therapeutics 4, 85-60 (1997)
ACUTE RENAL PAPILLARY NECROSIS INDUCED
BY IBUPROFEN
Mohamed G. Atta’ and Andrew Whelton**
Several specific renal syndromes may be induced by the interaction of nonsteroidal anti-
inflammatory drugs (NSAIDs) upon renal function. We report an NSAID-induced form of acute
renal failure that represents a dual mechanism of impact on renal function involving direct paren-
cchymal damage at a renal papillary level and mechanical outflow ureteric obstruction consequent
to acute papillary necrosis. This form of NSAID-related acute renal failure has been reported very
infrequently, We suspect the syndrome is not often recognized clinically. Clinicians and health care
‘workers need to remind constantly the general public concerning the standard steps to be taken to
censure the proper and safe use of over-the-counter drugs. This is especially important considering
the recent FDA approval of the over-the-counter sale of naproxen sodium, ketoprofen, and ibuprofen.
Keywords: acute renal failure, acute papillary necrosis, nonsteroidal antiinflammatory drugs, kidney
failure, analgesics
INTRODUCTION
The impact of nonsteroidal anti-inflammatory drugs
(NSAIDs) on renal function has recently been the sub-
ject of numerous reports and reviews [1-4]. Addition-
ally, the US. Food and Drug Administration (FDA)
approved over-the-counter (OTC) marketing of
naproxen sodium (1994), followed shortly thereafter
(October, 1995) by approval for OTC use of ketopro-
fen. These decisions have added the availability of two
more potent and effective NSAIDs other than ibupro-
fen, which was approved for similar use one decade
‘earlier. Specific renal syndromes have been identified
for NSAID-renal interactions and relevant risk factors
for these interactions have been identified (Table 1).
CASE REPORT
A 42-year-old African-American female was admitted
to the Johns Hopkins Hospital with a painful left
* Division of Nephrology, Johns Hopkins Univesity School of
‘Medicine, Baltimore, MD; * Finch University of Heath Sciences
The Chicago Medical School, North Chicago, IL, USA.
* To whom all correspondence should be addressed, at Finch Uni-
versity of Health Sciences/The Chicago Medica! Schol, 3333,
Green Bay Road, North Chicago, IL 60064-3095, USA.
1075-2765 © 1997 Chapman & Hall
breast abscess and the development of bilateral flank
pain 3 days prior to admission. The patient reported a
13-year history of depression and at the time of evalu-
ation, she was taking sertraline hydrochloride (Zoloft;
Roerig, New York, NY) for this condition. Her medical
records indicated that seven years earlier she had de-
veloped transient hepatitis, apparently secondary to
the use of fluphenazine hydrochloride (Prolixin;
Apothecon, Princeton, NJ). Otherwise, she had been in
‘good health,
Two weeks prior to admission, the patient noted the
development of redness, swelling, and superficial ul-
ceration of the medial aspect of her left breast. As this
became progressively more painful, she began to self-
medicate with OTC ibuprofen. Since this did not ini-
tially relieve the pain, she reported that she ingested
an average of 24 tablets for 3 consecutive days (each
tablet containing 200 mg ibuprofen). She then devel-
oped severe bilateral flank pain, colicky in nature and
radiating to the groin. She also noted the passage of
blood-stained “‘mucous-like” material on one occa-
sion. She did not note the development of gross he-
‘maturia. She denied the use of any other medications,
including intravenous recreational drug use. She pre-
sented to the Emergency Department of the Johns
Hopkins Hospital with combined breast and flank
pain.
During physical examination she was not in obvi-
ous distress and was oriented to time and place. Vital 56
MG ATTA and A WHELTON
Teble 1. Renal effects associated with NSAIDs and related analgesics.
Pathogenesis
‘Acetaminophen Risk factors
Renal effect NSAID
Fluid and electrolyte
disturbances
Sodium and water _4 Prostaglandins
retention
Hyperkalemia J Prostaglandins
Acute renal failure 1 Prostaglandins
Nephrotic syndrome with Acts as allergen -> lympho-
acute interstitial cyte-iymphokine activation
nephritis
‘Acute papillary necrosis/ Hypotension plus £ renal per:
analgesic nephropathy fusion; 4 prostaglandins
NA NSAID use; renal, cardiac,
hepatic impairment
NIA Renal, cardiac impairment,
‘multiple myeloma, DM, K
supplements, K-sparing
diuretic, ACE inti
CHF, renal or hepatic impai
‘ment, ascites, vascular
Unknown; in overdose situ
tions, ? secondary to acute
hepatic failuresinduced disease, volume contrac-
hypotension 3, SLE, shock, sepsis,
advanced age, hyper-
reninemia, hyperaldost
NA 2; female gender, advanced
age, use of fenoprofen
Long-term abuse with 7 dose Long-term, mixed analgesic
and concurrent use of abuse (acetaminophen,
salicylates and caffeine salicylates, and catfeine)
nt-nflammatory drug; SLE—syst
signs on admission were: blood pressure, 91/55 mm
Hg; pulse, 109/min; respiratory rate, 20/min; tem-
perature, 99°F; weight, 110 kg. She had a 10cm area of
shiny yellow ulceration on the medial aspect of her left
breast. There was no skin rash or lymphadenopathy.
Her abdominal examination was benign without cos-
tovertebral angle tenderness. The remainder of the
physical exam was unremarkable.
Admission serum electrolytes, chemistries, and he-
matology tests revealed: 136 mEq/L Na, 3.1 mEq/LK,
85 mEq/L Cl, 20 mEq/L HCO, 42 mg/dL blood urea
nitrogen (BUN), 3.3 mg/dL creatinine, 88 mg/dL glu-
cose, 20,200 WBC, 34.2% hematocrit, and 364,000/
mm’ platelets, At the time of admission, urine dem-
onstrated the presence of 1+ positivity for both heme
and protein on dipstick evaluation. Microscopic uri-
alysis demonstrated the presence of 5-10 erythro-
cytes/high power field and 10 leukocytes /high power
field.
‘The morning after admission, the renal service was
consulted and a repeat urine examination demon-
strated no protein but we did observe a trace heme
reaction on dipstick testing and rare tubular epithelial
cells on microscopic examination. A sonographic im-
age of the abdomen revealed normal size kidneys with
no signs of acute obstruction. Her prior records re-
American Journal of Therapeutics (1997) 4(1)
;Agiotensin-converting enzyme; CHF-congestive heart fallure; dlc—discontinue; OM— diabetes mein
ic lupus erythematosus; 1 indicates increase; L
vealed that her serum creatinine was 1.2 mg/dL sev-
‘eral months earlier.
Acute renal papillary necrosis (RPN) was suspected.
at the time of renal consultation. Initiation of vigorous
diuresis was undertaken by fluid hydration. This re-
sulted in an excellent response. Her serum creatinine
and BUN were reduced to 1.2 mg/dL and 12 mg/dL,
respectively, within 48 hours. During the time of vig-
orous diuresis, no further mucous or tissue-like mate-
rial was detected in her urine, She maintained her nor-
mal renal function upon discharge.
RESULTS
Clinical presentation of renal papillary necrosis
Renal papillary necrosis develops in a wide variety of
conditions (Table 2). Although the clinical course of
RPNis variable, it typically presents clinically in either
an acute or chronic fashion. Chronic RPN usually pur-
sues a protracted and often asymptomatic course over
months or years. It can be found unexpectedly on ex-
cretory urography or a5 an incidental lesion at post-
mortem in an otherwise asymptomatic patient, where-
in a diagnosis of RPN was not clinically entertained.
Acute RPN, by contrast, usually presents with flank ACUTE RENAL PAPILLARY NECROSIS INDUCED BY IBUPROFEN 87
Table 2. Clinical conditions associated with the
development of acute or chronic renal papillary necrosis.
Frequency of
Condition ‘association
Diabetes mellitus 50% to 60%
Urinary tract obstruction 10% to 40%
Analgesic abuse 18% to 20%
Sickle hemoglobinopathy 10% to 15%
Renal allograft rejection 5%
Pyelonephritis 5%
Less commonly:
Rapidly progressive glomerulonephritis
‘Amyloidosis
Cryoglobulinemia
Renal fungal infection
Retrograde radiocontrast injection
Acute pancreatitis
pain, colic, and urinary findings of gross or micro-
scopic hematuria. The passage of sloughed papillae
may be associated with severe lumbar pain that, due
to other causes, is difficult to distinguish clinically
from ureteral colic. Portions of necrotic papillae can be
recovered by straining the urine through a gauze filter
[5,6] The voiding of papillary tissue may be occasion-
ally associated with hematuria that can be massive
and difficult to control. Acute RPN usually, but not
invariably, involves both kidneys [78]. Despite bilat-
eral RPN, evidence of significant renal impairment is
not always present [9]. This is related to the fact that
damage may be limited to a small number of the pa-
pillae since a total of eight papillae are present in a
healthy human kidney. Additionally, despite the dam-
age to the papillary tips, the collecting ducts now dis-
charge their urine into the flattened viable portion of
the renal pyramid with the urine continuing through
the renal outflow tract. The dominant functional ab-
normality then becomes the inability to produce maxi-
mally concentrated urine.
Excretory urography remains the most useful ex-
amination in the diagnosis of RPN [10,11]. Unfortu-
nately, radiologic diagnosis cannot be made until
changes in the papillary region have progressed to a
point where the papillae have become shrunken or a
necrosed papilla appears as a translucent body within
radiocontrast filling the minor calyces. The latter ra-
diographic finding is designated as the ring finding of
renal papillary necrosis because the contrast within
the minor calyces assumes a ring-like appearance as it
surrounds the sloughed papilla. On occasion, radio-
graphic findings can be negative [12,13] despite recov-
ery of sloughed papillary tissue in the urine. In view of
the transient nature of the obstruction induced in the
ureter by the passage of a sloughed papilla (Fig. 1),
renal ultrasound study will not detect such a transient
episode of mechanical obstruction and renal failure
Such was the case in our patient.
Histology and pathophysiology
‘The basic pathophysiologic process in RPN appears to
be ischemic necrosis [14-17]. The sharp demarcation
of the renal papillary lesion and the tissue histology
disclosing coagulative necrosis closely resemble the
changes of infarction. The fact that necrosis is limited
to the distal segment of involved renal pyramids can
be attributed to the physiologic role of maximal uri-
nary concentrating ability displayed by this portion of
the kidney. The production of maximally-concen-
trated urine requires the unique vascular and ana-
tomical characteristics that are found in the renal pa-
pillae. A brief review of these features follows since it
will help explain the pathophysiologic circumstances
that contributed to the genesis of acute papillary ne-
crosis in our patient.
The kidney is divided into a pale outer region, the
cortex, and a darker inner region, the medulla (Fig. 1).
‘The human cortex develops as a multilobar entity. As
result, the medulla is divided into 8 to 18 (average, 8)
striated conical masses called the renal pyramids. The
base of each pyramid is positioned on the corticomed-
ullary boundary with the apex extending toward the
Fig. 1. Diagram of two renal pyra
kidney. One pyramidal tip or renal papilla has become
necrotic and sloughed off the pyramid, impacted within
the ureter, and caused acute outflow obstruction.
American Journal of Therapeutics (1997) 41) 58
renal pelvis to form a papilla. On the tip of each pa-
pilla are 10 to 25 small openings that represent the
distal ends of the collecting ducts. The individual
functioning units of the kidney, the nephrons, number
approximately one million per kidney and link into
these collecting ducts so that the final processing of
urine concentration can take place before the urine is
eliminated via the tips of the papillae. The renal pelvis
represents the extended portion of the upper urinary
tract. In humans, two and sometimes three outpouch-
ings called the major calyces extend outward from the
‘upper dilated end of the renal pelvis. From each of the
major calyces, several minor calyces extend toward
the papillae of the pyramids and drain the urine
formed by each pyramidal unit.
The blood supply to the renal papillae is derived
from two sources: the vasa recta, which arises from the
capillary network surrounding the proximal and di
tal segments of the nephron, and branches of the tor-
tuous arteries in the adventia of the minor calyces. The
vasa recta lie side-by-side and form vascular bundles
that are separated from each other by the intervening
tubules and the capillary plexus formed between the
descending and ascending limbs of the vasa recta. At
the base of the pyramid, or the outer medulla, the
vascular bundles are widest; they gradually decrease
in size and only discrete individual vessels remain
toward the tip of the papilla. The net effect is dimin-
ished blood supply to the papillary tip compared to
the rest of the kidney and pyramid. However, this is
essential for the physiologic operation of the counter-
current multiplier systems that permits the production
of maximally-concentrated or dilute urine [18-21]
This vascular supply is highly responsive to and de-
pendent on local prostaglandin production for its role
in the counter-current multiplier system [18-21]
Determination of the incidence of NSAID-induced
acute papillary necrosis,
‘The exact clinical frequency with which acute papil-
lary necrosis develops during NSAID therapy is un-
known. It appears likely that minor episodes of RPN
are frequently overlooked by both patients and phy-
sicians and that only the symptomatic episodes asso-
ciated with acute flank pain and gross hematuria re-
ceive clinical attention. Because of the infrequent clini-
cal presentation of the syndrome, itis not possible to
assess its rate of occurrence based on prospective clini-
cal trials. Hence, itis only from the literature and from
the database of spontaneous adverse drug reaction re-
ports, as collected by the FDA, that one can attempt to
define the clinical incidence of this problem.
The spontaneous reporting system (SRS) of the Di-
vision of Epidemiology and Surveillance (DES) of the
American Journal of Therapeutics (1997) 4(1)
MG ATTA and A WHELTON
FDA is a computerized database of adverse reactions
reported by health professionals. The present database
contains over 500,000 reports collected since 1969. The
system contains only adverse reactions detected and
reported after marketing the drug. The primary pur-
pose for maintaining the database is for it to serve as
an early warning system for adverse drug reactions
not detected during premarket testing. The SRS de-
pends on a health professional to detect a new clinical
event, attribute the appearance of the clinical event to
the administration of a drug, and report the clinical
event to a drug company or the FDA. The health pro-
fessional may choose to report the adverse reaction to
a drug firm who must, by law, report this to the FDA.
Ninety percent of DES reports are received from drug,
manufacturers and the remaining 10% are reported
directly from other sources (e.g., health professionals
and consumers). Data from all reports are entered into
the DES adverse drug reaction database and the report
images are scanned into an electronic filing system.
‘At our request, the DES retrieved the adverse
NSAID drug reports for the past decade (1985-1995),
as these would likely yield clinical reports of acute
papillary necrosis. Table 3 lists the clinical diagnostic
‘or symptomatic terms under which cases of renal side
effects of NSAID were reported to the FDA. Review of
this renal finding listing emphasizes the importance
of accurate and specific adverse drug reporting to the
FDA since these 18 diagnostic/symptomatic terms
Table 3. Ibuprofen-associated “renal” adverse
reactions spontaneously reported from within the USA
to the FDA 1985-1995.
Renal term (finding) Total reports
‘Acute kidney failure 41
Kidney failure 24
Kidney function abnormalities 20
Nephritis 16
Hematuria 10
Nephrosis
Uremia
Glomerulitis
Urinary frequency
Otiguria
Urine casts
Urine abnormalities
Anuri
Urinary retention
Urinary tract disease
Nocturia
Pain kidney
Kidney calculus
Total
B lassen ssenouee ACUTE RENAL PAPILLARY NECROSIS INDUCED BY IBUPROFEN 59
(Table 3) do not contain a specific reported term for
acute RPN. As a result, we can only describe the inci-
dence of NSAID-induced acute RPN as infrequent
DISCUSSION
The causative role of ibuprofen in the production of
acute papillary necrosis in our patient appears to be
beyond question. As demonstrated in Fig. 1, one or
more sloughed papillae caused transient bilateral ure-
teric obstruction and this resulted in the symptomatic
flank pain as reported by our patient. Rapid improve-
‘ment occurred as a consequence of forced fluid diure-
sis, which dislodged the obstructive sloughed papil-
lae, together with discontinuation of ibuprofen
therapy.
In our patient, itis likely that her short term (3 days)
ingestion of massive amounts (-5 g/d) of ibuprofen
led to a circumstance where prostaglandin-dependent
blood flow to her renal papillae was drastically re-
duced or eliminated as a result of the
of prostaglandin production inhi
therapy dehydration. These combined factors would
likely have produced exceedingly high local ibuprofen
concentrations within the tips of the renal papillae and
this may have provided a direct local tissue toxicity in
addition to the factors that would have set the stage
for drastic reduction in blood flow to the papillary
tips. These pathophysiologic and drug pharmacoki-
netic factors then produced acute renal papillary ne-
crosis.
A comprehensive literature search and in-house
data review yielded citations concerning ibuprofen-
associated renal papillary necrosis [22-25]. Essentially,
all commonly used NSAID have the ability to produce
RPN, characteristically at high dosing levels, as found
in animal toxicity studies. Information contained
within the Upjohn Worldwide Spontaneous database
was reviewed for us for reports of acute papillary ne-
tosis for all strengths of ibuprofen. There were 12
reports described as necrotizing papillitis, renal necro-
sis, or papillary necrosis. Such events have not been
reported with the 200 mg strength ibuprofen products.
Total daily dosage ranges from 400 mg/d to 2400
mg/d in 11 of the 12 reports; in eight of the 12, the
dose ranged from 1200 mg/d to 1800 mg/d. Several
were consumer reports that were not medically con-
firmed. Information concerning significant medical
history or confounding factors was not available in
‘most cases. One patient had a history of mild hyper-
tension. Partial or full recovery was reported in seven
of the 12 cases. Information from the Upjohn World-
wide Spontaneous database cannot be used to calcu-
late the incidence or estimates of drug risks. As with
all spontaneous reporting systems, there is not neces-
sarily a causal relationship between the use of a drug
and the occurrence of an event.
‘Our patient experience illustrates the importance of
continuing the educational efforts directed at the gen-
eral public that are undertaken by medical, regulatory,
and community groups to insure the proper and safe
use of OTC drugs.
ACKNOWLEDGMENT
We thank the Upjohn Company for performing the
literature search for this study,
REFERENCES.
1, Abraham PA, Keane WF: Glomerular and interstitial
disease induced by nonsteroidal anti-inflammatory
drugs. Am J Nephrol 1984-41
2. Clive DM, Stoff JS: Renal syndromes associated with
nonsteroidal anti-inflammatory drugs. N Engl J Med
1984;310:563
3. Whelton A, Hamilton CW: Nonsteroidal ant-inflamma-
tory drugs: Effects on kidney function. J Clin Pharmacol
1991;31:585-598,
4. Whelton A, Stout RL, Spilman PS, Klassen DK: Renal
cffects of ibuprofen, piroxicam, and sulindac in patients
with asymptomatic renal failure: A prospective, ran-
domized, crossover comparison. Ann Intern Med 1990;
112568.
5. Bergnes MA: Recovery of papillae in renal papillary ne-
crosis. Report of two cases. Arch Pathol 1963;75:501
6, Lindholm T: On renal papillary necrosis with special
reference to the diagnostic importance of papillary frag-
‘ments in the urine, therapy and prognosis. Acta Med
Scand 1960;167:319,
7. Lauler DP, Schreiner GE, David A: Renal medullary ne-
crosis, Am J Med 1960;29-132.
8, Sargent JC, Sargent JW: Unilateral renal papillary necro-
sis. J Urol 1955:73:757,
9. Eknoyan G, Quinibi WY, Grissom RT: Renal papillary
necrosis: An update. Medicine 1982;61:55,
10. Lindvall N: Renal papillary necrosis. A roentgeno-
‘graphic study of 155 cases. Acta Radiol (Stockholm)
1960;192{suppl 1):
11. Lindvall N: Radiological changes of renal papillary ne-
crosis. Kidney Int 1978;13:93
12, Failey KF, Kincaid-Smith P: Renal papillary necrosis
with a normal pyelogram. Br Med J 19681156.
13. Lalli AF: Renal papillary necrosis. Am J Roentgenol Rad
Ther Nucl Med 1972:114741.
14. Arruda JAL, Sabatani S, Mehta PK, Sodhi B, Baranowski
R: Functional characterization of drug-induced experi:
mental papillary necrosis. Kidney Int 1979;15:264.
American Journal of Therapeutics (1997) 41) 60
15,
16,
v7,
18.
18.
Kincaid-Smith P, Saker BM, Mckenzie IFC: Lesions in
the vasa recta in experimental analgesic nephropathy.
Lancet 1968;1:24
Nanra RS, Chirawong P, Kincaid-Smith P: Medullary
ischemia in experimental analgesic nephropathy. Aust
NZ J Med 1973:3:580,
Wylie RG, Hill GS, Murray G, Ramsden PW, Heptinstall
RH: Experimental papillary necrosis of the kidney IIL
Effects of reserpine and other pharmacological agents on.
the lesion. Am J Pathol 1972;68:236.
Beeuwkes R IIL, Bonventre JV: Tubular organization and
vascular-tubular relations in the dog kidney. Am J Phys-
Jol 1975,229:695,
Martinez-Maldonado M, Stitzer O: Urine concentration
and dilution in the rat: Contributions of papillary struc-
tures during high rates of urine flow. Kidney Int 1978;
13194,
American Journal of Therapeutics (1997) 4(1)
21.
2,
2,
24
25,
(MG ATTA and A WHELTON
Patrono C, Dunn MJ: The clinical significance of inhibi-
tion of renal prostaglandin synthesis. Kidney Int 1987;
32a
‘Stokes JB: Effect of prostaglandin E, on chloride trans-
port across the rabbit thick ascending limb of Henle:
Selective inhibition of the medullary portion. J Clin In-
‘vest 197964689.
Heaton JM, Bourke E: Papillary necrosis associated with
Vous aimerez peut-être aussi
- The Sympathizer: A Novel (Pulitzer Prize for Fiction)D'EverandThe Sympathizer: A Novel (Pulitzer Prize for Fiction)Évaluation : 4.5 sur 5 étoiles4.5/5 (121)
- A Heartbreaking Work Of Staggering Genius: A Memoir Based on a True StoryD'EverandA Heartbreaking Work Of Staggering Genius: A Memoir Based on a True StoryÉvaluation : 3.5 sur 5 étoiles3.5/5 (231)
- Grit: The Power of Passion and PerseveranceD'EverandGrit: The Power of Passion and PerseveranceÉvaluation : 4 sur 5 étoiles4/5 (588)
- Devil in the Grove: Thurgood Marshall, the Groveland Boys, and the Dawn of a New AmericaD'EverandDevil in the Grove: Thurgood Marshall, the Groveland Boys, and the Dawn of a New AmericaÉvaluation : 4.5 sur 5 étoiles4.5/5 (266)
- Never Split the Difference: Negotiating As If Your Life Depended On ItD'EverandNever Split the Difference: Negotiating As If Your Life Depended On ItÉvaluation : 4.5 sur 5 étoiles4.5/5 (838)
- The Emperor of All Maladies: A Biography of CancerD'EverandThe Emperor of All Maladies: A Biography of CancerÉvaluation : 4.5 sur 5 étoiles4.5/5 (271)
- The Little Book of Hygge: Danish Secrets to Happy LivingD'EverandThe Little Book of Hygge: Danish Secrets to Happy LivingÉvaluation : 3.5 sur 5 étoiles3.5/5 (400)
- The Subtle Art of Not Giving a F*ck: A Counterintuitive Approach to Living a Good LifeD'EverandThe Subtle Art of Not Giving a F*ck: A Counterintuitive Approach to Living a Good LifeÉvaluation : 4 sur 5 étoiles4/5 (5794)
- The World Is Flat 3.0: A Brief History of the Twenty-first CenturyD'EverandThe World Is Flat 3.0: A Brief History of the Twenty-first CenturyÉvaluation : 3.5 sur 5 étoiles3.5/5 (2259)
- Shoe Dog: A Memoir by the Creator of NikeD'EverandShoe Dog: A Memoir by the Creator of NikeÉvaluation : 4.5 sur 5 étoiles4.5/5 (537)
- The Gifts of Imperfection: Let Go of Who You Think You're Supposed to Be and Embrace Who You AreD'EverandThe Gifts of Imperfection: Let Go of Who You Think You're Supposed to Be and Embrace Who You AreÉvaluation : 4 sur 5 étoiles4/5 (1090)
- The Hard Thing About Hard Things: Building a Business When There Are No Easy AnswersD'EverandThe Hard Thing About Hard Things: Building a Business When There Are No Easy AnswersÉvaluation : 4.5 sur 5 étoiles4.5/5 (345)
- Team of Rivals: The Political Genius of Abraham LincolnD'EverandTeam of Rivals: The Political Genius of Abraham LincolnÉvaluation : 4.5 sur 5 étoiles4.5/5 (234)
- Her Body and Other Parties: StoriesD'EverandHer Body and Other Parties: StoriesÉvaluation : 4 sur 5 étoiles4/5 (821)
- Hidden Figures: The American Dream and the Untold Story of the Black Women Mathematicians Who Helped Win the Space RaceD'EverandHidden Figures: The American Dream and the Untold Story of the Black Women Mathematicians Who Helped Win the Space RaceÉvaluation : 4 sur 5 étoiles4/5 (895)
- The Unwinding: An Inner History of the New AmericaD'EverandThe Unwinding: An Inner History of the New AmericaÉvaluation : 4 sur 5 étoiles4/5 (45)
- Elon Musk: Tesla, SpaceX, and the Quest for a Fantastic FutureD'EverandElon Musk: Tesla, SpaceX, and the Quest for a Fantastic FutureÉvaluation : 4.5 sur 5 étoiles4.5/5 (474)
- On Fire: The (Burning) Case for a Green New DealD'EverandOn Fire: The (Burning) Case for a Green New DealÉvaluation : 4 sur 5 étoiles4/5 (74)
- The Yellow House: A Memoir (2019 National Book Award Winner)D'EverandThe Yellow House: A Memoir (2019 National Book Award Winner)Évaluation : 4 sur 5 étoiles4/5 (98)
