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1 redominantly in the distal intestine and the kidney.
2 e fate of monocytes recruited to the injured kidney.
3 ian rhythms, especially within the liver and kidney.
4 n the vascular endothelial cells of lung and kidney.
5 to characterize complex organs, such as the kidney.
6 es of the nephron, the filtering unit of the kidney.
7 of porcine donation after circulatory death kidneys.
8 find that TRPM7 expression increases in UUO kidneys.
9 late contrast enhancement, especially of the kidneys.
10 eogenic cells, and 0.17 +/- 0.15 cGy/MBq for kidneys.
11 of PSMA radiotracers in salivary glands and kidneys.
12 d amyloid deposits in the spleen, liver, and kidneys.
13 ment prevented the development of IRI in the kidneys.
14 vity were the adrenals (0.1835 mSv/MBq), the kidneys (0.1722 mSv/MBq), the submandibular glands (0.14
15 buffered saline (SCI + PBS), human embryonic kidney 293 (HEK293) cells, and hAFSCs transplantation.
16 eceptor isoform 2-expressing human embryonic kidney 293 cells) cells, biochemistry, dual Ca(2+)/volta
18 abnormal cardiolipin remodeling in diabetic kidneys, a cardinal sign of disrupted mitochondrial arch
19 activation of TFEB is the main driver of the kidney abnormalities and mTORC1 hyperactivity in a mouse
21 eceptor blocker telmisartan affected lung or kidney ACE2 or TMPRSS2, except for a small increase in k
24 ze the available literature on the causes of kidney allograft failure, both early and late, both noni
25 recipients enrolled in the Deterioration of Kidney Allograft Function (DeKAF) study were evaluated:
35 -nuclei mRNA sequencing of dissociated mouse kidneys and of dissected cortex, outer, and inner medull
36 rvived the first 3 months with a functioning kidney, and categorized as: deceased-donor kidney transp
38 cycles based on BED(max) for red marrow and kidneys, and a treatment having 4 cycles with optimized
39 involvement (80%-95%), as well as the hairy kidney appearance on computed tomography scan (63%), the
42 of NS8593, a known TRPM7 inhibitor, prevents kidney atrophy in UUO kidneys, retains tubular formation
44 n=581): Patients undergoing first for cause kidney biopsy (KTxBx) 1.7+/-1.4 (mean +/-SD) years postt
45 aradigm from patient stratification based on kidney biopsy findings towards personalized management b
47 ntegrative, multi-omics approaches since the kidney biopsy, blood and urine samples used to generate
49 h makes more efficient use of deceased donor kidneys but reduces access to transplantation for older
55 ereas it might function as an oncoprotein in kidney cancer, for example, by targeting phosphatase and
56 ce in, and potential for, addressing gaps in kidney care; and outlines avenues for conducting researc
58 isolated nuclear envelope lipids from human kidney cells, analyzed their composition and determined
59 lticellular monolayers of Madin-Darby canine kidney cells, highlighting its acuity in reconstructing
60 enge led to robust eGFP-L10a upregulation in kidney, confirming Mac(TRAP) responsiveness in vivo.
62 elayed myeloperoxidase inhibition suppressed kidney damage without augmenting adaptive immune respons
65 es in generating and maintaining NPCs during kidney development, but little is known about the molecu
68 r filtration rate and lowest rate of chronic kidney disease (>=stage 3) from year 1 onwards until stu
72 s been associated with lower risk of chronic kidney disease (CKD) progression, implicating mechanisms
76 r liver disease; 2.04 (95% CI 1.30-3.20) for kidney disease and 8.15 (95% CI 3.59-18.5) for lung absc
77 human cohorts: the African American Study of Kidney Disease and Hypertension and the Atherosclerosis
78 randomly assigned 777 patients with advanced kidney disease and moderate or severe ischemia on stress
79 tional sample of 1000 patients with advanced kidney disease between 2004 and 2014 who were followed u
81 d risk of cardiovascular disease and chronic kidney disease in those with gout, novel associations of
83 ctive for the treatment of anemia in chronic kidney disease patients and may also be beneficial for t
85 national transplant registry for 35 849 T2DM kidney disease patients who received transplant between
86 nt GSTM1 deletion variant is associated with kidney disease progression in human cohorts: the African
87 .67; 95% CI, 1.02, 2.72, P = .04), perceived kidney disease risk following donation (aOR, 1.68; 95% C
88 hin human BSND significantly associates with kidney disease severity in a patient cohort with CEP290
89 aimed to assess whether adding biomarkers of kidney disease to conventional risk factors improved 10-
90 to assess and address patient activation in kidney disease to facilitate best practices for supporti
91 obesity, hypertension, diabetes, and chronic kidney disease) and yielded additional insights into the
93 , albuminuria, autosomal dominant polycystic kidney disease, and ischemia/reperfusion-induced acute k
94 hen evaluated autoimmune disease parameters, kidney disease, and response to in vivo TLR7/9 pathogeni
95 ein PKD2 cause autosomal dominant polycystic kidney disease, but the function of PKD2 in cilia remain
96 2,8-DHA nephropathy, leading to progressive kidney disease, characterized by crystal deposits, tubul
97 coronary artery disease, stroke and chronic kidney disease, complemented by a systematic review of r
98 f LTBI testing (e.g., HIV, diabetes, chronic kidney disease, etc.) were identified from physician cla
99 s, and iii) altered ER Ca(2+) homeostasis in kidney disease, including podocytopathy, diabetic nephro
100 the most common being hypertension, chronic kidney disease, obstructive sleep apnoea, and metabolic
121 is a key aspect in the evaluation of living kidney donor candidates; however, data on performance of
122 ttle data on how kidney quality, measured by kidney donor profile index (KDPI), impacts KALT survival
123 recipients were allocated kidneys with lower Kidney Donor Profile Index (median 30% versus 35%, P < 0
125 SAs were associated with 3.52 fewer expected kidney donors per 100 eligible deaths than non-Gulf Stat
127 3(hu/hu) mice display elevated biomarkers of kidney dysfunction, glomerulosclerosis, C3/C5b-9 deposit
129 ent to induce detectable HIF activity in the kidney endothelium, in vitro experiments implicated a hu
131 ar gene transcripts as those observed in ECD kidneys, except that tumor necrosis factor alpha and mon
132 y significant difference in the incidence of kidney failure (31.7% with intervention vs 27.3% with pl
133 ge volumes of fluid removal in patients with kidney failure who are treated with intermittent haemodi
135 risk factor for the progression to end-stage kidney failure, cardiovascular morbidity, and premature
142 s after transplantation in recipients with a kidney from donors >=80 years was 0.54 (95% confidence i
143 t of adults (>=18 years of age) with reduced kidney function (>=2 measures of estimated glomerular fi
144 0.007) and, in the tertile with both normal kidney function (eGFR 84 +/- 11.7 ml/min/1.73m(2)) and n
145 03 is safe, and that it effectively promotes kidney function following IRI and survival of renal tran
147 phenol A (BPA) and phthalates on measures of kidney function, tubular injury, and oxidative stress ov
154 hypoxic injury compared to controls and the kidneys have reduced expression of the hypoxia-inducible
163 s isolates associated with severe UTI, i.e., kidney infection (pyelonephritis) or urinary-source bact
164 mplications during admission included: acute kidney injury (63%), transaminitis (31%), shock (31%), a
165 d with mortality in patients with both acute kidney injury (adjusted relative risk, 2.38; 95% CI, 1.7
167 alnutrition is common in patients with acute kidney injury (AKI) and the risk of mortality is high, e
169 likely to discard deceased donors with acute kidney injury (AKI) versus without AKI (30% versus 18%).
170 patients with ACLF diagnosed with HRS acute kidney injury (AKI) were randomized to albumin with infu
171 r process can result in recovery after acute kidney injury (AKI) with adaptive proliferation of tubul
176 n about the roles of myeloid cell subsets in kidney injury and in the limited ability of the organ to
177 omplement activation and acute post-ischemic kidney injury are prevented, with additional protection
178 orrelates with increased mortality and acute kidney injury early after transcatheter aortic valve rep
179 48 of 116 patients (41.4%) and severe acute kidney injury in 32 of 116 (27.6%) patients, which was m
181 as a therapeutic strategy to attenuate acute kidney injury in transgenic mice receiving contrast mate
183 of crucial injury response factors-including kidney injury molecule-1 (Kim1), lipocalin 2 (Lcn2), and
185 here was a trend toward higher risk of acute kidney injury requiring renal replacement therapy in SOT
187 rate (GFR) and urine albumin excretion, and kidney injury was evaluated by histopathology and gene e
189 raft dysfunction (EAD), L-GrAFT score, acute kidney injury, and comprehensive complication index were
191 .6; males: 113 [58.2%]); 163 (84%) had acute kidney injury, which was associated variously with dehyd
194 fficacy of transplantation of 30 HCV-viremic kidneys into HCV-negative recipients, followed by early
197 on levels in blood, brain, heart, intestine, kidney, liver, lung, muscle and spleen were determined o
198 different organs including the heart, liver, kidney, lungs, immune system, gastro-intestinal system,
199 RB was independently associated with altered kidney markers with an increased risk of +25 to +31% per
202 n transplant recipients (heart, lung, liver, kidney, multiorgan) at The Hospital for Sick Children (2
205 ristics of blood vessels, the heart, and the kidney of giraffes and how these functional and structur
207 of senescent cells in the lungs, heart, and kidneys of mice that were intraperitoneally injected wit
211 ns have been associated with severe advanced kidney pathologies, such as cystitis and pyelonephritis,
217 kidney tended to decline with the number of kidneys procured up to 549 kidneys per year and then inc
218 en the reassuring information from the first kidney provided by EVNP, the second kidney was not perfu
222 as the metabolic substrate for the heart and kidneys, reduced oxidative stress, lowered serum uric ac
224 which is associated with new-onset, adverse kidney-related outcomes.Study registered with Australian
226 tor Award, MSK's Ludwig Center, Weiss Family Kidney Research Fund, Novartis, The Sidney Kimmel Center
228 M7 inhibitor, prevents kidney atrophy in UUO kidneys, retains tubular formation, and reduces TRPM7 ex
229 However, the clinical significance of the kidney's clearance of tubular secretory solutes is uncer
230 y isolated from some lung, brain, liver, and kidney samples that were ZsG and/or PCR positive, and on
233 rapulmonary manifestations included hepatic, kidney, splenic, and bone marrow involvement, and microv
236 MED score category, the risk of developing a kidney stone was between 13% and 41% lower compared with
243 antation candidates who were offered a DCD50 kidney that was eventually accepted for transplantation.
244 could be accurately matched to very similar kidneys that had been transplanted in France; these disc
246 sible pathological changes in blood flow and kidney tissue, and provides retention of 20.5 +/- 3% of
247 ese effects, along with acid accumulation in kidney tissue, combine to accelerate progression of kidn
248 using multiphoton live cell imaging in mouse kidney tissue, FIB-SEM, and other complementary techniqu
251 g kidney, and categorized as: deceased-donor kidney transplant alone (DD-KA, 68%), living-donor kidne
253 roving knowledge among African American (AA) kidney transplant candidates compared to other races.
255 failure in patients (n = 181) who received a kidney transplant in Olmsted County, MN (January 1, 1998
256 We are reporting the first case of CG in a kidney transplant recipient with kidney disease of unkno
257 b (anti-PD-1) for ~9 months to a 57-year-old kidney transplant recipient with metastatic cutaneous sq
260 2014-December 2018) comprising 4 transgender kidney transplant recipients and 2 transgender living do
261 clinical and histologic phenotyping from 224 kidney transplant recipients between 2011 and 2017.
262 hould not be used in high-immunological risk kidney transplant recipients due to a perceived increase
264 evaluated 296 807 adult (age > 17) solitary kidney transplant recipients from the Scientific Registr
265 ation-09 study in which we randomized stable kidney transplant recipients to Tac withdrawal or mainte
270 with end-stage renal disease is longer after kidney transplantation (KT) compared with those remainin
273 ipients (SRTR) data to identify 92 081 adult kidney transplantation candidates who were offered a DCD
274 d racial and sex disparities in living donor kidney transplantation do not appear to be related to ne
275 are new trials in autoimmunity and heart and kidney transplantation to determine effectiveness of inh
276 mulative percentage of patients referred for kidney transplantation within 1 year of dialysis at the
282 rtality, and living-donor and deceased-donor kidney transplants (LDKT/DDKT) March 15-April 30, 2020 t
283 Whether donor leukocytes persist within kidney transplants or play any role in rejection is unkn
285 nism of sodium retention and its location in kidney tubules may vary with time in nephrotic syndrome
286 cords, intraoperative physiological signals, kidney ultrasound imaging, and digitized biopsy specimen
287 We recently demonstrated that removal of one kidney (uninephrectomy [UniNx]) in mice reduced high-fat
288 he first kidney provided by EVNP, the second kidney was not perfused with EVNP and was directly impla
289 rize the survival benefit of accepting DCD50 kidneys, we used 2010-2018 Scientific Registry for Trans
293 pressed genes (DEGs) in Pkd2 single-knockout kidneys, which were used to identify candidate pathways
298 cipients, post-KAS recipients were allocated kidneys with lower Kidney Donor Profile Index (median 30
299 is the dominant RAS peptide in healthy human kidneys with NEP rather than ACE2 being essential for it
300 been transplanted in France; these discarded kidneys would be expected to have allograft survival of