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of critical importance and consequence; "an acute (or critical) lack of research funds"
having or demonstrating ability to recognize or draw fine distinctions; "an acute observer of politics and politicians"; "incisive comments"; "icy knifelike reasoning"; "as sharp and incisive as the stroke of a fang"; "penetrating insight"; "frequent penetrative observations" (同)discriminating, incisive, keen, knifelike, penetrating, penetrative, piercing, sharp
extremely sharp or intense; "acute pain"; "felt acute annoyance"; "intense itching and burning" (同)intense
having or experiencing a rapid onset and short but severe course; "acute appendicitis"; "the acute phase of the illness"; "acute patients"
of an angle; less than 90 degrees
any physical damage to the body caused by violence or accident or fracture etc. (同)hurt, harm, trauma
an act that causes someone or something to receive physical damage
wrongdoing that violates anothers rights and is unjustly inflicted
an accident that results in physical damage or hurt (同)accidental injury
either of two bean-shaped excretory organs that filter wastes (especially urea) from the blood and excrete them and water in urine; "urine passes out of the kidney through ureters to the bladder"

PrepTutorEJDIC

(先の)『鋭い』,とがった / (痛み・感情などが)『激しい』,強い / (知力・感覚などが)『鋭い』,鋭敏な / (事態が)重大な / (病気が)急性の / (音が)高い,鋭い / 鋭角の
『負傷』,『損害』,損傷 / (名誉などを)傷つけること,侮辱《+『to』+『名』》
腎臓;(食品としての)羊(豚など)の腎臓 / 《文》気質,性質,たち(nature)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/08/15 09:31:00」(JST)

wiki en

Acute kidney injury (AKI), previously called acute renal failure (ARF),^[1]^[2] is a rapid loss of kidney function.

Its causes are numerous and include low blood volume from any cause, exposure to substances harmful to the kidney, and obstruction of the urinary tract. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce sufficient amounts of urine.

AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects to other organ systems. Management includes supportive care, such as renal replacement therapy, as well as treatment of the underlying disorder.

1 Signs and symptoms
2 Causes
- 2.1 Prerenal
- 2.2 Intrinsic
- 2.3 Postrenal
3 Diagnosis
- 3.1 Detection
- 3.2 Further testing
4 Classification
- 4.1 Definition
- 4.2 Staging
5 Treatment
- 5.1 Specific therapies
- 5.2 Diuretic agents
- 5.3 Renal replacement therapy
- 5.4 Complications
6 Prognosis
7 Epidemiology
8 History
9 See also
10 References

Signs and symptoms[edit source | edit]

The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea and vomiting.^[3] Marked increases in the potassium level can lead to irregularities in the heartbeat, which can be severe and life-threatening.^[4] Fluid balance is frequently affected, though hypertension is rare.^[5]

Pain in the flanks may be encountered in some conditions (such as thrombosis of the renal blood vessels or inflammation of the kidney); this is the result of stretching of the fibrous tissue capsule surrounding the kidney.^[6] If the kidney injury is the result of dehydration, there may be thirst as well as evidence of fluid depletion on physical examination.^[6] Physical examination may also provide other clues as to the underlying cause of the kidney problem, such as a rash in interstitial nephritis and a palpable bladder.^[6]

Inability to excrete sufficient fluid from the body can cause accumulation of fluid in the limbs (peripheral edema) and the lungs (pulmonary edema),^[3] as well as cardiac tamponade as a result of fluid effusions.^[5]

Causes[edit source | edit]

AKI can be caused by disease, crush injury, contrast agents, some antibiotics, and more.

The causes of acute kidney injury are commonly categorized into prerenal, intrinsic, and postrenal.

Classic laboratory findings in AKI
Type	U_Osm	U_Na	Fe_Na	BUN/Cr
Prerenal	>500	<10	<1%	>20
Intrinsic	<350	>20	>2%	<15^{[citation needed]}
Postrenal	<350	>40	>4%	>15

Prerenal[edit source | edit]

Prerenal causes of AKI ("pre-renal azotemia") are those that decrease effective blood flow to the kidney. These include systemic causes, such as low blood volume, low blood pressure, heart failure, and local changes to the blood vessels supplying the kidney. The latter include renal artery stenosis, or the narrowing of the renal artery which supplies the kidney with blood, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney.

Renal ischaemia ultimately results in functional disorder, depression of GFR, or both. These causes stem from the inadequate cardiac output and hypovolemia or vascular diseases causing reduced perfusion of both kidneys. Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function.

Intrinsic[edit source | edit]

Sources of damage to the kidney itself are dubbed intrinsic. Intrinsic AKI can be due to damage to the glomeruli, renal tubules, or interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively. A cause of intrinsic acute renal failure is tumor lysis syndrome.^[7]

Postrenal[edit source | edit]

Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stone, bladder, ureteral or renal malignancy. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. In post void residual, a catheter is inserted immediately after urinating to measure fluid still in the bladder. 50-100ml suggests neurogenic bladder. A renal ultrasound will demonstrate hydronephrosis if present. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis, however, in case of acute renal failure, the use of IV contrast is contraindicated. On the basic metabolic panel, the ratio of BUN to creatinine may indicate post renal failure.

Diagnosis[edit source | edit]

Detection[edit source | edit]

The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers has been proposed (such as NGAL, KIM-1, IL18 and cystatin C), but none are currently established enough to replace creatinine as a marker of renal function.^{[citation needed]}^[when?]

Sodium and potassium, two electrolytes that are commonly deranged in people with acute kidney injury, are typically measured together with urea and creatinine.^{[citation needed]}

Further testing[edit source | edit]

Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. These may include urine sediment analysis, renal ultrasound and/or kidney biopsy. Indications for renal biopsy in the setting of AKI include:^[8]

Unexplained AKI
AKI in the presence of the nephritic syndrome
Systemic disease associated with AKI

Classification[edit source | edit]

Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output, termed oliguria.

Definition[edit source | edit]

Introduced by the Acute Kidney Injury Network (AKIN), specific criteria exist for the diagnosis of AKI:^[9]

Rapid time course (less than 48 hours)
Reduction of kidney function
- Rise in serum creatinine, defined by either:
  - Absolute increase in serum creatinine of ≥0.3 mg/dl (≥26.4 μmol/l)
  - Percentage increase in serum creatinine of ≥50%
- Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours

Staging[edit source | edit]

The RIFLE criteria, proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in the staging of patients with AKI:^[10]^[11]

Risk: GFR decrease >25%, serum creatinine increased 1.5 times or urine production of <0.5 ml/kg/hr for 6 hours
Injury: GFR decrease >50%, doubling of creatinine or urine production <0.5 ml/kg/hr for 12 hours
Failure: GFR decrease >75%, tripling of creatinine or creatinine >355 μmol/l (with a rise of >44) (>4 mg/dl) OR urine output below 0.3 ml/kg/hr for 24 hours
Loss: persistent AKI or complete loss of kidney function for more than 4 weeks
End-stage renal disease: need for renal replacement therapy (RRT) for more than 3 months

Treatment[edit source | edit]

The management of AKI hinges on identification and treatment of the underlying cause. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances.^[12]

Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.

Specific therapies[edit source | edit]

In prerenal AKI without fluid overload, administration of intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid.

Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and hence renal perfusion. While a useful pressor, there is no evidence to suggest that dopamine is of any specific benefit,^[13] and may be harmful.

The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to Wegener's granulomatosis may respond to steroid medication. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as aminoglycoside, penicillin, NSAIDs, or paracetamol.^[6]

If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.

Diuretic agents[edit source | edit]

The use of diuretics such as furosemide, is widespread and sometimes convenient in ameliorating fluid overload, and is not associated with higher mortality (risk of death).^[14]

Renal replacement therapy[edit source | edit]

Renal replacement therapy, such as with hemodialysis, may be instituted in some cases of AKI. A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of intermittent hemodialysis and continuous venovenous hemofiltration (CVVH).^[15] Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.^[12]^[16]

Complications[edit source | edit]

Metabolic acidosis, hyperkalemia, and pulmonary edema may require medical treatment with sodium bicarbonate, antihyperkalemic measures, and diuretics.

Lack of improvement with fluid resuscitation, therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitate artificial support in the form of dialysis or hemofiltration.^[4]

Prognosis[edit source | edit]

Depending on the cause, a proportion of patients will never regain full renal function, thus entering end-stage renal failure and requiring lifelong dialysis or a kidney transplant. Patients with AKI are more likely to die prematurely after they were discharged from hospital even if their kidney function has recovered.^[2]

Epidemiology[edit source | edit]

New cases of AKI are unusual but not rare, affecting approximately 0.1% of the UK population per year (2000 ppm/year), 20x incidence of new ESRD. AKI requiring dialysis (10% of these) is rare (200 ppm/year), 2x incidence of new ESRD.^[17]

Acute kidney injury is common among hospitalized patients. It affects some 3-7% of patients admitted to the hospital and approximately 25-30% of patients in the intensive care unit.^[18]

History[edit source | edit]

Before the advancement of modern medicine, acute kidney injury was referred to as uremic poisoning while uremia was contamination of the blood with urine. Starting around 1847, uremia came to be used for reduced urine output, a condition now called oliguria, which was thought to be caused by the urine's mixing with the blood instead of being voided through the urethra.^{[citation needed]}

Acute kidney injury due to acute tubular necrosis (ATN) was recognised in the 1940s in the United Kingdom, where crush injury victims during the London Blitz developed patchy necrosis of renal tubules, leading to a sudden decrease in renal function.^[19] During the Korean and Vietnam wars, the incidence of AKI decreased due to better acute management and administration of intravenous fluids.^[20]

References[edit source | edit]

^ Webb S, Dobb G (December 2007). "ARF, ATN or AKI? It's now acute kidney injury". Anaesthesia and Intensive Care 35 (6): 843–4. PMID 18084974.
^ ^a ^b Dan Longo, Anthony Fauci, Dennis Kasper, Stephen Hauser, J. Jameson, Joseph Loscalzo (July 21, 2011). Harrison's Principles of Internal Medicine, 18 edition. McGraw-Hill Professional.
^ ^a ^b Skorecki K, Green J, Brenner BM (2005). "Chronic renal failure". In Kasper DL, Braunwald E, Fauci AS, et al.. Harrison's Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 1653–63. ISBN 0-07-139140-1.
^ ^a ^b Weisberg LS (December 2008). "Management of severe hyperkalemia". Crit. Care Med. 36 (12): 3246–51. doi:10.1097/CCM.0b013e31818f222b. PMID 18936701.
^ ^a ^b Tierney, Lawrence M.; Stephen J. McPhee and Maxine A. Papadakis (2004). "22". CURRENT Medical Diagnosis and Treatment 2005 (44 ed.). McGraw-Hill. p. 871. ISBN 0-07-143692-8. |accessdate= requires |url= (help)
^ ^a ^b ^c ^d Brady HR, Brenner BM (2005). "Chronic renal failure". In Kasper DL, Braunwald E, Fauci AS, et al.. Harrison's Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 1644–53. ISBN 0-07-139140-1.
^ Jim Cassidy, Donald Bissett, Roy A. J. Spence, Miranda Payne (1 January 2010). Oxford Handbook of Oncology. Oxford University Press. p. 706.
^ Papadakis MA, McPhee SJ (2008). Current Medical Diagnosis and Treatment. McGraw-Hill Professional. ISBN 0-07-159124-9.
^ Mehta RL, Kellum JA, Shah SV, et al. (2007). "Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury". Critical Care (London, England) 11 (2): R31. doi:10.1186/cc5713. PMC 2206446. PMID 17331245.
^ Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P (2004). "Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group". Crit Care 8 (4): R204–12. doi:10.1186/cc2872. PMC 522841. PMID 15312219.
^ Lameire N, Van Biesen W, Vanholder R (2005). "Acute renal failure". Lancet 365 (9457): 417–30. doi:10.1016/S0140-6736(05)17831-3. PMID 15680458.
^ ^a ^b Palevsky PM, Zhang JH, O'Connor TZ, et al. (July 2008). "Intensity of renal support in critically ill patients with acute kidney injury". The New England Journal of Medicine 359 (1): 7–20. doi:10.1056/NEJMoa0802639. PMC 2574780. PMID 18492867.
^ Holmes CL, Walley KR (2003). "Bad medicine: low-dose dopamine in the ICU". Chest 123 (4): 1266–75. doi:10.1378/chest.123.4.1266. PMID 12684320.
^ Uchino S, Doig GS, Bellomo R, et al (2004). "Diuretics and mortality in acute renal failure". Crit. Care Med. 32 (8): 1669–77. doi:10.1097/01.CCM.0000132892.51063.2F. PMID 15286542.
^ Pannu N, Klarenbach S, Wiebe N, Manns B, Tonelli M (February 2008). "Renal replacement therapy in patients with acute renal failure: a systematic review". JAMA : the Journal of the American Medical Association 299 (7): 793–805. doi:10.1001/jama.299.7.793. PMID 18285591.
^ Bellomo R, Cass A, Cole L, et al. (October 2009). "Intensity of continuous renal-replacement therapy in critically ill patients". The New England Journal of Medicine 361 (17): 1627–38. doi:10.1056/NEJMoa0902413. PMID 19846848.
^ "Renal Medicine: Acute Kidney Injury (AKI)". Renalmed.co.uk. 2012-05-23. Retrieved 2013-07-17.
^ Brenner and Rector's The Kidney. Philadelphia: Saunders. 2007. ISBN 1-4160-3110-3.
^ Bywaters EG, Beall D (1941). "Crush injuries with impairment of renal function.". Br Med J 1 (4185): 427–32. doi:10.1136/bmj.1.4185.427. PMC 2161734. PMID 20783577.
^ Schrier RW, Wang W, Poole B, Mitra A (2004). "Acute renal failure: definitions, diagnosis, pathogenesis, and therapy". J. Clin. Invest. 114 (1): 5–14. doi:10.1172/JCI22353. PMC 437979. PMID 15232604.

UpToDate Contents

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1. Evaluation of acute kidney injury (acute renal failure) among hospitalized patients
2. 急性腎障害（急性腎不全）のマネージメントの概要 overview of the management of acute kidney injury acute renal failure
3. 急性腎障害（急性腎不全）の定義 definition of acute kidney injury acute renal failure
4. Diagnostic approach to the patient with subacute kidney injury in an outpatient setting
5. 急性腎障害（急性腎不全）における腎前性疾患および急性尿細管壊死の病因および診断 etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury acute renal failure

English Journal

C-reactive protein promotes acute kidney injury by impairing G1/S-dependent tubular epithelium cell regeneration.

Tang Y, Huang XR, Lv J1, Chung AC, Zhang Y2, Chen JZ1, Szalai AJ3, Xu A1, Lan HY.Author information 1*Department of Nephrology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.2†Li Ka Shing Institute of Health Sciences and Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.3§Division of Clinical Immunology and Rheumatology, The University of Alabama at Birmingham, Birmingham, AL, U.S.A.AbstractCRP (C-reactive protein) is regarded as an inflammatory biomarker in AKI (acute kidney injury), but its exact role in AKI remains unclear. Thus we sought to investigate the role of CRP in AKI. Clinically, elevated serum CRP levels were found to associate closely with increased serum creatinine and urea levels (P<0.01) in patients with AKI, which then fell after recovery from AKI. To determine the role of CRP in AKI, an ischaemia/reperfusion mouse model of AKI was developed using Tg (transgenic) mice that express human CRP. Compared with the WT (wild-type) mice, CRP Tg mice developed more severe renal injury at 24 h after ischaemia as determined by significantly increased serum creatinine and tubular necrosis. This was associated with an impaired TEC (tubular epithelium cell) regeneration as shown by an over 60% reduction in PCNA+ (proliferating-cell nuclear antigen) and BrdU+ (bromodeoxyuridine) TECs in CRP Tg mice with AKI. In vitro, the addition of CRP to a human TEC line (HK-2) also largely suppressed the proliferation of TECs. The functional role of CRP in AKI was demonstrated further by the blocking of CRP binding to the FcγRII (Fcγ receptor II) with a neutralizing anti-CD32 antibody, which restored TEC proliferation and prevented AKI in CRP Tg mice. Moreover, we found that impaired G1/S transition by suppression of the phosphorylation of CDK2 (cyclin-dependent kinase 2) and expression of cyclin E may be a key mechanism by which CRP inhibits TEC regeneration during the AKI repair process. In conclusion, CRP plays a pathogenic role in AKI by inhibiting G1/S-dependent TEC regeneration. The results of the present study suggest that targeting CRP signalling may offer a new therapeutic potential for AKI.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 May;126(9):645-59. doi: 10.1042/CS20130471.
CRP (C-reactive protein) is regarded as an inflammatory biomarker in AKI (acute kidney injury), but its exact role in AKI remains unclear. Thus we sought to investigate the role of CRP in AKI. Clinically, elevated serum CRP levels were found to associate closely with increased serum creatinine and u
PMID 24206243

Effect of renal angioembolization on post-traumatic acute kidney injury after high-grade renal trauma: A comparative study of 52 consecutive cases.

Saour M1, Charbit J2, Millet I3, Monnin V4, Taourel P3, Klouche K5, Capdevila X6.Author information 1Department of Anesthesiology and Critical Care, Lapeyronie Hospital, Montpellier I University, Montpellier, France.2Department of Anesthesiology and Critical Care, Lapeyronie Hospital, Montpellier I University, Montpellier, France. Electronic address: j-charbit@chu-montpellier.fr.3Department of Radiology, Lapeyronie Hospital, Montpellier I University, Montpellier, France.4Department of Interventional Radiology, Arnaud de Villeneuve Hospital, Montpellier I University, Montpellier, France.5Department of Critical Care, Lapeyronie Hospital, Montpellier I University, Montpellier, France.6Department of Anesthesiology and Critical Care, Lapeyronie Hospital, Montpellier I University, Montpellier, France; Institut National de la Santé et de la Recherche Médicale, Equipe Inserm U1046, Montpellier F-34295 Cedex 5, France.AbstractBACKGROUND: Acute kidney injury (AKI) is associated with unfavourable outcomes and higher mortality after trauma. Renal angioembolization (RAE) has proved efficiency in the management of high-grade renal trauma (HGRT), but inevitably expose to unavoidable ischaemic areas or contrast medium nephrotoxicity which may impair renal function in the following hours. The aim of this study was to assess the potential acute impact of RAE on renal function in a consecutive series of HGRTs treated nonoperatively.
Injury.Injury.2014 May;45(5):894-901. doi: 10.1016/j.injury.2013.11.030. Epub 2013 Dec 2.
BACKGROUND: Acute kidney injury (AKI) is associated with unfavourable outcomes and higher mortality after trauma. Renal angioembolization (RAE) has proved efficiency in the management of high-grade renal trauma (HGRT), but inevitably expose to unavoidable ischaemic areas or contrast medium nephrotox
PMID 24456608

Biodistribution of mesenchymal stem cell-derived extracellular vesicles in a model of acute kidney injury monitored by optical imaging.

Grange C1, Tapparo M2, Bruno S3, Chatterjee D4, Quesenberry PJ4, Tetta C5, Camussi G1.Author information 1Department of Medical Sciences, University of Torino, Torino, Italy.2Translational Center for Regenerative Medicine, University of Torino, Torino, Italy.3Department of Molecular Biotechnology and Health Science, University of Torino, Torino, Italy.4Department of Medicine, The Warren Alpert Medical School of Brown University, Providence, RI, USA.5EMEA LA Medical Board, Fresenius Medical Care, Bad Homburg, Germany.AbstractMesenchymal stem cells (MSCs) contribute to the recovery of tissue injury, providing a paracrine support. Cell-derived extracellular vesicles (EVs), carrying membrane and cytoplasmatic constituents of the cell of origin, have been described as a fundamental mechanism of intercellular communication. We previously demonstrated that EVs derived from human MSCs accelerated recovery following acute kidney injury (AKI) in vivo. The aim of the present study was to investigate the biodistribution and the renal localization of EVs in AKI. For this purpose, two methods for EV labeling suitable for in vivo tracking with optical imaging (OI), were employed using near infrared (NIR) dye (DiD): i) labeled EVs were generated by MSCs pre-incubated with NIR dye and collected from cell supernatants; ii) purified EVs were directly labeled with NIR dye. EVs obtained with these two procedures were injected intravenously (i.v.) into mice with glycerol-induced AKI and into healthy mice to compare the efficacy of the two labeling methods for in vivo detection of EVs at the site of damage. We found that the labeled EVs accumulated specifically in the kidneys of the mice with AKI compared with the healthy controls. After 5 h, the EVs were detectable in whole body images and in dissected kidneys by OI with both types of labeling procedures. The directly labeled EVs showed a higher and brighter fluorescence compared with the labeled EVs produced by cells. The signal generated by the directly labeled EVs was maintained in time, but provided a higher background than that of the labeled EVs produced by cells. The comparison of the two methods indicated that the latter displayed a greater specificity for the injured kidney.
International journal of molecular medicine.Int J Mol Med.2014 May;33(5):1055-63. doi: 10.3892/ijmm.2014.1663. Epub 2014 Feb 20.
Mesenchymal stem cells (MSCs) contribute to the recovery of tissue injury, providing a paracrine support. Cell-derived extracellular vesicles (EVs), carrying membrane and cytoplasmatic constituents of the cell of origin, have been described as a fundamental mechanism of intercellular communication.
PMID 24573178

Japanese Journal

急性腎障害の予測バイオマーカー, urinary neutrophil gelatinase-associated lipocalin 測定値への影響因子の検討 : 便と白血球の混入および綿球による採尿

武藤秀和,石川健,小西雄[他]
岩手医学雑誌 65(3), 173-179, 2013-08-01
NAID 110009633574

症例脱水により腎障害を合併した薬剤性バゾプレシン分泌過剰症(SIADH)の1症例

山本尚範,足立裕史,高谷悠大 [他]
ICUとCCU = Japanese journal of intensive care medicine : 集中治療医学 37(6), 477-480, 2013-06
NAID 40019736963

Pretreatment of Renal Supscapular Administration of Adipose Tissue-derived Stem Cells Ameliorate Ischemiareperfusion-Induced Acute Kidney Injury

Yamamoto Tokunori,Funahashi Yasuto,Mastukawa Yoshihisa,Kato Masashi,Yoshino Yasushi,Gotoh Momokzu
弘前医学 64(Supplement), S6-S8, 2013-04-02
… BackgroundAcute renal ischemic injury （AKI） represents a major clinical problem with renal arterial clamp at partial nephrectomy. … Intravital videomicroscopy and measurement of red blood cell velocity in peritubular capillaries showed ASCs-injected kidneys displayed significant hemodynamic improvement.ConclusionsThe subscapular administration of ASCs to the kidney attenuates I/R renal injury though anti-inflammation, antiapotoyic effect and peritubular capillary microcirculation. …
NAID 120005230046

Related Pictures

★リンクテーブル★

リンク元	「急性腎障害」「AKI」
関連記事	「injury」「acute」「kidney」

「急性腎障害」

Acute kidney injury
	Classification and external resources
	; Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury.
ICD-10	N17
ICD-9	584
DiseasesDB	11263
MedlinePlus	000501
eMedicine	med/1595
MeSH	D058186

　　[★]

英: acute kidney injury
関: 急性腎不全、急性腎機能不全、acute renal insufficiency

「AKI」

　　[★] 急性腎障害 acute kidney injury

「injury」

　　[★]

n.

傷害、損傷、外傷、受傷
wound or trauma; harm or hurt; usually applied to damage inflicted on the body by an external force.

関: damage、injure、insult、lesion、spoilage、trauma、traumatic、traumatic injury、wound

「acute」

　　[★]

adj.

(疾患)急性の、急性型の、急性的な。(形状が)鋭い、鋭角の。(感覚、才知などが)鋭い。明敏な、鋭い眼識のある。

関: acutely、quick、sharp

「kidney」

　　[★] 腎臓

同: KUB

[aki-vs-arf-1] Webb S, Dobb G (December 2007). "ARF, ATN or AKI? It's now acute kidney injury". Anaesthesia and Intensive Care 35 (6): 843–4. PMID 18084974.

[harrison18-2] Dan Longo, Anthony Fauci, Dennis Kasper, Stephen Hauser, J. Jameson, Joseph Loscalzo (July 21, 2011). Harrison's Principles of Internal Medicine, 18 edition. McGraw-Hill Professional.

[Skorecki-3] Skorecki K, Green J, Brenner BM (2005). "Chronic renal failure". In Kasper DL, Braunwald E, Fauci AS, et al.. Harrison's Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 1653–63. ISBN 0-07-139140-1.

[Weisberg-4] Weisberg LS (December 2008). "Management of severe hyperkalemia". Crit. Care Med. 36 (12): 3246–51. doi:10.1097/CCM.0b013e31818f222b. PMID 18936701.

[cmdt-5] Tierney, Lawrence M.; Stephen J. McPhee and Maxine A. Papadakis (2004). "22". CURRENT Medical Diagnosis and Treatment 2005 (44 ed.). McGraw-Hill. p. 871. ISBN 0-07-143692-8. |accessdate= requires |url= (help)

[Brady-6] Brady HR, Brenner BM (2005). "Chronic renal failure". In Kasper DL, Braunwald E, Fauci AS, et al.. Harrison's Principles of Internal Medicine (16th ed.). New York, NY: McGraw-Hill. pp. 1644–53. ISBN 0-07-139140-1.

[7] Jim Cassidy, Donald Bissett, Roy A. J. Spence, Miranda Payne (1 January 2010). Oxford Handbook of Oncology. Oxford University Press. p. 706.

[isbn0-07-159124-9-8] Papadakis MA, McPhee SJ (2008). Current Medical Diagnosis and Treatment. McGraw-Hill Professional. ISBN 0-07-159124-9.

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Acute kidney injury
Classification and external resources
Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury.
ICD-10	N17
ICD-9	584
DiseasesDB	11263
MedlinePlus	000501
eMedicine	med/1595
MeSH	D058186

匿名

検索

案内

acute kidney injury