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Journal articles on the topic 'Acute kidney failure'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 August 2024

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1

Williams, Debra M., Sue S. Sreedhar, John J. Mickell, and James C. M. Chan. "Acute Kidney Failure." Archives of Pediatrics & Adolescent Medicine 156, no. 9 (September 1, 2002): 893. http://dx.doi.org/10.1001/archpedi.156.9.893.

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2

OKUDA, SEIYA. "Kidneys. 2. Acute kidney failure in old people." Nihon Naika Gakkai Zasshi 88, no. 3 (1999): 527–31. http://dx.doi.org/10.2169/naika.88.527.

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3

Pei, Juan, Yeoungjee Cho, Yong Pey See, Elaine M. Pascoe, Andrea K. Viecelli, Ross S. Francis, Carolyn van Eps, et al. "Impact of deceased donor with acute kidney injury on subsequent kidney transplant outcomes–an ANZDATA registry analysis." PLOS ONE 16, no. 3 (March 25, 2021): e0249000. http://dx.doi.org/10.1371/journal.pone.0249000.

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Background The need for kidney transplantation drives efforts to expand organ donation. The decision to accept organs from donors with acute kidney injury (AKI) can result in a clinical dilemma in the context of conflicting reports from published literature. Material and methods This observational study included all deceased donor kidney transplants performed in Australia and New Zealand between 1997 and 2017. The association of donor-AKI, defined according to KDIGO criteria, with all-cause graft failure was evaluated by multivariable Cox regression. Secondary outcomes included death-censored graft failure, death, delayed graft function (DGF) and acute rejection. Results The study included 10,101 recipients of kidneys from 5,774 deceased donors, of whom 1182 (12%) recipients received kidneys from 662 (11%) donors with AKI. There were 3,259 (32%) all-cause graft failures, which included 1,509 deaths with functioning graft. After adjustment for donor, recipient and transplant characteristics, donor AKI was not associated with all-cause graft failure (adjusted hazard ratio [HR] 1.11, 95% CI 0.99–1.26), death-censored graft failure (HR 1.09, 95% CI 0.92–1.28), death (HR 1.15, 95% CI 0.98–1.35) or graft failure when death was evaluated as a competing event (sub-distribution hazard ratio [sHR] 1.07, 95% CI 0.91–1.26). Donor AKI was not associated with acute rejection but was associated with DGF (adjusted odds ratio [OR] 2.27, 95% CI 1.92–2.68). Conclusion Donor AKI stage was not associated with any kidney transplant outcome, except DGF. Use of kidneys with AKI for transplantation appears to be justified.

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4

ISHIKAWA, ISAO. "Motion post-acute kidney failure." Nihon Naika Gakkai Zasshi 94, no. 9 (2005): 1949–55. http://dx.doi.org/10.2169/naika.94.1949.

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5

Qian, Qi, Karl A. Nath, Yiming Wu, Tarek M. Daoud, and Sanjeev Sethi. "Hemolysis and Acute Kidney Failure." American Journal of Kidney Diseases 56, no. 4 (October 2010): 780–84. http://dx.doi.org/10.1053/j.ajkd.2010.03.025.

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6

Dirkes, Susan M. "Acute Kidney Injury vs Acute Renal Failure." Critical Care Nurse 36, no. 6 (December 1, 2016): 75–76. http://dx.doi.org/10.4037/ccn2016170.

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7

Cho, Seong, Yu-Ji Lee, and Sung-Rok Kim. "Acute Peritoneal Dialysis in Patients with Acute Kidney Injury." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 37, no. 5 (September 2017): 529–34. http://dx.doi.org/10.3747/pdi.2016.00264.

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BackgroundThe purpose of this study was to evaluate the efficacy, complications, and mortality rate associated with acute peritoneal dialysis (PD) in patients with acute kidney injury (AKI).MethodsA total of 75 patients who were treated at Samsung Changwon Hospital between February 2005 and March 2016 were included in the study sample. The outcomes included in-hospital survival, renal recovery, metabolic and fluid control rates, and technical success rates.ResultsRefractory heart failure was the most frequent cause of acute PD (49.3%), followed by hepatic failure (20.0%), septic shock (14.7%), acute pancreatitis (9.3%), and unknown causes (6.7%). The hospital survival of patients in the acute PD was 48.0%. Etiologies of acute kidney injury (AKI) (refractory heart failure, acute pancreatitis compared with hepatic failure, septic shock or miscellaneous causes), use of inotropes, use of a ventilator, and simplified acute physiology score (SAPS) II were associated with survival differences. Maintenance dialysis required after survival was high (80.1% [29/36]) due to AKI etiologies (heart or hepatic failures). Metabolic and fluid control rates were 77.3%. The technical success rate for acute PD was 93.3%.ConclusionAcute PD remains a suitable treatment modality for patients with AKI in the era of continuous renal replacement therapy (CRRT). Nearly all patients who require dialysis can be dialyzed with acute PD without mechanical difficulties. This is particularly true in patients with refractory heart failure and acute pancreatitis who had a weak requirement for inotropes.

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8

Kwong, Y. Diana, Kathleen D. Liu, and Raymond K. Hsu. "Kidney Dysfunction After Acute Heart Failure: Is Acute Kidney Disease the New Acute Kidney Injury?" Kidney International Reports 7, no. 3 (March 2022): 378–80. http://dx.doi.org/10.1016/j.ekir.2021.12.034.

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9

Akhmedova Elena Alexandrovna. "Clinical and functional features of the bronchopulmonary system in chronic kidney disease." Texas Journal of Medical Science 16 (January 18, 2023): 57–59. http://dx.doi.org/10.62480/tjms.2023.vol16.pp57-59.

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Renal failure is a syndrome of reduced kidney function. It can happen suddenly (acute) or gradually (chronic). A lot of blood loss, a drop in blood pressure due to a mechanical injury or blood transfusion that does not match the patient's blood group, electric shock, septic abortion, etc.; damage to the kidney parenchyma due to poisoning from drugs and other metal salts; Obstruction of the ureter by tumors or kidney stones, damage to both kidneys due to trauma can cause acute kidney failure.

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10

Chen, Jia-Jin, Tao-Han Lee, George Kuo, Chieh-Li Yen, Shao-Wei Chen, Pao-Hsien Chu, Pei-Chun Fan, Victor Chien-Chia Wu, and Chih-Hsiang Chang. "Acute Kidney Disease After Acute Decompensated Heart Failure." Kidney International Reports 7, no. 3 (March 2022): 526–36. http://dx.doi.org/10.1016/j.ekir.2021.12.033.

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11

Wada, Takashi. "I. Acute Kidney Injury and Acute Renal Failure." Nihon Naika Gakkai Zasshi 103, no. 5 (2014): 1049–54. http://dx.doi.org/10.2169/naika.103.1049.

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12

Miller, Steven B., and Robert J. Anderson. "The kidney in acute respiratory failure." Journal of Critical Care 2, no. 1 (March 1987): 45–48. http://dx.doi.org/10.1016/0883-9441(87)90120-1.

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13

Templeton, Evelyn M., Moritz Lassé, Torsten Kleffmann, Leigh J. Ellmers, Suetonia C. Palmer, Trent Davidson, Nicola J. A. Scott, et al. "Identifying Candidate Protein Markers of Acute Kidney Injury in Acute Decompensated Heart Failure." International Journal of Molecular Sciences 23, no. 2 (January 17, 2022): 1009. http://dx.doi.org/10.3390/ijms23021009.

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One-quarter of patients with acute decompensated heart failure (ADHF) experience acute kidney injury (AKI)—an abrupt reduction or loss of kidney function associated with increased long-term mortality. There is a critical need to identify early and real-time markers of AKI in ADHF; however, to date, no protein biomarkers have exhibited sufficient diagnostic or prognostic performance for widespread clinical uptake. We aimed to identify novel protein biomarkers of AKI associated with ADHF by quantifying changes in protein abundance in the kidneys that occur during ADHF development and recovery in an ovine model. Relative quantitative protein profiling was performed using sequential window acquisition of all theoretical fragment ion spectra–mass spectrometry (SWATH–MS) in kidney cortices from control sheep (n = 5), sheep with established rapid-pacing-induced ADHF (n = 8), and sheep after ~4 weeks recovery from ADHF (n = 7). Of the 790 proteins quantified, we identified 17 candidate kidney injury markers in ADHF, 1 potential kidney marker of ADHF recovery, and 2 potential markers of long-term renal impairment (differential abundance between groups of 1.2–2.6-fold, adjusted p < 0.05). Among these 20 candidate protein markers of kidney injury were 6 candidates supported by existing evidence and 14 novel candidates not previously implicated in AKI. Proteins of differential abundance were enriched in pro-inflammatory signalling pathways: glycoprotein VI (activated during ADHF development; adjusted p < 0.01) and acute phase response (repressed during recovery from ADHF; adjusted p < 0.01). New biomarkers for the early detection of AKI in ADHF may help us to evaluate effective treatment strategies to prevent mortality and improve outcomes for patients.

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14

Sehic, Azra, and Russell W. Chesney. "Acute Renal Failure: Diagnosis." Pediatrics In Review 16, no. 3 (March 1, 1995): 101–6. http://dx.doi.org/10.1542/pir.16.3.101.

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Introduction Although acute renal failure (ARF) is relatively uncommon, its mortality rate is potentially so high that it is important to recognize this condition in children. Rapid deterioration of renal function is caused by numerous insults and results in typical findings, including extracellular volume expansion, hyperkalemia, hypertension, metabolic acidosis, and azotemia. It usually is reversible, with the majority of patients recovering completely. However, ARF can lead to residual impairment of renal function and progress to end-stage renal disease and death. Conservative medical treatment often is life-saving. Definition ARF represents the rapidly progressive (within several hours or days) cessation of renal function, which results in the inability of the kidney to control body homeostasis, manifesting in retention of nitrogenous waste products (azotemia) and fluid and electrolyte imbalance. On the basis of pathophysiologic process, ARF has been divided broadly into three diagnostic categories: prerenal, intrarenal (organic-intrinsic), and postrenal failure (Table 1). Prerenal and early postrenal failures are renal functional disorders and responses of a structurally intact kidney to extrarenal processes. These forms of renal dysfunction recover rapidly as soon as the cause is reversed. However, if these two disorders are not recognized in time, persist too long, or are treated inadequately, they can result in intrinsic renal failure.

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15

Dirkes, Susan. "Acute Kidney Injury: Not Just Acute Renal Failure Anymore?" Critical Care Nurse 31, no. 1 (February 1, 2011): 37–50. http://dx.doi.org/10.4037/ccn2011946.

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Until recently, no uniform standard existed for diagnosing and classifying acute renal failure. To clarify diagnosis, the Acute Dialysis Quality Initiative group stated its consensus on the need for a clear definition and classification system of renal dysfunction with measurable criteria. Today the term acute kidney injury has replaced the term acute renal failure, with an understanding that such injury is a common clinical problem in critically ill patients and typically is predictive of an increase in morbidity and mortality. A classification system, known as RIFLE (risk of injury, injury, failure, loss of function, and end-stage renal failure), includes specific goals for preventing acute kidney injury: adequate hydration, maintenance of renal perfusion, limiting exposure to nephrotoxins, drug protective strategies, and the use of renal replacement therapies that reduce renal injury.

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16

Arutyunov, A. G., R. A. Bashkinov, T. I. Batluk, E. S. Melnikov, and A. N. Ermilova. "Acute kidney injury in patients with chronic heart failure." South Russian Journal of Therapeutic Practice 2, no. 3 (October 3, 2021): 6–17. http://dx.doi.org/10.21886/2712-8156-2021-2-3-6-17.

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The problem of chronic heart failure (CHF) and especially CHF with reduced ejection fraction is one of the most significant for modern healthcare systems. This is due to the high mortality rate, reduced quality of life, frequent hospitalizations and marked comorbidity of patients with this pathology. Involvement of the kidneys in the pathological process is one of the most common comorbid conditions in cardiovascular disease. There are a large number of pathogenetic mechanisms of mutually negative impact of heart failure and renal dysfunction, reflected in the concept of «Cardiorenal syndrome». Moreover, drug therapy of CHF can be one of the causes of kidney damage. Episodes of acute circulatory decompensation as well as a new coronavirus infection (COVID-19) are particularly threatening conditions. The aim of this review is to consolidate the international literature on the problem of acute kidney injury in patients with CHF.

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17

Zaoral, Tomáš. "Acute renal failure and acute kidney injury in children." Pediatrie pro praxi 17, no. 1 (February 1, 2016): 32–36. http://dx.doi.org/10.36290/ped.2016.007.

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18

Moore, Joanna K., Eleanor Love, Darren G. Craig, Peter C. Hayes, and Kenneth J. Simpson. "Acute kidney injury in acute liver failure: a review." Expert Review of Gastroenterology & Hepatology 7, no. 8 (November 2013): 701–12. http://dx.doi.org/10.1586/17474124.2013.837264.

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19

Medar, Shivanand S., Daphne T. Hsu, Jacqueline M. Lamour, and Scott I. Aydin. "Acute Kidney Injury in Pediatric Acute Decompensated Heart Failure." Pediatric Critical Care Medicine 16, no. 6 (July 2015): 535–41. http://dx.doi.org/10.1097/pcc.0000000000000412.

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20

Villacrés, Sindy M., Shivanand S. Medar, and Scott I. Aydin. "Acute Kidney Injury in Children With Acute Respiratory Failure." Clinical Pediatrics 57, no. 11 (June 8, 2018): 1340–48. http://dx.doi.org/10.1177/0009922818779222.

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Background. Acute kidney injury (AKI) is common in critically ill children and develops in association with organ system dysfunction, with acute respiratory failure (ARF) one of the most common. We aim to study AKI in the pediatric ARF population. Methods. Data were retrospectively collected on children aged 1 day to 18 years admitted to the pediatric intensive care unit (PICU) with ARF between 2010 and 2013. Descriptive statistics and multivariate analyses utilizing Mann-Whitney U, Wilcoxon signed rank, χ2, or Fisher’s exact tests were performed to identify risk factors associated with AKI. Results. A total of 186 patients, with median age of 36 months (interquartile range 4-120 months) met the inclusion criteria. ARF was related to pulmonary disease in 49%. AKI was noted in 53% of patients. Patients with AKI had significantly higher serum creatinine ( P < .001) and lower estimated creatinine clearance ( P < .001) compared with those without AKI. Among patients with moderate and severe acute respiratory distress syndrome (ARDS), 64% had AKI versus 46% with mild or no ARDS ( P = .02). Patients with AKI had significantly lower PaO2/FiO2 ratio ( P = .03), longer PICU ( P = .03), and longer hospital length of stay ( P = .01). ARDS patients were less likely to be AKI free on day 7 of hospitalization, as compared with those without ARDS. Multivariate analysis revealed positive end expiratory pressure (odds ratio [OR] = 1.2, confidence interval [CI] = 1.0-1.4; P = .03) and admission serum creatinine (OR = 27.9, CI = 5.2-148.5; P < .001) to be independently associated with AKI. Conclusions. AKI is common in children with ARF. In patients with ARF and AKI, AKI is associated with ARDS and longer PICU and hospital length of stay. Positive end expiratory pressure and serum creatinine are independently associated with AKI.

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21

Maiwall, Rakhi, S. K. Sarin, and Richard Moreau. "Acute kidney injury in acute on chronic liver failure." Hepatology International 10, no. 2 (October 15, 2015): 245–57. http://dx.doi.org/10.1007/s12072-015-9652-y.

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22

Posadas, Maria Aurora, Vincent Yang, Bing Ho, Muhammad Omer, and Daniel Batlle. "Acute Renal Failure and Severe Hypertension from a Page Kidney Post-Transplant Biopsy." Scientific World JOURNAL 10 (2010): 1539–42. http://dx.doi.org/10.1100/tsw.2010.150.

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Page kidney refers to a clinical picture characterized by acute onset of hypertension due to external compression of the kidneys from hematoma, tumor, lymphocele, or urinoma. Hypertension is believed to result from renin-angiotensin-aldosterone activation triggered by renal hypoperfusion and microvascular ischemia. Renal failure, in addition to hypertension, may occur in the setting of a single functional kidney or a diseased contralateral kidney. We report a case of a patient who had a transplant kidney biopsy complicated by a subcapsular perinephric hematoma. The patient presented with an acute increase in blood pressure and a rapid rise in serum creatinine following a transplant kidney routine biopsy. He underwent emergent evacuation of the perinephric hematoma, with consequent decrease of his blood pressure and return of serum creatinine back to his baseline level. Early recognition and rapid intervention are needed in order to correct hypertension and reverse acute renal failure in Page kidney occurring in renal transplant recipients.

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23

Nikolova, M., I. Angelova, V. Kotseva, A. Kostadinova, D. Genov, C. Vutova, N. Koleva, et al. "Acute Kidney Injury and Acute Renal Failure in Coronaviral Infection." Acta Medica Bulgarica 49, no. 3 (October 1, 2022): 38–42. http://dx.doi.org/10.2478/amb-2022-0028.

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Abstract In December 2019 a newly described single-stranded coronavirus, later named SARS-CoV-2, started its expansion around the world and subsequently caused a global pandemic, affecting the lives of millions of people worldwide. SARS-CoV-2 can bind multiple receptors on different cells and thus invade many target organs, including the respiratory and gastrointestinal mucous membranes, lungs, central nervous system, heart, etc. This virus can affect the kidney tissue both directly and as a consequence of other organ involvement or of the treatment administered, causing acute kidney injury and leaving long term squeals that worsen the prognosis. We describe three patients with acute kidney injury and subsequent acute renal failure at the background of coronaviral infection.

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24

Chen, Shanshan, Yupei Li, and Baihai Su. "Acute Kidney Failure: Current Challenges and New Perspectives." Journal of Clinical Medicine 12, no. 10 (May 9, 2023): 3363. http://dx.doi.org/10.3390/jcm12103363.

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Acute kidney failure, also called acute kidney injury (AKI), is defined by a sudden loss of kidney function that is conventionally determined on the basis of increased serum creatinine levels and reduced urinary output [...]

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25

Kim, S. H., M. C. Han, S. Kim, and J. S. Lee. "Acute Renal Failure Secondary to Rhabdomyolysis." Acta Radiologica 33, no. 6 (November 1992): 573–76. http://dx.doi.org/10.1177/028418519203300616.

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MR imaging of the kidney was performed in 6 patients with acute renal failure (ARF) secondary to rhabdomyolysis caused by snake bite (n = 4), crush injury (n = 1), and carbon monoxide poisoning (n = 1). A test for urine myoglobin was positive in all 6 patients and MR imaging was done 6 to 18 days after the causative event of the rhabdomyolysis. MR images in all 6 patients showed globular swelling of the kidneys, preserved corticomedullary contrast on T1-weighted images, and obliteration of corticomedullary contrast on T2-weighted images. Unlike other medical renal diseases in which corticomedullary contrast is lost on T1-weighted images, preservation of the corticomedullary contrast on T1-weighted MR images with globular renal swelling was a constant finding in patients with ARF secondary to rhabdomyolysis.

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26

RUSCHITZKA, FRANK, SIDNEY SHAW, DANIEL GYGI, GEORG NOLL, MATTHIAS BARTON, and THOMAS F. LÜSCHER. "Endothelial Dysfunction in Acute Renal Failure." Journal of the American Society of Nephrology 10, no. 5 (May 1999): 953–62. http://dx.doi.org/10.1681/asn.v105953.

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Abstract. The kidney is an important target and source of the potent vasoconstrictor and mitogen endothelin-1 (ET-1). However, its exact role in acute renal failure (ARF) remains to be determined. ARF was induced in male Wistar-Kyoto rats (n = 7) in a 2-kidney, 2-clip model of 30-min clamping. Twentyfour hours after clamp release, contractions to angiotensin I (AngI) and II, ET-1, and big ET-1 were studied in isolated aortic and renal artery rings. Endothelium-dependent and -independent relaxations were assessed by acetylcholine and sodium nitroprusside. ET-1 clearance, tissue uptake, plasma levels, and vascular and kidney content were investigated. In addition, ETA and EtB receptor mRNA expression was determined. Sham-operated animals served as controls (n = 7). In ARF, ET-1 plasma levels and tissue content of the renal artery, the aorta, and the kidney markedly increased (P < 0.01). Plasma half-life of radiolabeled 125I-ET-1 was markedly prolonged, whereas 125I-ET-1 tissue uptake decreased in the kidney in ARF. Contractions to AngI and AngII were blunted (P < 0.05) and those to KC1 were unchanged, whereas vascular responses to big ET-1 and ET-1 were enhanced in the renal artery and also in the aorta in ARF (P < 0.05 to 0.001). Correspondingly, ETA and EtB receptor mRNA expression significantly increased in both vascular beds. In addition, endothelium-dependent relaxation to acetylcholine was diminished and inversely correlated with vascular ET-1 protein levels in the renal artery (r = -0.827, P < 0.001) and the aorta (r = -0.812, P < 0.001). In conclusion, the present study demonstrates that increase of circulating and tissue ET-1 protein levels and ETA and EtB receptor gene expression occurs, which induces endothelial dysfunction and enhanced vasoconstriction in different vascular beds in ARF.

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27

Gupta, Swarna, Punit Gupta, and Vishal Jain. "A study on outcome of malaria and acute gastroenteritis induced acute kidney injury requiring hemodialysis." International Journal of Advances in Medicine 5, no. 3 (May 22, 2018): 681. http://dx.doi.org/10.18203/2349-3933.ijam20182123.

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Background: Acute kidney injury previously known as acute renal failure, is characterized by the sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys. Acute Kidney Injury is usually manifested as multiorgan failure syndrome and extracorporeal support may also target fluid overload and heart failure, extracorporeal CO2 removal for combined kidney and lung support, albumin dialysis for liver support. Haemodialysis is more effective than peritoneal dialysis for management of Acute Kidney injury as Peritoneal dialysis is associated with clearance limitation and difficulties with fluid removal and is thus rarely used in adults in developed countries.Methods: The study was conducted in the Department of Medicine, Pt. J.N.M. Medical College and Dr. B.R.A.M. Hospital, Raipur (CG), India, from 2010 to 2012. All patients of both the sexes who were diagnosed as a case of Acute Kidney Injury due to Acute Gastroenteritis and Malaria and who were advised for Hemodialysis were included in the study. In our study, 32 patients of Acute Kidney Injury were included. The criteria used for AKI in the study was RIFLE criteria. Hemodialysis was done in all the cases. Quantitative variables are reported as means±SD and qualitative variables as percentage. Factor(s) determining outcome of AKI were tested by univariate analysis using “fisher’s exact test”. All variables with a P value <0.05 in the univariate analysis were defined statistically significant.Results: Out of 32 patients of Acute Kidney Injury in our study, 50% (n=16) were of Malaria associated AKI cases and other 50% (n=16) patients were of Acute Gastroenteritis associated AKI in which 87.5% males,12.5% Females were of Malaria and 75% male,25% Female were in AGE associated AKI. Maximum number of patients presented with features of AKI within first 3days of disease onset i.e. 56.25% (n=9) of malaria patients and 68.75% (n=11) of AGE patients. Mortality due to MOD was more common in Malaria patients as compared to AGE patients. AGE associated AKI patients had different level of deranged SOFA score.Conclusions: Acute kidney injury due to acute gastroenteritis differs from other causes of AKI by frequent occurrence of hypokalemia. Early diagnosis and prompt management can restore the kidney function.

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28

Fortin, Chantal, and Anne Boucher. "Acute Kidney Failure During SARS-CoV-2." Nephrology Nursing Journal 48, no. 5 (2021): 493. http://dx.doi.org/10.37526/1526-744x.2021.48.5.493.

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29

Van den Bergh, B., R. Oyen, and D. R. Kuypers. "Acute kidney failure and an epigastric mass." Clinical Kidney Journal 2, no. 1 (September 1, 2008): 78–79. http://dx.doi.org/10.1093/ndtplus/sfn140.

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30

Saliba, K. Ahmad, A. Colak, S. Gourishankar, and M. Mengel. "Acute Renal Failure in a Kidney Donor." American Journal of Transplantation 12, no. 11 (October 27, 2012): 3158–60. http://dx.doi.org/10.1111/j.1600-6143.2012.04280.x.

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31

Levinsky, Norman G. "Acute Kidney Failure Prerenal, Renal, or Postrenal?" Hospital Practice 20, no. 3 (March 15, 1985): 68G—68T. http://dx.doi.org/10.1080/21548331.1985.11703013.

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32

Oliveira Azevedo, Lília Mariana, Sergio Barroso Hernández, and Julian Valladares Alcobendas. "Acute kidney failure due to polyarteritis nodosa." Medicina Clínica (English Edition) 148, no. 2 (January 2017): 97–99. http://dx.doi.org/10.1016/j.medcle.2016.10.039.

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33

Palop-Larrea, Vicente, Asunción Sancho-Calabuig, José L. Gorriz-Teruel, Inocencia Martinez-Mir, and Luis M. Pallardó-Mateu. "Vasculitis with acute kidney failure and torasemide." Lancet 352, no. 9144 (December 1998): 1909–10. http://dx.doi.org/10.1016/s0140-6736(05)60401-1.

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34

Kao, Chih-Chin, Wei-Shun Yang, Ji-Tseng Fang, Kathleen D. Liu, and Vin-Cent Wu. "Remote organ failure in acute kidney injury." Journal of the Formosan Medical Association 118, no. 5 (May 2019): 859–66. http://dx.doi.org/10.1016/j.jfma.2018.04.005.

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35

Darmon, Michael, Matthieu Legrand, and Nicolas Terzi. "Understanding the kidney during acute respiratory failure." Intensive Care Medicine 43, no. 8 (September 12, 2016): 1144–47. http://dx.doi.org/10.1007/s00134-016-4532-z.

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36

Riley, Alyssa, Daniel J. Gebhard, and Ayse Akcan-Arikan. "Acute Kidney Injury in Pediatric Heart Failure." Current Cardiology Reviews 12, no. 2 (April 4, 2016): 121–31. http://dx.doi.org/10.2174/1573403x12666151119165628.

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37

Neubert, Z., P. Hoffmann, and D. Owshalimpur. "Acute kidney injury with hypoxic respiratory failure." Case Reports 2014, sep22 1 (September 22, 2014): bcr2014206582. http://dx.doi.org/10.1136/bcr-2014-206582.

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38

Šustić, Alan, Žarko Mavrić, Željko Fučkar, Damir Miletić, Vladimir Mozetič, and Boris Mlinarić. "Kidney length in postoperative acute renal failure." Journal of Clinical Ultrasound 26, no. 5 (June 1998): 251–55. http://dx.doi.org/10.1002/(sici)1097-0096(199806)26:5<251::aid-jcu4>3.0.co;2-b.

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39

Averbukh, Z., D. Modai, Y. Leonov, J. Weissgarten, G. Lewinsohn, L. Fucs, A. Golik, and E. Rosenmann. "Rhabdomyolysis and Acute Renal Failure Induced by Paraphenylenediamine." Human Toxicology 8, no. 5 (September 1989): 345–48. http://dx.doi.org/10.1177/096032718900800502.

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1 We present a 40-year-old healthy man who developed a typical clinical picture of rhabdomyolysis following the administration of paraphenylenediamine by a witchdoctor as a pain killer. 2 Two groups of 15 mice were given paraphenylenediamine 70 mg/kg and 35 mg/kg respectively. Biochemical and histological findings of rhabdomyolysis developed in both groups, without kidney damage. 3 Paraphenylenediamine may cause rhabdomyolysis resulting in acute renal failure in humans. In mice, however, it produces rhabdomyolysis, but the kidneys are not affected.

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MURZAKHMETOVA, A., V. KEMAIKIN, A. AINABAY, A. MEIRAMOVA, and B. AINABEKOVA. "ACUTE KIDNEY INJURY IN PATIENTS WITH ACUTE LEUKEMIA AFTER HEMATOPOIETIC STEM CELL TRANSPLANTATION: A SERIES OF CLINICAL CASES." Oncologia i radiologia Kazakhstana 65, no. 3 (September 30, 2022): 32–36. http://dx.doi.org/10.52532/2663-4864-2022-3-65-32-36.

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Relevance: Acute renal kidney injury is a severe complication in patients with acute leukemia who underwent hematopoietic stem cell transplantation (HSCT). According to statistics, acute renal dysfunction often occurs in the first 100 days after HSCT. This study aimed to evaluate kidney function in patients with acute leukemia after hematopoietic stem cell transplantation. Methods: The article presents clinical cases of patients with acute lymphoblastic leukemia who developed acute renal failure after HSCT. The dynamics of the functional state of kidneys in patients with acute lymphoblastic leukemia after HSCT are described. Results: The acute kidney disorder in the studied patients was mainly caused by HSCT complications. We have identified renal kidney damage in the form of acute tumor lysis and thrombotic microangiopathy. Conclusion: Patients with acute lymphoblastic leukemia risk developing acute kidney disorder during HSCT, which requires careful monitoring of kidney function, especially in the early post-transplant period

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41

Maltseva, L. A., L. V. Novytska-Usenko, V. V. Nykonov, and T. V. Kanchura. "Sepsis-associated acute kidney injury." EMERGENCY MEDICINE 17, no. 6 (January 10, 2022): 44–50. http://dx.doi.org/10.22141/2224-0586.17.6.2021.242326.

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Acute kidney injury (AKI) is a condition that develops as a result of a rapid decrease in the glomerular filtration rate, which leads to the accumulation of nitrogenous, including urea and creatinine, and non-nitrogenous metabolic products with electrolytic disorders, impairment of the acid-base balance, and the volume of fluid excreted by the kidneys. Objective: to provide a review of the literature concerning sepsis-associated acute kidney injury. We presented the problems of diagnosis, risk factors, the pathogenesis of sepsis-associated acute kidney injury, as well as to outline terminologically the clinical form of sepsis-associated acute kidney injury: the paradigm shifts from ischemia and vasoconstriction to hyperemia and vasodilation, from acute tubular necrosis to acute tubular apoptosis. Sepsis contributes significantly to the development of AKI: in sepsis, it occurs in 19 % of patients; nevertheless, it is much more frequent in septic shock (45 % of cases), the mortality of individuals with AKI is especially high in non-septic and septic conditions (45 and 73 %, respectively). To effectively diagnose the functional state of the kidneys and conduct nephroprotective therapy, stratification scales for assessing the severity of acute kidney damage are applied, which are based on the determination of plasma creatinine level and urine output: RIFLE (risk, injury, failure, loss of kidney function, and end-stage renal failure), AKIN (Acute Kidney Injury Network), KDIGO (Kidney Disease Improving Global Outcomes); the experts considered KDIGO scale more modern and perfect. It has been found that plasma creatinine is not an early biomarker of AKI that indicates the advisability of using other integral indicators. AKI biomarkers are substances that either participate in the pathological process or witness it allowing diagnose AKI even before an increase in plasma creatinine level. The characteristics of the structure, role of functions of such biomarkers as neutrophil gelatinase-associated lipocalin, cystatin C, interleukin-18, kidney injury molecule-1 and others are given. Intensive care for sepsis-associated acute kidney injury includes the standard therapy corresponding to 2016 Surviving Sepsis Campaign and KDIGO guidelines. Also, the paper focuses on renal replacement therapy (RRT): renal and extrarenal indications for the initiation, factors affecting the initiation of RRT, the timing of initiation, ways of optimization, the timing of RRT discontinuation, recommendations for the dose of RRT, the dose of renal replacement therapy in sepsis-associated AKI, choice of method, advantages and disadvantages of continuous RRT and intermittent hemodialysis, medication support for continuous therapy, the role of hemodialysis machine in the intensive care unit.

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Murzakhmetova, A., V. Kemaikin, A. Ainabay, A. Meiramova, and B. Ainabekova. "ACUTE RENAL DISORDER IN PATIENTS WITH ACUTE LEUKEMIA AFTER HEMATOPOIETIC STEM CELL TRANSPLANTATION: A SERIES OF CLINICAL CASES." Oncologia i radiologia Kazakhstana 65, no. 3 (September 30, 2022): 32–36. http://dx.doi.org/10.52532/2521-6414-2022-3-65-32-36.

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Relevance: Acute renal kidney disorder is a serious complication in patients with acute leukemia who underwent hematopoietic stem cell transplantation (HSCT). According to statistics, acute renal dysfunction often occurs in the first 100 days after HSCT. This study aimed to evaluate kidney function in patients with acute leukemia after hematopoietic stem cell transplantation. Methods: The article presents clinical cases of patients with acute lymphoblastic leukemia who developed acute renal failure after HSCT. The dynamics of the functional state of kidneys in patients with acute lymphoblastic leukemia after HSCT are described. Results: The acute kidney disorder in the studied patients was mainly caused by HSCT complications. We have identified renal kidney damage in the form of acute tumor lysis and thrombotic microangiopathy. Conclusion: Patients with acute lymphoblastic leukemia risk developing acute kidney disorder during HSCT, which requires careful monitoring of kidney function, especially in the early post-transplant period.

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Rose, Ashley, Samuel Slone, and Eric Padron. "Relapsed Acute Lymphoblastic Leukemia Presenting as Acute Renal Failure." Case Reports in Nephrology 2019 (May 13, 2019): 1–3. http://dx.doi.org/10.1155/2019/7913027.

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Acute lymphoblastic leukemia (ALL) is the second most common acute leukemia in adults. It is an aggressive hematologic neoplasm, with a bimodal age distribution typically presenting in childhood and the 6th decade of life (Terwilliger and Abdul-Hay, 2017). Renal injury in ALL is common and can occur through many different mechanisms, such as prerenal acute kidney injury, acute tubular necrosis, renovascular disease, obstruction, glomerulonephritis, and parenchymal infiltration of tumor cells (Luciano and Brewster, 2014). Infiltration of kidneys by leukemia cells is common; however a resultant injury only occurs in about 1% of patients, and renal failure is even more rare (Luciano and Brewster, 2014). Renal failure due to bilateral infiltration of tumor cells has been reported in only a few cases and is thought to be a poor prognostic indicator (Luciano and Brewster, 2014; Sherief et al., 2015). Biopsy is essential to the diagnosis of renal infiltration of leukemia. We present a case of acute renal failure secondary to bilateral renal infiltration of ALL presenting as the first sign of relapse in a young man.

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Magomedaliev, Magomedali, Daniil Korabelnikov, and Sergey Khoroshilov. "Acute Kidney Injury in patients with pneumonia." Russian Medical and Social Journal 1, no. 1 (July 1, 2019): 59–73. http://dx.doi.org/10.35571/rmsj.2019.1.006.

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Mutual complications of impaired lung and kidney function in severe pneumonia (SP) complicated by acute kidney damage (AKP) are considered. The lungs and kidneys perform some similar functions, such as detoxification and regulation of acid-base balance. Lung damage is complicated by dysfunction or impaired renal function, and vice versa, AKI depressively affects lung function. Initially, all organs and tissues, including the kidneys, suffer from hypoxemic respiratory failure. SP is characterized by increased production of inflammatory mediators, decay products of microorganisms and their toxins and ejection them into the bloodstream. Endothelial vascular insufficiency, disseminated microvascular thrombosis, central hemodynamic disorders develop, and as a result, multiple organ failure develops. With the development of AKI, the elimination of uremic toxins and water is disrupted, hyperhydration is formed with an increase in the volume of extravascular water in the lungs on the background of the already existing broken airborne barrier. Uremic toxins depressively affect the heart muscle on the background of an acute pulmonary heart. There is evidence of a negative effect of mechanical ventilation on kidney function, and, conversely, of an adverse effect of AKI on the need and duration of ventilation. The progression of TP and AKP disrupts the acid - base balance due to excess CO2, impaired H+ ion release, and impaired synthesis of HCO3. The pathophysiological mechanisms underlying these relationships are complex, and their effect on the course of the disease is significant.

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Kelly, Katherine J., Jizhong Zhang, Mingsheng Wang, Shaobo Zhang, and Jesus H. Dominguez. "Intravenous renal cell transplantation for rats with acute and chronic renal failure." American Journal of Physiology-Renal Physiology 303, no. 3 (August 1, 2012): F357—F365. http://dx.doi.org/10.1152/ajprenal.00680.2011.

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Acute kidney injury (AKI) and chronic renal failure (CKD) are the most challenging problems in nephrology. Multiple therapies have been attempted but these interventions have minimal effects on the eventual outcomes, and all too often the result is end-stage renal disease (ESRD). The only effective therapy for ESRD is renal transplantation but only a small fraction of patients receive transplants. In this work we introduce a novel approach to transplantation designed to regenerate kidneys afflicted by severe AKI or CKD: intravenous renal cell transplantation (IRCT) with adult rat primary renal cells reprogrammed to express the SAA gene localized and engrafted in kidneys of rat recipients that had severe AKI or CKD. IRCT significantly resolved renal dysfunction and limited kidney damage, inflammation, and fibrosis. Severe CKD was successfully improved by IRCT using kidney cells from donor rats or by renal cell self-donation in a form of autotransplantation. We propose that IRCT with adult primary renal cells reprogrammed to express the SAA gene can be used to effectively treat AKI and CKD.

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Kaur, Gurwant. "Acute Kidney Injury in a Case of Multiorgan Failure, Disseminated Intravascular Coagulation and Purpura Fulminans." International Journal of Clinical Case Reports and Reviews 6, no. 2 (January 8, 2021): 01–05. http://dx.doi.org/10.31579/2690-4861/088.

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Introduction Purpura fulminans (PF) is a life-threatening syndrome consisting of Disseminated Intravascular Coagulation (DIC), thrombotic occlusion of small- and medium-sized blood vessels with skin necrosis. Although there are few studies in the literature, only a minority of them discuss renal manifestations. Case Report We present a case of a 57-year-old Caucasian female with acute kidney injury (AKI) in the setting of multiorgan failure (MOF), DIC and PF. She presented with fever, exudative drainage from her port site, and skin changes concerning for bacteremia. Empiric antibiotics were started after blood, urine, and wound cultures were obtained. None of the cultures grew any organisms. Fever resolved after port removal. She exhibited thrombocytopenia, leukopenia, and neutropenia. Urinalysis showed hyaline casts and a fractional excretion of urea (FeUrea) ≤35% indicating a pre-renal state. Her hospital course was complicated by atrial fibrillation, acute hypoxic respiratory failure requiring mechanical ventilation, and hypovolemic shock requiring pressor support. Further, complicated by multiorgan failure including non-oliguric AKI and heart failure with reduced ejection fraction (HFrEF) of ≤65%. Acute skin findings included dusky, purple macules and patches involving all digits of both hands as well as gangrenous changes on the face and toes. It prompted further investigation by Hematology and Dermatology. Skin biopsy showed early leukocytoclastic vasculitis changes. Her laboratory markers were suggestive of DIC and Purpura Fulminans.

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Shah, Silvi, Anthony C. Leonard, Kathleen Harrison, Karthikeyan Meganathan, Annette L. Christianson, and Charuhas V. Thakar. "Mortality and Recovery Associated with Kidney Failure due to Acute Kidney Injury." Clinical Journal of the American Society of Nephrology 15, no. 7 (June 17, 2020): 995–1006. http://dx.doi.org/10.2215/cjn.11200919.

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Background and objectivesAKI requiring dialysis is a contributor to the growing burden of kidney failure, yet little is known about the frequency and patterns of recovery of AKI and its effect on outcomes in patients on incident dialysis.Design, setting, participants, & measurementsUsing the US Renal Data System, we evaluated a cohort of 1,045,540 patients on incident dialysis from January 1, 2005 to December 31, 2014, retrospectively. We examined the association of kidney failure due to AKI with the outcome of all-cause mortality and the associations of sex and race with kidney recovery.ResultsMean age was 63±15 years, and 32,598 (3%) patients on incident dialysis had kidney failure due to AKI. Compared with kidney failure due to diabetes mellitus, kidney failure attributed to AKI was associated with a higher mortality in the first 0–3 months following dialysis initiation (adjusted hazard ratio, 1.28; 95% confidence interval, 1.24 to 1.32) and 3–6 months (adjusted hazard ratio, 1.16; 95% confidence interval, 1.11 to 1.20). Of the patients with kidney failure due to AKI, 11,498 (35%) eventually recovered their kidney function, 95% of those within 12 months. Women had a lower likelihood of kidney recovery than men (adjusted hazard ratio, 0.86; 95% confidence interval, 0.83 to 0.90). Compared with whites, blacks (adjusted hazard ratio, 0.68; 95% confidence interval, 0.64 to 0.72), Asians (adjusted hazard ratio, 0.82; 95% confidence interval, 0.69 to 0.96), Hispanics (adjusted hazard ratio, 0.82; 95% confidence interval, 0.76 to 0.89), and Native Americans (adjusted hazard ratio, 0.72; 95% confidence interval, 0.54 to 0.95) had lower likelihoods of kidney recovery.ConclusionsKidney failure due to AKI confers a higher risk of mortality in the first 6 months compared with kidney failure due to diabetes or other causes. Recovery within 12 months is common, although less so among women than men and among black, Asian, Hispanic, and Native American patients than white patients.

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Mehta, Ravindra L. "From acute renal failure to acute kidney injury: Emerging concepts*." Critical Care Medicine 36, no. 5 (May 2008): 1641–42. http://dx.doi.org/10.1097/ccm.0b013e3181701481.

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Coelho, Silvia, José Nuno Fonseca, Joana Gameiro, Sofia Jorge, José Velosa, and José António Lopes. "Transient and persistent acute kidney injury in acute liver failure." Journal of Nephrology 32, no. 2 (December 19, 2018): 289–96. http://dx.doi.org/10.1007/s40620-018-00568-w.

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Klaus, Martin, Thomas Sitter, and John Michael Hoppe. "Acute kidney failure reveals primary renal non-Hodgkin lymphoma." BMJ Case Reports 17, no. 4 (April 2024): e259137. http://dx.doi.org/10.1136/bcr-2023-259137.

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A male patient in his 60s was admitted to our hospital with symptoms of dyspnoea, asthenia, diaphoresis and acute kidney failure. No tumour or infection was detected in initial screening. However, laboratory examination suggested that the acute kidney failure was due to an intrarenal cause, exhibiting a tubular injury pattern and indications of tumour lysis syndrome. Initial hydration therapy, paired with intravenous rasburicase, rapidly improved the kidney function. Unfortunately, the kidney function deteriorated once again, prompting a kidney biopsy that revealed an aggressive diffuse large B-cell non-Hodgkin lymphoma of the kidney. The chemotherapy, comprised of R-CHOP scheme, led to a full recovery of the kidney function and complete remission of the lymphoma. Primary renal non-Hodgkin lymphoma without nodal manifestation is rare, and its pathophysiology is poorly understood. Therapy schemes can vary significantly between cases, relying primarily on non-renal-specific haemato-oncological guidelines. Therefore, further studies are needed to develop the best therapeutic approaches.

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