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American Journal of Kidney Diseases :... Oct 2010Deposits of iron and hemosiderosis in the kidney have been observed in diseases with intravascular hemolysis, including paroxysmal nocturnal hemoglobinuria, and valvular...
Deposits of iron and hemosiderosis in the kidney have been observed in diseases with intravascular hemolysis, including paroxysmal nocturnal hemoglobinuria, and valvular heart diseases and prosthetic heart valve implants. However, the decrease in kidney function associated with hemolysis caused by cardiac valvular disease or prostheses is less well recognized. We present a case of intravascular hemolysis after repair and banding of the mitral valve that resulted in massive renal tubular deposition of hemosiderin with decreased kidney function. We discuss the pathophysiologic process of both acute and chronic tubular injury from heme and heme proteins, including injury to organelles resulting in autophagic vacuoles containing damaged organelles, such as mitochondria. We conclude that tubular injury resulting from heme proteins should be considered as a cause of decreased kidney function in all patients with a cardiac valvular disease or prosthesis.
Topics: Acute Kidney Injury; Aged; Biopsy, Needle; Combined Modality Therapy; Disease Progression; Drug Therapy, Combination; Follow-Up Studies; Heart Valve Prosthesis; Heart Valve Prosthesis Implantation; Hemolysis; Hemosiderin; Hemosiderosis; Humans; Immunohistochemistry; Kidney Diseases; Kidney Tubular Necrosis, Acute; Male; Mitral Valve Insufficiency; Renal Dialysis
PubMed: 20605299
DOI: 10.1053/j.ajkd.2010.03.025 -
ESC Heart Failure Oct 2020Acute kidney injury (AKI) during acute heart failure (AHF) is common and associated with increased morbidity and mortality. The underlying pathophysiological mechanism...
AIMS
Acute kidney injury (AKI) during acute heart failure (AHF) is common and associated with increased morbidity and mortality. The underlying pathophysiological mechanism appears to have prognostic relevance; however, the differentiation of true, structural AKI from hemodynamic pseudo-AKI remains a clinical challenge.
METHODS AND RESULTS
The Basics in Acute Shortness of Breath Evaluation Study (NCT01831115) prospectively enrolled adult patients presenting with AHF to the emergency department. Mortality of patients was prospectively assessed. Haemoconcentration, transglomerular pressure gradient (n = 231) and tubular injury patterns (n = 253) were evaluated to investigate pathophysiological mechanisms underlying AKI timing (existing at presentation vs. developing during in-hospital period). Of 1643 AHF patients, 755 patients (46%) experienced an episode of AKI; 310 patients (19%; 41% of AKI patients) presented with community-acquired AKI (CA-AKI), 445 patients (27%; 59% of AKI patients) developed in-hospital AKI. CA-AKI but not in-hospital AKI was associated with higher mortality compared with no-AKI (adjusted hazard ratio 1.32 [95%-CI 1.01-1.74]; P = 0.04). Independent of AKI timing, haemoconcentration was associated with a lower two-year mortality. Transglomerular pressure gradient at presentation was significantly lower in CA-AKI compared to in-hospital AKI and no-AKI (P < 0.01). Urinary NGAL ratio concentrations were significantly higher in CA-AKI compared to in-hospital AKI (P < 0.01) or no-AKI (P < 0.01).
CONCLUSIONS
CA-AKI but not in-hospital AKI is associated with increased long-term mortality and marked by decreased transglomerular pressure gradient and tubular injury, probably reflecting prolonged tubular ischemia due to reno-venous congestion. Adequate decongestion, as assessed by haemoconcentration, is associated with lower long-term mortality independent of AKI timing.
Topics: Acute Kidney Injury; Adult; Biomarkers; Heart Failure; Humans; Prognosis; Prospective Studies
PubMed: 32578962
DOI: 10.1002/ehf2.12788 -
Kidney International Dec 2023Acute kidney injury (AKI) is associated with adverse long-term outcomes, but many studies are retrospective, focused on specific patient groups or lack adequate... (Randomized Controlled Trial)
Randomized Controlled Trial
Acute kidney injury (AKI) is associated with adverse long-term outcomes, but many studies are retrospective, focused on specific patient groups or lack adequate comparators. The ARID (AKI Risk in Derby) Study was a five-year prospective parallel-group cohort study to examine this. Hospitalized cohorts with and without exposure to AKI were matched 1:1 for age, baseline kidney function, and diabetes. Estimated glomerular filtration rate (eGFR) and the urinary albumin:creatinine ratio (uACR) were measured at three-months, one-, three- and five-years. Outcomes included kidney disease progression, heart failure episodes and mortality. In 866 matched individuals, kidney disease progression at five years was found to be significantly increased in 30% of the exposed group versus 7% of those non-exposed (adjusted odds ratio 2.49 [95% confidence interval 1.43 to 4.36]). In the AKI group, this was largely characterized by incomplete recovery of kidney function by three months. Further episodes of AKI during follow-up were significantly more common in the exposed group (odds ratio 2.71 [1.94 to 3.77]) and had an additive effect on risk of kidney disease progression. Mortality and heart failure episodes were more frequent in the exposed group, but the association with AKI was no longer significant when models were adjusted for three-month eGFR and uACR. In a general hospitalized population, kidney disease progression after five years was common and strongly associated with AKI. Thus, the time course of changes and the attenuation of associations with adverse outcomes after adjustment for three-month eGFR and uACR suggest non-recovery of kidney function is an important assessment in post-AKI care and a potential future target for intervention. STUDY REGISTRATION: ISRCTN25405995.
Topics: Humans; Cohort Studies; Retrospective Studies; Prospective Studies; Acute Kidney Injury; Heart Failure; Glomerular Filtration Rate; Kidney; Disease Progression; Risk Factors
PubMed: 37611867
DOI: 10.1016/j.kint.2023.08.005 -
Kidney International Jan 2016Acute tubular necrosis causes a loss of renal function, which clinically presents as acute kidney failure (AKI). The biochemical signaling pathways that trigger necrosis... (Review)
Review
Acute tubular necrosis causes a loss of renal function, which clinically presents as acute kidney failure (AKI). The biochemical signaling pathways that trigger necrosis have been investigated in detail over the past 5 years. It is now clear that necrosis (regulated necrosis, RN) represents a genetically driven process that contributes to the pathophysiology of AKI. RN pathways such as necroptosis, ferroptosis, parthanatos, and mitochondrial permeability transition-induced regulated necrosis (MPT-RN) may be mechanistically distinct, and the relative contributions to overall organ damage during AKI in living organisms largely remain elusive. In a synchronized manner, some necrotic programs induce the breakdown of tubular segments and multicellular functional units, whereas others are limited to killing single cells in the tubular compartment. Importantly, the means by which a renal cell dies may have implications for the subsequent inflammatory response. In this review, the recent advances in the field of renal cell death in AKI and key enzymes that might serve as novel therapeutic targets will be discussed. As a consequence of the interference with RN, the immunogenicity of dying cells in AKI in renal transplants will be diminished, rendering inhibitors of RN indirect immunosuppressive agents.
Topics: Acute Kidney Injury; Animals; Clustered Regularly Interspaced Short Palindromic Repeats; Humans; Immunosuppressive Agents; Kidney Transplantation; Kidney Tubules; Necrosis; Receptor-Interacting Protein Serine-Threonine Kinases; Signal Transduction
PubMed: 26759047
DOI: 10.1016/j.kint.2015.10.008 -
Renal Failure Dec 2023Methods for early prediction of the occurrence of acute kidney injury (AKI) were limited. The relationship between triglyceride glucose index (TyG) and the incidence of...
BACKGROUND
Methods for early prediction of the occurrence of acute kidney injury (AKI) were limited. The relationship between triglyceride glucose index (TyG) and the incidence of acute kidney injury in ICU patients is unclear. This study aims to explore the relationship between the two.
METHODS
Based on their TyG index, participants from the Intensive Care Medical Information Market IV (MIMIC-IV) were divided into quartiles. A logistic regression model was constructed based on the risk of acute kidney injury as the main outcome, in order to detect a potential relationship that may exist between the TyG index and acute kidney injury in ICU patients. Finally, in order to confirm the relationship existing between the TyG index and the results, a restricted cubic spline model was used.
RESULTS
In total, 54,263 patients were involved in our present study, of whom 48.2% were male. The occurrence of acute kidney injury was 25.1%. An independent relationship was observed between the TyG index and an increased risk of acute kidney injury through multivariate logistic regression analysis (OR, 1.28 [95% CI 1.22-1.35] < 0.001). Q4 (5.344-9.911) of the TyG index quartiles was independently associated with an increase in the risk of acute kidney injury (OR, 1.43 [95% CI (1.32-1.54)] < 0.001). Through the restricted cubic spline regression model, the risk of acute kidney injury was also demonstrated to increase linearly with an increase in the TyG index.
CONCLUSION
The triglyceride glucose index is related to the risk of acute kidney injury in ICU patients. In the future, in order to further validate this finding, larger prospective studies are needed.
Topics: Humans; Male; Female; Cross-Sectional Studies; Acute Kidney Injury; Glucose; Triglycerides; Intensive Care Units; Blood Glucose; Risk Factors; Biomarkers
PubMed: 37563796
DOI: 10.1080/0886022X.2023.2238830 -
Nature Reviews. Nephrology Nov 2011Renal failure remains a principal cause of morbidity for patients with multiple myeloma. Once reversible factors such as hypercalcemia have been corrected, the most... (Review)
Review
Renal failure remains a principal cause of morbidity for patients with multiple myeloma. Once reversible factors such as hypercalcemia have been corrected, the most common cause of severe renal failure in these patients is a tubulointerstitial pathology that results from the very high circulating concentrations of monoclonal immunoglobulin free light chains. These endogenous proteins can result in isolated proximal tubule cell cytotoxicity, tubulointerstitial nephritis and cast nephropathy (myeloma kidney). Less frequently, high levels of free light chains can lead to immunoglobulin light chain amyloidosis and light chain deposition disease, although these conditions are usually associated with insidious progression of renal failure rather than acute kidney injury. Unless there is rapid intervention, progressive and irreversible damage occurs, particularly interstitial fibrosis and tubular atrophy. Despite advances in our understanding of the pathogenesis of these processes there has been a gap in translating these achievements into improved patient outcomes. The International Kidney and Monoclonal Gammopathy Research Group was formed to address this need. In this Review, we discuss the mechanisms of disease and diagnostic approaches to patients with acute kidney injury complicating multiple myeloma.
Topics: Acute Kidney Injury; Humans; Multiple Myeloma
PubMed: 22045243
DOI: 10.1038/nrneph.2011.168 -
BioMed Research International 2014It is well known that iodinated radiographic contrast media may cause kidney dysfunction, particularly in patients with preexisting renal impairment associated with... (Review)
Review
It is well known that iodinated radiographic contrast media may cause kidney dysfunction, particularly in patients with preexisting renal impairment associated with diabetes. This dysfunction, when severe, will cause acute renal failure (ARF). We may define contrast-induced Acute Kidney Injury (AKI) as ARF occurring within 24-72 hrs after the intravascular injection of iodinated radiographic contrast media that cannot be attributed to other causes. The mechanisms underlying contrast media nephrotoxicity have not been fully elucidated and may be due to several factors, including renal ischaemia, particularly in the renal medulla, the formation of reactive oxygen species (ROS), reduction of nitric oxide (NO) production, and tubular epithelial and vascular endothelial injury. However, contrast-induced AKI can be prevented, but in order to do so, we need to know the risk factors. We have reviewed the risk factors for contrast-induced AKI and measures for its prevention, providing a long list of references enabling readers to deeply evaluate them both.
Topics: Acute Kidney Injury; Contrast Media; Humans; Incidence; Radiography; Risk Factors
PubMed: 25197639
DOI: 10.1155/2014/362725 -
Israel Journal of Medical Sciences Jan 1979
Topics: Acute Kidney Injury; Diuresis; Diuretics; Humans; Ischemia; Kidney; Oliguria
PubMed: 422338
DOI: No ID Found -
British Medical Journal Jun 1980
Topics: Acute Kidney Injury; Central Venous Pressure; Humans; Kidney; Radiography; Renal Dialysis; Urea; Uremia
PubMed: 7388533
DOI: No ID Found -
Journal of the American College of... Apr 2008Cardiac angiography and coronary/vascular interventions depend on iodinated contrast media and consequently pose the risk of contrast-induced acute kidney injury (AKI).... (Review)
Review
Cardiac angiography and coronary/vascular interventions depend on iodinated contrast media and consequently pose the risk of contrast-induced acute kidney injury (AKI). This is an important complication that accounts for a significant number of cases of hospital-acquired renal failure, with adverse effects on prognosis and health care costs. The epidemiology and pathogenesis of contrast-induced AKI, baseline renal function measurement, risk assessment, identification of high-risk patients, contrast medium use, and preventive strategies are discussed in this report. An advanced algorithm is suggested for the risk stratification and management of contrast-induced AKI as it relates to patients undergoing cardiovascular procedures. Contrast-induced AKI is likely to remain a significant challenge for cardiologists in the future because the patient population is aging and chronic kidney disease and diabetes are becoming more common.
Topics: Acute Kidney Injury; Biomarkers; Contrast Media; Humans; Prognosis; Renal Dialysis; Risk Factors; United States
PubMed: 18402894
DOI: 10.1016/j.jacc.2007.12.035