Maladaptive repair following kidney tubular injury leads to the development of interstitial fibrosis, a pathology common to chronic kidney diseases (CKD). Dysfunctional DNA damage response plays an important role in the progression of CKD. We found that BRCA1 expression was increased in the kidneys of patients with CKD and fibrotic kidneys of mice. Exon 11 deletion of Brca1 in proximal tubule cells (PTCs) of mice subjected to ischemic or nephrotoxic (aristolochic acid) injury resulted in a reduced number of senescent cells, as assessed by a decrease in phospho-histone H3, p16INK4a, RAD51 recruitment, G2/M cell cycle phase cells, GATA4, and senescence-associated β-galactosidase. There was less production of inflammatory profibrotic mediators and reduced kidney fibrosis. After cisplatin exposure in vitro, human PTCs with reduced BRCA1 had increased apoptosis, decreased RAD51 nuclear foci, and fewer cells in the G2/M cell cycle phase, with reduced IL-6 and sonic hedgehog production. Thus, BRCA1 regulates nonmalignant tissue responses to kidney injury, a role hitherto unrecognized.

To test the hypothesis that ibuprofen ingestion exacerbates markers of acute kidney injury (AKI), gastrointestinal (GI) injury, and endotoxemia after running in the heat.

Using a randomized double-blind crossover design, 11 physically active individuals (six women) ingested 600 mg of ibuprofen or placebo 12- and 1-h before running 1 h in a heated chamber (35°C, 20%-60% R.H.) at an intensity of 60% V̇O 2peak . Blood and urine samples were collected preexercise, postexercise, and 1-h postexercise to assess cytokines and markers of AKI, GI injury, and endotoxemia.

One hour of running in the heat increased markers of AKI (urinary product of IGFBP7•TIMP2 [Placebo: ∆ 1.8 ± 0.8 log 10 (ng·mL 2 )/1000, Ibuprofen: ∆ 1.8 ± 0.9 log 10 (ng·mL 2 )/1000], urinary NGAL, and serum cystatin C), GI damage (I-FABP [Placebo: ∆ 631 ± 446 pg·mL -1 , Ibuprofen: ∆ 576 ± 455 pg·mL -1 ]), and inflammatory cytokines (TNFα [Placebo: ∆ 5.2 ± 3.5 pg·mL -1 , Ibuprofen: ∆ 6.2 ± 4.9 pg·mL -1 ], IL-6, IL-10, and MCP-1), but these changes were not exacerbated by ibuprofen ingestion. There were effects of time ( P < 0.001) and condition ( P = 0.03) for serum IL-8, with greater concentrations in the ibuprofen (pre: 11.4 ± 5.1 pg·mL -1 , post: 15.5 ± 7.3 pg·mL -1 ) trials than placebo (pre: 9.7 ± 4.2 pg·mL -1 , post: 11.7 ± 5.4 pg·mL -1 ). There were no effects of time or condition on markers of endotoxemia (LBP [Placebo: ∆ -1.2 ± 3.2 μg·mL -1 , Ibuprofen: ∆ 1.0 ± 1.6 μg·mL -1 ], sCD14).

These findings indicate that ibuprofen ingestion does not worsen intestinal or renal injury experienced during 1 h of exercise in the heat, but increases pro-inflammatory IL-8.

Elevated and dynamic high-sensitivity cardiac troponin T (hs-cTnT) concentrations are often observed in patients with acute kidney injury (AKI) without myocardial infarction (MI), yet their prognostic implications are unknown. This study investigated associations between hs-cTnT measurements and prognosis in patients with AKI in the emergency department (ED). All first visits to 7 EDs during 2010-2017 by patients without MI fulfilling AKI criteria and ≥1 hs-cTnT measured were included. Logistic and Cox regression analyses were applied to estimate short- and long-term risks of mortality and major adverse cardiovascular events (MACE) according to peak hs-cTnT and relative hs-cTnT change (Δhs-cTnT). A total of 12,136 patients were included. In-hospital- and long-term mortality was 15% and 49% (median follow-up: 3.8 years, IQR: 1.3-6.0). Adjusted in-hospital mortality risk increased with higher peak hs-cTnT, being >8-fold (aOR 8.68, 95% CI: 6.85-11.0) in the highest quintile of hs-cTnT, in whom long-term risk of cardiovascular mortality and MACE was 3-fold (HR: 3.01, 95% CI: 2.74-3.31) and 2-fold (HR: 2.12, 95% CI: 2.00-2.24). Associated risks were elevated already at intermediately elevated hs-cTnT and evident in patients with transient AKI and with normalized eGFR at discharge. Patients with the highest Δhs-cTnT experienced an increased short-term mortality risk, but Δhs-cTnT was not associated with long-term mortality and only weakly associated with the risk of MACE. In conclusion, in patients with AKI but without acute MI, peak hs-cTnT are associated with a worse prognosis in both the short and long term, whereas dynamic hs-cTnT changes may have less prognostic significance.

Extracellular vesicles present in urine (uEVs) are gaining considerable interest as biomarkers, to monitor and predict kidney physio-pathological state. Patients with single ventricle defects and hemodynamic stabilization by Fontan intervention may develop kidney dysfunction as one of the most prevalent extracardiac co-morbidity. Our study aimed to characterize uEVs in children with single ventricle heart defects who underwent Fontan surgery, focusing on markers for monitoring and predicting kidney function, to get physio-pathological insights on possible mechanisms of tissue damage and progression.

We isolated uEVs from urine of 60 paediatric patients affected by single ventricle defects, and from 10 healthy subjects. We analysed uEVs to assess the presence of the reno-protective hormone Klotho, using super resolution microscopy of single uEVs and ELISA. Moreover, we analysed the levels of markers of kidney regeneration, such as CD133 and CD24, and of inflammation using a bead-based cytofluorimetric multiplex analysis. The markers' levels were correlated with patients' demographical, clinical and surgical data.

uEVs from children with single ventricle defects showed reduced levels of Klotho and CD133, compared with the ones of healthy subjects. In parallel, the levels of inflammatory markers (CD3, CD56, and HLA-DR) were significantly higher. Interestingly, levels of inflammatory markers correlated with age of patients and distance from surgery.

This study demonstrates that single ventricle patients, who underwent Fontan's surgery, present altered levels of uEV biomarkers related to regeneration, inflammation and fibrosis, suggesting the presence of early signs of kidney damage and inflammation, compatible with the complexity of the pathology.

Acute kidney injury (AKI) is common in hospitalized adults and a risk factor for chronic kidney disease and mortality. The effect of angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARBs) post-AKI on mortality and long-term kidney function remains unclear.

Propensity-weighted retrospective observational cohort study.

A total of 3,289 patients with AKI admitted to a tertiary care hospital from November 2015-October 2016, with follow-up until September 2020.

ACEi/ARB use within 180 days post-AKI.

All-cause mortality, and major adverse kidney events (MAKE) as defined by composite of renal replacement therapy post-AKI, sustained estimated glomerular filtration rate (eGFR) decline >30% from baseline, or eGFR ≤15 mL/min/1.73 m2.

We generated propensity weights for ACEi/ARB use post-AKI, using age, sex, comorbid conditions, prior medication, intensive care unit admission, severe sepsis, and index AKI Kidney Disease: Improving Global Outcomes severity. Cox proportional hazard models were used to test associations of post-AKI ACEi/ARB with mortality, MAKE, and joint models for eGFR slopes.

A total of 2,309 (70.2%) participants died or experienced MAKE by end of follow-up. 161 (4.9%) and 406 (12.3%) patients initiated or resumed prior ACEi/ARB use within 180 days post-AKI, respectively. Although the overall cohort had no significant mortality association with post-AKI ACEi/ARB use, a significant association with lower mortality was observed in patients with KDIGO 3 AKI (HR, 0.40; 95% CI, 0.21-0.75; P interaction = 0.003). However, post-AKI ACEi/ARB use was associated with increased MAKE in patients without cardiovascular indications for ACEi/ARB use (HR, 1.52; 95% CI, 1.17-1.98; P interaction = 0.03). Although post-AKI use of ACEi/ARB was associated with acute eGFR decline (initial eGFR change -2.3 mL/min/1.73 m2/year; 95% CI, -3.1 to -1.5; P < 0.001), no association with longer-term eGFR decline was observed.

Retrospective observational study on heterogeneous AKI cohort without data on ACEi/ARB cumulative exposure.

Early ACEi/ARB post-AKI was not associated with better long-term survival or kidney function but was associated with lower mortality in patients with KDIGO 3 AKI.

Total hip arthroplasty and total knee arthroplasty are among the most successful orthopedic procedures, with increasing numbers performed annually in the United States. However, adverse perioperative complications like acute kidney injury (AKI) can adversely affect patient outcomes and increase health care costs. The incidence of AKI post-total joint arthroplasty varies widely, with large-scale studies reporting less than 2% and smaller studies indicating rates as high as 21.9%. Holding angiotensin converting enzyme inhibitors, aldosterone receptor blockers, NSAIDs, diuretics, and avoiding nephrotoxic antibiotics can help mitigate the risk.

Acute kidney injury (AKI) is common in critically ill children and associated with adverse short-term outcomes; however, long-term outcomes are not well described.

This longitudinal prospective cohort study examined the prevalence of chronic kidney disease (CKD) and hypertension (HTN) 11 vs. 6 years after pediatric intensive care unit (PICU) admission and association with AKI. We examined children (age < 19 years) without pre-existing kidney disease 11 ± 1.5 years after PICU admission at a single center. AKI was defined using serum creatinine criteria. The primary outcome was a composite of CKD or HTN. CKD was defined as estimated glomerular filtration rate (eGFR) < 90 mL/min/1.73 m2 or albuminuria. Multivariable analyses compared outcomes at 11- vs. 6-year follow-up and association with AKI during PICU admission.

Of 96 children evaluated 11 years after PICU admission, 16% had evidence of CKD or HTN (vs. 28% at 6 years, p < 0.05). Multivariable analysis did not show improvement in outcomes from 6- to 11-year follow-up. eGFR decreased from 6- to 11-year follow-up (adjusted coefficient - 11.7, 95% CI - 17.6 to - 5.9) and systolic and diastolic blood pressures improved. AKI was associated with composite outcome at 6-year (adjusted odds ratio (aOR) 12.7, 95% CI 3.2-51.2, p < 0.001), but not 11-year follow-up (p = 0.31). AKI was associated with CKD (aOR 10.4, 95% CI 3.1-34.7) at 11 years.

This study provides novel data showing that adverse kidney and blood pressure outcomes remain highly prevalent 10 years after critical illness in childhood. The association with AKI wanes over time.

Cardiogenic shock poses a critical challenge characterized by diminished cardiac output and organ perfusion. Timely recognition and risk stratification are essential for effective intervention. Liver cirrhosis adds complexity due to its diverse systemic manifestations. The effect of liver cirrhosis on in-hospital outcomes in cardiogenic shock remains underexplored.

We conducted a retrospective cohort study using the National Inpatient Sample database from 2016 to 2020, matching cirrhotic patients with non-cirrhotic counterparts using propensity scores. The Cochran-Mantel-Haenszel method was used to assess the impact of cirrhosis on in-hospital mortality and complications. Simple linear regression models were used to assess differences in length of stay and cost of hospitalization.

There were a total of 44,288 patients in the cohort, evenly distributed between the group with and without liver cirrhosis. Mean age of the cohort was 64 years (SD 12.5), 69.7 % were males, and 61.3 % were white. The overall in-hospital mortality rate in the cohort was 37.2 % with higher odds of in-hospital mortality in cirrhotic patients [OR = 1.3; 95 % CI (1.25, 1.35)]. Patients with cirrhosis exhibited increased risks of bowel ischemia, acute kidney injury, and sepsis compared to those without cirrhosis. Additionally, they had a heightened overall risk of major bleeding, particularly gastrointestinal bleeding, but a lower risk of intracranial hemorrhage and access site bleeding. Conversely, patients with cirrhosis had lower odds of deep vein thrombosis and pulmonary embolism, as well as arterial access site thrombosis and dissection, leading to reduced odds of peripheral angioplasty, thrombectomy, and amputation. Cirrhotic patients also had increased length of stay and cost of hospitalization.

Liver cirrhosis exacerbates outcomes in cardiogenic shock, necessitating tailored management strategies. Further research is warranted to optimize patient care and understand the underlying mechanisms.

Renal diseases, including glomerulonephritis, acute kidney injury, chronic kidney failure, and kidney tumors are all current global health challenges. Lesions in other systems can cause renal diseases and can affect other systems or even the whole body. Despite ongoing advancements in pharmaceutical and technological innovations, the prognosis for end-stage renal disease, encompassing renal failure and tumors, continues to be bleak. Follistatin-like protein 1 (FSTL1) is a secreted glycoprotein produced mainly by mesenchymal cells. FSTL1 is a glycoprotein that belongs to the family of secreted, cysteine-rich acidic proteins (SPARC). It plays a pivotal role in cell survival, proliferation, differentiation, and migration, as well as in modulating inflammation and immune responses. Research has shown that FSTL1 plays a crucial role in the onset and progression of renal diseases. This review explores the functions and underlying mechanisms of FSTL1 in kidney pathology. SIGNIFICANCE STATEMENT: This review highlights the pivotal role of FSTL1 in renal diseases, particularly its involvement in renal fibrosis, inflammation, and ischemia-reperfusion injury. By elucidating its dual roles across different pathologies, this work underscores FSTL1's potential as both a biomarker and a therapeutic target, offering novel insights for managing chronic kidney disease and associated complications.

Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are a specific class of drugs originally developed for treating type 2 diabetes mellitus. Subsequently, studies demonstrated that their action was not limited to glycemic control but could also have positive effects on other specific outcomes, particularly at the cardiovascular level. Indeed, due to their diuretic effect, SGLT2i improve the clinical control of chronic heart failure and reduce the risk of rehospitalization. In addition, other studies reported a protective effect on major cardiovascular events and mortality. More recently, it has been suggested that the prescription of SGLT2i after an acute myocardial infarction may have positive effects due to their possible effect on inflammation, arrhythmias, and ventricular remodeling. Here, we reviewed studies focused on SGLT2i after an acute myocardial infarction in patients treated with percutaneous coronary intervention.

It is well accepted that acute cognitive dysfunction and delirium can occur with severe acute kidney injury (AKI). Recent evidence has indicated AKI can contribute to incident dementia years later. However, these observations were limited by lack of adjudication in most of these studies and greater severity of AKI.

A retrospective cohort study.

8,148 older adults at high cardiovascular risk enrolled in the Systolic Blood Pressure Intervention Trial (SPRINT).

Adjudicated AKI as a time-varying predictor.

Incident mild cognitive impairment (MCI), probable dementia, and their composite.

Cox proportional hazard models.

Participants were 68 ± 9 years, 65% male, 28% with prevalent chronic kidney disease), with a median (interquartile range) follow-up time for the composite of 4.0 (2.1-5.4) and 4.6 (3.6-5.9) years in the AKI and non-AKI groups, respectively. The incidence rate of MCI, probable dementia, and their composite was higher in participants who experienced an AKI event (n = 270). In the fully adjusted model, AKI was positively associated with probable dementia (hazard ratio, 1.72; 95% CI, 1.07-2.75) and the composite outcome (1.43 [1.01-2.04]).

AKI before baseline was not captured; retrospective and associative.

Adjudicated AKI, which was largely mild and reversible, was independently associated with increased risk of probable dementia and the composite of probable dementia and MCI in older adults at high cardiovascular risk.

Acute kidney injury can lead to severe short- and long-term consequences. The majority of acute kidney injury outcome studies have focused on mortality and kidney-related outcomes, with very few studies considering the importance of a holistic approach to post-acute kidney injury care. In this review, we focus on the physical, emotional, cognitive, and social outcomes following acute kidney injury that may affect patients' quality of life, aiming to highlight the importance of assessing and managing patients both during their hospitalization as well as posthospital discharge. We conclude with specific key recommendations to ensure that health care providers consider all aspects of care for patients with acute kidney injury, and we advocate for a concerted effort to develop post-acute kidney injury care strategies that embrace a holistic approach, ensuring comprehensive care for acute kidney injury survivors.

Excessive inflammation and apoptosis in kidneys are critical players in the pathogenesis of acute kidney injury (AKI). Aromadendrin is a natural flavonoid characterized by anti-inflammatory, anti-apoptotic, and antioxidant actions. Thus, we investigated the roles and mechanisms of aromadendrin in the development of AKI.

Lipopolysaccharide (LPS) was used to induce AKI mice, and one hour after LPS challenge, the mice received oral administration of aromadendrin or vehicle. Renal functions were assessed by measuring blood urea nitrogen and creatinine in serum. Histological changes were determined by hematoxylin and eosin staining. Apoptotic cells of renal tissues were detected by TUNEL staining. Gene expression was measured by western blotting and RT-qPCR.

Aromadendrin alleviated LPS-induced renal dysfunctions and histological defects in mice. Additionally, aromadendrin suppressed excessive inflammation and tissue apoptosis in the kidneys of LPS-induced AKI mice. Mechanistically, aromadendrin blocked the activation of NF-κB and MAPK pathways in LPS-induced AKI mice.

Aromadendrin alleviates LPS-stimulated inflammation and tissue cell apoptosis in kidneys by inactivating the NF-κB and MAPK pathways.

The maintenance of fluid and electrolyte homeostasis by the kidney requires proper folding and trafficking of ion channels and transporters in kidney epithelia. Each of these processes requires a specific subset of a diverse class of proteins termed molecular chaperones. One such chaperone is GRP170, which is an Hsp70-like, endoplasmic reticulum (ER)-localized chaperone that plays roles in protein quality control and protein folding in the ER. We previously determined that loss of GRP170 in the mouse nephron leads to hypovolemia, electrolyte imbalance, and rapid weight loss. In addition, GRP170-deficient mice develop an acute kidney injury (AKI)-like phenotype, typified by tubular injury, elevation of kidney injury markers, and induction of the unfolded protein response (UPR). By using an inducible GRP170 knockout cellular model, we confirmed that GRP170 depletion induces the UPR, triggers apoptosis, and disrupts protein homeostasis. Based on these data, we hypothesized that UPR induction underlies hyponatremia and volume depletion in these rodents and that these and other phenotypes might be rectified by sodium supplementation. To test this hypothesis, control and GRP170 tubule-specific knockout mice were provided a diet containing 8% sodium chloride. We discovered that sodium supplementation improved electrolyte imbalance and kidney injury markers in a sex-specific manner but was unable to restore weight or tubule integrity. These results are consistent with UPR induction contributing to the kidney injury phenotype in the nephron-specific GR170 knockout model and indicate that GRP170 function in kidney epithelia is essential to both maintain electrolyte balance and ER homeostasis.NEW & NOTEWORTHY Loss of the endoplasmic reticulum chaperone, GRP170, results in widespread kidney injury and induction of the unfolded protein response (UPR). We now show that sodium supplementation is able to at least partially restore electrolyte imbalance and reduce kidney injury markers in a sex-dependent manner.

Acute kidney injury (AKI) is a well-known complication of critical illnesses, significantly affecting morbidity and the risk of death. Diuretics are widely used to ameliorate excess fluid accumulation and oliguria associated with AKI. Their popularity stems from their ability to reduce the energy demands of renal tubular cells by inhibiting transporters and flushing out intratubular casts. Numerous studies have assessed the effects of diuretics in the context of AKI prevention and treatment. However, a comprehensive systematic review addressing this topic has yet to be conducted.

This review aimed to explore the benefits and harms of diuretics for both the prevention and treatment of AKI.

The Cochrane Kidney and Transplant Register of Studies was searched up to May 2024 using search terms relevant to this review. Studies in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Registry Platform (ICTRP) Search Portal, and ClinicalTrials.gov.

We selected randomised controlled trials (RCTs) and quasi-RCTs in which diuretics were used to prevent or treat AKI.

Two authors independently extracted data using standardised data extraction forms. Dichotomous outcomes were expressed as risk ratios (RR) with 95% confidence intervals (CI). Where continuous scales of measurement were used to assess the effects of treatment, the standardised mean difference (SMD) was used. The primary review outcomes for AKI prevention studies were the incidence of AKI and any use of kidney replacement therapy (KRT). For treatment studies, the primary outcome was any use of KRT. The certainty of evidence was assessed per outcome using the Grades of Recommendation, Assessment, Development and Evaluation (GRADE) approach.

We included 64 studies (83 reports, 9871 participants): 53 prevention studies (8078 participants) and 11 treatment studies (1793 participants). Studies were conducted in the following World Health Organization regions: the Americas (15), Eastern Mediterranean (9), Europe (25), South-East Asia (2), and the Western Pacific (13). Thirty-six studies were single-centre studies, 19 were multicentre, and the setting was unclear in nine studies. Diuretics were compared to placebo, no treatment or conventional therapy, saline solutions (isotonic or hypotonic), 5% dextrose, 5% glucose, Hartmann's solution, and Ringer's acetate. Overall, the risk of bias was low in one study, high in 19 studies, and of some concern in 41 studies. Three studies could not be assessed because they did not report any outcomes of interest. For AKI prevention, compared to control, diuretics may reduce the risk of AKI (38 studies, 5540 participants: RR 0.75, 95%, CI 0.61 to 0.92; I2 = 77%; low-certainty evidence) and probably reduce any use of KRT (32 studies, 4658 participants: RR 0.63, 95% CI 0.43 to 0.91; I2 = 0%, moderate-certainty evidence) and death (33 studies, 6447 participants: RR 0.73, 95% CI 0.59 to 0.92; I2 = 0%; moderate-certainty evidence). The use of diuretics may result in little or no difference in the need for permanent dialysis (2 studies, 956 participants: RR 0.52, 95% CI 0.08 to 3.47; I2 = 21%; low-certainty evidence), hypotension (7 studies, 775 participants: RR 1.27, 95% CI 0.87 to 1.86; I2 = 0%; low-certainty evidence) and hypokalaemia (6 studies, 1383 participants: RR 1.20, 95% CI 0.88 to 1.73; I2 = 43%; low-certainty evidence), and had uncertain effects on arrhythmias (13 studies, 3375 participants: RR 0.77, 95% CI 0.57 to 1.04; I2 = 53%; very-low certainty evidence). Diuretics may make little or no difference to changes in SCr within 30 days (8 studies, 646 participants: SMD 0.41, 95% CI -0.01, to 0.83; I2 = 82%; low-certainty evidence) but it was uncertain whether diuretics increased urinary output (8 studies, 1155 participants: SMD 1.87, 95% CI -0.20 to 3.95; I2 = 99%; very low-certainty evidence). For AKI treatment, diuretics may make little or no difference to any use of KRT (8 studies, 1275 participants: RR 0.93, 95% CI 0.83 to 1.04; I2 = 2%; low-certainty evidence) or death (14 studies, 2052 participants: RR 1.08, 95% CI 0.96 to 1.22; I2 = 0%; low-certainty evidence). Diuretics may increase hypotension (2 studies, 720 participants: RR 1.99, 95% CI 1.16 to 3.41; I2 = 90%; low-certainty evidence) and probably increase arrhythmias (6 studies, 1011 participants: RR 1.62, 95% CI 1.12 to 2.33; I2 = 0%; moderate-certainty evidence). Diuretics may result in little or no difference in hypokalaemia (3 studies, 478 participants: RR 1.52, 95% CI 0.70 to 3.31; I2 = 0%; low-certainty evidence). It was uncertain whether diuretics increased urinary output (3 studies, 329 participants: SMD 4.40, 95% CI -0.94 to 9.74; I2 = 99%; very low-certainty evidence). The need for permanent dialysis and changes in serum creatinine were not reported.

When used for the prevention of AKI, diuretics may reduce the risk of AKI. However, our confidence in the effect estimate is limited. Diuretics probably reduce the incidence of KRT use, and we are moderately confident in the effect estimate. When used for the treatment of AKI, diuretics may make little or no difference to any use of KRT, and our confidence in the effect estimate is limited. More RCTs are needed to explore the role of diuretics for treating established AKI.

The recent rise in acute kidney injury (AKI) incidence, with approximately 30% attributed to potentially preventable adverse drug events (ADEs), poses challenges in evaluating drug-induced AKI due to polypharmacy and other risk factors. This study seeks to consolidate knowledge on the drugs with AKI potential from four distinct sources: (i) bio(medical) peer-reviewed journals; (ii) spontaneous reporting systems (SRS); (iii) drug information databases (DIDs); and (iv) NephroTox website. By harnessing the potential of these underutilised sources, our objective is to bridge gaps and enhance the understanding of drug-induced AKI.

By searching Medline, studies with lists of drugs with AKI potential established through consensus amongst medical experts were selected. A final list of 63 drugs was generated aggregating the original studies. For these 63 drugs, the AKI reporting odds ratios (RORs) using three SRS databases, the average frequency of ADEs from four different DIDs and the number of published studies identified via NephroTox was reported.

Drugs belonging to the antivirals, antibacterials, and non-steroidal anti-inflammatory pharmacological classes exhibit substantial consensus on AKI potential, which was also reflected in strong ROR signals, frequent to very frequent AKI-related ADEs and a high number of published studies reporting adverse kidney events as identified via NephroTox. Renin-angiotensin aldosterone system inhibitors and diuretics also display comparable signal strengths, but this can be attributed to expected haemodynamic changes. More variability is noted for proton-pump inhibitors.

By integrating four disjointed sources of knowledge, we have created a novel, comprehensive resource on drugs with AKI potential, contributing to kidney safety improvement efforts.

Community-acquired acute kidney injury (CA-acute kidney injury) is under-recognized in the outpatient setting and is associated with adverse outcomes.

We analyzed the incidence of CA-acute kidney injury in an academic primary care practice and community health center and assessed recognition and follow-up as determined by repeat creatinine measurement (closed-loop). We reviewed 93,259 specimens for 36,593 unique patients from January 1, 2018, through December 31, 2021.

There were 220 unique patients with CA-acute kidney injury, defined as a > 75% increase in creatinine from baseline (incidence: 150/100,000; 0.15% per year). One hundred thirty seven patients (62.3%) had repeat serum creatinine performed within 30 days. Chart reviews of the 83 (37.72%) patients with open loops found there was no follow-up creatinine ordered in 69/83 (83.1%) patients. Mean baseline creatinine was higher and estimated glomerular filtration rate (eGFR) was lower in the closed-loop group (0.92 ± 0.4 mg/dL; 84.45 ± 27.49 mL/min) vs the open-loop group (0.63 ± 0.34 mg/dL; 105.19 ± 26.67 mL/min) (P < .0001). Preexisting chronic kidney disease was more prevalent in closed-loop patients (35/137; 25.6%) compared with those with open loops (3/83; 3.6%). Patients with baseline chronic kidney disease were more likely to have closed loops. Progression to new chronic kidney disease was common among CA-acute kidney injury patients, occurring in 25% of open-loop and 24.1% of closed-loop patients. New baseline eGFR was lower in all groups.

Clinicians frequently overlooked a clinically significant change in eGFR, especially when the baseline creatinine and incident creatinine levels were in the "normal" range.

Acute Kidney Injury (AKI) is a multifaceted condition characterised by rapid deterioration of renal function, often precipitated by diverse etiologies. A comprehensive understanding of the molecular underpinnings of AKI is pivotal for identifying potential diagnostic markers and therapeutic targets. This study utilised bioinformatics to elucidate gene expression and immune infiltration in AKI. Publicly available mRNA and miRNA datasets were harnessed to discern differentially expressed genes (DEGs) and miRNAs in AKI. The CIBERSORT algorithm was employed to quantify immune cell infiltration in AKI samples. Functional enrichment analyses were conducted to unravel the implicated biological processes. Furthermore, the expression of identified genes and miRNAs was validated by quantitative real-time PCR in an AKI model. Our study revealed significant dysregulation of three genes (Aspn, Clec2h, Tmigd1) and two miRNAs (mmu-miR-21a-3p, mmu-miR-223-3p) in AKI, each with p < 0.0001. These molecular markers are implicated in immune responses, tissue remodelling, and inflammation. We observed notable disturbances in specific immune cells, including activated and immature dendritic cells, M1 macrophages, and subsets of T cells (Treg, Th1, Th17). These alterations correlated significantly with AKI pathology, with dendritic cells and M1 macrophages showing p < 0.01, and T cell subsets demonstrating p < 0.05. These results highlight the intricate involvement of the immune system in AKI and indicate significant enrichment of pathways related to immune response, inflammation, and tissue remodelling, pointing to their pivotal roles in AKI pathophysiology. Our study underscored the significance of immune cell infiltration and dysregulated gene and miRNA expression in AKI. The identified genes (Clec2h, Aspn, and Tmigd1) and miRNAs (mmu-miR-21a-3p and mmu-miR-223-3p) offer potential diagnostic markers and therapeutic avenues for AKI. Subsequent investigations targeting these genes and miRNAs, along with the elucidated pathways, may augment the clinical management and outcomes for AKI patients.

Acute kidney injury (AKI) is recognized as a common complication following cytoreductive surgery combined with hyperthermic intraperitoneal chemotherapy (CRS-HIPEC). Characterized by prolonged renal function impairment, acute kidney disease (AKD) is associated with a higher risk of chronic kidney disease (CKD) and mortality.

From January 2018 to December 2021, 158 patients undergoing CRS-HIPEC were retrospectively reviewed. Patients were separated into non-AKI, AKI, and AKD cohorts. Laboratory parameters and perioperative features were gathered to evaluate risk factors for both HIPEC-induced AKI and AKD, with the 90-day prognosis of AKD patients.

AKI developed in 21.5% of patients undergoing CRS-HIPEC, while 13.3% progressed to AKD. The multivariate analysis identified that ascites, GRAN%, estimated glomerular filtration rate (eGFR), and intraoperative (IO) hypotension duration were associated with the development of HIPEC-induced AKI. Higher uric acid, lessened eGFR, and prolonged IO hypotension duration were more predominant in patients proceeding with AKD. The AKD cohort presented a higher risk of 30 days of in-hospital mortality (14.3%) and CKD progression (42.8%).

Our study reveals a high incidence of AKI and AKI-to-AKD transition. Early identification of risk factors for HIPEC-induced AKD would assist clinicians in taking measures to mitigate the incidence.

Imbalances in blood potassium (K) homeostasis is a significant contributor to the emergence of severe complications, especially among critically ill patients. Hypokalemia and hyperkalemia are both associated with an increased risk of adverse events. However, it is not known about the impact of blood K levels on risk of intensive care units (ICU) mortality for Acute kidney injury (AKI) combined with sepsis patients. This study aimed to explore the relationship between admission blood K levels and ICU 30-day mortality in patients with AKI combined with sepsis.

We selected patients diagnosed with AKI and sepsis on their first ICU admission from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. The first blood K levels within 24 hours of admission were categorized into three groups according to tertiles (T1 < 3.9 mmol/L, 3.9 ≤ T2 < 4.5 mmol/L, and T3 ≥ 4.5 mmol/L), with T2 serving as the reference. We examined the association between blood K levels and ICU 30-day mortality using accelerated failure time (AFT) models and survival analysis.

A total of 8,242 ICU patients with AKI combined with sepsis were included. In multivariate AFT models, each 1 mmol/L increase in blood K levels was associated with a 13% increase in the risk of ICU 30-day mortality (p < 0.001, 95% confidence interval (CI): 1.06-1.20). Extended multivariable AFT models showed that, compared to the middle category, patients with high blood K levels (≥ 4.5 mmol/L) were associated with all-cause mortality (p = 0.002, adjusted hazard ratio (HR) = 1.22, 95% CI: 1.08-1.38), whereas those with low blood K levels (< 3.9 mmol/L) showed no significant difference (p = 0.385, adjusted HR = 1.06, 95% CI: 0.93-1.21). Kaplan-Meier curves indicated that patients with high blood K levels had higher mortality, and those with middle blood potassium levels (3.9 ≤ K < 4.5 mmol/L) had the lowest mortality.

The admission baseline blood K levels were significantly associated with ICU 30-day mortality in intensive care patients suffering from AKI in conjunction with sepsis. Therefore, immediate and careful correction of blood potassium imbalances may prove to be a crucial approach in improving outcomes for these patients.

Patients with diabetes are susceptible to acute kidney injury (AKI) as compared to counterparts without diabetes. However, data on the long-term clinical outcome of AKI specifically in people with diabetes are still scarce. We sought to study risk factors for and adverse cardio-renal outcomes of AKI in multi-ethnic Southeast Asian people with type 2 diabetes. 1684 participants with type 2 diabetes from a regional hospital were followed an average of 4.2 (SD 2.0) years. Risks for end stage kidney disease (ESKD), major adverse cardiovascular events (MACE) and all-cause death after AKI were assessed by survival analyses. 219 participants experienced at least one AKI episode. Age, cardiovascular disease history, minor ethnicity, diuretics usage, HbA1c, baseline eGFR and albuminuria independently predicted risk for AKI with good discrimination. Compared to those without AKI, participants with any AKI episode had a significantly high risk for ESKD, MACE and all-cause death after adjustment for multiple risk factors including baseline eGFR and albuminuria. Even AKI defined by a mild serum creatinine elevation (0.3 mg/dL) was independently associated with a significantly high risk for premature death. Therefore, individuals with diabetes and any episode of AKI deserve intensive surveillance for cardio-renal dysfunction.

Septic shock is defined as sepsis with hypotension requiring vasopressors to maintain a mean arterial pressure above 65 mmHg and having a serum lactate level of more than 2 mmol/L despite adequate volume resuscitation as per the Sepsis-3 criteria. Continuous renal replacement therapy (CRRT) is commonly utilized in septic shock patients for the treatment of acute kidney injury as well as for modulating immune response and maintaining hemodynamic stability.

We looked at the National Inpatient Sample database in 2019. We identified adult patients with septic shock as the primary diagnosis using the International Classification of Diseases, 10th revision, clinical modification codes R65.21 and R78.81, and subbranches of Aa41, A40, and R60. STATA 18 (StataCorp, College Station, TX) was used to perform logistic multivariate regression analyses.

A total of 15,794 adults who were admitted for septic shock as the primary diagnosis underwent CRRT. The mean age of the patients was 61.7 years. The overall mortality rate was 57% (N = 9,002). An increase in age by one year was associated with a 1% increase in mortality (p = 0.001). The presence of hypertension increased mortality by 29% (N = 6,391) (p = 0.028). Interestingly, preexisting diabetes mellitus improved mortality by 37% (N = 3331) (p = 0.001).The outcome of CRRT was better in patients with chronic kidney disease, with a 26% improvement in mortality (N = 2341) (p = 0.001). A significant improvement in outcome (29% decrease in mortality, p=0.013) and 31% reduction in hospital length of stay (p = 0.008) was noted with CRRT initiated on day 2 of hospitalization.

This study highlights that the approximate time of initiation of CRRT for optimal benefit of the treatment is between 24 and 48 hours of hospitalization. This study emphasizes the prognostic factors of a standard therapy, which can serve as a basis for clinical decision-making.

Acute kidney injury (AKI) following burns is associated with increased mortality and morbidity. Some patients require renal replacement therapy. There is limited large-scale data to sufficiently validate risk factors influencing the incidence and severity of early AKI, defined as AKI within the first 72 h since admission to a burn center following burn injury. The aims of this study were to compare the profile of adult patients admitted to Australian and New Zealand burn centers, with burns ≥10% total body surface area (TBSA) who developed early AKI with patients who did not develop AKI and to quantify the association between early AKI and in-hospital outcomes.

Data were extracted from the Burns Registry of Australia and New Zealand for adults (≥18 y), with burns ≥10% TBSA admitted to Australian or New Zealand burn centers between July 2016 and June 2021. All patients with two valid serum creatinine blood tests within the first 72 h were included. Differences in patient profiles and in-hospital outcomes were investigated. Univariable and multivariable logistic and linear regression models were used to quantify associations between early AKI and outcomes of interest.

There were 1297 patients who met the inclusion criteria for this study. Eighty-three patients (6.4%) developed early AKI. Compared to patients without AKI, patients with an AKI were older (P = 0.006), had a greater median %TBSA burned (P < 0.001), and had an inhalation injury (P < 0.001). In adjusted models, the development of early AKI was significantly associated with in-hospital mortality (adjusted odds ratio (aOR) [95% CI] 2.73 [1.33, 5.62], P < 0.001) and the need for mechanical ventilation (aOR [95% CI] 3.44 [1.77, 6.68], P = 0.001), but there was no significant increase in the hospital length of stay or intensive care unit length of stay.

This is the first large-scale study looking at early AKI in adult burns ≥10% TBSA. The incidence of AKI was lower than previously reported and AKI was associated with higher in-hospital mortality and increased need for mechanical ventilation. These findings support the notion that development of AKI in the immediate phase post burns injury can potentially have consequences and the appropriate care should be given to prevent its development.

Limited information exists regarding the impact of preoperative serum creatinine changes on cardiac surgery-associated acute kidney injury (CSA-AKI). This study aimed to investigate the development of AKI in patients with a baseline estimated glomerular filtration rate of ≥60 mL/min/1.73 m2 who present with an elevation in preoperative serum creatinine.

This retrospective cohort study assessed patients who underwent open-heart surgery. Preoperative serum creatinine change was calculated as the ratio of the maximum preoperative serum creatinine value to the baseline creatinine (MCR). Patients were categorized into three groups based on MCR: non-elevation (≤1.0), mild elevation (1.0 to 1.5), and pronounced elevation (≥1.5). Multivariable logistic regression was used to estimate the risk of AKI, severe AKI, and non-recovery from AKI.

There were significant increases in the odds of AKI (adjusted odds ratio [OR], 1.42; 95% confidence interval [CI], 1.29-1.57; per 0.1 increase in MCR), severe AKI (adjusted OR, 1.28; 95% CI, 1.15-1.41), and AKI non-recovery (adjusted OR, 1.29; 95% CI, 1.16-1.43). Pronounced elevation in preoperative serum creatinine was associated with a higher risk of AKI (adjusted OR, 15.45; 95% CI, 6.63-36.00), severe AKI (adjusted OR, 3.62; 95% CI, 1.20-10.87), and AKI non-recovery (adjusted OR, 4.74; 95% CI, 1.63-13.89) than non-elevation. Mild elevation in preoperative serum creatinine was also significantly associated with AKI (adjusted OR, 3.76; 95% CI, 1.92-7.37).

Elevation in preoperative serum creatinine from baseline was associated with an increased risk of AKI; even mild elevation significantly increased the risk of AKI.

Serum creatinine (SCr) is the primary biomarker for assessing kidney function; however, it may lag behind true kidney function, especially in instances of acute kidney injury (AKI). The objective of the work is to develop Nephrocast, a deep-learning model to predict next-day SCr in adult patients treated in the intensive care unit (ICU).

Nephrocast was trained and validated, temporally and prospectively, using electronic health record data of adult patients admitted to the ICU in the University of California San Diego Health (UCSDH) between January 1, 2016 and June 22, 2024. The model features consisted of demographics, comorbidities, vital signs and laboratory measurements, and medications. Model performance was evaluated by mean absolute error (MAE) and root-mean-square error (RMSE) and compared against the prediction day's SCr as a reference.

A total of 28 191 encounters met the eligibility criteria, corresponding to 105 718 patient-days. The median (interquartile range [IQR]) MAE and RMSE in the internal test set were 0.09 (0.085-0.09) mg/dL and 0.15 (0.146-0.152) mg/dL, respectively. In the prospective validation, the MAE and RMSE were 0.09 mg/dL and 0.14 mg/dL, respectively. The model's performance was superior to the reference SCr.

Our model demonstrated good performance in predicting next-day SCr by leveraging clinical data routinely collected in the ICU. The model could aid clinicians in in identifying high-risk patients for AKI, predicting AKI trajectory, and informing the dosing of renally eliminated drugs.

This comprehensive review examines the role of Fenoldopam, a selective dopamine-1 receptor agonist, in preventing and treating acute kidney injury (AKI) during cardiac surgery. AKI remains a significant complication in cardiac surgery, associated with increased morbidity, mortality, and healthcare costs. The review explores Fenoldopam's pharmacological properties, mechanism of action, and clinical applications, synthesizing evidence from randomized controlled trials, meta-analyses, and observational studies. While some studies have shown promising results in improving renal function and reducing AKI incidence, others have failed to demonstrate significant benefits. The review discusses these conflicting findings, explores potential reasons for discrepancies, and identifies areas requiring further research. It also compares Fenoldopam to other renoprotective strategies, including dopamine, diuretics, and N-acetylcysteine. The safety profile of Fenoldopam, including common side effects and contraindications, is addressed. Current guidelines and recommendations for Fenoldopam use in cardiac surgery are presented, along with a cost-effectiveness analysis. The review concludes by outlining future research directions and potential new applications of Fenoldopam in cardiac surgery. By providing a thorough overview of the current state of knowledge, this review aims to facilitate informed decision-making for clinicians and researchers while highlighting areas for future investigation.

Acute kidney injury (AKI) due to vitamin D therapy for osteoporosis is encountered in clinical practice, but epidemiological studies are scarce. We aimed to determine the association between AKI and vitamin D therapy and to identify risk factors for AKI using the Japanese Adverse Drug Event Report database. We used reporting odds ratios (RORs) to detect signals and evaluate risk factors using multiple logistic regression analysis. Among 298,891 reports from April 2004 to September 2023, 1071 implicated active vitamin D3 analogs as suspect drugs for adverse events. There was a significant association between AKI and active vitamin D3 analogs (ROR [95% confidence interval {CI}], eldecalcitol: 16.75 [14.23-19.72], P < 0.001; alfacalcidol: 5.29 [4.07-6.87], P < 0.001; calcitriol: 4.46 [1.88-10.59], P < 0.001). The median duration of administration before AKI onset was 15.4 weeks. Multiple logistic regression analysis showed a significant association between AKI and age ≥ 70 years (odds ratio [95% CI], 1.47 [1.04-2.07]; P = 0.028), weight < 50 kg (1.55 [1.12-2.13]; P = 0.007), hypertension (1.90 [1.42-2.54]; P < 0.001), and concomitant use of nonsteroidal anti-inflammatory drugs (1.58 [1.10-2.25], P = 0.012) and magnesium oxide (1.96 [1.38-2.78]; P < 0.001). Our results suggest that active vitamin D3 analogs are associated with AKI development. Physicians prescribing these medications to patients with risk factors should consider the possibility of AKI, especially during the first 6 months.

This study aimed to elucidate the association between IV contrast media CT and acute kidney injury (AKI) and in-hospital mortality among patients requiring emergency admission.

In this retrospective observational study, we examined AKI within 48 hours after CT, renal replacement therapy (RRT) dependence at discharge, and in-hospital mortality in patients undergoing contrast-enhanced CT or nonenhanced CT. We performed 1:1 propensity score matching to adjust for confounders in the association between IV contrast media use and outcomes. Subgroup analyses were performed according to age, sex, diagnosis at admission, ICU admission, and preexisting chronic kidney disease (CKD).

This study used the Medical Data Vision database between 2008 and 2019. This database is Japan's largest commercially available hospital-based claims database, covering about 45% of acute-care hospitals in Japan, and it also records laboratory results.

None.

The study included 144,149 patients with (49,057) and without (95,092) contrast media exposure, from which 43,367 propensity score-matched pairs were generated. Between the propensity score-matched groups of overall patients, exposure to contrast media showed no significant risk of AKI (4.6% vs. 5.1%; odds ratio [OR], 0.899; 95% CI, 0.845-0.958) or significant risk of RRT dependence (0.6% vs. 0.4%; OR, 1.297; 95% CI, 1.070-1.574) and significant benefit for in-hospital mortality (5.4% vs. 6.5%; OR, 0.821; 95% CI, 0.775-0.869). In subgroup analyses regarding preexisting CKD, exposure to contrast media was a significant risk for AKI in patients with CKD but not in those without CKD.

In this large-scale observational study, IV contrast media was not associated with an increased risk of AKI but concurrently showed beneficial effects on in-hospital mortality among patients requiring emergency admission.

Recently, ezetimibe (EZM) has been suggested to be a potent Nrf2 activator that is important for preventing oxidative stress. Interestingly, we found that its metabolite ezetimibe ketone (EZM-K) also has antioxidant effects. Thus, we investigated the role of EZM-K in preventing renal ischemia‒reperfusion injury (RIRI). Cultured NRK-52E cells were subjected to simulated IR with or without EZM-K. Rats were used to simulate in vivo experiments. EZM-K alleviated H2O2-induced apoptosis and reactive oxygen species (ROS) and upregulated Nrf2 and HO-1 levels in NRK-52E cells. A HO-1 and a Nrf2 inhibitor reversed the protective effects of EZM-K. In the rat RIRI model, pretreatment with EZM-K activated the Nrf2/HO-1 signaling pathway, suppressed tubular injury and inflammation, and improved renal function. EZM-K significantly prevented renal injury caused by ischemia‒reperfusion via the Nrf2/HO-1 signaling axis both in vivo and in vitro. The other metabolite of EZM, ezetimibe glucuronide (EZM-G) had no protective effects against ROS in RIRI. EZM-G also had no antioxidant effects and could not activate Nrf2/HO-1 signal pathway. Our findings also indicated the therapeutic potential of EZM-K in preventing RIRI.

Acute kidney injury (AKI) is a common surgical complication and is associated with intraoperative hypotension. However, the total duration and magnitude of intraoperative hypotension associated with AKI remains unknown. In this study, the causal relationship between the intraoperative arterial pressure and postoperative AKI was investigated among chronic hypertension patients undergoing non-cardiac surgery.

A retrospective cohort study of 6552 hypertension patients undergoing non-cardiac surgery (2011 to 2019) was conducted. The primary outcome was AKI as diagnosed with the Kidney Disease-Improving Global Outcomes criteria and the primary exposure was intraoperative hypotension. Patients' baseline demographics, pre- and post-operative data were harvested and then analyzed with multivariable logistic regression to assess the exposure-outcome relationship.

Among 6552 hypertension patients, 579 (8.84%) had postoperative AKI after non-cardiac surgery. The proportions of patients admitted to ICU (3.97 vs. 1.24%, p < 0.001) and experiencing all-cause death (2.76 vs. 0.80%, p < 0.001) were higher in the patients with postoperative AKI. Moreover, the patients with postoperative AKI had longer hospital stays (13.50 vs. 12.00 days, p < 0.001). Intraoperative mean arterial pressure (MAP) < 60 mmHg for >20 min was an independent risk factor of postoperative AKI. Furthermore, MAP <60 mmHg for >10 min was also an independent risk factor of postoperative AKI in patients whose MAP was measured invasively in the subgroup analysis.

Our work suggested that MAP < 60 mmHg for >10 min measured invasively or 20 min measured non-invasively during non-cardiac surgery may be the threshold of postoperative AKI development in hypertension patients. This work may serve as a perioperative management guide for chronic hypertension patients.

clinical trial number: ChiCTR2100050209 (8/22/2021). http://www.chictr.org.cn/showproj.aspx?proj=132277.

Background/Objectives: Patients with infective endocarditis (IE) are more susceptible to acute kidney injury (AKI). The presence of AKI increases in-hospital complications in these patients. Methods: The 2016-2020 National Inpatient Sample (NIS) database consisting of adult admissions with IE and AKI was utilized. The primary outcome was all-cause inpatient mortality. Secondary outcomes included fluid and electrolyte disorders, stroke, septic arterial embolism, septic shock, cardiogenic shock, valve surgery, vasopressor support, mechanical ventilation, length of stay (LOS), and total hospital charges. Results: Out of a total of 63,725 adult admissions with IE, 16,295 (25.5%) admissions had AKI. Patients with AKI were more likely to be males (63% vs. 57.6%, p < 0.001) and older (55.8 vs. 50.4, p < 0.001). A higher proportion of these patients were admitted to large hospitals (60.6 vs. 55.3%, p < 0.001) and urban teaching hospitals (81.9 vs. 75%, p < 0.001). Patients with AKI had higher LOS (17 ± 16.1 vs. 11.32 ± 11.7, p < 0.001) and hospital charges (USD 239,046.8 ± 303,977.3 vs. USD 124,857.6 ± 192,883.5, p < 0.001). Multivariable analysis showed higher odds of all-cause inpatient mortality (aOR: 2.22, 95% CI: 1.81-2.73, p < 0.001). They also had higher risk for fluid and electrolyte disorder (aOR: 2.31, 95% CI: 2.10-2.53, p < 0.001), septic arterial embolism (aOR: 1.61, 95% CI: 1.42-1.84, p < 0.001), septic shock (aOR: 3.78, 95% CI: 2.97-4.82, p < 0.001), cardiogenic shock (OR: 3.37, 95% CI: 2.65-4.28, p < 0.001), valve surgery (aOR: 1.52, 95% CI: 1.35-1.71, p < 0.001), vasopressor requirement (aOR: 1.99, 95% CI: 1.52-2.60, p < 0.001), and mechanical ventilation (aOR: 2.75, 95% CI: 2.33-3.24, p < 0.001). The association with stroke was elevated but not statistically significant. Conclusions: This large retrospective analysis demonstrated that patients with AKI and infective endocarditis had increased mortality, adverse hospital outcomes, increased LOS, and hospital costs.

Type 2 diabetes mellitus (T2DM) is a leading cause of chronic kidney disease (CKD) globally. Both conditions substantially worsen patients' prognosis. Current data on German in-hospital CKD cohorts are scarce. The multinational CaReMe study was initiated to evaluate the current epidemiology and healthcare burden of cardiovascular, renal and metabolic diseases. In this substudy, we share real-world data on CKD inpatients stratified for coexisting T2DM derived from a large German hospital network.

This study used administrative data of inpatient cases from 89 Helios hospitals from 01/01/2016 to 28/02/2022. Data were extracted from ICD-10-encoded discharge diagnoses and OPS-encoded procedures. The first case meeting a previously developed CKD definition (defined by ICD-10- and OPS-codes) was considered the index case for a particular patient. Subsequent hospitalizations were analysed for readmission statistics. Patient characteristics and pre-defined endpoints were stratified for T2DM at index case.

In total, 48,011 patients with CKD were included in the present analysis (mean age ± standard deviation, 73.8 ± 13.1 years; female, 44%) of whom 47.9% had co-existing T2DM. Patients with T2DM were older (75 ± 10.6 vs 72.7 ± 14.9 years, p < 0.001), but gender distribution was similar to patients without T2DM. The burden of cardiovascular disease was increased in patients with T2DM, and index and follow-up in-hospital mortality rates were higher. Non-T2DM patients were characterised by more advanced CKD at baseline. Patients with T2DM had consistently higher readmission numbers for all events of interest, except for readmissions due to kidney failure/dialysis, which were more common in non-T2DM patients.

In this study, we present recent data on hospitalized patients with CKD in Germany. In this CKD cohort, nearly half had T2DM, which substantially affected cardiovascular disease burden, rehospitalization frequency and mortality. Interestingly, non-diabetic patients had more advanced underlying renal disease, which affected renal outcomes.

The albumin-bilirubin (ALBI) grade has surfaced as a viable substitute for assessing liver functional reserve in individuals afflicted with hepatocellular carcinoma (HCC). ALBI grade also demonstrates the capacity to stratify distinct patient subcohorts bearing disparate prognostic implications in not only HCC but also other inflammatory diseases like acute pancreatitis. However, the association between ALBI grade and clinical outcomes of acute kidney injury (AKI) remains mysterious.

The dataset was sourced from the Multiparameter Intelligent Monitoring in Intensive Care Database IV (MIMIC-IV) version 2.0. ALBI grade was calculated in a nomogram utilizing albumin and bilirubin. In order to ascertain the connection between ALBI grades and clinical outcomes of patients with AKI, Cox proportional hazards regression analysis was employed with in-hospital, 30- and 90-day mortality as end points, respectively. The Kaplan-Meier (K-M) curve was employed to gauge the cumulative incidence of mortality based on various ALBI grades. To explore potential nonlinear relationships, the Restricted Cubic Spline (RCS) approach was adopted. Furthermore, a subgroup analysis was conducted to validate the durability of the correlation between ALBI grade and in-hospital mortality. Furthermore, equilibrium of confounding variables was also achieved through the application of propensity score matching (PSM).

The study encompassed a total of 12,518 patients (ALBI grade 1 : 2878, grade 2 : 6708, and grade 3 : 2932). Patients with heightened ALBI grades displayed a significant correlation with increased mortality in both univariate and various multivariate Cox regression models. RCS depicted a predominantly linear relationship. The robustness of the correlation was also affirmed across multifarious subpopulations through subgroup analysis. The association still remains after PSM.

Elevated ALBI grade was associated with worse clinical outcomes of critically ill patients with AKI.

Acute kidney injury (AKI) incidence is extremely high worldwide, and patients who develop AKI are at increased risk of developing chronic kidney disease (CKD), CKD progression, and end-stage kidney disease (ESKD). However, there is no established treatment strategy for AKI. Based on the idea that exercise has a stabilizing effect on hemodynamics, we hypothesized that rehabilitation would have beneficial renal outcomes in patients with AKI associated with cardiovascular disease. Therefore, the purpose of this study was to determine whether rehabilitation can stabilize hemodynamics and positively impact renal outcomes in patients with AKI associated with cardiovascular disease.

In total, 107 patients with AKI associated with cardiovascular disease were enrolled in this single-center retrospective study and were either assigned to the exposure group (n = 36), which received rehabilitation at least once a week for at least 8 consecutive weeks, or to the control group (n = 71). Estimated glomerular filtration rate was assessed at baseline before admission, at the lowest value during hospitalization, and at 3, 12, and 24 months after enrolment. Trends over time (group × time) between the two groups were compared using generalized estimating equations. Moreover, congestive status was assessed by amino-terminal pro-B-type natriuretic peptide (NT-proBNP), and the effect of rehabilitation on congestion improvement was investigated using logistical regression analysis.

The time course of renal function after AKI, from baseline to each of the three timepoints suggested significant differences between the two groups (p < 0.01). However, there was no significant difference between the two groups at any time point in terms of percentage of patients who experienced a 40% estimated glomerular filtration rate reduction from that at baseline. The proportion of patients with improved congestion was significantly higher in the exposure group compared with that in the control group (p = 0.018). Logistic regression analysis showed that rehabilitation was significantly associated with improved congestion (p = 0.021, OR: 0.260, 95%CI: 0.083-0.815).

Our results suggest that rehabilitation in patients with AKI associated with cardiovascular disease correlates with an improvement in congestion and may have a positive effect on the course of renal function.

The kidney epithelium, with its intricate arrangement of highly specialized cell types, constitutes the functional core of the organ. Loss of kidney epithelium is linked to the loss of functional nephrons and a subsequent decline in kidney function. In kidney transplantation, epithelial injury signatures observed during post-transplantation surveillance are strong predictors of adverse kidney allograft outcomes. However, epithelial injury is currently neither monitored clinically nor addressed therapeutically after kidney transplantation. Several factors can contribute to allograft epithelial injury, including allograft rejection, drug toxicity, recurrent infections and postrenal obstruction. The injury mechanisms that underlie allograft injury overlap partially with those associated with acute kidney injury (AKI) and chronic kidney disease (CKD) in the native kidney. Studies using advanced transcriptomic analyses of single cells from kidney or urine have identified a role for kidney injury-induced epithelial cell states in exacerbating and sustaining damage in AKI and CKD. These epithelial cell states and their associated expression signatures are also observed in transplanted kidney allografts, suggesting that the identification and characterization of transcriptomic epithelial cell states in kidney allografts may have potential clinical implications for diagnosis and therapy.

This study aims to assess the association between admission-corrected serum calcium phosphate (CaPO4) levels and the risks of in-hospital acute kidney injury (AKI) and mortality, hypothesizing a dose-dependent relationship between serum CaPO4 concentrations and the likelihood of developing AKI.

This large retrospective cohort study analyzed hospitalized adult patients who had serum calcium, phosphate, and albumin levels measured within 24 hours of admission between January 2014 and December 2018. Piecewise regression was employed to identify the optimal CaPO4 cutoff values for predicting in-hospital AKI and mortality. Subsequently, the odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the risks of in-hospital AKI and mortality associated with these cutoff values.

A total of 2,116 patients were included in the study. The incidence rates of AKI for patients with CaPO4 levels ≤27 and >27 mg2/dL2 were 9.6% and 10.9%, respectively. The bilinear association pattern revealed the lowest risk of AKI at a CaPO4 level of 27 mg2/dL2. Piecewise regression analysis showed that each 1 mg2/dL2 increase in CaPO4 level above the 27 mg2/dL2 cutoff was associated with increased risks of in-hospital AKI and mortality, with OR of 1.048 (95% CI: 1.030-1.065) and 1.048 (95% CI: 1.032-1.065), respectively.

Our findings indicate a critical relationship between elevated serum CaPO4 levels and increased risks of in-hospital AKI and mortality, with a notable cutoff at CaPO4 >27 mg2/dL2.