Acute kidney injury (AKI) is a frequent presentation in patients with infective endocarditis (IE), and is associated with poor outcomes. The primary aim of the study was to determine the risk factors for AKI in patients with IE.

A retrospective study was conducted in a tertiary hospital in China from August 2012 to April 2022. The primary outcome was AKI. Logistic regression was used to identify risk factors for AKI.

A total of 594 patients with IE were included, of which 256 (43.1%) experienced AKI. The following variables were found to be independent risk factors for AKI: hypertension (OR 1.96, p = 0.011), Staphylococcus aureus infection (OR 2.69, p = 0.008), heart failure (OR 5.99, p < 0.001), shock (OR 5.93, p = 0.015) and hematuria (OR 2.38, p < 0.001). The use of low-dose amikacin (400 mg daily) was associated with a lower incidence of AKI (OR 0.38, p < 0.001). Among patients with IE complicated by heart failure, surgery was associated with a lower incidence of AKI (OR 0.21, p = 0.010).

AKI is common in IE. Hypertension, Staphylococcus aureus infection, heart failure, shock and hematuria are risk factors of IE-associated AKI, whereas low-dose amikacin is a protective factor. Surgery is a protective factor of AKI in the setting of IE complicated by heart failure.

The Veterans Aging Cohort Study (VACS) Index is a summary measure of routinely obtained clinical variables that predicts numerous health outcomes. Because there are currently no tools to predict acute kidney injury (AKI) in people with HIV (PWH), we investigated the association of preadmission VACS Index with hospital AKI in PWH.

We conducted an observational study of PWH hospitalized in a New York City health system between 2010 and 2019. The VACS Index, calculated using outpatient laboratory values within 8-365 days of admission, was examined continuously and in quartiles. Multivariable Cox proportional hazards models, adjusting for sociodemographic factors, comorbidities, and ICU admission, determined the association of the VACS Index with AKI.

Among 1186 PWH, median age was 53 years, 43.5% were women, 86.2% were Hispanic or Black, 23.1% were coinfected with hepatitis C, and 65% were virally suppressed (<200 copies/mL). Overall AKI incidence was 20.9%. The proportion with AKI was higher by increasing VACS Index quartile: 10.7%, 18.6%, 28.1%, and 60.7% in quartiles 1-4, respectively. There was a graded, independent association of VACS Index quartile with AKI. Compared with those in the lowest quartile, the adjusted relative hazard of AKI was 1.55, 1.92, and 3.07 times higher in quartiles 2-4, respectively ( P for trend <0.001).

Preadmission VACS Index is associated with hospital AKI. Use of the VACS Index may allow for early identification of PWH at risk for AKI and initiation of preventative strategies. These findings should be externally validated in other health systems, including its predictive performance in specific hospital settings.

Evidence regarding the relationship between thyroid hormone levels within the normal range and the incidence of chronic kidney disease (CKD) in adults is scarce. This study aimed to identify the association between thyrotropin (TSH) and free thyroxine (FT4) levels with the incidence of CKD in a large cohort study over long-term follow-up.

This prospective cohort study, with an 18-year follow-up, included 4118 adults without CKD from the Tehran thyroid Study (TTS). Participants were categorized by tertiles of normal TSH levels (low-normal, middle-normal, and high-normal) and abnormal TSH. The study outcome was incident CKD, defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2. Multivariable Cox proportional hazard models were used to estimate hazard ratios (HRs) for CKD incidence based on thyroid hormone levels.

The HR for CKD development was 1.08 (95%CI: 1.01-1.15) per 1 SD increase in the TSH levels. Compared with participants with low-normal TSH levels, those with high-normal (HR:1.37; 95%CI: 1.03-1.84) and abnormal TSH (HR:1.24; 95%CI: 1.05-1.46) had a significantly higher risk of developing CKD. In subgroup analyses, the association between TSH level and CKD was significant in participants younger than 60 years, females, non-obese, non-smokers, and those without diabetes and hypertension. No association was observed between FT4 levels and incident CKD (HR: 0.92; 95%CI: 0.79-1.09). However, a significant association was observed between FT4 levels within the normal range and CKD development in those younger than 60 years old (HR: 0.77; 95% CI: 0.61-0.98).

Increased TSH levels, even within the normal range, linearly increased the risk of CKD even after adjustment for important risk factors. As a result, TSH may potentially be an independent risk factor for incident CKD.

Acute kidney injury after CRS + HIPEC is a serious postoperative complication, but only a few studies have reported its postoperative risk factors. In addition, there are large discrepancies in the results of available observational studies.

We searched The Cochrane Library, Embase, Web of Science,and PubMed to identify observational studies reporting risk factors for AKI after CRS + HIPEC. A meta-analysis was performed to investigate the effect of various preoperative and intraoperative risk factors on AKI after CRS + HIPEC.

A total of 7 studies were included in this study, comprising 1550 patients who developed AKI after CRS + HIPEC. The results of meta-analysis showed that the significant preoperative risk factors were age, sex, BMI, eGFR, Hb, PCI, diabetes mellitus, and hypertension. IO cisplatin, IO SBP < 100 was identified as an intraoperative risk factor, whereas IO mitomycin emerged as a protective factor for postoperative AKI. In addition, the risk of postoperative AKI varied by primary tumor site, with Appendix being less prone to AKI, while mesothelioma and ovarian, two sites with a greatly elevated risk of postoperative AKI.

This meta-analysis identified a number of risk factors for postoperative AKI after CRS + HIPEC. By identifying these risk factors, it is more beneficial for clinicians to perform early preoperative interventions and select the most appropriate treatment strategy for their patients, thus minimizing the risk of postoperative AKI.

PROSPERO CRD42024585269.

Multiple studies have identified risk factors for acute kidney injury (AKI) in hospitalized patients, but less is known about factors associated with AKI severity, including non-recovery of AKI.

Retrospective cohort study of adults (≥18 years) hospitalized between 2014 and 2017 at three US academic medical centers. Study outcomes included incidence of AKI and non-recovery from AKI at hospital discharge in those who survived hospitalization. AKI was defined by KDIGO serum creatinine criteria. Non-AKI recovery was defined as persistent AKI stage ≥1 at time of discharge. Multivariable models assessed the association of risk factors for each outcome, focusing on race, diabetes, and obesity (BMI ≥ 30 versus <30 kg/m2), and adjusting for potential confounders.

Among 56 056 patients included in the study (mean age 57, 25% Black, 48% women), 12 954 (23%) developed AKI. In adjusted models, Black race [odds ratio (OR) 1.26, 95% confidence interval (CI): 1.20, 1.32], diabetes (OR 1.14, 95% CI: 1.08, 1.19) and obesity (OR 1.14, 95% CI: 1.10, 1.20) were all associated with incident AKI. A total of 3591 of the 11 672 (30.8%) patients with AKI who survived until discharge had AKI non-recovery. In adjusted models, obesity (OR 1.27, 95% CI: 1.17, 1.39) was independently associated with higher risk of AKI non-recovery at hospital discharge.

Black race, diabetes, and obesity were associated with the development of AKI in hospitalized patients, but only obesity was associated with non-recovery from AKI at hospital discharge. These findings emphasize the growing relevance of obesity as an epidemiological risk factor of AKI.

Chronic Kidney Disease (CKD) is an escalating public health concern in the United States, linked with significant morbidity, mortality, and healthcare costs. Despite known risk factors like age, hypertension, and diabetes, comprehensive studies examining temporal trends in CKD prevalence are scarce. This study aims to analyze these trends using data from the National Health and Nutrition Examination Survey (NHANES).

This cross-sectional study analyzed NHANES data spanning 20 years (1999-2018), including 55,081 adults aged 20 years and above. Key renal function indicators like estimated glomerular filtration rate (eGFR) and albumin-to-creatinine ratio (ACR) were assessed, and CKD stages were categorized accordingly.

A fluctuating trend in CKD prevalence was observed, with early CKD stages (G1-G3) increasing from 9.28% in 1999-2000 to 12.93% in 2017-2018. Advanced CKD stages (G4-G5) showed a slight increase in prevalence from 0.3% in 1999-2000 to 0.51% in 2017-2018. Notable disparities were observed across age groups, diabetes status, and racial categories. Relatively, the elderly, women, and non-Hispanic whites have a higher prevalence of CKD, while individuals with diabetes have a consistently higher prevalence of early CKD from 1999 to 2018. The increasing prevalence of diabetes during the study period highlights its significant role as a CKD risk factor.

The prevalence of CKD in the U.S. has been rising over the period 1999-2018, and varying across demographic groups, underscoring significant disparities and risk factors. These insights are crucial for healthcare planning, policy formulation, and targeted interventions for CKD management.

Sodium-glucose cotransporter 2 inhibitors (SGLT2Is) and angiotensin receptor-neprilysin inhibitor (ARNI) may cause potential renal damage, the combined impact of SGLT2Is and ARNI on acute kidney injury (AKI) remains unclear. This pharmacovigilance study conducted a disproportionality analysis using reports from the FDA Adverse Event Reporting System database. The reporting odds ratio was used as an estimate for detecting AKI signal. A total of 659,573 reports on at least 1 glucose-lowering drug and/or ARNI were obtained. Of the 413 reports on cotherapy of SGLT2Is and ARNI, 99 (24.0%) reports mentioned AKI. Overall, the AKI reporting rate significantly increased in cotherapy (adjusted reporting odds ratio, 95% confidence interval: 8.04, 6.20-10.42, P < 0.001), with a stronger AKI signal in cotherapy of canagliflozin and ARNI (16.82, 3.75-75.57, P < 0.001). Specifically, no increased AKI signal was detected in patients with heart failure (HF) receiving cotherapy after adjustment for sex and age (HF: 1.27, 0.89-1.80, P = 0.189; HF plus diabetes: 2.08, 0.99-4.40, P = 0.055; or HF plus hypertension: 1.69, 0.53-5.35, P = 0.376), whereas enhanced AKI signals were detected in patients with diabetes (20.57, 11.93-35.46, P < 0.001), hypertension (4.30, 1.98-9.37, P < 0.001), or diabetes plus hypertension (5.44, 1.92-15.43, P = 0.001). This study reveals that superimposed renal impairment results from cotherapy with SGLT2Is and ARNI. It is necessary to be vigilant that the elderly patients with diabetes, hypertension, or chronic kidney disease are more susceptible to AKI, especially if they likewise receive diuretics. When cotherapy is unavoidable, early monitoring of renal function, blood volume, and blood pressure is excessively crucial. However, it is relatively safe in patients with HF.

The American Diabetes Association (ADA) "Standards of Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, an interprofessional expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations and a full list of Professional Practice Committee members, please refer to Introduction and Methodology. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.

The American Diabetes Association (ADA) "Standards of Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, an interprofessional expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations and a full list of Professional Practice Committee members, please refer to Introduction and Methodology. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.

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.

Chronic disease progression models are available for several highly prevalent conditions. For chronic kidney disease (CKD), the scope of existing progression models is limited to the risk of kidney failure and major cardiovascular (CV) events. The aim of this project was to develop a comprehensive CKD progression model (CKD-PM) that simulates the risk of CKD progression and a broad range of complications in patients with CKD. A series of literature reviews informed the selection of risk factors and identified existing risk equations/algorithms for kidney replacement therapy (KRT), CV events, other CKD-related complications, and mortality. Risk equations and transition probabilities were primarily sourced from publications produced by large US and international CKD registries. A patient-level, state-transition model was developed with health states defined by the Kidney Disease Improving Global Outcomes categories. Model validation was performed by comparing predicted outcomes with observed outcomes in the source cohorts used in model development (internal validation) and other cohorts (external validation). The CKD-PM demonstrated satisfactory modeling properties. Accurate prediction of all-cause and CV mortality was achieved without calibration, while prediction of CV events through CKD-specific equations required implementation of a calibration factor to balance time-dependent versus baseline risk. Predicted annual changes in estimated glomerular filtration rate (eGFR) and urine albumin-creatinine ratio were acceptable in comparison to external values. A flexible eGFR threshold for KRT equations enabled accurate prediction of these events. This CKD-PM demonstrated reliable modeling properties. Both internal and external validation revealed robust outcomes.

Diabetic kidney disease (DKD), a prevalent complication of diabetes mellitus, is often associated with acute kidney injury (AKI). Thus, the development of preventive and therapeutic strategies is crucial for delaying the progression of AKI and DKD.

The GSE183276 dataset, comprising the data of 20 healthy controls and 12 patients with AKI, was downloaded from the Gene Expression Omnibus (GEO) database to analyze the AKI group. For analyzing the DKD group, the GSE131822 dataset, comprising the data of 3 healthy controls and 3 patients with DKD, was downloaded from the GEO database. The common differentially expressed genes (DEGs) in renal tubular epithelial cells (TECs) were subjected to enrichment analyses. Next, a protein-protein interaction (PPI) network was constructed using the Search Tool for the Retrieval of Interacting Genes database to analyze gene-related regulatory networks. Finally, the AKI animal models and the DKD and AKI cell models were established, and the reliability of the identified genes was validated using quantitative real-time polymerase chain reaction analysis.

Functional analysis was performed with 40 common DEGs in TECs. Eight hub genes were identified using the PPI and gene-related networks. Finally, validation experiments with the in vivo animal model and the in vitro cellular model revealed the four common DEGs. Four DEGs that share molecular mechanisms in the pathogenesis of DKD and AKI were identified. In particular, the expression of Integrin Subunit Beta 6(ITGB6), a hub and commonly upregulated gene, was upregulated in the in vitro models.

ITGB6 may serve as a biomarker for early AKI diagnosis in patients with DKD and as a target for early intervention therapies.

Acute kidney injury (AKI) constitutes a common complication associated with liver or kidney transplantation, which may significantly impact the graft condition and perioperative mortality. Current AKI diagnostic criteria based on serum creatinine (sCr) and urine output alterations are widely utilized in routine clinical practice. However, the diagnostic value of sCr may be limited by various confounding factors, including age, sex, reduced or increased muscle mass, and pre-existing chronic kidney disease (CKD). Furthermore, sCr is rather a late indicator of AKI, as its concentration tends to increase only when the severity of the injury is enough to decrease the estimated glomerular filtration rate (eGFR). Recent expertise highlights the need for novel biomarkers in post-transplantation AKI diagnosis, prediction of event-associated mortality, or evaluation of indications for renal replacement treatment (RRT). Over the last decade, the diagnostic performance of various AKI biomarkers has been assessed, among which some showed the potential to outperform sCr in AKI diagnosis. Identifying susceptible individuals, early diagnosis, and prompt intervention are crucial for successful transplantation, undisturbed graft function in long-term follow-up, and decreased mortality. However, the research on AKI biomarkers in transplantation still needs to be explored. The field lacks consistent results, rigorous study designs, and external validation. Considering the rapidly growing prevalence of CKD and cirrhosis that are associated with the transplantation at their end-stage, as well as the existing knowledge gap, the aim of this article was to provide the most up-to-date review of the studies on novel biomarkers in the diagnosis of post-transplantation AKI.

The stress hyperglycemia ratio (SHR) is associated with poor outcomes in critically ill patients. However, the relationship between SHR and mortality in patients with sepsis-associated acute kidney injury (SA-AKI) remains unclear.

The data of patients with SA-AKI, identified based on the KDIGO criteria, were retrospectively collected from the Beth Israel Deaconess Medical Center between 2008 and 2019. SHR was calculated as follows: (glycemia [mmol/L]) / (1.59 × HbA1c [%] - 2.59). Primary outcomes were 30-day and 1-year mortality. The cumulative incidence of all-cause mortality was assessed using Kaplan-Meier survival analysis. Multivariable-adjusted logistic and Cox models and restricted cubic spline curves were used to analyze the correlation between SHR and all-cause mortality. Post-hoc subgroup analysis was performed to compare the effects of SHR across different subgroups.

1161 patients with SA-AKI were identified and categorized into four SHR quartiles as follows: Q1 (0.26, 0.90), Q2 (0.91, 1.08), Q3 (1.09, 1.30), and Q4 (1.31, 5.42). The median age of patients was 69 years, with 42.7% of the patients being women and 20.2% of the patients having chronic kidney disease. The 30-day and 1-year mortality were 22.1% and 35.0% respectively. Kaplan-Meier survival analysis indicated a gradual decrease in survival probability with increasing SHR quartiles. An increased SHR exhibited a strong correlation with 30-day mortality (hazard ratio [HR], 1.50; 95% confidence interval [CI], 1.18-1.90; P < 0.001) and 1-year mortality (HR, 1.32; 95% CI, 1.06-1.65; P = 0.014). SHR has a nonlinear relationship with 1-year mortality but not with 30-day mortality (P-nonlinear = 0.048 and 0.114, respectively). The results of subgroup analysis were mostly consistent with these findings.

An increased SHR is independently associated with 30-day and 1-year mortality in patients with SA-AKI. Therefore, SHR may serve as an effective tool for risk stratification in patients with SA-AKI.

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.

Acute kidney disease (AKD) is defined as subacute damage and/or loss of kidney function occurring 7 to 90 days after acute kidney injury (AKI), and bearing a high risk of progression to chronic kidney disease. Current management of AKD is non-specific and includes prevention of repeated AKI, early and regular follow-up by a nephrologist, resumption and dose adjustment of statins and renin-angiotensin system inhibitors, optimization of blood pressure control, nutrition management, and nephrotoxin avoidance. Recently, SGLT2i and GLP1- RAs have emerged as potential therapeutic tools preventing the transition from acute to chronic kidney disease due to their efficacy in preserving renal function.

The efficacy and safety of empagliflozin in the treatment of chronic kidney disease (CKD) were demonstrated in the EMPA-KIDNEY trial, which showed a 28% reduction in combined risks of kidney disease or death from cardiovascular causes (hazard ratio, 0.72; 95% confidence interval, 0.64-0.82; p < 0.001) compared with placebo. Based on these results, the present study aimed to assess the cost-effectiveness of empagliflozin + standard of care (SoC) compared with SoC alone in the treatment of CKD in France.

A Markov state microsimulation model was adapted to compare the health and economic outcomes in France, considering a healthcare system perspective, in patients treated with empagliflozin in addition to SoC versus patients treated with SoC alone. The model simulated the intention-to-treat population of the trial, transitioning between 18 mutually exclusive and collectively exhaustive health states defined based on the Kidney Disease: Improving Global Outcomes classification. For each arm, the model estimated (over a 25-year time horizon) the number of events and deaths, and the costs associated with these events, to calculate the incremental cost-effectiveness ratio. The resources used were derived using French authorities reports, literature, and French CKD guidelines. Both economic and health outcomes were discounted at a 2.5% annual rate according to French guidelines.

The model predicted that using empagliflozin + SoC to treat patients with CKD would prevent CKD-related complications and deaths associated with a cardiovascular event or all-cause deaths while in kidney replacement therapy, resulting on average in a discounted gain of 1.29 years in overall survival (9.48 years vs. 8.19 with SoC alone). Empagliflozin costs (treatment, events, and disease management) were completely offset by the cost savings from avoided kidney failure events. Overall, empagliflozin + SoC would be more effective and less costly than SoC alone and would therefore be the dominant treatment strategy. The sensitivity analyses conducted support the results' robustness in showing the dominance of empagliflozin + SoC over SoC alone.

The base-case results indicate that empagliflozin + SoC is a dominant strategy compared with the current SoC for the management of CKD in France. Empagliflozin + SoC would have a positive impact on patients with CKD by slowing CKD progression and leading to the prevention of kidney failure events on top of all-stages CKD complications.

Glomerular diseases, encompassing primary and secondary forms, pose significant morbidity and mortality risks. Despite their impact, little is known about critically ill patients with primary glomerulopathy admitted to the intensive care unit (ICU).

We conducted a case‒control study of patients with primary glomerulopathy using the Medical Information Mart for Intensive Care IV database. Demographic, clinical, and outcome data were collected. Logistic regression and mediation analysis were performed to identify predictors of hospital and long-term mortality.

Among 50,920 patients, 307 with primary glomerulopathy were included. Infectious and cardiovascular-related causes were the main reasons for ICU admission, with sepsis being diagnosed in more than half of the patients during their ICU stay. The hospital mortality rate was similar to that of the control group, with a long-term mortality rate of 29.0% three years post-ICU discharge. Reduced urine output and serum albumin were identified as independent predictors of hospital mortality, while serum albumin and the Charlson comorbidity index were significantly associated with long-term mortality. Notably, although acute kidney injury was frequent, it was not significantly associated with mortality. Additionally, reduced urine output mediates nearly 25% of the association between serum albumin and hospital mortality.

Critically ill patients with primary glomerulopathy exhibit unique characteristics and outcomes. Although hospital mortality was comparable to that of the control group, long-term mortality remained high. The serum albumin concentration and Charlson Comorbidity Index score emerged as robust predictors of long-term mortality, highlighting the importance of comprehensive risk assessment in this population. The lack of an association between acute kidney injury and mortality suggests the need for further research to understand the complex interplay of factors influencing outcomes in this patient population.

Acute kidney injury (AKI) is a common and serious complication in patients with acute non-variceal upper gastrointestinal bleeding (NVUGIB). Early prediction and intervention are crucial for improving patient outcomes.

Data for patients presenting with acute NVUGIB in this retrospective study were sourced from the MIMC-IV database. Patients were randomly allocated into training and validation cohorts for further analysis. Independent predictors for AKI were identified using least absolute shrinkage and selection operator regression and multivariable logistic regression analyses in the training cohort. Based on the logistic regression results, a nomogram was developed to predict early AKI onset in acute NVUGIB patients, and implemented as a web-based calculator for clinical application. The nomogram's performance was evaluated through discrimination, using the C-index, calibration curves, and decision curve analysis (DCA) to assess its clinical value.

The study involved 1082 acute NVUGIB patients, with 406 developing AKI. A multivariable logistic regression identified five key AKI predictors: CKD, use of human albumin, chronic liver disease, glucose, and blood urea nitrogen. The nomogram was constructed based on independent predictors. The nomogram exhibited robust accuracy, evidenced by a C-index of 0.73 in the training cohort and 0.72 in the validation cohort. Calibration curves demonstrated satisfactory concordance between predicted and observed AKI occurrences. DCA revealed that the nomogram offered considerable clinical benefit within a threshold probability range of 7% to 54%.

Our nomogram is a valuable tool for predicting AKI risk in patients with acute NVUGIB, offering potential for early intervention and improved clinical outcomes.

To assess the association between urinary albumin-to-creatinine ratio (UACR) categories within the normal range with mortality and adverse cardiovascular outcomes.

PubMed and Embase were systematically searched for real-world evidence studies. Studies were manually evaluated according to predefined eligibility criteria. We included prospective and retrospective cohort studies of the association between UACR categories <30 mg/g and cardiovascular outcomes or mortality. Published information regarding study design, participants, UACR categorization, statistical methods, and results was manually collected. Two UACR categorization approaches were defined: a two-category (UACR <10 mg/g vs. 10-30 mg/g) and a three-category division (UACR <5 mg/g vs. 5-10 and 10-30 mg/g). A random effects meta-analysis was performed on studies eligible for the meta-analysis.

In total, 22 manuscripts were identified for the systematic review, 15 of which were eligible for the meta-analysis. The results suggest an association between elevated UACR within the normal to mildly increased range and higher risks of all-cause mortality, cardiovascular death, and coronary heart disease, particularly in the range of 10-30 mg/g. Compared with UACR <10 mg/g, the hazard ratio [HR (95% confidence interval, CI)] for UACR between 10 and 30 mg/g was 1.41 (1.15, 1.74) for all-cause mortality and 1.56 (1.23, 1.98) for coronary heart disease. Compared with UACR <5 mg/g, the risk of cardiovascular mortality for UACR between 10 and 30 mg/g was more than twofold [HR (95% CI): 2.12 (1.61, 2.80)]. Intermediate UACR (5-10 mg/g) was also associated with a higher risk of all-cause mortality [HR (95% CI): 1.14 (1.05, 1.24)] and cardiovascular mortality [HR (95% CI): 1.50 (1.14, 1.99)].

We propose considering higher UACR within the normoalbuminuric range as a prognostic factor for cardiovascular morbidity and mortality. Our findings underscore the clinical significance of even mild increases in albuminuria.

Southern Hemisphere countries have been underrepresented in epidemiological studies on acute kidney injury (AKI). The objectives of this study were to determine the frequency, risk factors, and outcomes of AKI in adult hospitalized patients from the emergency department of a public high-complexity teaching hospital in the city of São Paulo, Brazil.

Observational and prospective study. AKI was defined by the KDIGO guidelines (Kidney Disease: Improving Global Outcomes) using only serum creatinine.

Among the 731 patients studied (age: median 61 years, IQR 47-72 years; 55% male), 48% had hypertension and 28% had diabetes as comorbidities. The frequency of AKI was 52.1% (25.9% community-based AKI [C-AKI] and 26.3% hospital-acquired AKI [H-AKI]). Dehydration, hypotension, and edema were found in 29%, 15%, and 15% of participants, respectively, at hospital admission. The in-hospital and 12-month mortality rates of patients with vs. without AKI were 25.2% vs. 11.1% (p<0.001) and 36.7% vs. 12.9% (p<0.001), respectively. The independent risk factors for C-AKI were chronic kidney disease (CKD), chronic liver disease, age, and hospitalization for cardiovascular disease. Those for H-AKI were CKD, heart failure as comorbidities, hypotension, and edema at hospital admission. H-AKI was an independent risk factor for death in the hospital, but not at 12 months. C-AKI was not a risk factor for death.

AKI occurred in more than half of the admissions to the clinical emergency department of the hospital and was equally distributed between C-AKI and H-AKI. Many patients had correctable risk factors for AKI, such as dehydration and arterial hypotension (44%) at admission. The only independent risk factor for both C-AKI and H-AKI was CKD as comorbidity.

Although community-acquired acute kidney injury (CA-AKI) represents a significant subset of all AKI incidence, evidence is limited due to the lack of comprehensive data prior to diagnosis. Here, we examined the risk of drug use for CA-AKI by using exhaustive pre-diagnostic prescription data. We included 78,754 working-age healthy individuals who underwent an annual health checkup program. We conducted a cohort study to assess the association between prevalent drug use and subsequent CA-AKI incidence using the Cox proportional hazard model. Subsequently, we conducted a case-crossover study to compare the new drug use in the case period directly before the CA-AKI incidence (- 3 to 0 months) with that in the control period far before the CA-AKI incidence (- 15 to - 12 months and - 9 to - 6 months) using the conditional Poisson regression model. The prevalent use of renin-angiotensin-aldosterone system (RAAS) inhibitors was associated with an increased CA-AKI incidence, but the new use was not. The new use of diuretics, anti-infectious drugs, and contrast medium was also associated with an increased CA-AKI incidence. These results suggest we need to pay attention for the incidence of AKI among the general population taking those common drugs.

Early detection is a key strategy to prevent kidney disease, its progression and related complications, but numerous studies show that awareness of kidney disease at the population level is low. Therefore, increasing knowledge and implementing sustainable solutions for early detection of kidney disease are public health priorities. Economic and epidemiological data underscore why kidney disease should be placed on the global public health agenda - kidney disease prevalence is increasing globally and it is now the seventh leading risk factor for mortality worldwide. Moreover, demographic trends, the obesity epidemic and the sequelae of climate change are all likely to increase kidney disease prevalence further, with serious implications for survival, quality of life and health care spending worldwide. Importantly, the burden of kidney disease is highest among historically disadvantaged populations that often have limited access to optimal kidney disease therapies, which greatly contributes to current socioeconomic disparities in health outcomes. This joint statement from the International Society of Nephrology, European Renal Association and American Society of Nephrology, supported by three other regional nephrology societies, advocates for the inclusion of kidney disease in the current WHO statement on major non-communicable disease drivers of premature mortality.

Introduction: Hypertension is a prevalent condition in the United States and leads to an increased risk of developing various comorbidities. However, the impact of new-onset hypertension after severe burns on patient outcomes is not known. We posit that hypertension onset after severe burn is associated with increased risk of developing comorbidities and mortality. Methods: Using the TriNetX database, burned patients diagnosed with essential hypertension after injury were compared with those who did not develop hypertension; neither had prior hypertension. Each cohort was grouped by sex, percent total body surface area (TBSA) burned, and age, then propensity matched for sex, race, ethnicity, and laboratory values. Outcomes assessed were acute kidney injury (AKI), hyperglycemia, heart failure, myocardial infarction (MI), and death. Results: Those diagnosed with hypertension after severe burn were 4.9 times more likely to develop AKI, 3.6 times for hyperglycemia, 5.3 times for heart failure, 4.7 times for acute MI, and 1.5 times for mortality. Sex analysis shows that men were at greater risk for AKI (1.5 times), heart failure (1.1 times), and death (1.4 times). Women were 1.3 times more likely to develop hyperglycemia. Percent TBSA burned grouping showed increased risk for all outcomes with increasing severity. Age grouping indicated an elevated risk of developing AKI, heart failure, acute MI, and death. Conclusion: New-onset hypertension diagnosis in severely burned patients is associated with acute kidney injury, heart failure, acute MI, and death. Overall, males, older patients, and those with a higher % TBSA burned are at a higher risk of developing these comorbidities.

Type 2 diabetes mellitus (T2DM) is a prevalent chronic disease and a leading cause of morbidity/mortality in Canada. We evaluated the burden of T2DM in Alberta, Canada, by estimating the 5-year period prevalence of T2DM and rates of comorbidities and complications/conditions after T2DM.

We conducted a population-based, retrospective study linking administrative health databases. Individuals with T2DM (≥18 years of age) were identified between 2008-2009 and 2018-2019 using a published algorithm, with follow-up data to March 2020. The 5-year period prevalence was estimated for 2014-2015 to 2018-2019. Individuals with newly identified T2DM, ascertained between 2010-2011 and 2017-2018 with a lookback period between 2008-2009 and 2009-2010 and a minimum 1 year of follow-up data, were evaluated for subsequent cardiovascular, diabetic, renal, and other complication/condition frequencies (%) and rates (per 100 person-years). Complications/conditions were stratified by atherosclerotic cardiovascular disease (ASCVD) status at index and age.

The 5-year period prevalence of T2DM was 11,051 per 100,000 persons, with the highest prevalence in men 65 to <75 years of age. There were 195,102 individuals included in the cohort (mean age 56.7±14.7 years). The most frequently reported complications/conditions (rates per 100 person-years) were acute infection (23.10, 95% confidence interval [CI] 23.00 to 23.30), hypertension (17.30, 95% CI 16.80 to 17.70), and dyslipidemia (12.20, 95% CI 11.90 to 12.40). Individuals who had an ASCVD event/procedure and those ≥75 years of age had higher rates of complications/conditions.

We found that over half of the individuals had hypertension or infection after T2DM. Also, those with ASCVD had higher rates of complications/conditions. Strategies to mitigate complications/conditions after T2DM are required to reduce the burden of this disease on individuals and health-care systems.

We observed transient elevations in creatinine levels among kidney recipients after three traditional holidays in Taiwan. This retrospective cohort study aimed to compare the changes in eGFR levels after Chinese New Year, Dragon Boat Festival, and Mid-Autumn Festival, all of which are associated with high-calorie and high-fat diets.

We conducted a retrospective analysis of 364 kidney recipients with stable graft function who were following at Chang Gung Memorial Hospital Linkou from 2018 to 2020. The graft function before and after the festival was determined by calculating the eGFR level using the serum creatinine measured during clinic visits prior to and following the festival. The patients were then categorized into subgroups based on their sex, BMI, and co-morbidities. The eGFR levels before and after the festival were evaluated and compared within these subgroups.

A total of 301 kidney recipients have been finally included in this retrospective cohort study. The analysis showed a significant decrease in overall eGFR levels after Chinese New Year (from 56.92 ± 29.70 to 55.14 ± 24.79, P = .006), Mid-Autumn Festival (from 54.03 ± 24.61 to 53.35 ± 24.33, P = .008), and Dragon Boat Festival only in 2020 (from 50.98 ± 24.35 to 49.99 ± 23.45, P = .018). The analysis of subgroups suggested a tendency of renal function decline after all 3 traditional holidays in patient groups with DM or hypertension or nonoverweight status.

In this study, we observed a significant decline in renal function among kidney recipients following traditional holidays in Taiwan, particularly among recipients with hypertension or diabetes mellitus or those who were not overweight.

Studies have demonstrated sodium-glucose cotransporter-2 (SGLT2) inhibitors are kidney protective; however, their ability to cause hemodynamic changes may predispose patients to acute kidney injury (AKI). An FDA warning recommends evaluating for factors that predispose patients to AKI before initiating a SGLT2 inhibitor. The primary objective of this study is to identify risk factors that may predispose persons with diabetes to AKI when initiating SGLT2 inhibitor therapy.

Multicenter retrospective cohort chart review.

Study patients were identified through an electronic medical record generated report if they had type 2 diabetes and were prescribed a SGLT2 inhibitor from January 2013 to September 2019.

Patients were included if they were receiving care at Advocate Medical Group and were confirmed to have taken one of the four SGLT2 inhibitors available at the time of study approval, canagliflozin, dapagliflozin, empagliflozin, or ertugliflozin, for at least 7 days. Patients were excluded if they did not have a basic metabolic panel or comprehensive metabolic panel recorded 1 year prior to or 6 months after SGLT2 inhibitor therapy initiation.

Data extraction from the electronic medical record identified 6425 patients receiving a SGLT2 inhibitor, of which 1962 met inclusion criteria and were included for analysis. Thirty-five (1.8%) patients experienced an AKI after SGLT2 inhibitor therapy initiation. There was no statistically significant difference between groups based on background medication use (p = 0.325). At baseline, patients experiencing an AKI after SGLT2 inhibitor initiation were more likely to be older in age (p = 0.010), have a higher serum potassium (p < 0.001), blood glucose (p = 0.018), SCr (p = 0.009) and UACR (p < 0.001), and a lower eGFR (p = 0.028) compared to those who did not experience AKI.

The transient eGFR decline with SGLT2 inhibitor initiation should be expected and is generally not an indication to discontinue therapy. Future initiatives should be directed at increasing knowledge of monitoring recommendations for these agents.

Kidneys have an amazing ability to adapt to adverse situations, both acute and chronic. In the presence of injury, the kidney is able to activate mechanisms such as autoregulation or glomerular hyperfiltration to maintain the glomerular filtration rate (GFR). While these adaptive mechanisms can occur in physiological situations such as pregnancy or high protein intake, they can also occur as an early manifestation of diseases such as diabetes mellitus or as an adaptive response to nephron loss. Although over-activation of these mechanisms can lead to intraglomerular hypertension and albuminuria, other associated mechanisms related to the activation of inflammasome pathways, including endothelial and tubular damage, and the hemodynamic effects of increased activity of the renin-angiotensin-aldosterone system, among others, are recognized pathways for the development of albuminuria. While the role of albuminuria in the progression of chronic kidney disease (CKD) is well known, there is increasing evidence of its negative association with cardiovascular events. For example, the presence of albuminuria is associated with an increased likelihood of developing heart failure (HF), even in patients with normal GFR, and the role of albuminuria in atherosclerosis has recently been described. Albuminuria is associated with adverse outcomes such as mortality and HF hospitalization. On the other hand, it is increasingly known that the systemic effects of congestion are mainly preceded by increased central venous pressure and transmitted retrogradely to organs such as the liver or kidney. With regard to the latter, a new entity called congestive nephropathy is emerging, in which increased renal venous pressure can lead to albuminuria. Fortunately, the presence of albuminuria is modifiable and new treatments are now available to reverse this common risk factor in the cardiorenal interaction.

The American Diabetes Association (ADA) "Standards of Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, an interprofessional expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations and a full list of Professional Practice Committee members, please refer to Introduction and Methodology. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.

Vancomycin (VAN) is widely used in neurosurgical patients for intracranial infections. We aimed to assess the incidence and risk factors for VAN-associated acute kidney injury (VA-AKI) in this population.

A case-control study of patients who treated with vancomycin in neurosurgery from January 2020 to December 2022 was conducted. Demographics and potential risk factors were collected. Multivariate logistic regression analyses were performed to identify risk factors for VA-AKI. AKI was defined according to the Kidney Disease Improving Global Outcomes Guidelines (KDIGO).

A total of 345 patients participated with a VA-AKI incidence of 17.1% (59 cases). Among them, 15 patients had renal impairment (Stage 2 or higher), and 2 required dialysis. With univariate analysis and binary logistic regression analysis, we found that the use of mannitol (OR: 4.164; 95% CI: 1.606-10.792; P = 0.003), loop diuretics (OR: 3.371; 95% CI: 1.633-6.958; P = 0.001), three or more antimicrobial applications (OR: 3.623; 95% CI: 1.600-8.206; P = 0.002), diastolic blood pressure 80-89 mm Hg (OR: 5.532; 95% CI: 1.677-18.250; P = 0.005) and diastolic blood pressure ≥ 90 mm Hg (OR: 6.845; 95% CI: 1.518-30.866; P = 0.012) were independent risk factors for VA-AKI. In addition, according to the Youden Index, the trough concentration of vancomycin should not exceed 15.845 mg/L.

The incidence of VA-AKI in neurosurgical patients was 17.1%. The concomitant use of mannitol and loop diuretics, along with higher diastolic blood pressure and the combined use of more than three antimicrobial agents, were associated with an increased risk of neurosurgical VA-AKI.

The American Diabetes Association (ADA) "Standards of Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, an interprofessional expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations and a full list of Professional Practice Committee members, please refer to Introduction and Methodology. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.

The sodium-glucose co-transporter-2 inhibitor empagliflozin was approved for treatment of adults with chronic kidney disease (CKD) on the basis of its demonstrated ability to slow CKD progression and reduce the risk of cardiovascular death. This analysis was performed to assess the cost-effectiveness of empagliflozin plus standard of care (SoC) vs SoC alone in the treatment of CKD in the UK.

A comprehensive, patient-level CKD progression model that simulates the evolution of risk factors for disease progression based on CKD-specific equations and clinical data was used to project a broad range of CKD-related complications. Patient baseline characteristics, distribution across Kidney Disease Improving Global Outcomes (KDIGO) health states, and changes in estimated glomerular filtration rate (eGFR), urine albumin-creatinine ratio (uACR), and other parameters while on treatment were derived from the EMPA-KIDNEY trial. UK cost and utilities/disutilities were sourced from the literature. Univariate and probabilistic sensitivity analyses were conducted. Annual discounting of 3.5% was applied on costs and outcomes.

Over a 50-year horizon, SoC resulted in per-patient costs, life years, and QALYs of £95,930, 8.55, and 6.28, respectively. Empagliflozin plus SoC resulted in an incremental gain in life years (+1.04) and QALYs (+0.84), while decreasing per-patient costs by £6,019. Empagliflozin was more effective and less costly (dominant) with a net monetary benefit of £22,849 at the willingness-to-pay threshold of £20,000. Although treatment cost was higher for empagliflozin, this was more than offset by savings in kidney replacement therapy. Empagliflozin remained highly cost-effective in patients with and without diabetes, and across scenario and sensitivity analyses.

This analysis is limited by reliance on short-term clinical trial data and by uncertainties in modelling CKD progression.

Empagliflozin as an add-on to SoC for treatment of adults with CKD represents cost-effective use of UK National Health Service (NHS) resources.

Diabetic kidney disease (DKD) is a chronic renal disease which could eventually develop into renal failure. Though albuminuria and estimated glomerular filtration rate (eGFR) are helpful for the diagnosis of DKD, the lack of specific biomarkers reduces the efficiency of therapeutic interventions.

Based on bulk-seq of 56 urine samples collected at different time points (including 11 acquired from DKD patients and 11 from healthy controls), in corporation of scRNA-seq data of urine samples and snRNA-seq data of renal punctures from DKD patients (retrieved from NCBI GEO Omnibus), urine-kidney specific genes were identified by Multiple Biological Information methods.

Forty urine-kidney specific genes/differentially expressed genes (DEGs) were identified to be highly related to kidney injury and proteinuria for the DKD patients. Most of these genes participate in regulating glucagon and apoptosis, among which, urinary PART1 (mainly derived from distal tubular cells) and PLA2R1 (podocyte cell surface marker) could be used together for the early diagnosis of DKD. Moreover, urinary PART1 was significantly associated with multiple clinical indicators, and remained stable over time in urine.

Urinary PART1 and PLA2R1 could be shed lights on the discovery and development of non-invasive diagnostic method for DKD, especially in early stages.

To combat the irreversible decline in renal function associated with kidney disease, it is essential to establish non-invasive biomarkers for assessing renal microcirculation. However, the limited resolution and/or vascular sensitivity of existing diagnostic imaging techniques hinders the visualization of complex cortical vessels. Here, a 3D renal ultrafast Doppler (UFD) imaging system that uses a high ultrasound frequency (18 MHz) and ultrahigh frame rate (1 KHz per slice) to scan the entire volume of a rat's kidney in vivo is demonstrated. The system, which can visualize the full 3D renal vascular branching pyramid at a resolution of 167 µm without any contrast agent, is used to chronically and noninvasively monitor kidneys with acute kidney injury (AKI, 3 days) and diabetic kidney disease (DKD, 8 weeks). Multiparametric UFD analyses (e.g., vessel volume occupancy (VVO), fractional moving blood volume (FMBV), vessel number density (VND), and vessel tortuosity (VT)) describe rapid vascular rarefaction from AKI and long-term vascular degeneration from DKD, while the renal pathogeneses are validated by in vitro blood serum testing and stained histopathology. This work demonstrates the potential of 3D renal UFD to offer valuable insights into assessing kidney perfusion levels for future research in diabetes and kidney transplantation.

Current demographic change leads to higher number of elderly patients admitted to an ICU. Among other organs also the kidneys show age-related changes, which are associated with a decline in various aspects of renal function. The purpose of this review is to provide an overview of structural and functional changes in elderly and also to specifically address the increased risk of acute kidney injury (AKI) in this population.

Ageing in the kidneys is affected by many different factors, such as low grade chronic inflammation, called inflammageing, and various comorbidities. Nevertheless, a decrease of glomerular filtration rate (GFR) occurs independent of the presence of comorbidities and a steady decline of GFR has been reported in both healthy men and women. Pharmacodynamic of many drugs is altered by these changes. Additionally the rate of diuretic resistance appears to be increased. The cause of AKI occurrence in older age is, multifactorial and includes preventable triggers (hypovolemia, hypotension, nephrotoxins) as well as changes associated with aging.

Age-related alterations of the kidneys were found at microscopic and macroscopic levels of the cell. These changes lead to a reduced renal reserve and subsequently to an increased vulnerability of aged kidneys when an additional stressor is added. Age is an independent risk factor for developing AKI. Physicians should take into account the altered renal function in elderly patients and take renal protective measures at an early stage.

Patients with chronic kidney disease (CKD) have high morbidity and mortality, and the disease progression has a significant impact on their survival and living standards. This research aims to analyze risk factors for CKD stage 1 and provide a reference for clinical decision making. The clinical data and peripheral blood samples of 300 patients with CKD stage 1 were collected retrospectively. Patients were randomly assigned into a training set (n = 210) and a validation set (n = 90). Patients' baseline characteristic levels were subjected to statistical tests for difference. Univariate and multivariate Cox regression analyses were utilized to identify risk factors influencing disease progression. Subsequently, a prediction model for disease progression was developed using a nomogram, and the model's accuracy was assessed using the C-index and calibration curve. The results revealed that hypertension, diabetes, and urinary albumin were essential factors in the progression of CKD stage 1. The nomogram was constructed and then the C-index was calculated. The calibration curve was utilized to assess the risk model. The C-index of the training set was 0.75, and the C-index of the validation set was 0.73, suggesting a good predictive ability of the model. The risk model accurately predicted the progression of CKD stage 1, which is of great significance to developing personalized treatment for patients in clinical practice.

Both diabetic and hypertensive nephropathy eventually progress to glomerulosclerosis. Previous studies revealed a potential role of endothelial-to-mesenchymal transition (EndMT) in the pathophysiology of glomerulosclerosis in diabetic rats. Therefore, we hypothesized that EndMT was also involved in the development of glomerulosclerosis in salt-sensitive hypertension. We aimed to explore the effects of high-salt diet on endothelial-to-mesenchymal transition (EndMT) in glomerulosclerosis in Dahl salt-sensitive (Dahl-SS) rats.

Eight-week-old male rats were fed high-salt (8%NaCl; DSH group) or normal salt (0.3%NaCl; DSN group) for eight weeks, with systolic blood pressure (SBP), serum creatinine, urea, 24-hour urinary protein/sodium, renal interlobar artery blood flow, and pathological examination measured. We also examined endothelial-(CD31) and fibrosis-related protein(α-SMA) expressions in glomeruli.

High-salt diet increased SBP (DSH vs. DSN, 205.2 ± 8.9 vs. 135.4 ± 7.9 mm Hg, P < 0.01), 24-hour urinary protein (132.55 ± 11.75 vs. 23.52 ± 5.94 mg/day, P < 0.05), urine sodium excretions (14.09 ± 1.49 vs. 0.47 ± 0.06 mmol/day, P < 0.05), and renal interlobar artery resistance. Glomerulosclerosis increased (26.1 ± 4.6 vs. 7.3 ± 1.6%, P < 0.05), glomerular CD31 expressions decreased while α-SMA expression increased in DSH group. Immunofluorescence staining showed that CD31 and α-SMA co-expressed in glomeruli of the DSH group. The degree of glomerulosclerosis negatively correlated with CD31 expressions (r = -0.823, P < 0.01) but positively correlated with α-SMA expressions (r = 0.936, P < 0.01).

We demonstrated that a high-salt diet led to glomerulosclerosis involving the EndMT process, which played an essential role in glomerulosclerosis in hypertensive Dahl-SS rats.

Diabetic kidney disease (DKD) is a major microvascular complication of type 2 diabetes mellitus (T2DM). Monitoring the early diagnostic period and disease progression plays a crucial role in treating DKD. In this study, to comprehensively elucidate the molecular characteristics of urinary proteins and urinary exosome proteins in type 2 DKD, we performed large-scale urinary proteomics (n=144) and urinary exosome proteomics (n=44) analyses on T2DM patients with albuminuria in varying degrees. The dynamics analysis of the urinary and exosome proteomes in our study provides a valuable resource for discovering potential urinary biomarkers in patients with DKD. A series of potential biomarkers, such as SERPINA1 and transferrin (TF), were detected and validated to be used for DKD diagnosis or disease monitoring. The results of our study comprehensively elucidated the changes in the urinary proteome and revealed several potential biomarkers reflecting the progression of DKD, which provide a reference for DKD biomarker screening.

We previously reported that induced type 1 diabetes mellitus (DM) increases the susceptibility of acute kidney injury in- duced by ischemia-reperfusion injury (IRI) in cynomolgus monkeys. In this follow-up study, we compared the expression of selected markers in the renal tissues of monkeys subjected to bilateral renal IRI with and without diabetes. All tissues were obtained from the original study. Renal biopsies were obtained before and 24 and 48 h after ischemia and were examined for expression of KI-67 (tubular proliferation), Na+ /K+ ATPase (sodium-potassium pump), TNF-α(tumor necrosis factor-α, inflammation), CD31 (microvessels), CD3 (T-cells), 2 fibrotic markers (fibroblast specific protein-1, FSP-1;α-smooth muscle actin,α -SMA), and cleaved caspase 3 (apoptosis). Generally, the expression of these markers differed in monkeys with and without DM. As compared with non-DM monkeys, DM monkeys had more cells that expressed KI-67 during progression of acute kidney injury (AKI). Na+ /K+ ATPase expression was clearly present at baseline in the basolateral tubular areas only in the non-DM monkeys. At 48 h, its expression in the basolateral area was not visible in DM monkeys, but was still present in intercellular junctions of non-DM monkeys. The expression of TNF-αwas higher in DM before and 48 h after ischemia. Before and 24 h after ischemia, the number of CD31-positive capillaries was not different between 2 groups, although more collapsed vessels were found at in DM at 24 h. At 48 h, the number of capillaries was less in DM compared with those from non-DM animals. DM monkeys had more interstitial CD3-positive cells than did non-DM monkeys at 24 and 48 h after ischemia. Finally, FSP-1-stained cells were more abundant in DM than non-DM at 24 and 48 h. Our results show that DM aggravates the recovery of renal ischemia/reperfusion injury by affecting tubular proliferation, capillary density, T cell infil- tration and by altering protein and mRNA expression of various genes involved in ion channel, inflammation, and fibrotic change. The results from this observational study demonstrate that DM aggravates the recovery of renal ischemia/reperfusion injury by affecting multiple events including tubular necrosis, proliferation, function, inflammation and by inducing capillary rarefaction in cynomolgus monkeys.