Rapid Kidney Function Decline Research Articles

Accessing the relationship between six surrogate insulin resistance indexes and the incidence of rapid kidney function decline and the progression to chronic kidney disease among middle-aged and older adults in China: Results from the China health and retirement longitudinal study

AimsInsulin resistance is closely related to kidney function decline, but which insulin resistance index could better predict rapid kidney function decline (RKFD) remains unclear. We aimed to evaluate the prospective association between six insulin resistance indexes: Chinese Visceral Adiposity Index (CVAI), Lipid Accumulation Product (LAP), Atherogenic Index of Plasma (AIP), triglyceride-glucose (TyG) index, triglyceride-glucose × Body Mass Index (TyGBMI) and triglyceride-glucose × waist circumference (TyGWC) with RKFD and further the progression to chronic kidney disease (CKD). Methods and measurementsData were obtained from the China Health and Retirement Longitudinal Study. Participants with normal kidney function (eGFRcr-cys ≥60 ml/min per 1.73 m2) and ≥45 years old were included at the baseline (year 2011). The eGFR was estimated by a combination of serum creatinine and cystatin C. The primary outcome was RKFD, defined as an annualized decline in eGFRcr-cys of 5 ml/min per 1.73 m2 or more. Secondary outcome was progression to CKD under the condition of RKFD, defined as an annualized decline in eGFRcr-cys of 5 ml/min per 1.73 m2 or more combined with eGFRcr-cys <60 ml/min per 1.73 m2 at the exit visit. Logistic analysis was applied for analysis of the association between six insulin resistance indexes and RKFD or progression to CKD. We use receiver operating characteristic curves to study the predictive performance of six insulin resistance indexes. Subgroup analysis were conducted by diabetes or hypertension status of the participants. ResultsA total of 3899 participants with normal kidney function were included in this study. After a 3.99 years follow-up, 191 of them ended up with RKFD. Among them, 66 participants progressed to CKD. Logistic analysis showed that per SD increase of all the six insulin resistance indexes were significantly associated with the incidence of RKFD (all P < 0.01), among which, TyGWC had the best predictive value for RKFD. There were significant association between per SD increase of CVAI, LAP, TyGBMI and TyGWC with progression to CKD (all P < 0.01), and CVAI had better predictive role than other indexes. In subgroup analysis, we found that the association between insulin resistance indexes and progression to CKD was more significant in subjects with hypertension or without diabetes. However, no significant differences were observed in the RKFD group. ConclusionsIn this study we proved six insulin resistance indexes were predictively associated with RKFD in Chinese with normal renal function over age 45. TyGWC is the best insulin resistance index for predicting RKFD. CVAI is the best index for predicting further progression to CKD.

Association of plasma ceramide with decline in kidney function in patients with type 2 diabetes

Circulating ceramide levels are dysregulated in kidney disease. However their associations with rapid decline in kidney function (RDKF) and end-stage kidney disease (ESKD) in patients with type 2 diabetes (T2D) are unknown. In this prospective study of 1746 T2D participants, we examined the association of plasma ceramide Cer16:0, Cer18:0, Cer24:0 and Cer24:1 with RDKF, defined as an estimated glomerular filtration rate (eGFR) decline of 5ml/min/1.73m2/yr or greater, and ESKD defined as eGFR <15/min/1.73m2 for at least three months, on dialysis, or renal death at follow-up. We performed multivariable logistic and cox regression analyses adjusted for traditional cardio-renal risk factors, including baseline renal functions. During a median (interquartile range) follow-up period of 7.7 (4.7-8.9) years, 197 (11%) patients experienced RDKF. Ceramide Cer24:0 (odds ratio [OR]=0.71, 95%CI 0.56-0.90) and ratios Cer16:0/Cer24:0 (OR=3.54, 95%CI 1.70-7.35), Cer18:0/Cer24:0 (OR=1.89, 95%CI 1.10-3.25) and Cer24:1/Cer24:0 (OR=4.01, 95%CI 1.93-8.31) significantly associated with RDKF in multivariable analysis. 124 patients developed ESKD. The ratios Cer16:0/Cer24:0 (hazard ratio [HR]=3.10, 95%CI 1.44-6.64), and Cer24:1/Cer24:0 (HR=4.66, 95%CI 1.93-11.24) significantly associated with a higher risk of ESKD. The Cer24:1/Cer24:0 ratio improved risk discrimination for ESKD beyond traditional risk factors by small but statistically significant margin (Harrell C-index difference 0.01; P=0.022). A high ceramide risk score, constructed using individual ceramide level and ceramide ratios, also associated with RDKF (OR=2.28, 95%CI 1.26-4.13) compared to lower risk score. In conclusion, specific ceramide levels and their ratios are associated with RDKF and conferred an increased risk of ESKD, independently of traditional risk factors in patients with T2D.

Effect of proteinuria on the rapid kidney function decline in chronic kidney disease depends on the underlying disease: A post hoc analysis of the BRIGHTEN study

AimsIt is unclear whether the effect of proteinuria on rapid kidney function decline is equivalent among diabetic kidney disease (DKD), non-DKD with diabetes (NDKD+DM), and nephrosclerosis without diabetes (NS-DM), particularly in advanced chronic kidney disease patients. MethodsIn total, 1038 chronic kidney disease patients who participated in the BRIGHTEN study were included in the present study. A linear mixed effect model was applied to estimate the annual estimated glomerular filtration rate decline in each disease group. ResultsThe prevalence of rapid decliners (rapid kidney function decline, defined as an eGFR loss of > 5 mL/min/1.73 m2/year) in the DKD group (44.6 %) was significantly higher compared with the NDKD+DM (27.9 %) and NS-DM (27.0 %) groups. By contrast, the prevalence of rapid decliners in different urine total protein to creatinine ratio (UPCR) categories (<0.5, 0.5 to < 1.0, 1.0 to < 3.5, and ≥ 3.5 g/g) were equivalent between the DKD and NS-DM groups. Moreover, the prevalence of a UPCR < 1.0 g/g in rapid decliners of the NS-DM group was more than double than in those of the DKD and NDKD+DM groups. ConclusionsThe risk of rapid kidney function decline in NS-DM patients with low levels of proteinuria may be greater than initially predicted.

COVID-19−Associated Acute Kidney Injury and Longitudinal Kidney Outcomes

COVID-19 infection is associated with a high incidence of acute kidney injury (AKI). Although rapid kidney function decline has been reported in the first few months after COVID-19-associated AKI (COVID-AKI), the longer-term association of COVID-AKI with kidney function remains unknown. To assess long-term kidney outcomes of patients who had COVID-19-associated AKI. This was a retrospective longitudinal multicenter cohort study conducted in a large hospital system using electronic health records data on adult hospitalized patients with AKI and COVID-19 or other illnesses. Included patients were hospitalized during the COVID-19 pandemic (March 2020-June 2022), were screened for SARS-CoV-2, had AKI, and survived to discharge, or had been hospitalized during the 5 years before the pandemic (October 2016-January 2020), had a positive influenza A or B test result, had AKI, and survived to discharge. Patients were followed up for a maximum of 2 years after hospital discharge. Data analyses were performed from December 2022 to November 2023. COVID-19 and influenza. The primary outcome was major adverse kidney events (MAKE), defined as a composite of mortality and worsened kidney function (estimated glomerular filtration rate [eGFR] decline by ≥25% from discharge eGFR or kidney failure requiring dialysis). Multivariable time-to-event analyses were performed to compare MAKE between individuals with COVID-AKI and those who had AKI associated with other illnesses hospitalized during the same period. For further comparison, this outcome was assessed for a historic cohort of patients with influenza-associated AKI. The study cohort included 9624 hospitalized patients (mean [SD] age, 69.0 [15.7] years; 4955 [51.5%] females) with AKI, including 987 patients with COVID-AKI, 276 with influenza-associated AKI, and 8361 with AKI associated with other illnesses (other-AKI). Compared with the other 2 groups, patients with COVID-19-associated AKI were slightly younger in age, had a higher baseline eGFR, worse baseline comorbidity scores, higher markers of illness severity, and longer hospital stay. Compared with the other-AKI group, the COVID-AKI group had lower MAKE (adjusted hazard ratio [aHR], 0.67; 95% CI, 0.59-0.75) due to lower all-cause mortality (aHR, 0.31; 95% CI, 0.24-0.39) and lower rates of worsened kidney function (aHR, 0.78; 95% CI, 0.69-0.88). The findings of this multicenter cohort study indicate that survivors of hospitalization with COVID-AKI experience lower rates of MAKE, long-term kidney function decline, and mortality compared with patients with AKI associated with other illnesses.

The role of non-protein-coding RNAs in ischemic acute kidney injury.

Acute kidney injury (AKI) is a condition characterized by a rapid decline in kidney function within a span of 48 hours. It is influenced by various factors including inflammation, oxidative stress, excessive calcium levels within cells, activation of the renin-angiotensin system, and dysfunction in microcirculation. Ischemia-reperfusion injury (IRI) is recognized as a major cause of AKI; however, the precise mechanisms behind this process are not yet fully understood and effective treatments are still needed. To enhance the accuracy of diagnosing AKI during its early stages, the utilization of innovative markers is crucial. Numerous studies suggest that certain noncoding RNAs (ncRNAs), such as long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), play a central role in regulating gene expression and protein synthesis. These ncRNAs are closely associated with the development and recovery of AKI and have been detected in both kidney tissue and bodily fluids. Furthermore, specific ncRNAs may serve as diagnostic markers and potential targets for therapeutic interventions in AKI. This review aims to summarize the functional roles and changes observed in noncoding RNAs during ischemic AKI, as well as explore their therapeutic potential.

Association between pulmonary function and rapid kidney function decline: a longitudinal cohort study from CHARLS

BackgroundPulmonary function has been reported to be associated with chronic kidney disease. However, the relationship between lung function and rapid kidney function decline remains unclear.MethodsParticipants aged ≥45 years with complete...

Association Between Trimethylamine N-oxide and Adverse Kidney Outcomes and Overall Mortality in Type 2 Diabetes Mellitus.

Type 2 diabetes (T2D) is the major contributor to chronic kidney disease and end-stage kidney disease (ESKD). The influence of trimethylamine N-oxide (TMAO) on kidney outcomes in T2D remains unclear. To examine the association between fasting serum TMAO levels and adverse kidney outcomes in patients with T2D. Between October 2016 and June 2020, patients with T2D were recruited and monitored every 3 months until December 2021. Serum TMAO levels were assessed using liquid chromatography-mass spectrometry. The primary kidney outcomes were doubling of serum creatinine levels or progression to ESKD necessitating dialysis; the secondary kidney outcome was a rapid 30% decline in estimated glomerular filtration rate within 2 years. All-cause mortality was also evaluated. Among the 440 enrolled patients with T2D, those in the highest serum TMAO tertile (≥0.88 μM) were older, had a longer diabetes duration, elevated blood urea nitrogen, and lower estimated glomerular filtration rate. Over a median follow-up period of 4 years, 26 patients (5.9%) had a doubling of serum creatinine level or progression to ESKD. After propensity score weighting, the patients in the highest serum TMAO tertile had a 6.45-fold increase in the risk of doubling of serum creatinine levels or progression to ESKD and 5.86-fold elevated risk of rapid decline in kidney function compared with those in the lowest tertile. Additionally, the stepwise increase in serum TMAO was associated with all-cause mortality. Patients with T2D with elevated circulating TMAO levels are at higher risk of doubling serum creatinine, progressing to ESKD, and mortality. TMAO is a potential biomarker for kidney function progression and mortality in patients with T2D.

Poor glycemic control is associated with more rapid kidney function decline after the onset of diabetic kidney disease.

The role of glycemic control and its variability on the rate of kidney function decline after the onset of diabetic kidney disease (DKD) remains unclear. The association between baseline HbA1c and rates of estimated GFR (eGFR) loss during follow-up was examined by mixed-effects linear regression in 530 individuals with type 1 diabetes and early-to-moderate DKD from the Preventing Early Renal Loss (PERL) trial, and 2,378 individuals with type 2 diabetes and established DKD from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. The benefit of intensive vs. standard glycemic control in slowing eGFR decline was examined in ACCORD. The associations between continuous glucose monitoring-derived short-term glycemic variability indices and rate of GFR decline were also evaluated in PERL. A higher baseline HbA1c was associated with a more negative eGFR slope in both PERL and ACCORD (-0.87 and -0.27 ml/min/1.73m2/year per Hba1c unit increment, p<0.0001 and p=0.0002, respectively). In both studies, the strength of this association progressively increased with increasing levels of albuminuria (p for interaction <0.05). Consistent with this, the benefit of intensive glycemic control on eGFR decline was greater in ACCORD participants with severe than in those with moderate albuminuria (+1.13 vs. +0.26 ml/min/1.73 m2/year, p=0.01). No independent associations were found in PERL between short-term glycemic variability indices and rate of eGFR decline. In both type 1 and type 2 diabetes, poor glycemic control is associated with a more rapid rate of GFR decline after DKD onset, especially in persons with severe albuminuria.

Reno-protective effect of protocatechuic acid is independent of sex-related differences in murine model of UUO-induced kidney injury.

Obstructive nephropathy is a condition often caused by urinary tract obstruction either anatomical (e.g., tumors), mechanical (e.g., urolithiasis), or compression (e.g., pregnancy) and can progress to chronic kidney disease (CKD). Studies have shown sexual dimorphism in CKD, where males were found to have amore rapid decline in kidney function following kidney injury compared to age-matched females. Protocatechuic acid (PCA), an anti-oxidant and anti-inflammatory polyphenolic compound, has demonstrated promising effects in mitigating drug-induced kidney injuries. The current study aims to explore sexual dimorphism in kidney injury after unilateral ureteral obstruction (UUO) and assess whether PCA treatment can mitigate kidney injury in both sexes. UUO was induced in 10-12weeks old male and female C57BL/6J mice. Mice were categorized into four groups (n = 6-8/group); Sham, Sham plus PCA (100mg/kg, I.P daily), UUO, and UUO plus PCA. After 2 weeks of induction of UUO, markers of kidney oxidative stress (TBARs), inflammation (IL-1α and IL-6), tubular injury (neutrophil gelatinase-associated lipocalin, NGAL and urinary kidney injury molecule-1, KIM-1), fibrosis (Masson's trichrome staining, collagen IV expression, MMP-2 and MMP-9) and apoptosis (TUNEL+ cells, active caspase-1 and caspase-3) were significantly elevated in both males and females relative to their sham counterparts. Males exhibited significantly greater kidney oxidative stress, inflammation, fibrosis, and apoptosis after induction of UUO when compared to females. PCA treatment significantly attenuated UUO-induced kidney injury, inflammation, fibrosis, and apoptosis in both sexes. Our findings suggest adifferential gender response to UUO-induced kidney injury with males being more sensitive to UUO-induced kidney inflammation, fibrosis, and apoptosis than age-matched females. Importantly, PCA treatment reduced UUO-induced kidney injury in a sex-independent manner which might be attributed to its anti-oxidant, anti-inflammatory, anti-fibrotic, and anti-apoptotic properties.

Circadian syndrome is associated with the development of chronic kidney disease and rapid decline in kidney function in middle-aged and elder adults: a China nationwide cohort study.

The correlation between circadian syndrome (CircS) and kidney outcomes is currently supported by limited empirical evidence. Thus, the objective of this study was to determine the potential relationship between CircS and the development of chronic kidney disease (CKD), as well as the rapid decline in renal function. We utilized data from the 2011 China Health and Retirement Longitudinal Study (CHARLS), which involved 6002 Chinese adults ≥40 years of age. Among these participants, 3670 subsequently had follow-up evaluations in the 2015 survey. The primary outcome was the development of CKD, as defined by an estimated glomerular filtration rates decrease to a level <60ml/min/1.73m2, while the secondary outcome was rapid decline in renal function, as defined by an estimated glomerular filtration rates decrease of >5ml/min/1.73m2 per year. Multivariable logistic regression analysis was utilized to determine the association between CircS and kidney outcomes. Compared to participants without CircS, those with CircS had a higher risk of CKD in the cross-sectional studies conducted in 2011 (OR, 1.292; 95% CI, 1.053-1.585) and 2015 (OR, 1.860; 95% CI, 1.469-2.355). Participants with CircS in the longitudinal cohort study had a higher risk of progressing to CKD (OR, 3.050; 95% CI, 2.052-4.534) and a rapid decline in renal function (OR, 1.959; 95% CI, 1.433-2.677) after 4 years of follow-up evaluations and adjustment for covariates. Moreover, participants who had CircS with ≥6 CirS components had the highest risk of a rapid decline in renal function (OR, 1.703; 95% CI, 1.054-2.753). CirS significantly increased the risk of CKD progression and rapid decline in renal function among middle-aged and elder individuals. Our study findings highlights the importance of recognizing and managing CirC as a preventative strategy for CKD.

Epidemiology and Clinical Outcomes of Community-Acquired Acute Kidney Injury in the Emergency Department: A Multisite Retrospective Cohort Study

The prevalence of community-acquired acute kidney injury (CA-AKI) in the United States and its clinical consequences are not well described. Our objective was to describe the epidemiology of CA-AKI and the associated clinical outcomes. Retrospective cohort study. 178,927 encounters by 139,632 adults at 5 US emergency departments (EDs) between July 1, 2017, and December 31,2022. CA-AKI identified using KDIGO (Kidney Disease: Improving Global Outcomes) serum creatinine (Scr)-based criteria. For encounters resulting in hospitalization, the in-hospital trajectory of AKI severity, dialysis initiation, intensive care unit (ICU) admission, and death. For all encounters, occurrence over 180 days of hospitalization, ICU admission, new or progressive chronic kidney disease, dialysis initiation, and death. Multivariable logistic regression analysis to test the association between CA-AKI and measured outcomes. For all encounters, 10.4% of patients met the criteria for any stage of AKI on arrival to the ED. 16.6% of patients admitted to the hospital from the ED had CA-AKI on arrival to the ED. The likelihood of AKI recovery was inversely related to CA-AKI stage on arrival to the ED. Among encounters for hospitalized patients, CA-AKI was associated with in-hospital dialysis initiation (OR, 6.2; 95% CI, 5.1-7.5), ICU admission (OR, 1.9; 95% CI, 1.7-2.0), and death (OR, 2.2; 95% CI, 2.0-2.5) compared with patients without CA-AKI. Among all encounters, CA-AKI was associated with new or progressive chronic kidney disease (OR, 6.0; 95% CI, 5.6-6.4), dialysis initiation (OR, 5.1; 95% CI, 4.5-5.7), subsequent hospitalization (OR, 1.1; 95% CI, 1.1-1.2) including ICU admission (OR, 1.2; 95% CI, 1.1-1.4), and death (OR, 1.6; 95% CI, 1.5-1.7) during the subsequent 180 days. Residual confounding. Study implemented at a single university-based health system. Potential selection bias related to exclusion of patients without an available baseline Scr measurement. Potential ascertainment bias related to limited repeat Scr data during follow-up after an ED visit. CA-AKI is a common and important entity that is associated with serious adverse clinical consequences during the 6-month period after diagnosis. Acute kidney injury (AKI) is a condition characterized by a rapid decline in kidney function. There are many causes of AKI, but few studies have examined how often AKI is already present when patients first arrive to an emergency department seeking medical attention for any reason. We analyzed approximately 175,000 visits to Johns Hopkins emergency departments and found that AKI is common on presentation to the emergency department and that patients with AKI have increased risks of hospitalization, intensive care unit admission, development of chronic kidney disease, requirement of dialysis, and death in the first 6 months after diagnosis. AKI is an important condition for health care professionals to recognize and is associated with serious adverse outcomes.

Role of Histone Modifications in Acute Kidney Injury Progressing to Chronic Kidney Disease

Acute kidney injury (AKI), a clinical syndrome caused by various factors, is characterized by a rapid decline in kidney function in a short period of time. AKI affects the short-term prognosis of patients and may also induce chronic kidney disease (CKD). However, the current treatment options for AKI mainly focus on symptom management. Specific therapeutic measures available for the prevention of transition from AKI to CKD are very limited in number. Histones are basic proteins that intricately bind the DNA in chromosomes. After translation, histones undergo various modifications on their amino-terminal tails, such as methylation, acetylation, phosphorylation, ubiquitination, and lactylation, collectively forming the "histone code", which affects the expression of genes mainly by regulating the elastic structure of chromatin or recruiting specific proteins. Extensive research conducted in recent years on histone post-translational modifications (PTMs) has also sparked continuous interest in their association with the AKI-to-CKD transition. Therefore, this paper highlights the significant role of PTMs in the process of AKI developing and progressing to CKD, with a view to finding new approaches to preventing the progression of AKI to CKD.

Rapid decline of kidney function increases fracture risk in the general population: Insights from TLGS

BackgroundAlthough the association between Chronic Kidney Disease (CKD) and all-cause fractures was addressed in previous studies, the association between estimated glomerular filtration rate (eGFR) decline and fractures was poorly addressed. For the first time we examined the association between rapid kidney function decline (RKFD) and fracture incidence among Iranian general population. MethodsIn a Tehranian community-based cohort, RKFD was defined as a 30 % decline in eGFR over 2–3 years. Cox proportional hazards models, adjusted for age, sex, current eGFR, diabetes mellitus, hypertension, dyslipidemia, current smoking, obesity status, waist circumference, prevalent cardiovascular diseases, aspirin, steroid use, education level, and marital status, were used to examine the association of RKFD with different fracture outcomes. ResultsAmong 5305 (3031 women) individuals aged ≥30 years, during the median follow-up of 9.62 years, 226 fracture events were observed. The multivariable hazard ratio of RKFD for any-fracture events, lower-extremity, and major osteoporotic fractures were 2.18 (95 % CI, 1.24–3.85), 2.32 (1.15–4.71), and 2.91 (1.29–6.58), respectively. These associations remained significant after accounting for the competing risk of death. The impact of RKFD on the development of incident all-cause fractures was not modified by gender [men: 2.64 (1.11–6.25) vs. women: 2.11 (1.00–4.47)] and according to current CKD status [without CKD: 2.34 (1.00–5.52) vs. with CKD: 2.59 (1.04–6.44)] (all P for interaction >0.5). ConclusionsRKFD can increase the incidence of fractures among general population, the issue that was equally important among non-CKD individuals, emphasizing the need for early identification and management in those with rapidly declining eGFR.

Mitochondrial DNA copy number is associated with incident chronic kidney disease and proteinuria in the AIDS linked to the intravenous experience cohort

We evaluated the prospective association of mitochondrial DNA copy number (mtDNA CN) with markers of kidney function among a cohort of persons who inject drugs (PWID). This is a Prospective cohort study nested in the AIDS linked to the intravenous experience cohort (community-based cohort of PWID in Baltimore, MD). mtDNA CN was measured at two time-points 5 years apart using a real-time polymerase chain reaction. Kidney function (estimated glomerular filtration rate [eGFR], serum creatinine, urine protein) was measured annually. We used linear mixed effects models to evaluate kidney function trajectories (N = 946) and Cox regression models to assess hazard of incident CKD (eGFR < 60 at two consecutive visits, N = 739) and proteinuria (urine protein:creatinine ratio > 200, N = 573) by level of mtDNA CN (Low [lowest quartile], vs high [other three quartiles]. Models were adjusted for demographic and behavioral characteristics, HIV and/or HCV infection, and comorbidity burden. Low mtDNA CN was independently associated with higher hazard of incident CKD (aHR: 2.33, 95% CI 1.42, 3.80) and proteinuria (aHR: 1.42, 95% CI 1.04, 1.96). Participants with low mtDNA CN had greater declines in eGFR and greater increases in serum creatinine over time. Low mtDNA CN is associated with more rapid kidney function decline and risk of incident CKD and proteinuria.

The Effect of Oral N-Acetyl Cysteine Administration on Acute Kidney Injury Patients at Dr. Mohammad Hoesin General Hospital, Palembang, Indonesia

Background: Acute kidney injury (AKI) is a clinical condition characterized by a rapid decline in kidney function that includes structural damage (injury) or malfunction (impairment). AKI is a common complication that occurs in 5-10% of patients due to various underlying etiologies. One of the underlying pathophysiology of AKI is the role of discharge reactive oxygen species (ROS), which causes injury to kidney cells. From various studies, it has been reported that N-acetylcysteine (NAC) has anti-inflammatory and antioxidant effects and has an effect on reducing serum creatinine values.&#x0D; Methods: This research is an open randomized clinical trial without control involving 30 patients at Dr. Mohammad Hoesin General Hospital, Palembang, who were all given intervention in the form of NAC 1200 mg/day, starting in September – October 2023. This study aimed to determine the role of NAC in reducing serum creatinine values in patients with acute kidney injury at Dr. Mohammad Hoesin General Hospital, Palembang, Indonesia. Data analysis was carried out using SPSS 21 univariate and bivariate.&#x0D; Results: From the research results, it was found that the average age of patients was 53.9 years, involving 21 males (70%, N=30) and 9 females (30%, N=30). The most common causes were prerenal and then renal (53.3% and 46.7%). The initial serum creatinine level was found to be 2.12± 0.79 mg/dL (n = 30 samples), and after administration of the intervention, the mean serum creatinine level was 1.28± 0.63 mg/dL (n = 30 samples). By using a paired t-test, there was a decrease in serum creatinine levels significant (p=0,012).&#x0D; Conclusion: NAC administration to patients with acute kidney injury of pre-renal or post-renal causes has a statistical effect on reducing serum creatinine values in patients with acute kidney injury at Dr. Mohammad Hoesin General Hospital, Palembang, Indonesia.

Medication profiling in women with type 1 diabetes highlights the importance of adequate, guideline-based treatment in low-risk groups

Effective treatment may prevent kidney complications, but women might be underprescribed. Novel, data-driven insights into prescriptions and their relationship with kidney health in women with type 1 diabetes may help to optimize treatment. We identified six medication profiles in 1164 women from the FinnDiane Study with normal albumin excretion rate based on clusters of their baseline prescription data using a self-organizing map. Future rapid kidney function decline was defined as an annual estimated glomerular filtration rate (eGFR) loss > 3 ml/min/1.73 m2 after baseline. Two profiles were associated with future decline: Profile ARB with the highest proportion of angiotensin receptor blockers (odds ratio [OR] 2.75, P = 0.02) and highly medicated women in profile HighMed (OR 2.55, P = 0.03). Compared with profile LowMed (low purchases of all), profile HighMed had worse clinical characteristics, whereas in profile ARB only systolic blood pressure was elevated. Importantly, the younger women in profile ARB with fewer kidney protective treatments developed a rapid decline despite otherwise similar baseline characteristics to profile ACE & Lipids (the highest proportions of ACE inhibitors and lipid-modifying agents) without a future rapid decline. In conclusion, medication profiles identified different future eGFR trajectories in women with type 1 diabetes revealing potential treatment gaps for younger women.

Association of sarcopenia with rapid kidney function decline and chronic kidney disease in adults with normal kidney function.

The association between sarcopenia and kidney function remains poorly investigated. We aimed to evaluate the associations between sarcopenia status and kidney function (rapid kidney function decline and chronic kidney disease (CKD)) in middle-aged and older Chinese population. A total of 9375 participants from the China Health and Retirement Longitudinal Study 2011 were included in the cross-sectional analyses. A total of 5864 participants with eGFRcr-cys ≥ 60 ml/min per 1·73 m2 at baseline were included in the longitudinal analyses and were followed up in 2015. Sarcopenia status was defined according to the Asian Working Group for Sarcopenia 2019 criteria. In the cross-sectional analyses, possible sarcopenia and sarcopenia were significantly associated with an increased risk of CKD. During the 4 years of follow-up, 359 (6·12 %) participants experienced rapid decline in kidney function and 126 (2·15 %) participants developed CKD. After multivariable adjustment of baseline eGFRcr-cys level and other risk factors, possible sarcopenia (OR, 1·33; 95 % CI 1·01, 2·12) and sarcopenia (OR, 1·49; 95 % CI 1·05, 2·12) were associated with an increased risk of primary outcome (composite of rapid decline in kidney function (annualised decline in eGFRcr-cys ≥ 5 ml/min per 1·73 m2) and progression to CKD (eGFRcr-cys < 60 ml/min per 1·73 m2). Individuals with low muscle mass or low muscle strength alone also had an increased risk of rapid decline in kidney function and progression to CKD.

Apoptosis-related prognostic biomarkers and potential targets for acute kidney injury based on machine learning algorithm and in vivo experiments.

Acute kidney injury (AKI) is a common critical illness in hospitalized patients, characterized by a rapid decline in kidney function over a short period, which can seriously endanger the patient's life. Currently, there is a lack of precise and universal AKI diagnostic biomarkers in clinical practice. In this study, weighted gene coexpression network analysis (WGCNA), differential expression analysis, univariate and multivariate logistic regression analyses, receiver operating characteristic (ROC) curves, and immune cell infiltration were performed to identify apoptosis-related biomarkers that can be used for AKI diagnosis. Three core apoptosis-related genes (ARGs), CBFB, EGF and COL1A1, were identified as AKI biomarkers. More importantly, an apoptosis-related signature containing three hub ARGs was validated as a diagnostic model. The hub genes exhibited good correlations with glomerular filtration rate (GFR) and serum creatinine (SCr) in the Nephroseq kidney disease database. Additionally, CIBERSORT immune infiltration analysis indicated that these core ARGs may affect immune cell recruitment and infiltration in AKI patients. Subsequently, we investigated the alteration of the expression levels of three core ARGs in AKI samples using single-cell RNA sequencing analysis and analyzed the cell types that mainly expressed these ARGs. More importantly, the expression of core ARGs was validated in folic acid- and cisplatin-induced AKI mouse models. In summary, our study identified three diagnostic biomarkers for AKI, explored the roles of ARGs in AKI progression and provided new ideas for the clinical diagnosis and treatment of AKI.

Kidney function decline is associated with mortality events: over a decade of follow-up from Tehran Lipid and Glucose Study.

To investigate the association between estimated glomerular filtration rate (eGFR) change and mortality risk in a cohort from the Middle East and North Africa region with increasing chronic kidney disease burden. We included 2210 participants aged ≥ 50 years from the prospective cohort of the Tehran Lipid and Glucose Study. The interval for eGFR measurement was between the examinations in 2002-2005 to 2009-2011, and participants were followed through March 2018. Glomerular filtration rate was estimated from serum creatinine using the CKD-EPI creatinine equation. We assessed the association of rapid kidney function decline, (defined as annual eGFR decline ≥ 3 ml/min/1.73m2 per year); ≥ 30% eGFR decline over six years; and certain drop in kidney function (≥ 25% eGFR decline plus drop in eGFR category) with mortality outcomes. During a median follow-up of 14.3years after recruitment, 315 all-cause and 112 cardiovascular disease deaths were recorded. The multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) of all-cause death for rapid kidney function decline, ≥ 30% decline in eGFR over 6 years, and drop in kidney function were 1.68 (1.24-2.27), 2.01 (1.46-2.78), and 1.49 (1.11-1.98), respectively. The HRs of all-cause death andfor rapid kidney function decline in those without and with chronic kidney disease were 1.41 (1.03-1.91) and 3.38 (1.69-6.76), respectively. Similar findings were observed regarding cardiovascular disease-related and non-cardiovascular disease-related mortality. Estimated GFR decline is associated with an increased mortality risk, indicating its ability to provide additional prognostic information beyond traditional risk predictors in the general population.

CKD and Rapid Kidney Function Decline During the COVID-19 Pandemic

The direct and indirect effects of the coronavirus disease 2019 (COVID-19) pandemic on kidney function in the chronic kidney disease (CKD) population are not well understood. Cohort study. Retrospective study of kidney function trajectories using deidentified administrative claims and laboratory data for Medicare Advantage and commercially insured enrollees with CKD stages G3-4 between 2018 and2021. COVID-19 infection. Rapid kidney function decline defined as annual estimated glomerular filtration rate (eGFR) decline of≥40%. Propensity score matching was used to identify individuals without COVID-19 infection matched 1:1 to a COVID-19 infected cohort and indexed on the date of diagnosing COVID-19 infection, age, sex, race or ethnicity, and Charlson comorbidity index score. Outpatient kidney function was compared during the prepandemic period (January 1, 2018, to February 29, 2020) with the pandemic period (March 1, 2020, to August 31, 2021). Two creatinine measurements, after the infection date and≥60 days apart, were required to reduce correlation with acute infection. Of 97,203 enrollees with CKD G3-4, 9% experienced a COVID-19 infection. Characteristics of 8,901 propensity matched enrollees include mean age 74 years, 58% women, 67% White, and 63% CKD G3a, 28% CKD G3b, and 9% CKD G4. Median overall annual eGFR change was -2.65ml/min/1.73m2, with 76% of the cohort experiencing worsened eGFR in the pandemic period. Rapid kidney function decline was observed in 1.9% and 2.0% of enrollees in the prepandemic and pandemic periods, respectively. Rapid kidney function decline was observed in 2.5% of those with COVID-19 infection and 1.5% of those without COVID-19 infection (P<0.05). Factors associated with increased odds of rapid kidney function decline during pandemic included Asian race, higher Charlson comorbidity index, advancing CKD stage, prepandemic rapid kidney function decline, and COVID-19 infection. Retrospective study design with potential bias. COVID-19 infection increased odds of rapid kidney function decline during the pandemic. The downstream impact of pandemic-related eGFR decline on health outcomes, such as kidney failure or mortality, requires further study. We used a cohort of insured individuals with moderate-to-severe chronic kidney disease (CKD) to compare the rates of rapid kidney function decline in prepandemic and pandemic periods and to evaluate the impact of the coronavirus disease 19 (COVID-19) on kidney function decline. We found that overall rates of rapid kidney function decline did not change during the prepandemic and pandemic periods but were significantly higher in both periods among individuals with a COVID-19 infection. As CKD severity increased, rates of both rapid kidney function decline and COVID-19 increased. Advancing CKD, higher comorbid condition, Asian race, prepandemic rapid kidney function decline, and COVID-19 were all associated with higher odds of rapid kidney function decline in the pandemic. These findings suggest close monitoring is warranted for individuals with CKD and COVID-19.