Chronic Kidney Disease Group Research Articles

An examination of co-existence of metabolic dysfunction-associated liver disease and chronic kidney disease and its effect on long-term mortality in patients with acute myocardial infarction

Abstract Background Metabolic dysfunction-associated liver disease (MASLD) and chronic kidney disease (CKD) are both diseases that can cause increased cardiovascular risk. Recent studies have revealed that the combination of both is a more potent risk factor for ischemic heart disease. However, the mortality and outcomes of patients presenting with acute myocardial infarction (AMI) with varying combination of these two risk factors have yet to be examined. Aims Our research aims to examine the effects of concomitant MASLD and CKD on mortality in patients presenting with AMI. Methods This research examined the features and outcomes of individuals experiencing AMI at our institution. The patients were stratified into 4 groups – patients without MASLD or CKD (MASLD(-)/CKD(-)), patients with MASLD without CKD (MASLD(+)/CKD (-)), patients with CKD without MASLD (MASLD(-)/CKD(+)), and patients with both MASLD and CKD (MASLD(+)/CKD(+)). MASLD was identified as hepatic steatosis along with at least one of five metabolic criteria, and hepatic steatosis was assessed using the Hepatic Steatosis Index. CKD is defined as estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m². A Kaplan-Meier curve was generated to analyse long-term all-cause mortality, and Cox regression analysis was used to identify independent predictors of mortality. Results A total of 6757 patients who presented with AMI were examined over 3.2 ± 2.4 years. Of whom, 3766 (55.7%) individuals were in the MASLD(-)/CKD(-) group, 1945 (28.8%) in the MASLD(+)/CKD (-) group, 675 (10.0%) in the MASLD(-)/CKD(+) group and 371 (5.5%) in the MASLD(+)/CKD(+) group. The MASLD(+)/CKD(+) group had the highest risk of cardiogenic shock compared to their counterparts (p<0.001). The highest 30-day mortality rates were found in the MASLD(+)/CKD(+) group (17.8%), followed by MASLD(-)/CKD(+) (11.6%), MASLD(+)/CKD(-) (4.6%) and MASLD(-)/CKD(-) (4.0%) (p<0.001). In terms of long-term mortality, the Kaplan-Meier curve demonstrated that both MASLD(-)/CKD(+) and MASLD(+)/CKD(+) groups had unfavorable survival following an AMI. Conclusions Patients with AMI, in the presence of concomitant MASLD and CKD, had the highest 30-day mortality rates. They were at the highest risks of AMI-related complications such as heart failure and cardiogenic shock. This study highlights the prognostic impact of cardiovascular-liver-kidney-metabolic health on AMI, and future studies are warranted to mitigate this risk.Figure 1:30 – day all cause mortalityFigure 2:Long term mortality

Elevation of circulating FGF23 in chronic kidney disease promotes atrial fibrosis through the AKT pathway

Abstract Background The relationship between chronic kidney disease (CKD) and atrial fibrillation (AF) remains unclear. Elevated level of fibroblast growth factor 23 (FGF23) is highly associated with increased cardiovascular disease and mortality in patients suffering from CKD. In recent years, studies have shown that FGF23 promotes cardiac hypertrophy through FGFR4, suggesting that FGF23 may be an important bridge between the heart and kidney. Purpose In this study, we sought to use a well-established rat model of CKD to further characterize the effects of CKD on AF and to identify potential drivers of CKD-induced AF. Methods 14 SD rats were randomly selected to undergo 5/6 nephrectomy and fed for 15 weeks to establish a CKD model, while the SHAM group (8 rats) underwent the same surgery without removing kidney tissue. Body weight, blood pressure, renal function, cardiac ultrasound, epicardial electrocardiography, and pathological indices were monitored in both groups. Gene sequencing was performed on the left atria to search for differentially expressed genes. Rat atrial fibroblasts were selected for further mechanism exploration. We chose TGF-β to stimulate fibroblasts to mimic the process of fibrosis in vivo, and then administered FGFR inhibitors to explore the downstream molecular mechanisms. Results Systolic blood pressure and creatinine were elevated in the CKD group. Compared with the SHAM group, the incidence of AF was significantly higher, left atrial diameter was significantly larger, and epicardial electrical markers showed that left atrial electrical conduction velocity was significantly slower and conduction heterogeneity was significantly increased in the CKD group. Pathologic staining of the left atrium showed significant fibrosis in the CKD group. Consistent with previous findings, FGF23 was significantly elevated in CKD rats. Transcriptomic sequencing revealed that FGFR4 expression was significantly upregulated in the left atrium of CKD rats, The results in rat atrial fibroblasts showed that blocking FGFR4 expression inhibited TGF-β-induced fibrosis and was mediated by the AKT pathway. Conclusions The mechanism of CKD-induced AF is that CKD promotes both structural and electrical remodeling of the atria. Further investigation of its possible downstream molecules revealed that elevated FGF23 in the CKD circulation promotes the development of atrial fibrosis by binding to FGFR4 through the AKT pathway.

Impact of neutrophil-to-lymphocyte ratio on clinical outcomes in patients with or without chronic kidney disease undergoing percutaneous coronary intervention

Abstract Background Neutrophil-to-lymphocyte ratio (NLR) has recently emerged as inexpensive inflammatory biomarker associated with worse cardiovascular outcomes. However, little is known about its role in risk stratification of patients with both chronic kidney disease (CKD) and coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI). Purpose We aimed to evaluate the clinical impact of baseline NLR in patients with and without CKD undergoing PCI. Methods We retrospectively evaluated all consecutive patients undergoing PCI between 2012-2022 in a large tertiary US center. We excluded patients without available NLR and those who were deemed to have active hematological or infective diseases, including patients with extremely low or high lymphocyte and neutrophil counts or with hs-CRP above 10 mg/L. Quartiles of NLR were derived in the overall population and patients were stratified according to presence of CKD (eGFR < 60 ml/min). Within each group, we estimated the risk of adverse events using the lowest NLR quartile as reference. The primary endpoint was 12-month incidence of major adverse cardiovascular events (MACE), defined as the composite of all-cause death, myocardial infarction, or stroke. Secondary endpoints included incidence of clinically relevant bleeding and contrast-associated acute kidney injury (CA-AKI), defined as ≥ 0.3 mg/dL or ≥ 50% serum creatinine increase from baseline. Results A total of 7,287 patients were included in the analysis; of these 2,008 (27.6%) had CKD and 5,279 (72.4%) did not. CKD patients (mean eGFR 40.8±16.1 ml/min) were older, had more comorbidities, and presented with higher hs-CRP levels and a greater estimated risk of CA-AKI. Overall, patients with elevated NLR had more severe CAD and underwent more complex PCI. In CKD patients, incidence of adverse events increased stepwise and those in the 4th NLR quartile had the highest adjusted risks of MACE (HRadj 1.86, 95% CI 1.12-3.08; P=0.012), all cause death (HRadj 2.44, 95% CI 1.18-5.05; P=0.003) and bleeding (HRadj 1.74, 95% CI 1.07-2.84; P=0.002) at 1 year, as compared to those in the lowest quartile (Table 1). In patients without CKD, MACE and all-cause death incidences were numerically higher in the 4th quartile but risk estimates were no longer statistically significant after adjustment. The overall incidence of CA-AKI was much greater in the CKD group. When compared to the lowest quartile, patients in the 4th NLR quartile showed a trend for higher risk of CA-AKI in CKD group, while they had a significant increased risk in non-CKD group (Figure 1). Conclusions Elevated NLR is strongly associated with higher risk of MACE and all-cause mortality in CKD patients. Conversely, the risk of bleeding and CA-AKI is increased with elevated NLR in both CKD and non-CKD patients. Thus, NLR may further inform risk stratification of CKD patients undergoing PCI.

Does gut microbiota dysbiosis impact the metabolic alterations of hydrogen sulfide and lanthionine in patients with chronic kidney disease?

BackgroundChronic Kidney Disease (CKD) is characterized by a methionine-related metabolic disorder involving reduced plasma levels of hydrogen sulfide (H2S) and increased lanthionine. The gut microbiota influences methionine metabolism, potentially impacting sulfur metabolite dysfunctions in CKD. We evaluated whether gut microbiota dysbiosis contributes to H2S and lanthionine metabolic alterations in CKD.MethodsThe gut microbiota of 88 CKD patients (non-dialysis, hemodialysis, and transplant patients) and 26 healthy controls were profiled using 16 S-amplicon sequencing. H2S and lanthionine concentrations were measured in serum and fecal samples using the methylene blue method and LC-MS/MS, respectively.ResultsThe CKD population exhibited a tenfold increase in serum lanthionine associated with kidney dysfunction. Despite lanthionine retention, hemodialysis and transplant patients had significantly lower serum H2S than healthy controls. Fecal H2S levels were not altered or related to bloodstream H2S concentrations. Conversely, fecal lanthionine was significantly increased in CKD compared to healthy controls and associated with kidney dysfunction. Microbiota composition varied among CKD groups and healthy controls, with the greatest dissimilarity observed between hemodialysis and transplant patients. Changes relative to the healthy group included uneven Ruminococcus gnavus distribution (higher in transplant patients and lower in non-dialysis CKD patients), reduced abundance of the short-chain fatty acid-producing bacteria Alistipes indistinctus and Coprococcus eutactus among transplant patients, and depleted Streptococcus salivarius in non-dialysis CKD patients. A higher abundance of Methanobrevibacter smithii, Christensenella minuta, and Negativibacillus massiliensis differentiated hemodialysis patients from controls. No correlation was found between differentially abundant species and the metabolic profile that could account for the H2S and lanthionine alterations observed.ConclusionsThe metabolic deregulation of H2S and lanthionine observed in the study was not associated with alterations in the gut microbiota composition in CKD patients. Further research on microbial sulfur pathways may provide a better understanding of the role of gut microbiota in maintaining H2S and lanthionine homeostasis.

Propolis Extract Attenuates NF-κB Activation and Chronic Kidney Disease Progression in a Rat Model: Potential Surgical Adjuvant?

Background: Chronic kidney disease (CKD) is a global health concern often complicated by cardiovascular diseases like atherosclerosis. Both conditions share an inflammatory pathogenesis, with nuclear factor kappa B (NF-κB) playing a central role. Propolis, a natural bee product with anti-inflammatory properties, has shown potential in mitigating CKD progression. This study aimed to investigate the effects of propolis extract on NF-κB activation in a rat model of CKD, exploring its potential benefits as a surgical adjuvant. Methods: Male white rats (Rattus norvegicus) were divided into three groups: a control group, a CKD group, and a CKD+Propolis group receiving propolis extract (200 mg/kg body weight) daily for 20 days. CKD was induced using the unilateral ureteral obstruction (UUO) method. NF-κB levels were measured weekly using ELISA. Results: Propolis extract significantly reduced NF-κB levels in the CKD+Propolis group compared to the CKD group (p<0.05). This effect was consistently observed across all time points, indicating a sustained reduction in NF-κB activation with propolis treatment. Conclusion: Propolis extract effectively attenuates NF-κB activation in a rat model of CKD, suggesting its potential as an adjunctive therapy for CKD management, particularly in the context of surgical interventions. Further research is needed to elucidate the underlying mechanisms and evaluate its efficacy in human subjects.

Comparison of Shear-Wave Elastography USG and CT: Composition Analysis of Rectus Femoris Muscle in Healthy Adults and Chronic Kidney Disease Patients.

This study aimed to compare shear-wave elastography (SWE) USG and composition analysis of CT on the right mid-rectus femoris muscle (RF) in both healthy adults and chronic kidney disease (CKD) patients. Sixty-three healthy adults and 22 CKD patients were included. One musculoskeletal radiologist performed right RF SWE USG, while two radiologists measured shear-wave velocity (SWV) from the same SWE images. CT scan was performed, and muscle composition was measured using imageJ, categorized into four HU-based compositions. Interobserver agreement for SWV between two readers was evaluated. Correlations between SWV and CT compositions were analyzed using Pearson's or Spearman's correlation. SWV of healthy group was significantly higher than CKD group by each reader (p = 0.030 and 0.038). The percentage of low-density muscle was higher in CKD group than healthy group (p < 0.001), and the percentage of normal density muscle was higher in healthy group than CKD (p < 0.001) by each reader. Interobserver agreement of SWV by the two readers was almost perfect in both groups (k = 0.957-0.984, 0.959-0.993). There was a statistically significant correlation between SWV and the percentage of normal density muscle on CT in both healthy adults and CKD patient groups (Reader 1, r = 0.318-0.480, p = 0.001 and 0.024; Reader 2, r = 0.511-0.518, p < 0.001 and p = 0.013). SWV demonstrated a significant correlation with the percentage of normal density muscle on CT in both healthy adults and CKD patients by each reader. SWE provides a radiation-free approach that may offer an objective method for evaluating muscle quality, potentially making it an option for muscle monitoring.

Real-world fracture risk, osteoporosis treatment status, and mortality of Japanese non-dialysis patients with chronic kidney disease stages G3-5.

Few studies have investigated fracture risk and mortality in a Japanese chronic kidney disease (CKD) stages G3-5 population using a large-scale clinical database. This retrospective cohort study extracted data from 1 April 2008 to 30 April 2023. A single age-sex-matched control without CKD was matched with each non-dialysis CKD (estimated glomerular filtration rate < 60mL/min/1.73m2) patient. The incidences of all and hip fractures and all-cause mortality after the index date were calculated. Among 76,598 (38,299 per group) individuals matched, the incidence of all fractures did not differ between the CKD and control groups (5.7% vs 5.8%; hazard ratio [HR] 1.022 [95% confidence interval CI 0.952-1.098], P = 0.542). The CKD group had higher risk of hip fracture than the control group (incidence of hip fracture, 1.7% vs 1.3%; HR 1.415 [95% CI 1.234-1.622], P < 0.001). Multivariable regression analysis showed an increased risk for hip fracture in the CKD vs control groups, and a greater difference in this risk was observed with younger age. Osteoporosis treatment and bone mineral density (BMD) measurements were 10.0% and 5.3% in the CKD group and 4.4% and 4.4% in the control group, respectively. Mortality was also higher in the CKD group (HR 1.413 [95% CI 1.330-1.501], P < 0.001). Japanese patients with CKD had higher risk of hip fracture than those without. Treatment and BMD measurement for fracture are insufficient in Japanese patients with CKD, and more adequate management of fracture risk is needed.

Changes in Skeletal Muscle Atrophy over Time in a Rat Model of Adenine-Induced Chronic Kidney Disease

This study evaluated changes over time in skeletal muscle atrophy, expressions of skeletal muscle anabolic and catabolic genes, and mitochondrial activity by skeletal muscle type in an adenine-induced chronic kidney disease (CKD) model. A CKD model was successfully established by feeding male Wistar rats a 0.75% adenine diet for 4 weeks starting at 8 weeks of age. Control and CKD groups were sacrificed at 12 and 20 weeks of age. The back muscles were analyzed histologically, and succinate dehydrogenase (SDH) staining was performed to evaluate mitochondrial activity. Gene expressions of myogenic determination gene number 1 and myogenin as indicators of muscle anabolism, atrogin-1 and muscle RING-finger protein-1 (MuRF1) as indicators of muscle catabolism, and peroxisome proliferator-activated receptor-γ coactivator-1-α as a marker of mitochondrial biogenesis were assessed. Type I and type II muscle cross-sectional areas (CSAs) were decreased at 12 weeks, but type I muscle CSA was recovered at 20 weeks. SDH staining was lower in CKD than in control rats at 12 weeks, but no significant difference was observed at 20 weeks. Increased expressions of myogenin, atrogin-1, and MuRF-1 were observed only at 12 weeks, but no differences were observed at 20 weeks. The adenine-induced CKD rat model appears to show changes in muscle atrophy over time.

Urinary cyclophilin A as an early marker of chronic kidney disease with underlying type 2 diabetes

Cyclophilin A (CypA) is a novel renal inflammation biomarker, with levels altered in various diseases, particularly in patients with diabetes mellitus (DM) and kidney damage. This study aimed to investigate the correlation between urinary cyclophilin A (uCypA) and chronic kidney disease (CKD) conditions with and without type 2 diabetes mellitus (T2DM) using an in-house enzyme-linked immunoassay (ELISA) method. A uCypA strip-test prototype was also developed. An indirect ELISA was performed to determine the uCypA levels. A 0.48 µg/mL uCypA cutoff differentiated healthy patients from those with early-stage CKD (stages I and II). The uCypA levels were significantly increased in patients with progression of renal deterioration, especially in the T2DM with late-stage CKD group, compared to the control group. Fasting blood sugar (FBS), estimated glomerular filtration rate (eGFR), albumin/creatinine ratio, and metformin use were associated with uCypA levels. Multinomial logistic regression analysis revealed an association between uCypA levels and T2DM diagnosed for over five years and early-stage CKD. This finding shows that uCypA could be used as a biomarker for distinguishing early-stage CKD as well as T2DM complications, which is beneficial for patients to be aware of their health status and change their behavior to slow kidney deterioration.

Dietary protein intake and the tubular handling of indoxyl sulfate.

Chronic kidney disease (CKD) patients are advised to limit their protein intake. A high protein diet is known to induce glomerular hyperfiltration, as well as hypertrophy of the remnant kidney, and glomerulosclerosis. Whether the diet causes changes in kidney tubule transport via gut microbiome metabolites is still unknown. We hypothesized that protein intake affects not only the intestinal generation and absorption, but also the kidney disposal of microbial amino acid metabolites. We combined data from animal models and human studies. 5/6th nephrectomy rats were administered a high (HP) or low-protein (LP) diet for 7 weeks. Plasma and urine concentration of the uremic toxins (UTs) indoxyl sulfate (IS), p-cresyl sulfate (PCS), and p-cresyl glucuronide (PCG) were measured. Their fractional excretion (FE) was calculated. The expression of kidney membrane transporters OAT1, OAT3, BCRP, OCT2 and MRP4 was analyzed. Differences in FE of UTs between individuals with higher and lower protein intake in two CKD cohorts were sought. CKD rats on an HP diet showed increased plasma levels of PCS and PCG but not IS compared to rats on a LP diet. Conversely, urinary excretion and FE of IS were higher in the HP CKD group. BCRP, MRP4 and OCT2 were not influenced by the diet. OAT1 and OAT3 were upregulated in the HP CKD group. In two independent cohorts of CKD patients, individuals with a high dietary protein intake showed a significantly higher FE of IS. A HP diet leads to a higher generation and/or absorption of aminoacid-derived UT precursors in CKD rodent models and humans, most likely via gut microbiome modulation. We demonstrate that dietary protein intake modulates transcription and expression of OAT1 and OAT3, corroborating the existence of the remote sensing and signaling hypothesis. Dietary protein intake influences kidney physiology beyond glomerular filtration.

The Addition of a Non-Steroidal Anti-Inflammatory Drug (NSAID) in Local Infiltration Analgesia During Total Knee Arthroplasty Increases the Risk of Acute Kidney Injury in Patients Who Have Renal Impairment: A Propensity-Matched Retrospective Cohort Study

BackgroundLocal infiltration analgesia (LIA) is a crucial component of pain management during total knee arthroplasty (TKA). Various formulations of the LIA drug cocktail have been described, with non-steroidal anti-inflammatory drugs (NSAIDs) commonly included. Although NSAIDs are highly effective in improving postoperative pain, they are associated with adverse renal, gastrointestinal, and cardiovascular effects. This study aimed to investigate whether the addition of an NSAID in LIA affects the incidence of acute kidney injury (AKI) in TKA patients, especially those who have pre-existing renal impairment. The secondary aim was to determine overall AKI incidence. MethodsA retrospective cohort study was conducted on elective, primary TKA patients in a single tertiary institution between January 2020 and April 2024. Data was obtained from a prospectively collected institutional knee arthroplasty registry. Patients were administered LIA intraoperatively, with or without an NSAID (30 mg of ketorolac). The study population was divided into two subpopulations, patients who did or did not have chronic kidney disease (CKD), and analyzed separately. Propensity matching was performed on the CKD group, correcting for age, sex, BMI, ASA score, and presence of diabetes mellitus/hypertension. The outcome of interest was the incidence of AKI. A t-test or Chi-square test was used, where appropriate, to determine the statistical significance of the results. ResultsIn patients who had CKD (n = 114), the presence of ketorolac in LIA was associated with a higher AKI incidence (12.7 versus 2.0%, P = 0.041). In patients who did not have CKD (n = 870), the presence of ketorolac in LIA was not associated with a higher AKI incidence (2.0 versus 1.9%, P = 1.0). Overall AKI incidence was 2.6%. ConclusionIn patients who have CKD, orthopaedic surgeons should be highly cautious of administering ketorolac in LIA during TKA, as it is associated with a higher risk of AKI. Patients who have normal renal function can be safely given ketorolac in LIA without an elevated risk of AKI. Further studies are needed to examine AKI incidence when other NSAIDs are used in LIA.

Glucagon Clearance Is Decreased in Chronic Kidney Disease but Preserved in Liver Cirrhosis.

It is not completely clear which organs are responsible for glucagon elimination in humans, and disturbances in the elimination of glucagon could contribute to the hyperglucagonemia observed in chronic liver disease and chronic kidney disease (CKD). Here, we evaluated kinetics and metabolic effects of exogenous glucagon in individuals with stage 4 CKD (n =16), individuals with Child-Pugh A-C cirrhosis (n = 16) and matched control individuals (n = 16), before, during and after a 60-minute glucagon infusion (4 ng/kg/min). Individuals with CKD exhibited a significantly lower mean metabolic clearance rate of glucagon (14.0 [95% CI 12.2;15.7] mL/kg/min) both compared to individuals with cirrhosis (19.7 [18.1;21.3] mL/kg/min, P < 0.001) and to control individuals (20.4 [18.1;22.7] mL/kg/min, P < 0.001). Glucagon half-life was significantly prolonged in the CKD group (7.5 [6.9;8.2] minutes) compared to individuals with cirrhosis (5.7 [5.2;6.3] minutes, P = 0.002) and control individuals (5.7 [5.2;6.3] minutes, P < 0.001). No difference in the effects of exogenous glucagon on plasma glucose, amino acids, or triglycerides was observed between groups. In conclusion, chronic kidney disease, but not liver cirrhosis leads to a significant reduction in glucagon clearance, supporting the kidneys as a primary site for human glucagon elimination.

Ultrasound viscoelastic imaging in the noninvasive quantitative assessment of chronic kidney disease

Background This study aims to evaluate the clinical application value of ultrasound viscoelastic imaging in noninvasive quantitative assessment of chronic kidney disease (CKD). Methods A total of 332 patients with CKD and 190 healthy adults as a control group were prospectively enrolled. Before kidney biopsy, ultrasound viscoelastic imaging was performed to measure the mean stiffness value (Emean), mean viscosity coefficient (Vmean), and mean dispersion coefficient (Dmean) of the renal. CKD patients were divided into three groups based on estimated glomerular filtration rate. The differences in clinic, pathology, ultrasound image parameters between the control and patient groups, or among different CKD groups were compared. The correlation between viscoelastic parameters and pathology were analyzed. Results Emean, Vmean, and Dmean in the control group were less than the CKD group (p < 0.05). In the identification of CKD from control groups, the area under curve of Vmean, Dmean, Emean, and combining the three parameters is 0.90, 0.79, 0.69, 0.91, respectively. Dmean and Vmean were increased with the decline of renal function (p < 0.05). Vmean and Dmean were positively correlated with white blood cell, urea, serum creatinine, and uric acid (p < 0.05). Vmean is positively correlated with interstitial fibrosis and inflammatory cell infiltration grades (p < 0.001). Conclusions Ultrasound viscoelastic imaging has advantages in noninvasive quantitative identification and evaluating renal function of CKD. Emean > 6.61 kPa, Vmean > 1.86 Pa·s, or Dmean > 7.51 m/s/kHz may suggest renal dysfunction. Combining Vmean, Dmean, and Emean can improve the efficiency of identifying CKD.

Association Of Hyperkalemia With T-Wave Changes In Chronic Kidney Disease Patients Versus Hemodialysis Patients.

Hemodialysis (HD) patients often face hyperkalemia due to various reasons. Level of hyperkalemia and ECG changes may be discordant among HD patients in a significant number of patients. This study was conducted to investigate whether or not there is a unique ECG characteristic that predicts hyperkalemia in individuals with chronic kidney disease (CKD). OBJECTIVE: To determine an association between hyperkalemia (raised serum potassium) and T- (atypical T-wave) changes on ECG in CKD patients versus HD patients. METHODOLOGY 200 patients on HD and CKD 4 &amp; 5 not on HD, fulfiling the inclusion criteria were enrolled in the study. Sampleing for seum potassium levels were done and ECG obtained. RESULTS Mean age in HD and CKD groups respectivley was 51.46 ± 26.96 and 56.16 ± 21.68 years. In HD group there were 61 males and 39 females whereas in CKD group there were 57 males and 43 females. Mean serum potassium levels were 5.20 ± 0.85 (mEq/L) in HD group whereas in CKD group mean serum potassium levels were 5.50 ± 0.62 (mEq/L). The mean T-wave duration in HD group was 168.01 ± 2.94 (msec), while in CKD group the mean T-wave duration was 173.76 ± 2.33 (msec). In HD group Pearson correlation coefficient was -0.779 with a P -value of 0.000, whereas in CKD group Pearson correlation coefficient was -0.02 with P -value was 0.985. CONCLUSION In our study, there was a negative correlation between serum K+ levels and duration of T-wave in patients on maintenance HD. T

Chronic Kidney Disease and Frailty: Insights from a Cross-Sectional Study in Older Adults

Abstract Background Chronic Kidney Disease (CKD) and frailty are prevalent conditions among older adults, contributing to increased healthcare utilisation and adverse outcomes. The aim of this study was to examine CKD prevalence and associated factors in older adults attending a Community Specialist Team (CST) for older persons for Comprehensive Geriatric Assessment (CGA). Methods A cross-sectional study was conducted of all adults aged ≥65 years who had a CGA from October 2023 to March 2024. Variables recorded on an Excel spreadsheet included age, gender, Clinical Frailty Scale (CFS) score, Modified Barthel Index (mBI), presence of probable sarcopenia, Malnutrition Screening Tool (MST) and Dementia Screening Interview (AD8) outcomes. CKD was defined as estimated Glomerular Filtration Rate (eGFR) &amp;lt;60ml/min/1.73m2. The presence of frailty was defined as CFS ≥4. Functional impairment was defined by mBI&amp;lt;15 and MST ≥2 defined malnutrition risk. Regression analysis was used to identify associations. Results Ninety-one patients, 59 (64.8%) female and 32 (35.2%) male, with a mean age of 81.83 (SD=7.19) years were included. The prevalence of frailty was 90% (n=82) and of CKD was 53.8% (n=49). Age was a significant predictor of CKD and with each additional year, the odds of having CKD increased by 10% (p=0.004). Twelve (24.5%) of the CKD group had MST ≥2 compared with 17 (40.5%) without CKD (p=0.120). The odds of having probable sarcopenia was non-significantly higher (OR=1.09, p=0.8444) in CKD compared to without CKD. The odds of a positive AD8 was also non-significantly higher (OR=1.24, p=0.605) in CKD compared with no CKD. There was no difference in prevalence of functional impairment between the 2 groups (p=0.466). Conclusion CKD is common chronic condition in frail older persons referred to a CST. It is frequently unrecognised. Identification of CKD through CGA should facilitate an integrated interdisciplinary approach to care which may contribute to better overall health and quality of life.

Short- and long- term outcomes of mechanical thrombectomy in acute ischemic stroke patients with chronic kidney disease.

Chronic kidney disease (CKD) is a risk factor of acute ischemic stroke (AIS). Outcomes of treatment with mechanical thrombectomy (MT) in patients with CKD seem to be poorer than in the general population. Long‑term follow‑up studies are lacking. Our aim was to asses short- and long‑term outcomes (up to 365 days after stroke) in MT‑treated AIS patients with concomitant CKD. The study included all AIS patients treated with MT at the Comprehensive Stroke Center in Kraków, Poland, from 2019 to 2021. The patients were divided into the CKD group (best glomerular filtration rate [GFR] during hospitalization <60 ml/min/1.73 m2 or diagnosed CKD) and the controls. In‑hospital, 90‑day, and 365‑day mortality and rate of good functional outcomes (defined as modified Rankin Scale ≤2) were compared between the CKD patients and controls as well as between patients with CKD stages 1-3 (GFR ≥30 ml/min/1.73 m2) and 4-5 (GFR <30 ml/min/1.73 m2). Factors associated with the abovementioned outcomes were identified using univariable logistic regression analyses and then added to multivariable analyses. The CKD patients had higher 90- and 365‑day mortality and lower 90- and 365‑day good functional outcome rates than the controls. The patients with CKD stage 4-5 had significantly higher in‑hospital, 90‑day, and 365‑day mortality than the patients with CKD stage 1-3. Neither CKD nor its late stages (4-5) were independently associated with short- and long‑term mortality and functional outcomes of MT. MT outcomes in CKD patients are worse, especially in advanced stages of the disease, but CKD is not independently associated with poor prognosis. CKD alone should not be a contraindication for MT in otherwise eligible patients, although patients with impaired kidney function require more careful postprocedural monitoring.

Features of preeclampsia in patients with chronic kidney disease

Aims: to study the characteristics of preeclampsia (PE) in women with chronic kidney disease (CKD) compared to PE in the general population.Method: a prospective observational study analyzed the course of PE in 24 women with a previously established diagnosis of CKD (Group 1) and 39 women in the general population (Group 2) without a complicating somatic history. In patients with CKD with a known pregestational creatinine level, the physiological response of the kidneys to pregnancy was assessed, defined as a decrease in serum creatinine by more than 10% in the first trimester. The angiogenic ratio (sFlt-1/PLGF) was studied in 13 patients with CKD.Results: the two groups did not differ in age or parity. In the first group, 16 patients had CKD stage 1-2, 5 had CKD 3A, and one patient each had CKD 3B, 4 and 5 (the later receiving hemodialysis). Nineteen (79%) of women with CKD had hypertension, proteinuria (PU), renal impairment or a combination of these factors before conception. Only 3 out of 16 patients had a physiological renal response. Early PE developed in 58.3% of patients with CKD compared to 35.3% in second group (p = 0.082). The duration of PE inversely correlated with the stage of CKD (r = -0.630; p = 0.001). As pregnancy progressed in patients with CKD, PU increased, reaching nephrotic level in 54% of women by the time of PE. HELLP syndrome or isolated hematological signs of TMA were noted in 8 patients in the general population group, and in 1 in the CKD group. The average sFlt-1/PLGF value in patients with early stages of CKD (n = 9) was 81.0±24.0, with late stages (n = 4) it was 14±8.Conclusion: the study identified the features of PE in CKD: early onset, increased PU reaching nephrotic level in half of the cases by the time PE is diagnosed, and the absence of a histological renal response to pregnancy in the 1st trimester. The lack of changes in the angiogenic coefficient in women with PE and late-stage CKD requires further study in a larger group of patients.

Outcomes for older people with screening detected versus existing chronic kidney disease: Cohort study with data linkage

BackgroundChronic Kidney Disease (CKD) is a common health problem, associated with increased risk of cardiovascular disease (CVD), end stage kidney disease (ESKD), and premature death. A third of people aged≥70 years have CKD, many of whom are undiagnosed, but little is known about the value of screening.AimTo compare the risk of adverse health outcomes between people with an existing diagnosis of CKD and those identified on screening. To identify factors associated with mortality in CKD.Design &amp; settingProspective cohort study of 892 primary care patients aged≥60 years with CKD (existing and screening detected) in Oxfordshire, with data linkage to civil death registry and secondary care.MethodHazard Ratios (HR) and 95% Confidence Intervals (CI) were estimated using Cox proportional-hazard models to compare the risk of all-cause mortality, hospitalisation, CVD, ESKD separately, and as a composite between CKD groups, as well as to identify factors associated with mortality.ResultsAfter a median follow-up of 3-5 years, 49 people died, 493 were hospitalised, 57 had an incident CVD event, and 0 had an ESKD event. There was no difference in the composite outcome between those existing CKD and those identified on screening (HR 0.94, CI 0.67-1.33). Older age (HR 1.10, CI 1.06-1.15), male sex (HR 2.31, CI 1.26-4.24), and heart failure (HR 5.18, CI 2.45-10.97) were associated with increased risk of death.ConclusionScreening older people for CKD may be of value, as their risk of short-term mortality, hospitalisation, and CVD is comparable to people routinely diagnosed. Larger studies with longer follow-up in more diverse and representative populations of older adults are needed to corroborate these findings.

Evaluation of platelet indices in chronic kidney disease

Objective: Chronic kidney disease (CKD) is characterized by an irreversible decrease in kidney functions and accumulation of uremic toxins in the body. Platelet indices have the potential to predict the inflammatory status and disease progression in patients with CKD. In this study it was aimed to investigate platelet indices and their relations with renal function and comorbid conditions in CKD patients. Method: In this study it was included 411 CKD patients. We looked for associations between platelet indices and estimated glomerular filtration rate (eGFR). We generated linear regression models for platelet indices that may be associated with eGFR. We evaluated CKD patients for possible associations between platelet indices and comorbid conditions such as diabetes, hypertension, and cardiovascular diseases. Results: The mean age of CKD patients was 60.5 and the GFR value was 40.1+24.8 mL/min/1.73m2. While the mean platelet count, MPV, PCT, PDW, P-LCR values were lower in the advanced CKD group, hematocrit adjusted platelet count (HAPC), MPV/Lymphocyte ratio and SII parameters were higher in the advanced CKD group (p

A clinical comparative study on carbamylated haemoglobin as a surrogate marker to differentiate acute kidney injury from chronic kidney disease.

Carbamylated haemoglobin is the result of reaction of isocyanate with N-terminal valine residues of the α and β chains of haemoglobin. Carbamylated haemoglobin concentration is dependent on the degree and duration of uraemia and thus may potentially serve as a marker to differentiate acute kidney injury (AKI) and chronic kidney disease (CKD). A hospital-based prospective clinical comparative study was conducted in an urban tertiary medical care centre. Carbamylated haemoglobin was estimated in a total of 60 patients, 30 each of chronic kidney disease and acute kidney injury. The comparison of the carbamylated haemoglobin levels among the CKD and AKI groups was done using Mann-Whitney test. The mean value of carbamylated haemoglobin among the CKD group was 240.71 ± 75.64 μgVH/g, whereas among the AKI group, it was 67.15 ± 17.05 μgVH/g. These values are statistically significant with P < 0.001. Carbamylated haemoglobin values were elevated in relation to renal dysfunction, and it significantly correlated with chronicity of kidney disease. Mean CarHb among the CKD group was significantly high in comparison to the AKI group with statistical significance, with a P value of <0.001. It was significantly attributed in this study that carbamylated haemoglobin >100 μgVH/g is diagnostic of CKD and a value <100 μgVH/g is diagnostic of AKI. Thus, in this study, it can be concluded that carbamylated haemoglobin is a useful marker to differentiate AKI from CKD.