Renoprotective Effects of Daprodustat in Patients with Chronic Kidney Disease and Renal Anemia.

Many large-scale studies revealed that exogenous erythropoietin, erythropoiesis-stimulating agents, have no renoprotective effects. We reported the renoprotective effects of endogenous erythropoietin production on renal function in ischemic reperfusion injury (IRI) of the kidney using the prolyl hydroxylase domain (PHD) inhibitor, Roxadustat. The purpose of this study was to investigate the effects of daprodustat on the progression of chronic renal failure. We retrospectively investigated the effects of daprodustat on the progression of chronic renal failure and renal anemia in patients with stages 3a-5 chronic kidney diseases (estimated glomerular filtration rate, eGFR < 60 mL/min/1.73 m2). The results show that daprodustat largely slowed the reduction in eGFR. The recovery of renal function was observed in some patients. Daprodustat is useful not only for renal anemia but also for the preservation of renal function. The renoprotective effect of daprodustat was small in patients with serum creatinine larger than 3-4 mg/dL because of low residual renal function. The appearance of renal anemia would be a sign of the time to start using daprodustat.

Effects of soluble Klotho and Wnt/ß-catenin signaling pathway in vascular calcification in chronic kidney disease model rats and the intervention of Shenyuan granules.

OBJECTIVE: This study aimed to investigate the effect of the soluble Klotho (sKlotho)/Wnt/ß-catenin signaling pathway on vascular calcification in rat models of chronic kidney disease (CKD) and the intervention effect of Shenyuan granules. METHODS: Rats with 5/6 nephrectomy and high phosphorus feeding were used to establish the vascular calcification model. The rats were given gradient doses of Shenyuan granules aqueous solution and calcitriol solution by gavage for 8 weeks, which were divided into experimental group and positive control group. RESULTS: The 5/6 nephrectomy combined with high phosphorus feeding induced thoracic aortic calcification in rats. Shenyuan granules intervention increased the serum sKlotho level, inhibited the mRNA and protein expression of Wnt1, ß-catenin, and Runx2 in the thoracic aorta, and alleviated thoracic aortic media calcification in rats. CONCLUSION: Shenyuan granules may partially regulate the Wnt/ß-catenin signaling pathway via serum sKl to interfere with the expression of Runx2, thereby improving vascular calcification in CKD.

Dietary counseling, meal patterns, and diet quality in patients with type 2 diabetes mellitus with/without chronic kidney disease.

BACKGROUND: Aim to this study is to investigate the association of Dietary Counseling, Meal Patterns, and Diet Quality (DietQ) in Patients with Type 2 Diabetes Mellitus (T2DM) with/without chronic kidney disease (CKD) in primary healthcare. METHODS: Cross-sectional study acquired data on dietary counseling and meal patterns by direct interview with a food-frequency questionnaire and one 24-h food-recall. The Healthy Eating Index (HEI) was used to classify DietQ ["good" DietQ (GDietQ, score ≥ 80) and "poor" DietQ (PDietQ, score < 80)]. PARTICIPANTS/SETTING: This study included 705 patients with T2DM: 306 with normal kidney function; 236 with early nephropathy, and 163 with overt nephropathy (ON). STATISTICAL ANALYSES PERFORMED: Multivariate linear-regression models for predicting HEI and χ2 tests for qualitative variables and one-way ANOVA for quantitative variables were employed. Mann-Whitney U and independent Student t were performed for comparisons between GDietQ and PDietQ. RESULTS: Only 18 % of the population was classified as GDietQ. Patients with ON and PDietQ vs. with GDietQ received significantly less dietary counseling from any health professional in general (45 % vs 72 %, respectively), or from any nutrition professional (36 % vs. 61 %, respectively). A better HEI was significantly predicted (F = 42.01; p = 0.0001) by lower HbA1C (ß -0.53, p = 0.0007) and better diet diversity (ß 8.09, p = 0.0001). CONCLUSIONS: Patients with more advanced stages of CKD had less nutritional counseling and worse dietary patterns, as well as more frequent PDietQ. Our findings reinforce the need for dietitians and nutritionists in primary healthcare to provide timely nutritional counseling.

Differences in mortality and risk factors, two years after endovascular repair of ruptured abdominal aortic aneurysms - Reassessment analysis.

OBJECTIVE: The prevalence of abdominal aortic aneurysms (AAA) increases with age. Elective intervention for AAA is critical to prevent rupture associated with very high mortality among older males. METHODS: The aim of this study was to address the impact of post-contrast acute kidney-PC-AKI injury among patients treated with endovascular repair of ruptured AAA-EVAR on outcomes such as new onset chronic kidney disease-CKD and mortality among patients within a two-year trial. RESULTS: The same study group (of n = 192 patients) underwent reassessment, two years after EVAR treatment. The overall mortality rate was 16.67%, and it was higher in the AKI group - 38.89%. CKD patients had a mortality rate of 23.88% (n = 16). Among patients with an aneurysm diameter >67 mm mortality rate reached 20% (n = 6), while in the previously reported diabetes mellitus group 37.93% (n = 11). New onset of CKD was diagnosed in 23% of cases. Preexisting CKD patients with PC- AKI contributed to a 33.33% mortality rate (n = 8). CONCLUSION: This study concludes that PC-AKI impacts outcomes and survival in endovascularly treated AAAs. Type 2 diabetes and preexisting chronic kidney disease are associated with higher mortality within a 2-year follow-up, however gender factor was not significant. A larger aneurysm diameter is related with a higher prevalence of PC-AKI. These factors should be taken into account during screening, qualifying patients for the treatment and treating patients with AAA. It may help to identify high-risk individuals and tailor preventive measurements and treatment options accordingly, improving treatment results and reducing mortality.

Inflammatory indexes and anemia in chronic kidney disease: correlation and survival analysis of the National Health and Nutrition Examination Survey 2005-2018.

BACKGROUND: There is currently no research on the correlation between novel inflammatory indexes systemic immune-inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and the risk of anemia in chronic kidney disease (CKD) population, as well as survival analysis in CKD with anemia. METHODS: This investigation encompassed 4444 adult subjects out of the National Health and Nutrition Examination Survey (NHANES) between 2005 and 2018. The study utilized multi-variable logistic regression to assess the relationship between SII, NLR, PLR, and anemia risk occurrence in CKD population. Survival differences in CKD patients with anemia, based on varying levels of SII, NLR, and PLR were evaluated employing Kaplan-Meier and Cox proportional hazards models. RESULTS: The adjusted logistic regression model demonstrates that SII, NLR, and PLR are associated with the risk of anemia occurrence in CKD population. Kaplan-Meier's analysis reveals significant differences in survival rates among CKD patients with anemia stratified by NLR levels. The adjusted Cox proportional hazards model shows that the higher NLR group has a 30% elevated risk of all-cause mortality contrasted with lower group (hazard ratio, HR: 1.30, confidence interval (CI) [1.01, 1.66], p value <.04). Restricted cubic spline (RCS) demonstrates no nonlinear relationship between NLR and all-cause mortality. Lastly, sub-cohort analysis indicates that in populations with diabetes, hypertension, and hyperuricemia, NLR levels have a greater impact on all-cause mortality. CONCLUSIONS: Controlling inflammation may reduce the occurrence of anemia in CKD populations, with NLR serving to be a potential prognostic indicator for survival results within CKD patients suffering from co-morbid anemia.

Evaluation of complications in patients with mandible fractures undergoing chronic kidney disease in the United States.

BACKGROUND: This research aims to assess the demographic characteristics, prevalence, outcomes, and complications in chronic kidney disease (CKD) patients following mandible fractures in the United States using a nationally representative database. METHODS: We analyzed data from the National Inpatient Sample from 2010 to 2019 in the United States. Patients with mandible fractures were categorized into three groups based on the International Classification of Diseases, Ninth and Tenth Revisions (ICD-9-CM and ICD-10-CM): end-stage renal disease (ESRD), non-ESRD CKD, and healthy kidney function. Chi-squared tests and analysis of variance (ANOVA) were used to compare these groups. Additionally, multivariate regression analysis was performed to determine whether CKD is an independent risk factor for complications in patients with mandible fractures. RESULTS: A total of 38,481 patients in the United States were estimated to have experienced mandible fractures between 2010 and 2019. The incidence rate of non-ESRD CKD in patients with mandible fractures significantly increased over time, while the prevalence of ESRD remained stable during the ten-year period. Compared to the healthy kidney function group, patients with chronic kidney disease exhibited higher hospital costs, longer hospitalization durations, and higher in-hospital mortality rates. Additionally, they had greater odds ratios for most of the investigated complications. CONCLUSIONS: This study revealed a steady annual increase in the morbidity rate of non-ESRD CKD among patients with mandible fractures, while ESRD prevalence remained stable over ten years. We observed a close association between chronic kidney disease and the prognosis of patients with mandible fractures. Clinicians should prioritize preventive measures and appropriate management of mandibular fractures in patients with CKD.

Massive cerebral tuberculomas, Pott's disease and hypercalcaemia secondary to Mycobacterium bovis in a patient with chronic kidney disease on peritoneal dialysis.

Tuberculosis (TB) is still a health problem in developing countries. Pulmonary involvement remains the most common clinical presentation. However, multiorgan involvement can be life-threatening. We present the case of a young woman on peritoneal dialysis who was admitted to hospitalisation for hypercalcaemia and low back pain. In his biochemical evaluation, suppressed intact parthyroid hormone (iPTH) and elevated 1,25-hydroxyvitamin D were detected. On a lumbar CT scan, a hypodense lesion in vertebral bodies compatible with Pott's disease was found. Positive cultures for Mycobacterium bovis were obtained in bronchoalveolar lavage and peritoneal fluid, for which specific treatment was initiated. Due to neurological deterioration, a CT scan was performed showing the presence of multiple tuberculomas. Retrospectively, the lack of an etiological diagnosis of chronic kidney disease, the initiation of dialysis 8 months before and the clear evidence of long-standing TB strongly suggest mycobacterium infection as the cause or trigger for the rapid decline in kidney function.

Key regulators of vascular calcification in chronic kidney disease: Hyperphosphatemia, BMP2, and RUNX2.

Vascular calcification is quite common in patients with end-stage chronic kidney disease and is a major trigger for cardiovascular complications in these patients. These complications significantly impact the survival rate and long-term prognosis of individuals with chronic kidney disease. Numerous studies have demonstrated that the development of vascular calcification involves various pathophysiological mechanisms, with the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) being of utmost importance. High phosphate levels, bone morphogenetic protein 2 (BMP2), and runt-related transcription factor 2 (RUNX2) play crucial roles in the osteogenic transdifferentiation process of VSMCs. This article primarily reviews the molecular mechanisms by which high phosphate, BMP2, and RUNX2 regulate vascular calcification secondary to chronic kidney disease, and discusses the complex interactions among these factors and their impact on the progression of vascular calcification. The insights provided here aim to offer new perspectives for future research on the phenotypic switching and osteogenic transdifferentiation of VSMCs, as well as to aid in optimizing clinical treatment strategies for this condition, bearing significant clinical and scientific implications.

Increased Lymphatic Vessels: A Risk Factor for Severe Renal Function Loss in Obstructive Nephropathy Patients.

Background: Obstructive nephropathy (ON), resulting from hindered urine flow, significantly contributes to both acute kidney injury (AKI) and chronic kidney disease (CKD). Research has consistently highlighted increased lymphatic vessels (LVs) density in diverse kidney diseases. However, the precise involvement of LVs in ON remains unclear. Methods: Patients diagnosed with ON were enrolled in this study from January 2020 to December 2023. LVs and histological pathology in renal biopsy tissues were detected through immunohistochemistry and Periodic Acid-Schiff staining. Patients were categorized into two cohorts based on their estimated glomerular filtration rate (eGFR) levels: one cohort included patients with eGFR < 90, while the other encompassed those with eGFR ≥ 90. Univariate and multivariable logistic regression analyses were conducted to determine the odds ratio (OR) and 95% confidence interval (CI) for the association between the two cohorts. Results: 239 patients were enrolled in the study. The density of LVs was elevated in ON, with even higher densities observed in patients with severe renal impairment. Additionally, several risk factors contributing to the deterioration of renal function in ON patients have been identified, including age, ureteral calculi (UC), alanine aminotransferase (ALT), and uric acid (UA). Furthermore, by leveraging LVs density, multiple robust models have been established to predict severe renal impairment in ON. Conclusions: Lymphatic vessels density is significantly elevated in ON, serving as an independent risk factor for the decline in renal function.

The systemic inflammatory response index is associated with chronic kidney disease in patients with hypertension: data from the national health and nutrition examination study 1999-2018.

BACKGROUND: Studies have shown that in hypertensive patients, chronic kidney disease (CKD) is associated with a poor prognosis. Inflammation is a highly important factor in the progression of CKD. Detecting systemic inflammation and intervening promptly in patients with hypertension may help reduce the risk of CKD. The systemic inflammatory response index (SIRI) is a tool used to measure the systemic inflammatory response, but its relationship with CKD in patients with hypertension remains uncertain. METHODS: We utilized data from the National Health and Nutrition Examination Survey (NHANES), which was conducted between 1999 and 2018. The analysis included a total of 20,243 participants, categorized into three groups based on SIRI tertiles. Logistic regression analysis and restricted cubic spline analysis were used to examine the relationship between the SIRI and CKD. RESULTS: In patients with hypertension, there was a notable relationship between the SIRI and the odds of developing CKD. After full adjustment, there was a 31% greater likelihood of developing CKD associated with each incremental increase of 1 unit in the SIRI (OR: 1.31, 95% CI: 1.24-1.39, p < 0.001). The groups with greater SIRI values exhibited greater odds of developing CKD than did the T1 group (T2: OR: 1.20, 95% CI: 1.04-1.38, p = 0.015; T3: OR: 1.69, 95% CI: 1.47-1.94, p < 0.001). CONCLUSION: A high SIRI is associated with an increased risk of CKD in hypertensive patients. The greater the SIRI is, the greater the risk of CKD in hypertensive patients.

Impact of Serum Phosphorus on Hemoglobin: A Literature Review.

Phosphorus is a macroelement found in the body, mostly in the bones as crystals of hydroxyapatite. Higher levels are found in patients affected by chronic kidney disease (CKD). Since the early stage of CKD phosphorous excretion is impaired, but the increase of PTH and FGF23 maintains its level in the normal range. In the last decades, the role of FGF23 in erythropoiesis was studied, and now it is well known for its role in anemia genesis in patients affected by conservative CKD. Both Hyperphosphatemia and anemia are two manifestations of CKD, but many studies showed a direct association between serum phosphorous and anemia. Phosphorus can be considered as the common point of more pathogenetic ways, independent of renal function: the overproduction of FGF23, the worsening of vascular disease, and the toxic impairment of erythropoiesis, including the induction of hemolysis.

Association of ACEI/ARB therapy with total and cardiovascular death in coronary artery disease patients with advanced chronic kidney disease: a large multi-center longitudinal study.

INTRODUCTION: Advanced chronic kidney disease (CKD) is common among patients with coronary artery disease (CAD), and angiotensin­converting enzyme inhibitors (ACEI) or angiotensin­receptor blockers (ARB) can improve cardiac and renal function, but whether ACEI/ARB therapy improves long-term prognosis remains unclear among these high-risk patients. Therefore, this research aimed to investigate the relationship between ACEI/ARB therapy and long-term prognosis among CAD patients with advanced CKD. METHODS: CAD patients with advanced CKD were included in five hospitals. Advanced CKD was defined as estimated glomerular filtration rate (eGFR)<30 ml/min per 1.73 m2. Cox regression models and competing risk Fine and Gray models were used to examine the relationship between ACEI/ARB therapy and all-cause and cardiovascular death, respectively. RESULTS: Of 2527 patients, 47.6% population of our cohort was discharged on ACEI/ARB. The overall all-cause and cardiovascular mortality were 38.6% and 24.7%, respectively. Multivariate Cox regression analyses indicated that ACEI/ARB therapy was found to be associated with lower rates of both all-cause mortality (hazard ratio (HR)=0.836, 95% confidence interval (CI): 0.738-0.948, p = 0.005) and cardiovascular mortality (HR = 0.817, 95%CI: 0.699-0.956, p = 0.011). In the propensity-matched cohort, the survival benefit was consistent, and significantly better survival was observed for all-cause mortality (HR = 0.856, 95%CI: 0.752-0.974, p = 0.019) and cardiovascular mortality (HR = 0.830, 95%CI: 0.707-0.974, p = 0.023) among patients treated with ACEI/ARB. CONCLUSION: ACEI/ARB therapy showed a better survival benefit among high-risk CAD patients with advanced CKD at long-term follow-up, which manifested that strategies to maintain ACEI/ARB treatment may improve clinical outcomes among these high-risk populations.

What is the current knowledge on the topic? Advanced CKD is highly prevalent and strongly associated with higher mortality risk and worse outcomes among CAD patients, and patients with advanced CKD have often been excluded from randomized controlled trials, creating an evidence gap for these high-risk CAD patients. ACEI/ARB are beneficial for greater survival among CAD patients, but the effect of ACEI/ARB therapy on long-term prognosis is unclear among CAD patients with advanced CKD.What does this study add to our knowledge? ACEI/ARB treatment showed a better survival benefit among high-risk CAD patients with advanced CKD at long-term follow-up.How might this change clinical pharmacology or translational science? CAD patients with advanced CKD are not only have worse outcomes but also limited in their choice of therapy strategies. Our study may prompt an important reference for the subsequent improvement of long-term prognosis among these high-risk populations.

Ferric citrate hydrate improves transferrin saturation in patients with low levels of transferrin saturation undergoing hemodialysis.

Although it has been established that patients with chronic kidney disease and iron deficiency, as indicated by a transferrin saturation of < 20%, are at increased risk of all-cause mortality and cardiovascular events, the optimal management of such patients has not yet been determined. In this post hoc subgroup analysis, we aimed to clarify the effect of ferric citrate hydrate on transferrin saturation in patients with chronic kidney disease and low transferrin saturation (< 20%) undergoing hemodialysis. To accomplish this, we extracted the relevant data on a subset of patients drawn from two previous studies: the ASTRIO study (A Study examining the contribution to Renal anemia treatment with ferric citrate hydrate, Iron-based Oral phosphate binder, UMIN000019176) and a post-marketing surveillance study. The subset of patients used for the present study were those with baseline transferrin saturation < 20%. We found that administration of ferric citrate hydrate increased transferrin saturation and maintained transferrin saturation at approximately 30%. However, because we did not have access to data on all-cause mortality or cardiovascular events, we could not ascertain whether the frequency of these outcomes was reduced in parallel with improvements in transferrin saturation. Further large studies are required.

BRCC36 regulates ß-catenin ubiquitination to alleviate vascular calcification in chronic kidney disease.

BACKGROUND: The prevalence of vascular calcification (VC) in chronic kidney disease (CKD) patients remains substantial, but currently, there are no effective pharmaceutical therapies available. BRCA1/BRCA2-containing complex subunit 36 (BRCC36) has been implicated in osteoblast osteogenic conversion; however, its specific role in VC remains to be fully elucidated. The aim of this study was to investigate the role and underlying mechanisms of BRCC36 in VC. METHODS: The association between BRCC36 expression and VC was examined in radial arteries from patients with CKD, high-adenine-induced CKD mice, and vascular smooth muscle cells (VSMCs). Western blotting, real-time polymerase chain reaction, immunofluorescence, and immunohistochemistry were used to analyse gene expression. Gain- and loss-of-function experiments were performed to comprehensively investigate the effects of BRCC36 on VC. Coimmunoprecipitation and TOPFlash luciferase assays were utilized to further investigate the regulatory effects of BRCC36 on the Wnt/ß-catenin pathway. RESULTS: BRCC36 expression was downregulated in human calcified radial arteries, calcified aortas from CKD mice, and calcified VSMCs. VSMC-specific BRCC36 overexpression alleviated calcium deposition in the vasculature, whereas BRCC36 depletion aggravated VC progression. Furthermore, BRCC36 inhibited the osteogenic differentiation of VSMCs in vitro. Rescue experiments revealed that BRCC36 exerts the protective effects on VC partly by regulating the Wnt/ß-catenin signalling pathway. Mechanistically, BRCC36 inhibited the Wnt/ß-catenin pathway by decreasing the K63-linked ubiquitination of ß-catenin. Additionally, pioglitazone attenuated VC partly through upregulating BRCC36 expression. CONCLUSIONS: Our research results emphasize the critical role of the BRCC36-ß-catenin axis in VC, suggesting that BRCC36 or ß-catenin may be promising therapeutic targets to prevent the progression of VC in CKD patients.

Torsemide in Edema Associated with Chronic Kidney Disease.

Torsemide is a loop diuretic used to manage edema associated with chronic kidney disease (CKD) and acute kidney injury (AKI). It acts by inhibiting sodium and chloride ions reabsorption in the ascending limb of the loop of Henle, thereby increasing urine output and reducing fluid accumulation. Compared to other diuretics, torsemide has an extended duration of action, higher bioavailability, and its elimination route is primarily through the hepatic route, making it effective in patients with CKD and AKI. Clinical studies indicate that torsemide can improve symptoms of fluid overload and potentially enhance renal function.

Statin therapy and upper tract urothelial carcinoma risk in hyperlipidemic patients with chronic kidney disease and end-stage kidney disease, a population-based 17-year follow-up study.

BACKGROUND: The upper tract urothelial carcinoma (UTUC) risk associated with statin therapy in hyperlipidemic patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD) remains obscure. AIM: This retrospective cohort study investigated the UTUC risk for hyperlipidemic patients with CKD or ESKD associated with statin therapy. METHODS: From the national insurance claims data of Taiwan, we identified hyperlipidemic patients and established three pairs of statin users and non-users sub-cohorts matched by propensity scores: 401,490 pairs with normal kidney function, 37,734 pairs with CKD, and 6271 pairs with ESKD. Incidence rates and hazard ratio (HR) of UTUC were estimated, by the end of 2016, between statin and non-statin cohorts, and between hydrophilic statins users and lipophilic statins users. Time-dependent model estimated adjusted HR, and sub-distribution HR (sHR) accounting for the competing risk of deaths. RESULTS: The statin-users with ESKD were at increased UTUC risk (sHR 1.98; 95% confidence interval (CI), 1.28-3.06), significant for younger patients (40-64 years). The incidence was twofold greater in women than in men (31.8 versus 15.9 per 10,000 person-years). Receiving lipophilic statins was associated with increased UTUC risk in CKD and ESKD patients, while receiving hydrophilic statins was associated with increased UTUC risk in ESKD patients. CONCLUSIONS: Patients with ESKD receiving statin were at an increased UTUC risk, significant for younger group (<65 y/o). The positive associations between UTUC and statin persisted in both genders with ESKD, and in therapy with either lipophilic statins or hydrophilic statins. Statin users with ESKD deserve attention for UTUC prevention.

Association between malnutrition-inflammation score (MIS) and quality of life in elderly hemodyalisis patients.

INTRODUCTION: The malnutrition-inflammation process is one of the main causes of morbidity and mortality in patients with chronic kidney disease (CKD), influencing quality of life. The aim of this study was to identify the inflammatory and nutritional status of elderly hemodialysis (HD) and its association with quality of life. METHODS: This study was carried out in health services in three different cities. The Malnutrition-Inflammation Score (MIS) was used to assess the inflammatory and nutritional status, with anthropometric measurements, protein status, lean mass and function. The quality of life was assessed using KDQOL-SFTM. Data were analyzed using multivariate analysis and the Poisson model to evaluate the factors that increased the risk of developing malnutrition and inflammation. RESULTS: The MIS identified a 52.2% prevalence of malnutrition and inflammation in the population. In univariate analysis, most KDQOL-SFTM domains presented higher scores for nourished elderly. Anthropometric measures associated with muscle mass and functionality were lower in the malnourished elderly. Multivariate modeling revealed a higher nutritional risk of 50.6% for women and older age, since with each additional year of life the risk of malnutrition increased by 2.4% and by 0.4% with each additional month on HD. Greater arm muscle circumference (AMC) and higher serum albumin were factors for reducing malnutrition by 4.6% and 34.7%, respectively. CONCLUSION: Higher serum albumin and preserved AMC have been shown to be good indicators of better nutritional status. Higher MIS was associated with poorer quality of life, older age, lower income and education, longer time on dialysis, and presence of comorbidities.

Examining the Potential Correlation Between Periodontal Disease and Chronic Kidney Disease.

Chronic kidney disease (CKD) refers to any abnormalities in kidney structure or function that remain longer than 3 months and negatively impact health. Characterized by a loss of nephrons and a decline in the glomerular filtration rate, CKD can stem from various diseases, such as glomerular, vascular, and others, with treatment options including dialysis or kidney transplantation. Many patients with CKD go undetected because they exhibit no symptoms. Periodontal disease is an inflammatory reaction that results in destruction in the periodontium's connective tissues and alveolar bone, potentially leading to such clinical signs and symptoms as edema, erythema, bleeding on probing, suppuration, tooth mobility and migration, alveolar bone loss, and tooth loss. Recent studies point to a connection between periodontal disease and systemic conditions, including CKD. Periodontal disease severity and presence may correlate with the occurrence of CKD. While various bacteria can cause periodontal disease, specific ones, such as Gram-negative bacilli, are linked to the beginning and progression of CKD, especially in people with compromised immune systems. It is beneficial, therefore, for clinicians to understand the association between CKD and periodontal disease.