Advanced Stages Of Chronic Kidney Disease Research Articles

Development of a preliminary conceptual model of the patient experience of chronic kidney disease: a targeted literature review and analysis

BackgroundPatient-reported outcome (PRO) instruments should capture the experiences of disease and treatment that patients consider most important in order to inform patient-centred care and product development. The aim of this study was to develop a preliminary conceptual model of patient experience in chronic kidney disease (CKD) based on a targeted literature review and to characterize existing PRO instruments used in CKD.MethodsPubMed, EMBASE and Cochrane databases and recent society meetings were searched for publications reporting signs/symptoms and life impacts of CKD. Concepts identified in the literature review were used to develop a preliminary conceptual model of patient experience of CKD, overall, and within patient subpopulations of differing CKD causes, severities and complications. PRO instruments, identified from PRO databases, CKD literature and CKD clinical trials, were assessed for content validity, psychometric strength and coverage of concepts in the literature review.ResultsIn total, 100 publications met criteria for analysis; 56 signs/symptoms and 37 life impacts of CKD were identified from these sources. The most frequently mentioned signs/symptoms were pain/discomfort (57% of publications) and tiredness/low energy/lethargy/fatigue (42%); the most commonly reported life impacts were anxiety/depression (49%) and decrements in physical functioning (43%). Signs/symptoms and life impacts varied across the subpopulations and were more frequent at advanced CKD stages. The preliminary conceptual model grouped signs/symptoms into seven domains (pain/discomfort; energy/fatigue; sleep-related; gastrointestinal-related; urinary-related; skin−/hair−/nails-related; and other) and life impacts into six domains (psychological/emotional strain; cognitive impairment; dietary habit disruption; physical function decrements; interference with social relationships; and other). Eleven PRO instruments were considered to be promising for use in CKD; all had limitations.ConclusionsAlthough preliminary, the proposed conceptual model highlights key PROs for people with CKD and is intended to spur development of more tailored PRO instruments to assess these concepts.

Vascular Calcification in Patients with Early-Stage Chronic Kidney Disease: The Pivotal Role of Estimated Glomerular Filtration Rate

Background: Vascular calcification in advanced chronic kidney disease (CKD) is correlated with uremic toxins and severely impaired calciumphosphate- parathyroid metabolism. The association factors of vascular calcification in early-stage CKD are still unestablished. Objective: To identify the risk factors for vascular calcification in the early-stage CKD, which was the non-target population, different from other previous studies that explored this association in advanced stage CKD. Materials and Methods: The present study was a longitudinal study conducted to examine the risk factors of vascular calcification in CKD stage G2 and G3 patients who had no previous cardiovascular diseases. All parameters including coronary artery calcification (CAC) and abdominal aortic calcification (AAC) at baseline and after twelve months were evaluated. Results: Twenty-two patients without established cardiovascular diseases were included and completed the follow-up period. Mean baseline LDL was 99 mg/dL and no patient received statin. At 12-month, the median CAC score was significantly increased to 266 (126 to 956) versus 282 (198 to 846), (p=0.024]. By multivariable analysis in generalized estimating equations, only estimated glomerular filtration rate (eGFR) was associated with CAC score greater than 400 (aOR 0.92, p=0.041), and AAC score greater than 5 (aOR 0.90, p=0.023). Conclusion: In early-stage CKD, eGFR was associated with vascular calcification. Further studies should explore the potential benefits of delaying CKD progression on vascular calcification in the early-stage CKD patients. Keywords: Chronic kidney disease; Vascular calcification; Coronary artery calcification; Abdominal aortic calcification; Glomerular filtration rate; Renal function

MO470PATIROMER PHARMACOUTILIZATION IN REAL-WORLD GERMAN CKD PATIENTS WITH MODERATELY TO SEVERELY REDUCED EGFR

Abstract Background and Aims Hyperkalemia (HK) (serum K>5.0 mEq/L) is a chronic condition in patients with chronic kidney disease (CKD) associated with high morbidity and mortality, and it is a frequent reasons for renin angiotensin aldosterone inhibition (RAASi) discontinuation. Patiromer is a non-absorbed, sodium-free, K+ binder that has been shown to reduce serum K+ in patients with HK, and thereby enable RAASi therapy, which is supported by randomized trial evidence. The description of patiromer utilization in patients with moderate to advanced CKD in the real-world setting in Europe is lacking. The objective of this analysis was to describe predictors of patiromer initiation and time to discontinuation among CKD patients using contemporary (April 2018-October 2020) data from German participants in CKD Outcomes and Practice Patterns Study (CKDopps). Method We identified 136 patiromer users (116 with matching K measurement) during the observation period. Patients with eGFR <60ml/min/1.73m2 and a serum potassium ≥4mEq/L who never initiated patiromer during the follow up were used as a comparison. We used the most recent lab and drug use information available within the 6-month period prior to baseline, which was defined as either first use of patiromer, April 1, 2018, or entry into the PDOPPS study. The median time between the most recent K+ measurement and baseline was 45 days for non-patiromer users and 4 days for patiromer users. Logistic regression models were used to test associations between patient factors and whether the patient was in the patiromer initiation group or the comparison group. Time on patiromer was estimated using a Kaplan-Meier curve, censoring for death, dialysis, transplantation, or loss of follow-up. Results Patiromer was prescribed to ≥2 patients in 11 clinics, one patient in 19 clinics, and zero patients in 57 clinics. Patients prescribed patiromer had lower eGFR (23.2 [15.8, 28.6] vs 36.9 [27.7, 46.3]ml/min) and higher serum K levels (5.6 [5.4, 6.1] vs 4.6 [4.3, 5.0]ml/min). There were no major differences according to patiromer use in other demographic, clinical, and biochemical characteristics. Despite the differences in serum K, use of RAAS inhibitors was similar in patiromer users (83%) versus non-users (80%). Thirty three percent of patiromer users were prescribed polystyrene sulfonate (SPS) before patiromer initiation. In a multiple logistic regression models (including serum K, CKD stage, gender, age, prescription of RAASi, diabetes, coronary artery disease, heart failure), patiromer use was strongly associated more advanced CKD stage (independently of high serum K), with odds ratios of initiation >3 for CKD stage 4 or 5 versus CKD stage 3. Among new users, 90% of patients had active prescription at 30 days and about one-half had active prescription at one year (Figure). Conclusion The main predictors of Patiromer initiation were advanced CKD stage and hyperkalemia. Treatment decisions did not appear to be based on other patient or clinical characteristics. Patiromer was often prescribed to patients already receiving alternative HK treatment (SPS), suggesting use for chronic hyperkalemia rather than response to acute event. Further analysis with a larger population and measurements of K+ before and after patiromer initiation may improve the understanding of its pharmacoutilization in moderate to advanced CKD.

MO751OXIDATIVE STRESS IN PATIENTS WITH CHRONIC RENAL FAILURE AND CARDIOVASCULAR COMPLICATIONS

Abstract Background and Aims The atherosclerosis process is highly accelerated in patients with chronic kidney disease (CKD). Oxidative stress is considered as one of the pro-atherogenic factors involved in accelerating the atherosclerosis process of the carotid artery. The aim of the present study was to determine the relationship between oxidative stress markers and the progression of carotid atherosclerosis in CKD patients. Method The study was conducted on 220 patients with CKD and 40 controls, and the disease stage was scored between 2 and 5D. Blood samples were taken and myeloperoxidases, malondialdehyde, nitric oxide, glutathione, and oxidised low-density lipoprotein were measured. Furthermore, we studied the correlations between these biomarkers and clinical and para-clinical cardiovascular complications. Results The average age of patients was 60.5 years. The oxidative stress markers average ± SD levels in CKD groups compared to the control were as follows: myeloperoxidase (49.89 ±1.98 vs. 38.45 ±1.98 UI/ml), malondialdehyde (5.2 ±0.12 vs. 3.26 ±0.03 µmol/l), nitric oxide (56.82 ±1.06 vs. 42.19 ±2.1 µmol/l), glutathione (42.21 ±1.3 vs. 79.4 ±2.6 IU/ml), and oxLDL (15.57 ±1.07 vs. 1.72 ±0.82 µmol/l). While the glutathione level decreased significantly in advanced CKD stage (p < 0.05), the concentrations of all the other biomarkers increased significantly in accordance with CKD score (p < 0.05). Patients with high IMD (> 1 mm) had higher values of the prooxidant markers (NO, oxLDL, MDA, MPO) but lower antioxidant marker values (glutathione), compared to other patients with lower IMD Conclusion Cardiovascular diseases, mainly atherosclerosis, can be diagnosed indirectly by measuring oxidative stress markers. Furthermore, theses markers can be used to predict the progression of CKD, for better management of the disease.

Insulin Withdrawal in Diabetic Kidney Disease: What Are We Waiting for?

The prevalence of type 2 diabetes mellitus worldwide stands at nearly 9.3% and it is estimated that 20–40% of these patients will develop diabetic kidney disease (DKD). DKD is the leading cause of chronic kidney disease (CKD), and these patients often present high morbidity and mortality rates, particularly in those patients with poorly controlled risk factors. Furthermore, many are overweight or obese, due primarily to insulin compensation resulting from insulin resistance. In the last decade, treatment with sodium–glucose cotransporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP1-RA) have been shown to be beneficial in renal and cardiovascular targets; however, in patients with CKD, the previous guidelines recommended the use of drugs such as repaglinide or dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitors), plus insulin therapy. However, new guidelines have paved the way for new treatments, such as SGLT2i or GLP1-RA in patients with CKD. Currently, the new evidence supports the use of GLP1-RA in patients with an estimated glomerular filtration rate (eGFR) of up to 15 mL/min/1.73 m2 and an SGLT2i should be started with an eGFR > 60 mL/min/1.73 m2. Regarding those patients in advanced stages of CKD, the usual approach is to switch to insulin. Thus, the add-on of GLP1-RA and/or SGLT2i to insulin therapy can reduce the dose of insulin, or even allow for its withdrawal, as well as achieve a good glycaemic control with no weight gain and reduced risk of hypoglycaemia, with the added advantage of cardiorenal benefits.

Association of Renal and Cardiovascular Safety With DPP-4 Inhibitors vs. Sulfonylureas in Patients With Type 2 Diabetes and Advanced Chronic Kidney Disease.

This study assessed the effects of dipeptidyl peptidase-4 inhibitors (DPP4is) vs. sulfonylureas (SUs) on composite renal, cardiovascular, and hospitalized hypoglycemia outcomes in type 2 diabetes (T2D) patients with advanced chronic kidney disease (CKD) who were underrepresented in previous clinical studies. The National Health Insurance Research Database was utilized. Patients with T2D and advanced CKD (stages 3b-5) with stable use of DPP4is or SUs were identified during 2011-2015 and followed until death or December 31, 2016. The primary outcome was the composite renal outcome. Secondary outcomes included hospitalized heart failure (HHF), major adverse cardiovascular event (MACE), hospitalized hypoglycemia, and all-cause death. Subdistribution hazard models were employed to assess treatment effects on clinical outcomes. A total of 1,204 matched pairs of DPP4i and SU users were analyzed. Compared with SUs, DPP4is had no significant difference in the risks of the composite renal outcome, HHF, and three-point and four-point MACE (hazard ratios (95% confidence intervals): 1.10 (0.93-1.31), 1.11 (0.95-1.30), 0.97 (0.79-1.19), and 1.08 (0.94-1.24), respectively), but reduced risks of hospitalized hypoglycemia (0.53 (0.43-0.64)) and all-cause death (0.71 (0.53-0.96)). In conclusion, among patients with T2D and advanced CKD, the use of DPP4is vs. SUs was associated with comparable safety profiles on renal and cardiovascular outcomes, and reduced risks of hospitalized hypoglycemia and all-cause death. DPP4is may be preferred for patients with T2D and advanced CKD, and the regular monitoring on cardiac function remains crucial among this population who are at a higher risk of HHF.

Illness perceptions predict distress in patients with chronic kidney disease

BackgroundPatients diagnosed with chronic kidney disease (CKD) report increased distress associated with their clinical diagnosis. Distress in patients with predialysis CKD, has been linked to several adverse events; including increased risk of hospitalisation, early dialysis initiation and even death, suggesting that distress is a matter of great concern during routine care in predialysis CKD.AimsThe present study aimed to assess the nature of illness perceptions and the level of distress in a CKD cohort diagnosed with different stages of kidney disease. It also aimed to explore the correlates of distress and to create a model for distress and its associated predictors making use of hierarchical regression analysis.MethodsA sample of 200 patients diagnosed with Chronic Kidney Disease were recruited for this study from the nephrology outpatient clinics of Mater Dei Hospital, Malta. The participants were assessed for their; illness perceptions, treatment beliefs, level of depression and anxiety, coping style, as well as treatment adherence. Routine clinical information was also collected for participants, including a co-morbidity score.ResultsA percentage of 33.5% of the participants reported moderate distress, whilst 9.5% reported severe distress. Stronger illness identity, a perception of timeline as being increasingly chronic or cyclical in nature, greater consequences and higher emotional representations were associated with more advanced stages of CKD. In contrast, lower personal and treatment control and poorer illness coherence were associated with more advanced stages of CKD. Results from the hierarchical regression analysis showed that illness perceptions contributed significantly to distress over and above the clinical kidney factors. Being female, having low haemoglobin and specific illness perceptions including; perceptions of greater symptomatology, longer timeline, low personal control and strong emotional representations, as well as resorting to maladaptive coping, were all significantly associated with distress symptoms. Nevertheless, illness perceptions accounted for the greatest variance in distress thus indicating that the contribution of illness perceptions is greater than that made by the other known covariates.ConclusionIllness perceptions hold a principal role in explaining distress in CKD, relative to other traditional covariates. For this reason, illness perceptions should be addressed as a primary modifiable component in the development of distress in CKD.

Factors associated with the absence of pharmacological treatment for common modifiable complications in children with chronic kidney disease.

Chronic kidney disease (CKD) is associated with many comorbidities requiring complex management. We described treatment patterns for common modifiable CKD complications (high blood pressure, anemia, hyperphosphatemia, and acidosis) according to severity of CKD and examined factors associated with the absence of drug therapy, among participants with a persistent comorbidity, for 1 year in children enrolled in the CKiD study. A total of 703 CKiD participants contributed 2849 person-visits over a median 3.5 years of follow-up. Using pairs of annual visits, we examined whether participants with abnormal biomarker levels at the first (index) visit persisted in the abnormal levels 1 year later according to CKD risk stage. Multivariate analyses identified demographic and clinical factors associated with the absence of drug therapy among those with persistent comorbid conditions for 1 year. The overall proportions of person-visits prescribing therapy at 1-year follow-up for treating anemia, acidosis, hyperphosphatemia, and high blood pressure were 54%, 45%, 29%, and 81%, respectively. The frequency of therapy increased with advanced CKD risk stage for all comorbidities; however, 19-23% of participants with acidosis, 24-27% with anemia, and 30-39% with hyperphosphatemia at high-risk stages (E and F) were not prescribed appropriate therapy despite the persistence of abnormal levels of these biomarkers for at least 1 year. The resolution of comorbidities at advanced CKD stages without treatment was unlikely. Many children with CKD in the CKiD cohort did not receive pharmacological treatment for common and persistent modifiable comorbidities, even in severe CKD risk stages.

Association of Pre-ESRD Serum Bicarbonate with Post-ESRD Mortality in Patients with Incident ESRD

Background: Serum bicarbonate or total carbon dioxide (CO₂) concentrations decline as chronic kidney disease (CKD) progresses and rise after dialysis initiation. While metabolic acidosis accelerates the progression of CKD and is associated with higher mortality among patients with end stage renal disease (ESRD), there are scarce data on the association of CO₂ concentrations before ESRD transition with post-ESRD mortality. Methods: A historical cohort from the Transition of Care in CKD (TC-CKD) study includes 85,505 veterans who transitioned to ESRD from October 1, 2007, through March 31, 2014. After 1,958 patients without follow-up data, 3 patients with missing date of birth, and 50,889 patients without CO₂ 6 months prior to ESRD transition were excluded, the study population includes 32,655 patients. Associations between CO₂ concentrations averaged over the last 6 months and its rate of decline during the 12 months prior to ESRD transition and post-ESRD all-cause, cardiovascular (CV), and non-CV mortality were examined by using hierarchical adjustment with Cox regression models. Results: The cohort was on average 68 ± 11 years old and included 29% Black veterans. Baseline concentrations of CO₂ were 23 ± 4 mEq/L, and median (interquartile range) change in CO₂ were −1.8 [−3.4, −0.2] mEq/L/year. High (≥28 mEq/L) and low (<18 mEq/L) CO₂ concentrations showed higher adjusted mortality risk while there was no clear trend in the middle range. Consistent associations were observed irrespective of sodium bicarbonate use. There was also a U-shaped association between the change in CO₂ and all-cause, CV, and non-CV mortality with the lowest risk approximately at −2.0 and 0.0 mEq/L/year among sodium bicarbonate nonusers and users, respectively, and the highest mortality was among patients with decline in CO₂ >4 mEq/L/year. Conclusion: Both high and low pre-ESRD CO₂ levels (≥28 and <18 mEq/L) during 6 months prior to dialysis transition and rate of CO₂ decline >4 mEq/L/year during 1 year before dialysis initiation were associated with greater post-ESRD all-cause, CV, and non-CV mortality. Further studies are needed to determine the optimal management of CO₂ in patients with advanced CKD stages transitioning to ESRD.

Health-Related Quality of Life Profiles in Dialyzed Patients With Varying Health Literacy. A Cross-Sectional Study on Slovak Haemodialyzed Population.

Objectives: Chronic kidney disease (CKD) strongly affects patients’ health-related quality of life (HRQoL), mostly in the advanced stages of CKD. Health literacy (HL) may affect this association, in particular for some aspects of HRQoL. The aim of this study is to compare the profiles of HRQoL in dialyzed patients with varying HL. Methods: We obtained data on HL using the Health Literacy Questionnaire (HLQ) and on HRQoL using the Kidney Disease Quality of Life – Short Form (KDQoL-SF 1.3) in a multicentre cross-sectional study in 20 dialysis clinics in Slovakia (n = 542; mean age = 63.6 years; males: 60.7%). We compared HRQoL for three HL groups using ANOVA and the Kruskal-Wallis test. Results: Patients with low HL reported worse HRQoL than patients with moderate and high HL. The greatest differences between HL groups were found in the scales Effect of kidney disease, Cognitive function, Quality of social interaction, Social support, Dialysis staff encouragement, Patient satisfaction, Physical functioning, Pain, Emotional well-being and Social function. p-values in all cases were <0.001. Conclusion: Patients with low HL have a worse HRQoL in several domains than patients with a higher HL. Increasing HL capacities and better supporting patients with low HL should thus be given priority to support their HRQoL and at least maintain its level.

Effects of fetuin-A-containing calciprotein particles on posttranslational modifications of fetuin-A in HepG2 cells

Fetuin-A is an inhibitor of ectopic calcification that is expressed mainly in hepatocytes and is secreted into the circulation after posttranslational processing, including glycosylation and phosphorylation. The molecular weight (MW) of fully modified fetuin-A (FM-fetuin-A) is approximately 60 kDa in an immunoblot, which is much higher than the estimated MW by amino acid sequence. Under conditions of calcification stress such as advanced stage chronic kidney disease, fetuin-A prevents calcification by forming colloidal complexes, which are referred to as calciprotein particles (CPP). Since the significance of CPP in this process is unclear, we investigated the effect of synthetic secondary CPP on the level of FM-fetuin-A in HepG2 cells. Secondary CPP increased the level of FM-fetuin-A in dose- and time-dependent manners, but did not affect expression of mRNA for fetuin-A. Treatment with O- and/or N-glycosidase caused a shift of the 60 kDa band of FM-fetuin-A to a lower MW. Preincubation with brefeldin A, an inhibitor of transport of newly synthesized proteins from the endoplasmic reticulum to the Golgi apparatus, completely blocked the secondary CPP-induced increase in FM-fetuin-A. Treatment with BAPTA-AM, an intracellular calcium chelating agent, also inhibited the CPP-induced increase in the FM-fetuin-A level. Secondary CPP accelerate posttranslational processing of fetuin-A in HepG2 cells.

Hyperkalemia in chronic heart failure with renal dysfunction or diabetes mellitus: Results from the TREAT HF study.

Chronic kidney disease (CKD) and diabetes mellitus (DM) are common comorbidities in heart failure (HF). Patients with HF are at a high risk of hyperkalemia, and are therefore undertreated with respect to disease-modifying therapies. The Turkish Research Team-Heart Failure (TREAT HF) data were analyzed for the evaluation of hyperkalemia in real-life clinical practice in HF patients with CKD or DM. The TREAT HF is a multicenter, national, observational registry. In this study, potassium levels of 1028 patients with HF were analyzed. Hyperkalemia is defined as blood potassium levels >5 mEq/L and evaluated based on the CKD, DM, HF medications, and New York Heart Association (NYHA) classes. Overall, 14.3% of patients (n=147) were found to have hyperkalemia. Hyperkalemia was more prevalent in patients with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 than those with eGFR ≥60 mL/min/1.73 m2 (17.7% and 12%, respectively, p=0.010). Hyperkalemia was present in 10.9% (n=23) of patients with stage 1, 12.6% (n=50) with stage 2, 17.0% (n=52) with stage 3, and 19.5% (n=22) with stage 4-5 CKD. Hyperkalemia was higher in patients with DM (20.5% vs 12.3%, p=0.001). Furthermore, hyperkalemia was much higher in patients with DM with eGFR <60 mL/min/1.73 m2 (25.2%). The rate of hyperkalemia increased across NYHA categories (NYHA-I: 9.8%, NYHA-II: 12.8%, NYHA-III: 14.4%, and NYHA-IV: 23.4%, p=0.030). In patients with stage 4-5 CKD who were receiving renin-angiotensin-aldosterone system (RAAS) inhibitor therapy, more patients had hyperkalemia than those not receiving RAAS inhibitor therapy (23.4% and 12.5%, respectively). In clinical practice, 14.3% of all patients with HF, 17.7% of all patients with CKD, and 20.5% of all patients with DM have hyperkalemia. The risk of hyperkalemia increases with advanced stages of CKD or NYHA and the risk is higher in patients receiving RAAS inhibitor therapy.

Cardiovascular Disease in Chronic Kidney Disease: Pathophysiological Insights and Therapeutic Options.

Patients with chronic kidney disease (CKD) exhibit an elevated cardiovascular risk manifesting as coronary artery disease, heart failure, arrhythmias, and sudden cardiac death. Although the incidence and prevalence of cardiovascular events is already significantly higher in patients with early CKD stages (CKD stages 1–3) compared with the general population, patients with advanced CKD stages (CKD stages 4–5) exhibit a markedly elevated risk. Cardiovascular rather than end-stage kidney disease (CKD stage 5) is the leading cause of death in this high-risk population. CKD causes a systemic, chronic proinflammatory state contributing to vascular and myocardial remodeling processes resulting in atherosclerotic lesions, vascular calcification, and vascular senescence as well as myocardial fibrosis and calcification of cardiac valves. In this respect, CKD mimics an accelerated aging of the cardiovascular system. This overview article summarizes the current understanding and clinical consequences of cardiovascular disease in CKD.

Approach to stable angina in patients with advanced chronic kidney disease.

Chronic kidney disease is one of the major risk factors for coronary artery disease. Both end-stage renal disease (ESRD) and advanced chronic kidney disease patients have atypical presentations of coronary artery disease (CAD) due to modifications in cardinal symptoms and clinical presentation. Data on evaluation and management of coronary artery or stable angina is limited in advanced chronic kidney disease (CKD) patients due to a limited number of trials. There are sparse data supporting either percutaneous coronary intervention (PCI) or coronary artery bypass graft in advanced CKD patients. The ISCHEMIA-CKD trial to date is the most extensive prospective randomized study looking at advanced CKD patients study looking at advanced CKD stage 4/5 patients randomized to medical treatment alone vs. invasive strategy for moderate to severe myocardial ischemia. There was no evidence found that an initial invasive strategy compared with conservative strategy with maximal medical management resulted in reduced risk of death or nonfatal myocardial infarction in patients with advanced CKD and coronary artery disease with stable angina. In this review, we will discuss the existing data on assessment and management of stable coronary artery disease/stable angina. And how this extrapolates to the application in advanced CKD patients awaiting kidney transplant.

Elderly Patients in a Large Nephrology Unit: Who Are Our Old, Old-Old and Oldest-Old Patients?

The world population is aging, and the prevalence of chronic kidney disease (CKD) is increasing. Whether this increase is also due to the methods currently being used to assess kidney function in the elderly is still a matter of discussion. We aimed to describe the actual referral pattern of CKD patients in a large nephrology unit and test whether the use of different formulae to estimate kidney function could affect the staging and the need for specialist care in the older subset of our population. In 2019, 1992 patients were referred to our center. Almost 28% of the patients were aged ≥80 and about 6% were ≥90 years old. Among the causes of kidney disease, glomerulonephritis displayed a higher prevalence in younger patients whereas hypertensive or diabetic kidney disease were more prevalent in older patients. The prevalence of referred patients in advanced CKD stages increased with age; estimated glomerular filtration rate (eGFR) decreased with age regardless of which equation was used (chronic kidney disease epidemiology collaboration (CKD-EPI), Lund–Malmö Revised (LMR), modification of diet in renal disease (MDRD), Full Age Spectrum (FAS), or Berlin Initiative Study 1 (BIS)). With CKD-EPI as a reference, MDRD and FAS underestimated the CKD stage while LMR overestimated it. The BIS showed the highest heterogeneity. Considering an eGFR threshold limit of 45 mL/min for defining “significant” CKD in patients over 65 years of age, the variability in CKD staging was 10% no matter which equation was used. Our study quantified the weight of “old” and “old-old” patients on follow-up in a large nephrology outpatient unit and suggested that with the current referral pattern, the type of formula used does not affect the need for CKD care within the context of a relatively late referral, particularly in elderly patients.

Bone metabolic disorder and its contributing factors in patients with chronic kidney disease; a three-year cohort study

Introduction: The prevalence of bone mineral disorder is best known in end-stage renal disease (ESRD) patients, but less data is available for the earlier stages. Objectives: We aimed to compare the prevalence of bone metabolic disorder at all stages of chronic kidney disease (CKD) and assess its contribution to CKD progression and patients’ outcome. Patients and Methods: In a retrospective cohort study, CKD patients who were under treatment for three years were selected from a nephrology clinic in Tehran, Iran. Patients’ demographic and laboratory data, as well as the outcome of their treatment were gathered and analyzed. Results: In 473 patients with an average age of 61.5, 60.1% were at stage III, 35.8% were at stage IV, and 4.1% were at stage V of CKD. There was a significant relationship between CKD stage and serum phosphate, calcium-phosphate product, and systolic blood pressure (SBP). Furthermore, the patients’ outcome was significantly related to advanced stages of CKD, higher first phosphate level, diabetes mellitus in medical history, and higher stages of SBP. By multiple Cox regression analysis, after adjustment for glomerular filtration rate (GFR), the first serum phosphate level, and the calcium-phosphate product did not contribute to the undesirable outcome. Conclusion: Although bone metabolic disorder is more frequently seen in advanced stages of chronic kidney disease, these changes can be seen even in earlier stages of the disease. The influence of phosphate abnormality in the patients’ outcome should be studied more in earlier stages for better control.

Improved Awareness of Tuberculosis Infection in Advanced Stage Chronic Renal Disease Could Reduce Cases of Active TB: Lessons from Four Challenging Cases

Patients with chronic kidney disease (CKD) have an increased risk of developing tuberculosis (TB) compared to those with normal renal function. The reasons for this are well described, but include impaired cellular immunity, a high incidence of co-morbid conditions as well as the concomitant use of immunosuppressive medications. Ethnicity as well as socio-economic factors also prevail. Expert guidelines recommend TB chemoprophylaxis in renal transplant recipients deemed at high risk – invariably those from ethnic minorities or recent arrivals from areas with high endemic rates of TB. However, in most renal centres within the UK including our own, high risk patients with advanced CKD (stages 4 and 5) are not routinely screened for latent TB infection (LTBI) prior to transplantation, thus contributing to missed opportunities for preventing TB disease. We report four challenging cases of patients diagnosed with TB disease on a background of advanced CKD, who all presented within an 18-month period whilst under the care of a large tertiary renal centre. Two of the cases were patients with well-functioning renal transplants and two were on renal replacement therapy. We describe our experience and share practical considerations on how to manage TB in CKD including the role of therapeutic drug monitoring in peritoneal dialysis. These cases highlight the need for a better awareness of the possibility of TB reactivation and underscore the arguments in favour of screening programmes for LTBI in patients with advanced CKD.

Cardiovascular calcifications in kidney transplant recipients.

Vascular and valvular calcifications are highly prevalent in kidney transplant recipients (KTRs) and are associated with an increased risk of cardiovascular events, which represent the leading cause of long-term mortality in these patients. However, cardiovascular calcification has been traditionally considered as a condition mostly associated with advanced chronic kidney disease stages and dialysis, and comparatively fewer studies have assessed its impact after kidney transplantation. Despite partial or complete resolution of uraemia-associated metabolic derangements, KTRs are still exposed to several pro-calcifying stimuli that favour the progression of pre-existing vascular calcifications or their de novo development. Traditional risk factors, bone mineral disorders, inflammation, immunosuppressive drugs and deficiency of calcification inhibitors may all play a role, and strategies to correct or minimize their effects are urgently needed. The aim of this work is to provide an overview of established and putative mediators involved in the pathogenesis of cardiovascular calcification in kidney transplantation, and to describe the clinical and radiological features of these forms. We also discuss current evidence on preventive strategies to delay the progression of cardiovascular calcifications in KTRs, as well as novel therapeutic candidates to potentially prevent their long-term deleterious effects.

Association between albuminuria and thyroid function in patients with chronic kidney disease

PurposeThe relationship between proteinuria and thyroid function remains controversial in patients with chronic kidney disease (CKD). We prospectively investigated the association between kidney and thyroid function in thyroid antibody-negative patients through all CKD stages.MethodsWe enrolled 184 nondialysis patients (mean age: 63.1 ± 16.9 years) without previous thyroid disease or thyroid-specific antibodies. Kidney function was assessed by estimating the glomerular filtration rate (eGFR) classified according KDIGO (CKD G1–5). Kidney damage was assessed by albuminuria (albumin-to-creatinine ratio, ACR) and classified as mild, moderate, or severe (ACR1: <300, ACR2: 300–3000, and ACR3: 3000 mg/g). To evaluate thyroid function, TSH, T4, fT4, T3, fT3, reverse T3 (rT3), and thyroxine-binding globulin (TBG) were measured.ResultsrT3 concentrations correlated negatively with albuminuria (r = −0.286, p < 0.001) and were significantly lower in patients with severe albuminuria than in those with mild or moderate albuminuria (ACR3: 0.28 vs. ACR2: 0.32 vs. ACR1: 0.36 nmol/l, p < 0.001). The severity of albuminuria revealed no impact on TSH, fT4, T3, fT3, and TBG. EGFR correlated with increasing T4, fT4, T3, fT3, and TBG (T4: r = 0.289, p < 0.01; fT4: r = 0.196, p < 0.01; T3: r = 0.408, p < 0.01; fT3: r = 0.390, p < 0.01) but not with rT3.ConclusionsIn thyroid antibody-negative patients presenting advanced CKD (stages 4 and 5), even severe kidney protein loss failed to influence thyroid hormone status. However, albuminuria severity correlated negatively with rT3, which was significantly lower in patients with albuminuria in the nephrotic range.

STUDY THE SERUM VITAMIN D LEVELS IN PATIENTS OF CHRONIC KIDNEY DISEASE

INTRODUCTION: Chronic Kidney Disease (CKD) is dened as a disease characterized by alterations in either kidney structure or function or both for a minimum of 3 months duration. Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney 1 function over a period of months or years. Early on there are typically no symptoms. Later, leg swelling, feeling tired, vomiting, loss of appetite, or 1 confusion may develop. Complications may include heart disease, high blood pressure, bone disease, or anemia. AIM AND OBJECTIVES: Study of Prevalence of hypovitaminosis D in patients of chronic kidney diseases. Search for commonest etiology of hypovitaminosis D in CKD. MATERIALAND METHOD: A Cross-sectional study on 100 cases of newly diagnosed Chronic Kidney Disease patients and matched control subjects is undertaken to study the prevalence of Vitamin D deciency in CKD population and correlation between their serum 25-OH-vitamin D level. 100 Patients who are newly diagnosed as CKD are selected after proper initial screening at Midnapore Medical College, Paschim Medinipur. RESULT AND ANALYSIS: Our study showed that in non-dialysis Syndrome the mean VitD (mean± s.d.) of patients was 25.6620 ± 8.5476. In dialysis the mean VitD (mean± s.d.) of patients was 10.9476 ± 2.6508. Difference of mean VitD in Dialysis vs Non-Dialysis was statistically signicant (p&lt;0.0001). In eGFR 1 (&lt;15) the mean VitD (mean± s.d.) of patients was 11.1130 ± 2.9562. In eGFR2 (15-30) the mean VitD (mean± s.d.) of patients was 24.0750 ± 8.2995. In eGFR3 (31-45) the mean VitD (mean± s.d.) of patients was 26.8296 ± 7.3646. In eGFR4 (&gt;45) the mean VitD (mean± s.d.) of patients was 36.3167 ± 4.9898. Difference of mean VitDin eGFR was statistically signicant (p&lt;0.0001). SUMMARYAND CONCLUSION: Vitamin-D deciency more pronounced in advanced stages of CKD. Vitamin-D deciency was most prevalent in female gender, younger age group and connective tissue disorder. Vitamin-D deciency was more marked in hemodialysis patients compared to non-dialysis CKD patients.