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CKD (Chronic Kidney Disease) Case Report

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Open Access

Peer-reviewed

Research Article

A multicentral prospective cohort trial of a pharmacist-led nutritional intervention on serum potassium levels in outpatients with chronic kidney disease: The MieYaku-Chronic Kidney Disease project

Roles Conceptualization, Data curation, Formal analysis, Funding acquisition, Investigation, Methodology, Project administration, Resources, Writing – original draft

* E-mail: [email protected]

Affiliations Department of Pharmacy, Faculty of Medicine, Mie University Hospital, Mie University, Tsu, Mie, Japan, Pharmacy, National Hospital Organization Mie Chuo Medical Center, Tsu, Mie, Japan

Roles Conceptualization, Methodology, Project administration

Affiliation Nutrition Management Office, National Hospital Organization Mie Chuo Medical Center, Tsu, Mie, Japan

Roles Data curation, Investigation, Project administration

Affiliation Mie Pharmaceutical Association Kaiei Hisai Dispensing Pharmacy, Tsu, Mie, Japan

Affiliation Hisai Center Pharmacy, Tsu, Mie, Japan

Roles Conceptualization, Data curation, Investigation, Project administration

Affiliation Konan Pharmacy, Tsu, Mie, Japan

Affiliation Ai Pharmacy Myojin Store, Tsu, Mie, Japan

Affiliation Sugi Pharmacy Hisai Intergarden Store, Tsu, Mie, Japan

Roles Conceptualization, Investigation, Methodology, Project administration

Affiliation Department of Cardiology, National Hospital Organization Mie Chuo Medical Center, Tsu, Mie, Japan

Roles Conceptualization, Data curation, Investigation, Methodology, Project administration

Affiliation Pharmacy, National Hospital Organization Mie Chuo Medical Center, Tsu, Mie, Japan

Roles Conceptualization, Investigation, Methodology, Project administration, Writing – review & editing

Affiliation Mie Pharmaceutical Association, Tsu, Mie, Japan

Roles Conceptualization, Methodology, Project administration, Writing – review & editing

Affiliation Department of Pharmacy, Mie Heart Center Hospital, Taki, Mie, Japan

Roles Conceptualization, Formal analysis, Methodology, Writing – review & editing

Affiliation Department of Pharmacy, Faculty of Medicine, Mie University Hospital, Mie University, Tsu, Mie, Japan

• Yuki Asai, 
• Asami Muramatsu, 
• Tatsuya Kobayashi, 
• Ikuhiro Takasaki, 
• Toshiki Murasaka, 
• Ai Izukawa, 
• Kahori Miyada, 
• Takahiro Okazaki, 
• Tatsuki Yanagawa, 

• Published: May 31, 2024
• https://doi.org/10.1371/journal.pone.0304479
• Peer Review
• Reader Comments

Although dietary potassium restriction is an acceptable approach to hyperkalemia prevention, it may be insufficient for outpatients with chronic kidney disease (CKD). Most outpatients with CKD use community pharmacies owing to the free access scheme in Japan. The MieYaku-CKD project included a community pharmacist-led nutritional intervention for dietary potassium restriction, with the goal of determining its efficacy for patients’ awareness of potassium restriction and serum potassium levels in outpatients with CKD. This was a five-community pharmacy multicenter prospective cohort study with an open-label, before-and-after comparison design. Eligible patients (n = 25) with an estimated glomerular filtration rate (eGFR) < 45 mL/min/1.73 m 2 received nutritional guidance from community pharmacists. The primary outcome was a change in serum potassium levels at 12 weeks post-intervention. The eligible patients’ knowledge, awareness, and implementation of potassium restriction were evaluated using a questionnaire. The median value of serum potassium was significantly reduced from 4.7 mEq/L before to 4.4 mEq/L after the intervention [ p < 0.001, 95% confidence interval (CI): 0.156–0.500], with no changes in eGFR ( p = 0.563, 95% CI: -2.427–2.555) and blood urine nitrogen/serum creatinine ratio ( p = 0.904, 95% CI: -1.793–1.214). The value of serum potassium had a tendency of attenuation from 5.3 to 4.6 mEq/L ( p = 0.046, 95% CI: 0.272–1.114) in the eGFR < 30 mL/min/1.73 m 2 group. A questionnaire revealed that after the intervention, knowledge and attitudes regarding dietary potassium restriction were much greater than before, suggesting that the decrease in serum potassium levels may be related to this nutritional guidance. Our findings indicate that implementing a dietary potassium restriction guidance program in community pharmacies is feasible and may result in lower serum potassium levels in outpatients with CKD.

Citation: Asai Y, Muramatsu A, Kobayashi T, Takasaki I, Murasaka T, Izukawa A, et al. (2024) A multicentral prospective cohort trial of a pharmacist-led nutritional intervention on serum potassium levels in outpatients with chronic kidney disease: The MieYaku-Chronic Kidney Disease project. PLoS ONE 19(5): e0304479. https://doi.org/10.1371/journal.pone.0304479

Editor: Amir Hossein Behnoush, Tehran University of Medical Sciences, ISLAMIC REPUBLIC OF IRAN

Received: November 10, 2023; Accepted: May 11, 2024; Published: May 31, 2024

Copyright: © 2024 Asai et al. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: The raw laboratory data supporting the findings of this study are openly available in repository Mendeley Data at https://data.mendeley.com/datasets/c9kydmj6c2/1 . DOI is 10.17632/c9kydmj6c2.1 .

Funding: This work was supported by grant of Japan Pharmaceutical Association "Yakuzaishi shokuno shinko kenkyu josei jigyo"(grant for research and studies which seek to develop pharmacy profession and function in healthcare and pharmaceutical affairs) (Grant No. jpa2022-03). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

1 Introduction

Hyperkalemia is a life-threatening metabolic problem that can lead to cardiac arrest in extreme cases [ 1 ]. Patients with chronic kidney disease (CKD) often acquire this condition, with an incidence rate of 14–20% in patients with CKD [ 2 ]. Serum potassium levels ≥ 5.5 mEq/L in CKD may be associated with increases in acute- [ 3 ] and long-term [ 4 ] mortality. Therefore, hyperkalemia is the most important adverse event that shortens lifetime in patients with CKD. The mechanism of developing hyperkalemia is attributed to be reduced kidney function because serum potassium is primarily extracted via urine. In fact, during CKD stage 3b [ 5 ], urinary excretion rate is substantially reduced, and the occurrence of hyperkalemia events is elevated [ 3 ]. While the prevalence of hyperkalemia in patients with CKD has recently increased due to increased prescription of renin-angiotensin system inhibitors (RASi) [ 6 , 7 ], discontinuation of RASi [ 8 ], or mineralocorticoid receptor antagonists [ 9 ] due to hyperkalemia may be associated with a higher risk of death and major adverse cardiovascular events; therefore, even drugs that cause hyperkalemia should be continued for the long-term prognosis of patients with CKD.

Dietary potassium restriction is a reasonable approach for preventing hyperkalemia and has been advised for patients with CKD worldwide [ 10 ]. A meta-analysis revealed that dietary potassium restriction can lower serum potassium levels [ 11 ]. However, because of influencing factors that alter serum potassium levels, such as hydration level, acid-base status, glycemic management, and gastrointestinal complications, it is challenging to identify the appropriate potassium intake for specific patients with CKD [ 12 ]. Further complicating potassium restriction is the fact that different foods have different potassium contents [ 13 ], and severe potassium restriction in the diet (restricting vegetable and fruit intake) has been associated with death regardless of CKD stage [ 14 ]. Various lifestyle habits (cigarette smoking, infrequent alcohol consumption, and low physical activity) and characteristics (younger age, higher body mass index, male gender, and lower educational attainment) may be involved in low-adherence to CKD-specific dietary recommendations, including potassium restriction [ 15 ], indicating that guidance regarding potassium restriction needs to be individualized to fit the patient’s lifestyle and characteristics. Therefore, it is crucial that dietary potassium restriction be managed by healthcare workers in conjunction with patients with CKD.

The role of the pharmacist extends beyond dispensing medications and plays an essential role in health promotion and screening [ 16 ]. There are 61,715 community pharmacies in United States, and 48.1% people live within 1 mile of any pharmacy [ 17 ]. Therefore, it goes without saying that community pharmacies are highly accessible healthcare locations for many outpatients with CKD. Hyperkalemia episodes occurred in 47.3% of the outpatients [ 3 ], indicating that community pharmacists can help outpatients with CKD in restricting their potassium intake. To the best of our knowledge, no information exists on the effects of community pharmacist-led nutritional interventions on serum potassium levels in outpatients with CKD, therefore, we hypothesized that the nutritional guidance provided by community pharmacists for outpatients with CKD may be a useful technique for dietary potassium restriction.

The present study aims to investigate the influence of community pharmacist-led nutritional guidance about dietary potassium restriction on the patient awareness and serum potassium levels in outpatients with CKD in a community setting (MieYaku Chronic Kidney [MY-CKD] Project).

2 Martials and methods

2.1 study design.

This was a multicenter prospective cohort study with an open-label, before-and-after comparison design. This study was conducted in five community pharmacies belonging to the Tsu Pharmaceutical Association. Cardiologists, registered dieticians, and pharmacists from the National Hospital Organization Mie Chuo Medical Center (Mie, Japan) participated in this study.

2.2 Participants

Urinary potassium excretion decreases estimated glomerular filtration rate (eGFR) < 45 mL/min/1.73 m 2 in the Japanese population [ 5 ], therefore, the cut-off value for eligible patients with CKD was set at eGFR < 45 mL/min/1.73 m 2 . The inclusion criterion was adult outpatients (age ≥18 years old) at Mie Chuo Medical Center with eGFR < 45 mL/min/1.73 m 2 . As a result, the following patients were excluded from the study: patients (a) below the age of 18, (b) with communication difficulties, (c) with hypokalemia (serum potassium level < 4.0 mEq/L), (d) undergoing hemodialysis, (e) taking potassium preparations, and (f) who received a refill prescription If the patient brought a refill prescription, serum potassium level could not be evaluated because there is no need to visit the Mie Chuo Medical center during or after the 12-week follow-up period. Therefore, “those who received a refill prescription” was set as an exclusion criterion.

2.3 Outcomes

All registered patients were followed up for 12 weeks. The following patients were excluded from the outcome evaluation during the observation period: those with (1) changes in the dosage of drugs affecting serum potassium levels, such as RASi, mineralocorticoid receptor antagonists, loop diuretics, or potassium-binding agents; (2) hemodialysis introduction; and (3) failure to complete the questionnaires at 12 weeks.

The primary outcome was the change in serum potassium levels from baseline (pre-intervention, day 1) to 12 weeks (post-intervention, day 84). eGFR and blood urine nitrogen (BUN)/serum creatinine ratio were assessed as indicators of renal function and hydration [ 18 ], respectively. The development of acute kidney injury (AKI) was elucidated during the 12-week follow-up period. An AKI was defined as an increase of at least 0.3 mg/dL in creatinine within 48 h or a 1.5-fold increase in creatinine, which is known or presumed to have occurred within 7 days [ 19 ]. Additionally, the difference between sodium and chloride levels (Na-Cl) mEq/L as a surrogate marker of metabolic acidosis in the present study [ 20 ]. In a subgroup study, the reduction of serum potassium levels was compared between eGFR < 30 and eGFR ≥ 30 mL/min/1.73 m 2 . Laboratory data were collected from Mie Chuo Medical Center’s elective medical records.

The secondary outcome was the change in patients’ attitudes toward potassium restriction at 12 weeks. Information about the questionnaire survey were listed in the S1 Methods . Questions 1 and 2 inquired about their understanding of hyperkalemia and potassium restrictions, respectively. Questions 3 and 4 were designed to address attitudes toward potassium restriction. Changes in the ratio between pre- and post-intervention were evaluated from questions 1 to 4. In the post-intervention period, questions 5 and 6 were meant to assess future awareness of potassium restriction.

2.4 Adverse event

The systolic and diastolic blood pressures (SBP and DBP) were monitored before and after the intervention. Cases of hypokalemia that required treatment were also collected.

2.5 Pharmacist intervention strategy

The intervention scheme is shown in Fig 1 .

• PPT PowerPoint slide
• PNG larger image
• TIFF original image

CKD, chronic kidney disease. DBP, diastolic blood pressure. SBP, systolic blood pressure.

https://doi.org/10.1371/journal.pone.0304479.g001

2.5.1 Training.

On November 1, 2022, a cardiologist (TO), registered dietician (AM), and pharmacist (YA) gave a seminar to community pharmacists on potassium control in CKD. This educational program included a 60-min classroom session as well as a web-based component. Thirty-six community pharmacists attended the lectures and discussed their participation in the MY-CKD project. The purpose of this training was to standardize the quality of pharmacist interventions and eliminate study bias. Details of the lecture contents are provided in S1 Table .

2.5.2 Intervention.

All the following interventions were implemented at each community pharmacy:

On the first intervention day (day 1), community pharmacists met with patients to describe the goals of the MY-CKD project, how to gather laboratory data, and lifestyle adjustments to avoid dialysis. Using a nutritional guidance sheet, community pharmacists lectured on dietary techniques for potassium restriction ( S1 Fig ). These nutritional guidance documents were mostly prepared by a registered dietician (AM) in consultation with healthcare workers. Following the lecture, a questionnaire was used to assess baseline awareness of potassium restriction, and SBP and DBP were measured at rest. Adherence was assessed if the patient was taking potassium-binding agents.

We continued to monitor the patient for dietary changes, kidney function, and serum potassium levels during the follow-up period.

A questionnaire survey to evaluate the awareness of potassium restriction was conducted 12 weeks after the intervention. SBP and DBP were measured at rest.

2.6 Sample size

In a prior study, nutritional advice for a potassium-restricted diet resulted in a decrease of up to 0.5 mEq/L in serum potassium levels [ 11 ]. The maximum standard deviation for serum potassium levels among individuals has been reported to be 0.8 mmol/L [ 21 ]. With a standard deviation of serum potassium levels of 1.0 mEq/L, and a mean difference of 0.5 mEq/L due to intervention, using a corresponding t-test (α = 0.05 and β = 0.20), the number of cases necessary for the trial was calculated to be n = 34. Although similar reports have not existed, the estimated percentage dropouts over the observation period were set as 15.0% [ 22 ], the target number of registered patients was established as 40.

2.7 Statistical analysis

The Wilcoxon signed-rank test was used to examine differences in continuous variables, such as serum potassium, eGFR, BUN/creatinine ratio, Na-Cl, SBP, and DBP between pre- and post-intervention because respective variables followed a non-normal distribution. In the questionnaire survey, the rate of responses on the 4-point scale were compared pre- and post-intervention for questions 1 to 4, using the McNemar test. The effect size of changes in serum potassium level mediated by this intervention was calculated. All statistical analyses were performed using SPSS Statistics version 27 (IBM Japan, Tokyo, Japan), and the significance level was set at two-sided p < 0.05.

2.8 Ethics approval statement

This study was conducted in accordance with the Ethical Guidelines for Medical and Health Research Involving Human Subjects. The study protocol was approved by the National Hospital Organization, Mie Chuo Medical Center (approval ref. MCERB-202238) and Mie Pharmaceutical Association (approval ref. 2022–3). When community pharmacists referred to the value of eGFR on the prescription issued by Mie Chuo Medical Center, if they met the inclusion criteria, consent to participate in this study was obtained from the patients by each community pharmacist using a written consent document. All data were analyzed anonymously. We registered the protocol for this study in the University Hospital Medical Information Network Clinical Trials Registry (UMIN000049814).

3.1 Characteristics of the participants

Enrolment in the MY-CKD project began on December 28, 2022, with five community pharmacies, and terminated on March 28, 2023. A total of 35 patients with CKD were resistant to treatment. Fig 2 shows that during the observation period, 25 patients were eligible for outcome evaluation based on the exclusion criteria, and the required number of patients was reached.

CKD, chronic kidney disease. RASi, renin-angiotensin system inhibitors.

https://doi.org/10.1371/journal.pone.0304479.g002

The baseline patient characteristics are presented in Table 1 . There were 19 patients (64.0%) who were men, with a median age of 78 and a body mass index of 22.6 kg/m 2 . The median eGFR was 35.0 mL/min/1.73 m 2 (range: 30.5–36.7 mL/min/1.73 m 2 ), which corresponds to the G3b stage. The baseline serum potassium level was 4.7 mEq/L (range: 4.3–5.1 mEq/L), which was close to the upper reference limit. While all patients cooked largely for themselves, only 8.0% (n = 2) requested advice from registered dietitians. Medication was self-managed by 80.0% of respondents. Only 12.0% (n = 3) of patients were taking potassium-binding agents.

https://doi.org/10.1371/journal.pone.0304479.t001

3.2 Outcomes

Fig 3A shows that the median value of serum potassium significantly decreased from 4.7 mEq/L before intervention to 4.4 mEq/L post-intervention [ p < 0.001, 95% confidence interval (CI): 0.156–0.500], and its effect size was -0.67. In contrast, eGFR ( p = 0.563, 95%CI: -2.427–2.555) ( Fig 3B ) and BUN/creatinine ratio ( p = 0.904, 95%CI: -1.793–1.214) ( Fig 3C ) did not change. In addition, the developed AKI was not observed during the 12-week follow-up period. There was no significant difference in the value of Na-Cl between pre- and post-intervention ( p = 0.377, 95%CI: -1.324–0.444). In subgroup analysis, serum potassium levels had a tendency of attenuation in the eGFR < 30 mL/min/1.73 m 2 group (n = 6), from 5.3 mEq/L to 4.6 mEq/L ( p = 0.046, 95%CI: 0.272–1.114) ( Fig 4A ). On the other hand, patients with eGFR ≥ 30 mL/min/1.73 m 2 showed a significant decrease in serum potassium levels ( p = 0.009, 95%CI: 0.057–0.364) ( Fig 4B ).

Effect of nutritional intervention on (A) serum potassium levels, (B) eGFR, and (C) BUN/creatinine ratio. The number of patients included in the analysis of each parameter was 25. BUN, blood urine nitrogen; eGFR, estimated glomerular filtration rate. The differences in respective variables between pre- and post-intervention were compared using the Wilcoxon signed-rank test.

https://doi.org/10.1371/journal.pone.0304479.g003

Changes in serum potassium levels in (A) eGFR < 30 mL/min/1.73 m 2 and (B) eGFR ≥ 30 mL/min/1.73 m 2 . The number of patients in eGFR < 30 mL/min/1.73 m 2 and eGFR ≥ 30 mL/min/1.73 m 2 were six and 19, respectively. eGFR, estimated glomerular filtration rate. The differences in respective variables between pre- and post-intervention were compared using the Wilcoxon signed-rank test.

https://doi.org/10.1371/journal.pone.0304479.g004

The percentage of responses changed significantly for all questions ( Fig 5 ). For questions 1 and 2, no patients answered "Not at all" when asked about their understanding of the risk of hyperkalemia and potassium-rich foods ( p < 0.001). Concerning routine potassium restriction awareness (question 3), the percentage of “Every time” increased ( p = 0.143), while the percentage of “Not at all” decreased ( p = 0.008). For question 4, “Is it bothersome to be aware of your potassium intake?” the percentages who replied “Not at all” ( p < 0.001) and “Not much” ( p = 0.012) decreased, while the percentage who answered “Slightly” ( p = 0.136) and “Extremely” increased ( p = 0.122). "Frequently" was the most prevalent response to the question “Has this guidance made you more careful about your intake of foods containing potassium?”, (56.0%, 14/25), followed by “Not that much,” “Sometimes,” and “Not at all.” Finally, 68.0% (17/25) of respondents claimed they will continue to avoid consuming potassium-containing foods in the future.

The number of patients that responded to each question of the questionnaire was 25. The rate of responses on the 4-point scale were compared pre- and post-intervention for question 1 to 4, respectively, using the McNemar test.

https://doi.org/10.1371/journal.pone.0304479.g005

3.3 Adverse event

Although the SBP and DBP of the six patients could not be followed in post-intervention, there were no significant changes in the median values of SBP or DBP following intervention ( S2 Fig ). Furthermore, there were no cases of hypokalemia requiring potassium supplementation.

4 Discussion

In the present study, serum potassium levels decreased without any changes in hydration levels, kidney function, or developing AKI. Furthermore, patients who underwent dose modification with concomitant drugs that affected serum potassium levels were excluded, suggesting that the decrease in serum potassium levels could be attributed to nutritional guidance. The results of our questionnaire survey also support this hypothesis.

Although hyperkalemia is commonly defined as serum potassium levels ≥ 5.5 mEq/L, levels > 5.0 mEq/L have been linked to an increased risk of mortality in CKD stages 4–5 [ 23 ]. The reduction of serum potassium levels to less than 5.0 mEq/L in patients with eGFR < 30 mL/min/1.73 m 2 may help improve the prognosis of CKD patients; therefore, stricter control of serum potassium levels is required in the CKD stage of the patients in this study.

Patient knowledge of CKD is often minimal, with only 26.5% of patients with an eGFR < 60 mL/min/1.73 m 2 reporting awareness [ 24 ]. Moreover, even among hemodialysis patients, the level of knowledge acquisition regarding potassium restriction was poor [ 25 ]. Following the current nutritional intervention, 0.0% of patients answered "Not at all" when asked about the risk of hyperkalemia and foods with high potassium content ( Fig 5 ), indicating increased knowledge among patients with CKD. Terlizzi et al. [ 26 ] found that multidisciplinary team support could help patients maintain a healthy nutritional status while delaying dialysis. The MY-CKD project’s strengths were that community pharmacists learned the basics through lectures from cardiologists, registered dietitians, and hospital pharmacists ( S1 Table ), and community pharmacists then passed on their knowledge to patients with CKD. Additionally, community pharmacists shared the goal of lowering serum potassium levels in patients with CKD, and constant follow-up on cooking procedures for potassium reduction was deemed important during the observation period. As all patients enrolled in this trial cooked for themselves ( Table 1 ), this intervention strategy may result in a change in attitude toward routine potassium restriction. However, the percentage of patients with problematic potassium restriction increased ( Fig 5 ). The MY-CKD project is thought to have provided the patient with information about the pathogenesis of CKD and potassium restriction. However, this may lead to patients needing nutritional management.

It is well-known that potassium intake is responsible for the dose-dependent reduction of blood pressure [ 27 ]. However, severe potassium restriction may cause blood pressure fluctuation in patients with CKD [ 28 ]. Therefore, the effect of dietary potassium restriction on SBP and DBP was classified as a negative event in this study. Neither SBP nor DBP changed significantly after the intervention ( S2 Fig ), suggesting that the degree of potassium restriction had no effect on blood pressure.

Our study had several limitations. First, the long-term persistence of the dietary potassium restriction could not be determined. Second, because the sample size was limited, and required sample size could not be reached, there could be unexplained confounding factors, such as patient selection bias. Third, in patients with eGFR < 60 mL/min/1.73 m 2 in Japan, the frequency of hyperkalemia was considerably higher in the winter (December–February) than that in the summer (June–August) [ 29 ]. Seasonal changes may have had an impact on 52.0% (13/25) of patients whose observation end date was in summer, indicating that seasonal variations cannot be ruled out. Fourth, the efficiency of this intervention strategy in patients undergoing hemodialysis remains unknown. Fifth, although the quality of the intervention method may be elevated with the participation of nephrologists, the National Hospital Organization Mie Chuo Medical Center did not have staff nephrologists. Therefore, it was considered necessary to construct a project with the participation of nephrologists in future investigations. Sixth, because the questionnaire used in the present study was developed originally, the relationship between changes in awareness/knowledge and specific dietary changes through questionnaires was not validated. Therefore, the extent to which the patients’ diets have changed by the present questionnaire would not be fully evaluated. Finally, because this study only included patients with CKD who were outpatients at a secondary hospital in Japan, the impact on patients who attended hospitals with different characteristics, such as tertiary hospitals or clinics, is unknown. A cluster-randomized controlled study in Japan found that a lifestyle advising program in community pharmacies can lower SBP [ 30 ] and hemoglobin A1c [ 31 ]. Given these limitations and evidence, a cluster-randomized controlled design with long-term follow-up of potassium restriction is needed to evaluate the variability in serum potassium levels when patients are supported by community pharmacists.

CKD is one of the most important global public health problems that shortens the lifetime by increasing the requirement for dialysis treatment and risk of cardiovascular events [ 32 ]. The number of community pharmacies in Japan is comparable to those in the United States [ 17 , 33 ], therefore, the evidence from the MY-CKD project of dietary potassium restriction by community pharmacist will provide great benefit for patients with CKD. Therefore, the present intervention strategy may serve as a model case in the world for nutritional guidance provided to CKD patients by community pharmacists.

5 Conclusion

This is the first study to show that a community pharmacist-led nutritional intervention mediated through the MY-CKD project improves dietary potassium restriction attitudes and lowers serum potassium levels in patients with CKD. Although few studies have demonstrated the benefits of community pharmacist activities in practice, the implementation of nutritional interventions, such as potassium restriction, for patients with CKD by educated community pharmacists certainly contributes directly to the improvement of community populations’ health.

Supporting information

S1 checklist. consort checklist..

https://doi.org/10.1371/journal.pone.0304479.s001

S2 Checklist. STROBE statement—checklist of items that should be included in reports of cohort studies .

https://doi.org/10.1371/journal.pone.0304479.s002

S1 File. Study protocol in English.

https://doi.org/10.1371/journal.pone.0304479.s003

S2 File. Study protocol in Japanese.

https://doi.org/10.1371/journal.pone.0304479.s004

S1 Methods. The questionnaire contents in MY-CKD project.

https://doi.org/10.1371/journal.pone.0304479.s005

S1 Table. Lecture contents in the MY-CKD project.

https://doi.org/10.1371/journal.pone.0304479.s006

S1 Fig. The nutritional guidance document of MY-CKD project.

https://doi.org/10.1371/journal.pone.0304479.s007

Changes in (A) SBP and (B) DBP by dietary potassium restriction. The number of patients in pre-intervention and in post-intervention were 25 and 19, respectively. DBP, diastolic blood pressure. SBP, systolic blood pressure. CI, confidence interval. The differences in respective variables between pre- and post-intervention were compared using the Wilcoxon signed-rank test.

https://doi.org/10.1371/journal.pone.0304479.s008

Acknowledgments

We thank Tomoharu Hasebe, Hiroya Inui, Chie Suezawa, Zyun Niato, Akira Sato, Yuji Nakagawa, Yuko Niimi, Yasuki Ogino, Hiroki Sugino, Ryota Kobayashi, Yoshihiro Kinoshita, Takahiro Fukuyama, Koji Terada, Shinichi Maegawa, Kosuke Miyachi, Tomohiko Aoki, Taisuke Matsumuro, and Nobuyuki Nakagawa for their institutional enrollment in the MY-CKD project.

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• 19. Kidney Disease Improving Global Outcomes: KDIGO Clinical Practice Guideline for Acute Kidney Injury. Section 2: AKI Definition. 2012. [Cited 2024 Feb 10]. Available from: https://kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-Guideline-English.pdf .
• 33. Ministry of Health, Labour and Welfare. First Working Group on the Work of Pharmacy Pharmacists and the Functions of Pharmacies. [Cited 2023 Oct 7]. Available from: https://www.mhlw.go.jp/content/11121000/000896856.pdf

Chronic Kidney Disease

Nov 27, 2014

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Chronic Kidney Disease. Progressive, irreversible damage to the nephrons and glomeruli. Chronic Kidney Disease. Major causes are. Diabetes and high blood pressure Type 1 and type 2 diabetes mellitus High blood pressure (hypertension) Glomerulonephritis Polycystic kidney disease

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• kidney disease
• fluid removal
• urine tests
• high blood pressure
• blood compartment decrease pressure

Presentation Transcript

Progressive, irreversible damage to the nephrons and glomeruli Chronic Kidney Disease

Major causes are • Diabetes and high blood pressure • Type 1 and type 2 diabetes mellitus • High blood pressure (hypertension) • Glomerulonephritis • Polycystic kidney disease • Use of analgesics - acetaminophen(Tylenol) and ibuprofen (Motrin, Advil • Clogging and hardening of the arteries(atherosclerosis)  • Obstruction of the flow of urine by stones, an enlarged prostate, strictures (narrowings), or cancers.  • HIV infection, sickle cell disease, heroin abuse, amyloidosis, kidney stones, chronic kidney infections, and certain cancers.

Kidney functions - monitored regularly • Diabetes mellitus type 1 or 2  • High blood pressure  • High cholesterol • Heart disease • Liver disease  • Amyloidosis  • Sickle cell disease  • Systemic Lupus erythematosus  • Vascular diseases such as arteritis, vasculitis, or fibromuscular dysplasia  • Vesicoureteral reflux (a urinary tract problem in which urine travels the wrong way back toward the kidney)  • Require regular use of anti-inflammatory medications  • A family history of kidney disease

Protein and waste metabolism accumulates in the blood (azotemia) 90% of kidney function is lost (kidney cannot adequately function) Hypothesis: Nephrons remains intact, others progressively destroyed. Adaptive response maintains function until ¾ are destroyed Hypertrophy continues kidneys begin to lose their ability to concentrate the urine adequately Chronic Renal FailureEnd Stage Renal Disease (ESRD)

Table 1. Stages of Chronic Kidney Disease *GFR is glomerular filtration rate, a measure of the kidney's function.

Modifiable Factors -Diabetic Mellitus -Hypertension -Increase Protein and Cholesterol Intake -Smoking -Use of analgesics Non-Modifiable Factors -Hereditary -Age greater than 60 years old -Gender -Race Decreased renal blood flow Primary kidney disease Damage from other diseases Urine outflow obstruction Chronic Kidney Disease - Pathophysiology BUN Serum Creatinine Decreased glomerular filtration Hypertrophy of remaining nephrons Dilute Polyuria Loss of Sodium in Urine Hyponatremia Inability to concentrate urine Dehydration Further loss of nephron function Loss of nonexcretory renal function 2a Failure to convert inactive forms of calcium Failure to produce eryhtropoietin Impaired insulin action Production of lipids Immune disturbances Disturbances in reproduction Erratic blood glucose levels Advanced atherosclerosis Anemia Pallor Calcium absorption Delayed wound healing Infection Libido Infertility 1

2a 1 Hypocalcemia Osteodystrophy Loss of excretory renal function Excretion of nitrogenous waste Decreased sodium reabsorption in tubule Decreased potassium excretion Decreased phosphate excretion Decreased hydrogen excretion Uremia Hyperkalemia Hyperphosphatemia Metabolic acidosis Water Retention BUN, Creatinine Uric Acid Decreased calcium absorption Hypertension Heart Failure Edema Proteniuria Hypocalcemia Peripheral nerve changes Hyperparathyroidism Decreased potassium excretion Pericarditis Increased potassium CNS changes Pruritus Altered Taste Bleeding Tendencies

Weakness and tiredness/ fatigue. • Nocturia is often an early symptom • Itchiness of the skin which can progressively worsen • Pale skin which is easily bruised • Muscular twitches, cramps and pain • Pins and needles in the hands and feet • Nausea

As the condition worsens the symptoms progress to: • Oedema (swelling of the face, limbs and abdomen) • Oliguria (greatly reduced volume of urine) • Dyspnoea (breathlessness) • Vomiting • Confusion • Seizures • Severe lethargy • Very itchy skin • Breath that smells of ammonia

Associated complications of chronic Kidney Disease would be: • Anaemia, mostly due to deficiency of erythropoietin • Bleeding which is caused by impairment of platelet function • Metabolic Bone Disease (known as Renal Osteodystrophy)

Associated complications of chronic Kidney Disease would be: • Cardiovascular Disease - hypertension, (which may further exacerbate the renal failure) -accelerated atherosclerosis -pericarditis. 80% of those with chronic renal failure develop hypertension which must be treated

Associated complications of chronic Kidney Disease would be: • Nervous system – neuropathy caused by the loss of myelin from nerve fibres – may improve when dialysis is established • Gastrointestinal complications - anorexia, nausea and vomiting, and a higher incidence of peptic ulcer disease

Associated complications of chronic Kidney Disease would be: • Skin disease – itching, which is attributed to the retention of metabolic waste products. It often improves with dialysis. Dry skin can also occur • Muscle dysfunction - myopathy leading to muscle cramps and the “restless leg” syndrome

Associated complications of chronic Kidney Disease would be: • Metabolic dysfunction - involving lipids, insulin and uric acid (gout). Metabolic acidosis is also associated

Diagnosis • Urine Tests • Urinalysis • Twenty-four hour urine tests  • Glomerular filtration rate (GFR) • Blood Tests • Creatinine and urea (BUN) in the blood • Estimated GFR (eGFR) • Electrolyte levels and acid-base balance   • Blood cell counts  • Other tests • Ultrasound: • Biopsy

Decrease fluid 1000ml/day Decrease protein (.5-1kg body weight) Decrease sodium (1-4gm variable) Decrease potassium Decrease phosphorous (<1000mg/day) Dialysis (periotoneal, hemodialysis) RBC, Vitamin D (calcitrol replacement) etc. Treatment Modalities

General Principal: Movement of fluid and molecules across a semi permeable membrane from one compartment to another Hemodialysis – Move substances from blood through a semi permeable membrane and into a dialysis solution (dialysate –bath) (synethetic membrane) Peritoneal – Peritoneal membrane is the semi permeable membrane Dialysis Hemodialyis(Hemo)Peritoneal (PD)

Diffusion - movement of solutes (particles) from an area of > concentration to area of < concentration [Remove urea, creatinine, uric acid and electrolytes, from the blood to the dialystate bath] RBC, WBC, Large plasma proteins do not go through Ultrafiltration – Water and fluid removed when the pressure gradient across the membrane is created, by increase pressure in the blood compartment & decrease pressure in the dialysate compartment Osmosis-Diffusion-Ultrafiltration Osmosis - movement fluidfrom an area of< to > concentration of solutes(particles)

Catheter placement – anterior abdominal wall Tenckoff (25cm length with cuff anchor and migration) Dialysis solution (1-2 liters sometimes smaller) Three phases of PD Inflow (fill) approximately 10 minutes, could be in cycles) Dwell (equilibration) (approximately 20-30 min or 8 hours+) Drain (approximately 15 minutes) These 3 phases are called Exchanges Peritoneal Dialysis

Peritoneal Dialysis

Vascular access for high blood flow Shunts, (teflon, external) Arteriovenous fistulas and grafts (AV) Anastomosis between an artery and vein Fistulas are native vessels (4-6 wks maturity) Grafts are artificial/synthetic material Hemodialysis

Hemodialysis AV Fistula Communication AV Graph Access

Hemodialysis Hemodialysis Circuit Hemodialysis Machine

Immediate initiation Less complicated Portable (CAPD) Fewer dietary restrictions Short training time Less cardio stress Choice for diabetics Bacterial/chemical peritonitis Protein loss Exit site of catheter Self image Hyperglycemia Surgical placement of catheter Multiple abdominal surgery PD Advantages and Disadvantages Advantages Disadvantages

Rapid fluid removal Rapid removal of urea & creatinine Effective K+ removal Less protein loss Lower triglycerides Home dialysis possible Temporary access at the bedside Vascular access problems Dietary & fluid restrictions Heparinization Extensive equipment Hypotension Added blood lost Trained specialist Hemo Advantages & Disadvantages Advantages Disadvantages

Fluid removal and decrease in BUN during hemodilaysis which cause changes in blood osmolarity.These changes trigger a fluid shift from the vascular compartment into the cells. In the brain, this can cause cerebral edema, resulting in increase intracranial pressure and visible signs of decreasing level of consciousness. Symptoms: Sudden onset of headache, nausea and vomiting, nervousness, muscle twitching, palpitation, disorientation and seizures Treatment: Hypertonic saline, Normal saline Disequalibrium Syndrome

The following are general dietary guidelines:  • Protein restriction: • Salt restriction • Fluid intake: • Potassium restriction: • Phosphorus restriction: • Control blood pressure and/or diabetes;  • Stop smoking; and • Lose Excess Weight

Avoided or used with caution: • Certain analgesics: Aspirin; ibuprofen • Fleets or phosphosoda enemas because of their high content of phosphorus  • Laxatives and antacids containing magnesium and aluminum such as magnesium hydroxide • Ulcer medication H2-receptor antagonists: cimetidine, ranitidine • Decongestants such as pseudoephedrine  especially if they have high blood pressure  • Herbal medications

Weigh before & after Assess site before & after (bruit, thrill, infection, bleeding etc.) Medications (precautions before & after) Vital signs before and after etc. Nursing Care Pre, Post Dialysis

Living and Cadaveric donors Predialysis: obtain a dry weight free of excess fluids and toxins More preparation time from a living donor vs. cadaveric – transplant within 36 hours of procurement Delay may increase ATN Pre-transplant: Immunotherapy (IV methylprednisolone sodium succinate, (A –methaPred, Solu-Medrol), cyclosporine (Sandimmune and azathioprine ((Imuran) Renal Transplant

Rejection is a major problem Hyperacute rejection: occurs within minutes to hours after transplantation Renal vessels thrombosis occurs and the kidney dies There is no treatment and the transplanted kidney is removed Complications Post Transplant

Done to minimize the destruction (rejection) of the transplanted kidney HUMAN LEUKOCYTE ANTIGEN (HLA) This gives you your genetic identity (twins share identical HLA) HLA compatibility minimizes the recognition of the transplanted kidney as foreign tissues. Immunological Compatibility of Donor and Recipient

WHITE CELL CROSS MATCH (the recipient serum is mixed with donor lymphocytes to test for performed cytotoxic (anti-HLA) antibodies to the potential donor kidney A positive cross match indicates that the recipient has cytotoxic antibodies to the donor and is an absolute contraindication to transplantation Immunological Analysis

MIXED LYMPHOCYTE CULTURE The donor and recipient lymphocytes are mixed. Result = HIGH SENTIVITY, this is contraindicated for renal transplantation. ABO BLOOD GROUPING ABO blood group must be compatible Immulogical Analysis

LLQ of the abdomen outside of the peritoneal cavity Renal artery and vein anastomosed to the corresponding iliac vessels Donor ureters are tunneled into the recipients’ bladder. Surgery

Acute Rejection: occurs 4 days to 4 months after transplantation It is not uncommon to have at least one rejection episode Episodes are usually reversible with additional immunosuppressive therapy (Corticosteroids, muromonab-CD3, ALG, or ATG) Signs: increasing serum creatinine, elevated BUN, fever, wt. gain, decrease output, increasing BP, tenderness over the transplanted kidneys Complications Post Transplant

Chronic Rejection: occurs over months or years and is irreversible. The kidney is infiltrated with large numbers of T and B cells characteristic of an ongoing , low grade immunological mediated injury Gradual occlusion renal blood vessels Signs: proteinuria, HTN, increase serum creatinine levels Supportive treatment, difficult to manage Replace on transplant list Complications Post Transplant

Infection Hypertension Malignancies (lip, skin, lymphomas, cervical) Recurrence of renal disease Retroperiotneal bleed Arterial stenosis Urine leakage Complications Post Transplant

100 patients with eGFR < 60 (Tuesday morning in Outpatients)

Tuesday morning 1 year later: 1 patient needs RRT, 10 patients have died (> 50% CV death)

Tuesday morning 10 years later: 8 patients need RRT, 65 patients have died, 27 have ongoing CKD

The majority of patients with CKD 1-3 do not progress to ESRF. Their risk of cardiovascular death is higher than their risk of progression.

Cardiovascular disease Proteinuria Hypertension Diabetes Smoking Obesity Exercise tolerance Optimise risk factors TAKE HOME MESSAGE

Nursing Care Plan of a Patient With ESRD • Nursing diagnosis: Excess fluid volume related to decreased urine output, dietary excesses, and retention of sodium and water. • Goal: Maintenance of ideal body weight without excess fluid.

Assess fluid status (Daily weight, intake and output balance, skin turgor and presence of edema, distention of neck veins, blood pressure, pulse rate, and rhythm, respiratory rate and effort). • Limit fluid intake to prescribed volume. • Identify potential sources of fluid (medications and fluids used to take medications; oral and intravenous, foods). • Explain to patient and family rationale for restriction.

Nursing Care Plan of a Patient With ESRD (Cont…) • Nursing diagnosis: Imbalanced nutrition; less than body requirements related to anorexia, nausea, vomiting, and dietary restrictions. • Goal: Maintenance of adequate nutritional intake.

Interventions: The nurse should: • Assess nutritional status (weight changes, serum electrolyte, BUN, creatinine, protein, transferrin, and iron levels). • Assess patient’s nutritional dietary patterns (diet history, food preferences, calorie counts). • Assess for factors contributing to altered nutritional intake (Anorexia, nausea, or vomiting, diet unpalatable to patient, depression, lack of understanding of dietary restrictions, stomatitis). • Provide patient’s food preferences within dietary restrictions. • Promote intake of high biologic value protein foods

Nursing Care Plan of a Patient With ESRD (Cont…) • Nursing diagnosis: Deficient knowledge regarding condition and treatment. • Goal: Increased knowledge about condition and related treatment.

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