Organizational support, training and equipment are key determinants of burnout among dialysis healthcare professionals during the COVID-19 pandemic.

INTRODUCTION: Burnout was already found to be an important factor in the professional landscape of nephrology prior to the COVID-19 outbreak and is expected to worsen during the pandemic. OBJECTIVES: The aim of our study was to assess pandemic experiences, perceptions, and burnout among Polish dialysis unit professionals in the COVID-19 period. PARTICIPANTS AND METHODS: A survey, which consisted of a Pandemic Experiences and Perceptions Survey (PEPS) and a Maslach Burnout Inventory was distributed online to Polish dialysis units. The study group comprised 379 participants (215 nurses, 148 physicians, and 16 respondents of other professions). RESULTS: The pandemic largely affected or completely dominated the work of dialysis units according to 53.4% and 25.5% of nurses responding to the PEPS, respectively. Among physicians, the prevalence was 55.5% and 15.4% of participants, respectively. Serious or life-threatening risk was perceived by 72.1% and 11.9% of dialysis healthcare professionals, respectively. Furthermore, 74.6% of the study participants stated that their work in a dialysis setting amidst the pandemic was felt to be associated with serious risk for their relatives. Adequate personal protective equipment and information from management decreased burnout among dialysis staff. Burnout was lower in all dimensions among those participants who felt more in control of their exposure to infection, provided by proper training, equipment, and support (p = 0.0004 for emotional exhaustion, p = 0.0007 for depersonalization, and p < 0.0001 for feelings of personal accomplishment). CONCLUSIONS: The COVID-19 pandemic has largely affected the work in dialysis units. Providing proper training, equipment, and support may decrease burnout among dialysis staff.

Vitamin D Metabolites, Body Composition, and Nutritional Status in Patients in the Long Term After Kidney Transplantation.

BACKGROUND The aim of the study was to assess the relationship between body composition and nutritional status with the level of vitamin D metabolites 25(OH)D and 1,25(OH)2D in patients in the long term after kidney transplantation (KTx). MATERIAL AND METHODS During 2 routine outpatient visits in summer and winter, the anthropometric and body composition measurements and laboratory data from 105 stable KTx patients were taken and the annual averages were analyzed. RESULTS Data of 64 patients (26 F, 38 M) at mean age 49.3±12.2 years and 5.6±2.7 years after KTx with mean BMI 26.9 kg/m² were included for final analysis. Mean annual 25(OH)D concentration was 18.76±6.32 ng/dl and 1,25(OH)2D 86.65±18.0 pg/ml. A reverse relationship between 25(OH)D level and fat tissue index was observed (r=-0.26; P=0.039). 25(OH)D level increased together with body cell mass (r=0.30, P=0.017) and lean tissue mass values (r=0.30, P=0.015). The body weight and BMI were not associated with 25(OH)D or 1,25(OH)2D level. A reverse relationship was found between: 25(OH)D and total cholesterol (r=-0.31, P=0.012) and LDL level (r=-0.25, P=0.049), and between 1,25(OH)2D and HDL level (r=-0.25, P=0.046). No significant correlations between biochemical nutritional parameters, graft function and 25(OH)D or 1,25(OH)2D were noted. CONCLUSIONS Body composition is one of the factors affecting the vitamin D status in KTx patients. Fat tissue index is a negative predictor of 25(OH)D level in patients in the long term after KTx. A low level of 25(OH)D predisposes to lipids disturbances in KTx recipients.

Different Effects of Empagliflozin on Markers of Mineral-Bone Metabolism in Diabetic and Non-Diabetic Patients with Stage 3 Chronic Kidney Disease.

Background and objectives: Treatment with sodium-glucose co-transporter 2 (SGLT2) inhibitors decrease tubular reabsorption of phosphate, which may explain the reduction of bone mineral density and an excess of bone fractures observed in some studies with this class of drugs. Since an increased risk of bone fractures may also be a result of diabetes itself, our study aimed to compare the effect of empagliflozin on the markers of mineral-bone metabolism between diabetic (DKD) and non-diabetic (ND-CKD) patients with stage 3 chronic kidney disease (CKD). Materials and Methods: Forty-two patients with stage 3 CKD and A2 albuminuria, including 18 with DKD and 24 ND-CKD, were investigated. All subjects received 10 mg empagliflozin for 7 days. Serum calcium, phosphate, parathormone (PTH), calcitriol, bone alkaline phosphatase (BAP), FGF-23 and urine calcium, phosphate, albumin and the renal tubular maximum reabsorption rate of phosphate to the glomerular filtration rate (TmP-GFR) were measured before and after empagliflozin administration. Differences in biomarkers response to empagliflozin between DKD and ND-CKD were the main measures of outcome. Results: There was a significant increase of PTH, FGF-23 and phosphate in DKD but not in ND-CKD whereas BAP and TmP/GFR did not change in either group. The reduction of albuminuria was only significant in ND-CKD. Conclusions: The effect of SGLT2 inhibitor on serum mineral and bone markers and on albuminuria in patients with CKD may be differently modified by the presence of diabetes mellitus.

Different Effect of Lanthanum Carbonate and Sevelamer Hydrochloride on Calcium Balance in Patients with Moderate to Advanced Chronic Kidney Disease.

OBJECTIVE: Opposite to lanthanum carbonate (LC), sevelamer hydrochloride (SH) may increase intestinal calcium absorption. The study compared the effects of LC and SH on serum and urine phosphate and calcium, and on hormones regulating mineral-bone metabolism. PATIENTS AND METHODS: A prospective randomized crossover study included 34 patients with eGFR <60 mL/min. A single oral dose of LC (1,000 mg) or SH (2,400 mg) was administered in random order 15 minutes after a standardized meal fortified with 5 g calcium carbonate. Serum calcium, phosphate, and parathormone were measured before and 3, 6, 12, and 24 hours after each medication. Bone alkaline phosphatase (BAP), sclerostin, calcitriol, and FGF-23 were measured at baseline and after 12 and 24 hours. A 24-hour calcium and phosphate excretion was measured after each drug. RESULTS: Serum calcium increased 3 and 6 hours after SH then returned to baseline. After LC calcium was unchanged for up to 3 hours then transiently increased and eventually returned to baseline. The area under curve (AUC) of serum calcium for 12 hours after SH was larger than after LC (p=0.04). Serum phosphate decreased after each drug with a nadir 3 hours post-SH and 6 hours post-LC. AUC of serum phosphate was similar after both medications. PTH decreased transiently after both drugs. BAP did not change. FGF-23 was constant for the first 12 hours but later decreased after each drug. CONCLUSION: A 2,400 mg SH and 1,000 mg LC are similarly effective in lowering serum phosphate in CKD, but LC induce in less intestinal calcium absorption after a meal. The trial was registered on February 23, 2018 in the clinicaltrial.gov database - NCT03451019.

Varying Patterns of Biomarkers of Mineral and Bone Metabolism After Kidney Transplantation.

Sclerostin inhibits Wnt/ß-catenin signaling pathway, thereby decreasing bone formation. Osteoblast stimulating actions of parathyroid hormone (PTH) are mediated by suppression of sclerostin. Thus, sclerostin may reflect both bone metabolism and parathyroid function. The study was aimed to analyze the patterns of the changes of mineral and bone biomarkers for 9 months following kidney transplantation (KTx). Thirty-five patients after KTx were included into a 9-month observational study. Serum creatinine, calcium, phosphorus, 25-OH vitamin D, PTH, fibroblast growth factor 23 (FGF-23), sclerostin, and bone-specific alkaline phosphatase (BAP) were measured before KTx, and 1, 2 weeks, and 1, 2, 3, 4, 5, 6, and 9 months thereafter. Urine sclerostin/creatinine ratio was assessed in parallel from month 1 after KTx. Following KTx most serum markers significantly decreased till the end of observation including PTH (by 58%), phosphorus (37%), sclerostin (31%), BAP (28%), and FGF-23 (82%). Most of the decrease was observed during first 2 months after KTx. Serum calcium was increased by 17%. Urine sclerostin/creatinine ratio increased from month 1 till month 6. At KTx serum FGF-23 correlated only with phosphate (r=0.62, p=0.01) and PTH with BAP (r=0.49, p=0.04) but not with sclerostin. At the end of the study neither serum sclerostin nor FGF-23 correlated with other parameters of mineral and bone metabolism. Sclerostin shows the limited utility as the marker of the resolution of bone and mineral metabolism after KTx.

Prescription-medication sharing among family members: an unrecognized cause of a serious drug adverse event in a patient with impaired renal function.

Many medications need to be avoided in chronic kidney disease (CKD) because of increased toxicity. Metformin - an oral hypoglycemic drug universally recommended as the first-line treatment for type 2 diabetes mellitus (T2DM) - undergoes significant accumulation in advanced CKD that may ultimately lead to lactic acidosis. Recently, it has been found that side effects of the therapy may occasionally neither be linked to improper prescription nor lack of dose adjustment by the physician, but can result from borrowing and sharing of drugs with relatives and friends. This poorly recognized problem has never been studied in renal patients. This work contains a discussion on the diagnostic problems associated with proper diagnosis of the etiology of severe acidosis in an elderly woman with advanced CKD and diabetes. The patient developed severe lactic acidosis by taking metformin that was prescribed by another doctor to her son, who was also diabetic. The diagnosis of lactic acidosis was delayed since the initial laboratory assessments had focused mostly on dehydration and substance abuse.

A comparison of the antihypertensive and anti-inflammatory effects of aliskiren and ramipril add-on therapy in peritoneal dialysis patients--a pilot open label study.

Most hypertensive dialysis patients are currently treated with angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB). Aliskiren, the direct renin inhibitor, has not been specifically studied in peritoneal dialysis patients. The aim of the study was to compare hypotensive effects of aliskiren and ramipril and their influence on serum potassium and inflammatory parameters in hypertensive peritoneal dialysis patients. Eighteen hypertensive patients on chronic peritoneal dialysis were enrolled in an open-label comparative fixed-order study. The patients had been off RAAS blocking drugs for ≥4 weeks prior to an inclusion. At each of 3 study visits (baseline and after each of the treatment periods) blood pressure, serum lipids, potassium, renin, aldosterone, C-reactive protein (CRP) and monocyte chemotactic protein-1 (MCP-1) were measured. After the baseline visit aliskiren was started (150 mg/d) and after 12 weeks replaced with ramipril (5 mg/d) for the next 12 weeks. Blood pressure was 142/88±15/11 mmHg at baseline, 137/84±10/8 mmHg after aliskiren (ns) and 126/81±11/7 mmHg after ramipril (p<0.05 vs baseline and aliskiren). No incidents of hyperkalemia were observed. Plasma renin concentration increased significantly during aliskiren treatment compared to ramipril (227,6±844 vs. 58,3±765 pg/mL). CRP was similar after both therapies (8,8±34 vs. 8,4±32 µg/mL) but MCP-1 concentration was significantly lower after aliskiren than after ramipril (294,0±172,6 vs. 358,9±183,3 pg/mL). Aliskiren 150 mg/day decreases blood pressure less effectively than ramipril 5 mg/day in peritoneal dialysis patients. It does not influence serum potassium. The decrease of MCP-1 concentration after aliskiren treatment may provide an indirect evidence for its blood pressure independent cardioprotective and anti-inflammatory effects.

Treatment of chronic hemodialysis patients with low-dose fenofibrate effectively reduces plasma lipids and affects plasma redox status.

Dyslipidemia is common in chronic hemodialysis patients and its underlying mechanism is complex. Hemodialysis causes an imbalance between antioxidants and production of reactive oxygen species, which induces the oxidative stress and thereby may lead to accelerated atherosclerosis. Statins have been found to be little effective in end-stage kidney disease and other lipid-lowering therapies have been only scarcely studied. The study aimed to assess the effect of low-dose fenofibrate therapy on plasma lipids and redox status in long-term hemodialysis patients with mild hypertriglyceridemia.Twenty seven chronic hemodialysis patients without any lipid-lowering therapy were included in a double-blind crossover, placebo-controlled study. The patients were randomized into two groups and were given a sequence of either 100 mg of fenofibrate per each hemodialysis day for 4 weeks or placebo with a week-long wash-out period between treatment periods. Plasma lipids, high sensitive C-reactive protein (CRP), urea, creatinine, electrolytes, phosphocreatine kinase (CK), GOT, GPT and plasma thiols (total and free glutathione, homocysteine, cysteine and cysteinylglycine) were measured at baseline and after each of the study periods. Plasma aminothiols were measured by reversed phase HPLC with thiol derivatization with 2-chloro-1-methylquinolinium tetrafluoroborate.Fenofibrate therapy caused a significant decrease of total serum cholesterol, LDL cholesterol and triglycerides and an increase of HDL cholesterol. The treatment was well tolerated with no side-effects but there was a small but significant increase of CK not exceeding the upper limit of normal range. There were no changes of serum CRP, potassium, urea, and creatinine and liver enzymes during the treatment. Neither total nor total free cysteinylglycine and cysteine changed during the study but both total and free glutathione increased during the therapy with fenofibrate and the same was observed in case of plasma homocysteine.The study shows that a treatment with reduced fenofibrate dose is safe and effective in reducing serum triglycerides and cholesterol in chronic dialysis patients and may shift plasma aminothiol balance towards a more antioxidative pattern.

[Respiratory tract diseases in the elderly]. / Choroby ukladu oddechowego w wieku podeszlym.

According to recent definitions the person enters a senile age after 65. Each person starts ageing after the completion of maturation. The phenomenon of ageing is highly individual and differs among people with respect to its rate and affected systems and organs. This may be responsible for a frequent inequality of metrical and biological age. Ageing is a multisystem process which also leads to alterations in symptomatology of many diseases. The process of ageing has been very well described, especially in the cardiovascular system. In contrast, ageing of the respiratory tract is far less recognised and still remains a subject of debates. The elderly are affected by the same diseases as younger individuals. The most common diseases at this age are respiratory tract infections, tuberculosis, chronic obstructive pulmonary diseases and bronchial asthma. Their course may be, however, different in the elderly not only due to the physiologic process of ageing but also frequent comorbidities. This fact should be taken into account when establishing a diagnosis and treatment regimens. A therapy of the older person usually requires a highly individualized approach.