Objective:To analyze the risk factors of hypocalcemia in 3-5 stages of chronic kidney disease (CKD) patients with hyperkalemia and non-dialysis after potassium lowering therapy.Methods:Clinical data of 3-5 stages of CKD patients with hyperkalemia and non-dialysis treated in Linyi Central Hospital from January 2019 to November 2024 were collected through the electronic medical record system. According to whether the corrected calcium level after potassium lowering treatments was lower than 2.12 mmol/L, the patients were divided into hypocalcemia group and non-hypocalcemia group. The gender, age, body mass index, primary disease, disease duration, comorbidity, use of potassium lowering drugs, concomitant medication, and blood potassium, corrected calcium, carbon dioxide binding capacity, blood magnesium, blood phosphorus, estimated glomerular filtration rate, and total parathyroid hormone before potassium lowering treatments between the 2 groups were compared. Multiple logistic regression analysis was used to identify the risk factors for hypocalcemia in 3-5 stages of CKD patients with hyperkalemia and non-dialysis after potassium lowering therapy.Results:A total of 260 patients were entered, including 58 with blood calcium lower than 2.12 mmol/L, and incidence of hypocalcemia was 22.3%. The differences in the baseline corrected calcium, blood phosphorus, carbon dioxide binding capacity, estimated glomerular filtration rate, and total parathyroid hormone between the hypocalcemia group and the non-hypocalcemia group were statistically significant ( P<0.05). The factors with P<0.1, including primary disease, baseline corrected calcium, blood phosphorus, carbon dioxide binding capacity, estimated glomerular filtration rate, and total parathyroid hormone, were included in the multivariate logistic regression analysis. The results showed that the probability of hypocalcemia at baseline corrected calcium levels of 2.12-2.21, 2.22-2.31, and 2.32-2.41 mmol/L was 49.306 times, 13.651 times, and 13.342 times that of at ≥2.42 mmol/L, respectively. Low carbon dioxide binding capacity (odds ratio=0.909, 95% confidence interval: 0.836-0.987) was also a risk factor of hypocalcemia in 3-5 stages CKD patients with hyperkalemia and non-dialysis after potassium lowering therapy. Conclusions:Three to five stages of CKD patients with hyperkalemia and non-dialysis are prone to hypocalcemia after potassium lowering therapy. The low levels of baseline corrected calcium and carbon dioxide binding may be closely related to the occurrence of hypocalcemia in 3-5 stages of CKD patients with hyperkalemia and non-dialysis after potassium lowering therapy.

Objective:To investigate the effects of roxadustat on thyroid function in patients with renal anemia undergoing peritoneal dialysis.Methods:After applying the inclusion and exclusion criteria, a retrospective analysis was conducted on the clinical data of 151 patients undergoing peritoneal dialysis who were treated with either roxadustat or erythropoietin at Linyi Central Hospital from January 2019 to December 2023. The patients were divided into two groups based on their treatment: roxadustat group ( n = 88) and erythropoietin group ( n = 63). Patient age, sex, body mass index, urine output, duration of illness, primary disease, comorbidities, estimated glomerular filtration rate, total parathyroid hormone levels, and thyroid nodule status were recorded. Thyroid-stimulating hormone (TSH), free triiodothyronine, and free thyroxine levels before and after treatment were compared between the two groups. A decrease in TSH of more than one-third after treatment compared with the pre-treatment level was defined as a significant decrease in TSH. Multivariate logistic regression analysis was conducted to investigate the independent risk factors associated with a significant decrease in TSH in patients with renal anemia undergoing peritoneal dialysis. Results:After treatment, the roxadustat group showed significant decreases in TSH [1.84 (1.06, 2.67) U/L] and FT4 [(11.82 ± 3.56) pmol/L] compared with pre-treatment levels [2.58 (1.67, 3.42) U/L, (14.89 ± 3.27) pmol/L, Z = -3.42, t = -5.97, both P < 0.05]. After treatment, both TSH and FT4 levels were significantly lower in the roxadustat group than those in the erythropoietin group [2.80 (1.61, 3.78) U/L, (15.49 ± 3.24) pmol/L, Z = -3.36, t = 6.49, both P < 0.05]. Multivariate logistic regression analysis indicated that the use of roxadustat was an independent risk factor for a significant decrease in TSH in patients with renal anemia undergoing peritoneal dialysis [ OR = 7.621, 95% CI (3.195, 18.178)]. Conclusions:Roxadustat may lower TSH and FT4 levels in patients with renal anemia undergoing peritoneal dialysis.

Objective:To investigate the effects of roxadustat on thyroid function in patients with renal anemia undergoing peritoneal dialysis.Methods:After applying the inclusion and exclusion criteria, a retrospective analysis was conducted on the clinical data of 151 patients undergoing peritoneal dialysis who were treated with either roxadustat or erythropoietin at Linyi Central Hospital from January 2019 to December 2023. The patients were divided into two groups based on their treatment: roxadustat group ( n = 88) and erythropoietin group ( n = 63). Patient age, sex, body mass index, urine output, duration of illness, primary disease, comorbidities, estimated glomerular filtration rate, total parathyroid hormone levels, and thyroid nodule status were recorded. Thyroid-stimulating hormone (TSH), free triiodothyronine, and free thyroxine levels before and after treatment were compared between the two groups. A decrease in TSH of more than one-third after treatment compared with the pre-treatment level was defined as a significant decrease in TSH. Multivariate logistic regression analysis was conducted to investigate the independent risk factors associated with a significant decrease in TSH in patients with renal anemia undergoing peritoneal dialysis. Results:After treatment, the roxadustat group showed significant decreases in TSH [1.84 (1.06, 2.67) U/L] and FT4 [(11.82 ± 3.56) pmol/L] compared with pre-treatment levels [2.58 (1.67, 3.42) U/L, (14.89 ± 3.27) pmol/L, Z = -3.42, t = -5.97, both P < 0.05]. After treatment, both TSH and FT4 levels were significantly lower in the roxadustat group than those in the erythropoietin group [2.80 (1.61, 3.78) U/L, (15.49 ± 3.24) pmol/L, Z = -3.36, t = 6.49, both P < 0.05]. Multivariate logistic regression analysis indicated that the use of roxadustat was an independent risk factor for a significant decrease in TSH in patients with renal anemia undergoing peritoneal dialysis [ OR = 7.621, 95% CI (3.195, 18.178)]. Conclusions:Roxadustat may lower TSH and FT4 levels in patients with renal anemia undergoing peritoneal dialysis.

Objective:To analyze the risk factors of hypocalcemia in 3-5 stages of chronic kidney disease (CKD) patients with hyperkalemia and non-dialysis after potassium lowering therapy.Methods:Clinical data of 3-5 stages of CKD patients with hyperkalemia and non-dialysis treated in Linyi Central Hospital from January 2019 to November 2024 were collected through the electronic medical record system. According to whether the corrected calcium level after potassium lowering treatments was lower than 2.12 mmol/L, the patients were divided into hypocalcemia group and non-hypocalcemia group. The gender, age, body mass index, primary disease, disease duration, comorbidity, use of potassium lowering drugs, concomitant medication, and blood potassium, corrected calcium, carbon dioxide binding capacity, blood magnesium, blood phosphorus, estimated glomerular filtration rate, and total parathyroid hormone before potassium lowering treatments between the 2 groups were compared. Multiple logistic regression analysis was used to identify the risk factors for hypocalcemia in 3-5 stages of CKD patients with hyperkalemia and non-dialysis after potassium lowering therapy.Results:A total of 260 patients were entered, including 58 with blood calcium lower than 2.12 mmol/L, and incidence of hypocalcemia was 22.3%. The differences in the baseline corrected calcium, blood phosphorus, carbon dioxide binding capacity, estimated glomerular filtration rate, and total parathyroid hormone between the hypocalcemia group and the non-hypocalcemia group were statistically significant ( P<0.05). The factors with P<0.1, including primary disease, baseline corrected calcium, blood phosphorus, carbon dioxide binding capacity, estimated glomerular filtration rate, and total parathyroid hormone, were included in the multivariate logistic regression analysis. The results showed that the probability of hypocalcemia at baseline corrected calcium levels of 2.12-2.21, 2.22-2.31, and 2.32-2.41 mmol/L was 49.306 times, 13.651 times, and 13.342 times that of at ≥2.42 mmol/L, respectively. Low carbon dioxide binding capacity (odds ratio=0.909, 95% confidence interval: 0.836-0.987) was also a risk factor of hypocalcemia in 3-5 stages CKD patients with hyperkalemia and non-dialysis after potassium lowering therapy. Conclusions:Three to five stages of CKD patients with hyperkalemia and non-dialysis are prone to hypocalcemia after potassium lowering therapy. The low levels of baseline corrected calcium and carbon dioxide binding may be closely related to the occurrence of hypocalcemia in 3-5 stages of CKD patients with hyperkalemia and non-dialysis after potassium lowering therapy.

Objective:To explore the occurrence and risk factors of piperacillin sodium and tazobactam sodium (TZP)-related hypokalemia.Methods:The clinical data of adult inpatients treated with TZP in Linyi Central Hospital from January 2022 to January 2023 were collected through the hospital′s electronic medical record system, including patient demographic information, infection sites, major underlying diseases, laboratory tests, TZP use information and concomitant drugs, and patients with TZP-related hypokalemia were screened. The occurrence of TZP-related hypokalemia was analyzed by descriptive statistics. According to whether or not having TZP-related hypokalemia, the patients were divided into hypokalemia group and non-hypokalemia group, and the clinical characteristics were compared. The clinical characteristics with statistically significant differences between 2 groups were included in the multivariate logistic regression, and the risk factors of TZP-related hypokalemia were analyzed.Results:A total of 363 patients were included in the analysis, of which 86 (23.7%) were with hypokalemia and were judged to be associated with TZP, 46 (53.5%) were male and 40 (46.5%) were female; the age was 76 (68, 83) years. Of the 86 patients, 76 (88.4%) had mild hypokalemia, 10 (11.6%) had moderate hypokalemia, and none had severe hypokalemia. Through clinical characteristic comparison between the hypokalemia group and the non-hypokalemia group, statistically significant differences were found in patient gender, age, body mass index, the proportion of patients with pulmonary infection, abdominal/gastrointestinal infection, and urinary tract infection, the proportion of patients with coronary atherosclerotic heart disease and without major underlying diseases, baseline hemoglobin, serum total protein, serum albumin, blood calcium, blood magnesium, and the proportion of patients using potassium preserving diuretics and other diuretics during TZP treatment (all P<0.05). The above variables were included in the multivariate logistic regression, and the results showed that only the baseline level of blood magnesium was an independent influencing factor of TZP-related hypokalemia, and the lower the level, the higher the risk (odds ratio=0.105, 95% confidence interval: 0.012-0.956, P=0.045). Conclusions:Hypokalemia is a common adverse reaction of TZP, which should be paid attention to in clinic. The lower level of blood magnesium at baseline may be related to the increased risk of hypokalemia during TZP treatment.

Objective:To explore the occurrence and risk factors of piperacillin sodium and tazobactam sodium (TZP)-related hypokalemia.Methods:The clinical data of adult inpatients treated with TZP in Linyi Central Hospital from January 2022 to January 2023 were collected through the hospital′s electronic medical record system, including patient demographic information, infection sites, major underlying diseases, laboratory tests, TZP use information and concomitant drugs, and patients with TZP-related hypokalemia were screened. The occurrence of TZP-related hypokalemia was analyzed by descriptive statistics. According to whether or not having TZP-related hypokalemia, the patients were divided into hypokalemia group and non-hypokalemia group, and the clinical characteristics were compared. The clinical characteristics with statistically significant differences between 2 groups were included in the multivariate logistic regression, and the risk factors of TZP-related hypokalemia were analyzed.Results:A total of 363 patients were included in the analysis, of which 86 (23.7%) were with hypokalemia and were judged to be associated with TZP, 46 (53.5%) were male and 40 (46.5%) were female; the age was 76 (68, 83) years. Of the 86 patients, 76 (88.4%) had mild hypokalemia, 10 (11.6%) had moderate hypokalemia, and none had severe hypokalemia. Through clinical characteristic comparison between the hypokalemia group and the non-hypokalemia group, statistically significant differences were found in patient gender, age, body mass index, the proportion of patients with pulmonary infection, abdominal/gastrointestinal infection, and urinary tract infection, the proportion of patients with coronary atherosclerotic heart disease and without major underlying diseases, baseline hemoglobin, serum total protein, serum albumin, blood calcium, blood magnesium, and the proportion of patients using potassium preserving diuretics and other diuretics during TZP treatment (all P<0.05). The above variables were included in the multivariate logistic regression, and the results showed that only the baseline level of blood magnesium was an independent influencing factor of TZP-related hypokalemia, and the lower the level, the higher the risk (odds ratio=0.105, 95% confidence interval: 0.012-0.956, P=0.045). Conclusions:Hypokalemia is a common adverse reaction of TZP, which should be paid attention to in clinic. The lower level of blood magnesium at baseline may be related to the increased risk of hypokalemia during TZP treatment.

Objective:To evaluate the relationship between protein kinase C-delta (PKCδ) and pyroptosis during ventilator-induced lung injury (VILI) in rats.Methods:Thirty-six clean-grade healthy adult male Sprague-Dawley rats, weighing 200-250 g, were divided into 3 groups ( n=12 each) using a random number table method: control group (group C), group VILI, and VILI plus specific PKCδ inhibitor KAI 9803 group (group K). Phosphate buffer solution 200 μl was injected through the tracheal tube after intubation in group VILI, and KAI 9803 200 μg/kg was given instead in group K. The patients were mechanically ventilated (tidal volume 40 ml/kg, respiratory rate 60 breaths/min, inspiratory/expiratory ratio 1∶2, fraction of inspired oxygen 21%, positive end-expiratory pressure 0) for 4 h. Blood samples were taken from the femoral artery at the end of mechanical ventilation for blood gas analysis, and PaO 2 was recorded.Animals were sacrificed at the end of ventilation, lung tissues were removed, and bronchoalveolar lavage fluid (BALF) was prepared.The total protein concentrations in BALF were measured by coomassie blue staining, and concentrations of interleukin-18 (IL-18) and IL-1β in BALF by enzyme-linked immunosorbent assay.Lung tissues were obtained for microscopic examination of the pathological changes which were scored and for determination of wet/dry weight ratio (W/D ratio) and expression of PKCδ and gasdermin D N terminal fragment (GSDMD-N) protein and mRNA (by Western blot or by quantitative real-time polymerase chain reaction). Results:Compared with group C, the lung injury score, W/D ratio, and concentrations of total protein, IL-18 and IL-1β in BALF were significantly increased, PaO 2 was decreased, and the expression of PKCδ and GSDMD-N protein and mRNA was up-regulated in VILI and K groups ( P<0.01). Compared with group VILI, the lung injury score, W/D ratio, and concentrations of total protein, IL-18 and IL-1β in BALF were significantly decreased, PaO 2 was increased, and the expression of PKCδ and GSDMD-N protein and mRNA was down-regulated in group K ( P<0.05 or 0.01). Conclusion:PKCδ can mediates the pathophysiological process of VILI in which pyrolysis is involved in rats.

Objective:To evaluate the effect of rapamycin on the activity of NOD-like receptor C4 (NLRC4) inflammasomes in the rats with ventilator-induced lung injury (VILI).Methods:Thirty-six healthy clean-grade male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 3 groups ( n=12 each) using a random number table method: control group (group C), VILI group and rapamycin group (group RAPA). In group RAPA, rapamycin 4 mg·kg -1·d -1 was intraperitoneally injected once a day for 3 consecutive days before establishing the model, while the equal volume of normal saline was given instead in group C and group VILI.The patients were mechanically ventilated for 4 h (tidal volume 20 ml/kg, respiratory rate 80 breaths/min, inspiratory/expiratory ratio 1∶1, fraction of inspired oxygen 21%) in VILI and RAPA groups.Blood samples were collected from the femoral artery after the end of ventilation for blood gas analysis and for determination of serum interleukin-1β (IL-1β) and interleukin-18 (IL-18) concentrations (by enzyme-linked immunosorbent assay), and PaO 2 was recorded.The bronchoalveolar lavage fluid (BALF) was collected for determination of the neutrophil count and IL-1β and IL-18 concentrations by enzyme-linked immunosorbent assay.The lung tissues were obtained for examination of the pathological changes (under the light microscope) after HE staining which were scored and for determination of wet to dry weight (W/D) ratio, and expression of mammalian target of rapamycin (mTOR), NLRC4 and caspase-1 (by Western blot) and expression of NLRC4 mRNA (by real-time polymerase chain reaction). Results:Compared with group C, the W/D ratio, lung injury score, neutrophil counts in BALF, and concentrations of IL-1β and IL-18 in serum and BALF were significantly increased, PaO 2 was decreased, and the expression of mTOR, NLRC4, caspase-1 and NLRC4 mRNA was up-regulated in group VILI and group RAPA ( P<0.01). Compared with group VILI, the W/D ratio, lung injury score, neutrophil counts in BALF, and concentrations of IL-1β and IL-18 in serum and BALF were significantly decreased, PaO 2 was increased, and the expression of mTOR, NLRC4, caspase-1 and NLRC4 mRNA was down-regulated in group RAPA ( P<0.05). Conclusion:The mechanism by which rapamycin alleviates VILI may be related to inhibiting activation of mTOR signaling pathway and inhibiting the activity of NLRC4 inflammasomes in rats.

AIM: To investigate the role of angiopoietin-1 (Ang1) and Tie2 receptor in angiogenesis after myocardial infarction through detecting their mRNA expression in normal and infracted myocardium. METHODS: The experiment was conducted in the laboratory of Biochemistry and Molecular Biology, Medical Department of Peking University from April 2006 to April 2007. Forty male SD rats were randomly divided into acute myocardial infarction model group and sham-operation group. The myocardial infarction model was established in the rats of model group through the ligation of left anterior descending artery, while the rats in sham operation group were braided of the left anterior descending artery without ligation. Five rats in both groups were executed at 3, 7, 14, and 28 days after model establishment. RNA was extracted from the same site of left anterior wall, and the polymerase chain reaction was used to semiquantitatively analyze the Ang1 and Tie2 receptor mRNA expression with GAPDH gene as internal control; meanwhile, the immunohistochemistry was used to detect vascular density in and around infarction area. All the treatments for animals were accorded with the animal ethical standards. RESULTS: All 40 rats were included in the final analysis. Both Ang1 and Tie2 receptor were expressed in normal myocardium. In the 28 days after myocardial infarction, Ang1 expression kept at almost the same level without changing, but Tie2 receptor expression was slightly elevated at 3 days, reached peak value at 7 days, and returned to the baseline value at 14 days. The vascular density increased both infarction and peri-infarction area at 7 days after acute myocardial infarction, and did not change with time. CONCLUSION: Tie2 receptor expression is elevated and coincided with angiogenesis after myocardial infarction. It may play a role in the development and stabilization of the blood vessel after myocardial infarction.

Objective To explore the clinical character istics of bile reflux gastritis. Methods We observed 1328 patients with bile reflux gastritis(excluding gastritis of the remnant stomach),and selected 425 superficial gastritis as control group.All the patients took helicobacter pylori(Hp) rapid urease examination. 664 cases in observed group and all in patients of control group were examined for bile disease by UB. Results In 1328 patients,there were 797 male and 531 female,and the ratio of male and female was 1.5/1.The detecting rate of bile reflux gastritis was decreased along with aging. Among all the patients,there were 651 simple superficial gastritis(49%),86 gastric ulcer(6.5%),412 duodenal ulcer (31%),122 combined ulcer(9.2%) and 57 other disease(4.7%).In observed group,1030 HP(77.56%) were regative; 298 Hp(22.44%) were positive,and in control group,282 Hp(66.35%) were regative,147 Hp(33.65%) were positive.The amount of gallbladder disease resection was 221(33.3%),which was more than that of control group(16.9%). Conclusion The detecting rate of bile reflux gastritis was decreased along with aging.Bile reflux gastritis is more often combined with ulcer disease or gallbladder disease. The Hp infection rate of bile reflux gastritis is significant lower than that of non-bile reflux gastritis.