Kidney & blood pressure research最新文献

Introduction: Chronic kidney disease (CKD) is closely linked to high blood pressure (HBP), which is its leading cause in developing countries. Hypertension affects 1.2 billion people worldwide. However, a significant portion of individuals with HBP are undiagnosed, and their kidney function is even less known. The objective of this study was to determine the prevalence and associated factors of CKD among three sub-groups of blood pressure status (normotensive, diagnosed hypertension, and undiagnosed hypertension) individuals.

Patients and methods: We conducted a cross-sectional study in the general population of three northern regions in Senegal using a two-level cluster sampling method. The sample was constituted with a precision of 5% and a power of 80%, with an additional 10% attrition margin. Individuals aged 18-80 years were included in the study after consent. Pregnant women, hospitalized persons within the past 3 months, patients with general or urinary symptoms within the past 7 days and individuals undergoing renal replacement therapy were excluded. Investigators collected clinical and biological data at participants' homes using a modified version of the WHO's STEPwise questionnaire. Samples were collected for biochemical analysis (serum creatinine, lipid profile, and blood sugar). Estimated glomerular filtration rate was calculated using the CKD-EPI 2021 formula.

Results: A total of 2,441 participants were included in the study with a mean age of 45.4 ± 16.0 years and a sex ratio M/F of 0.4. The overall prevalence of HBP and CKD were, respectively, 52.0% and 17.8%. Three out of every five hypertensive patients were undiagnosed. CKD was more frequent among known hypertensive patients (30.5%) compared to individuals with undiagnosed hypertension (19.1%) and normotensive individuals (10.9%). Multivariate analysis showed that CKD was associated with older age and female sex.

Conclusion: Undiagnosed hypertension is common among populations in northern Senegal. A high prevalence of CKD was found among both diagnosed and undiagnosed individuals with hypertension. Extending strategies for early detection and management in the general population could help prevent or reduce morbidity and mortality associated with CKD.

Introduction: Patients with idiopathic membranous nephropathy (IMN) are particularly susceptible to thromboembolism (TE). The phospholipase A2 receptor (PLA2R) antibody (Ab) has been indicated to work as an independent risk predictor for venous TE in IMN. This study aimed to further explore the predictive value of PLA2R Ab for both venous and arterial TE in IMN patients.

Methods: A total of 91 IMN patients were retrospectively selected and divided into anti-PLA2R-positive or anti-PLA2R-negative groups according to the anti-PLA2R Ab titer (cutoff: 20 RU/mL). Serum PLA2R Abs were estimated using ELISA. Anti-PLA2R-positive IMN patients were further assigned into two groups based on the presence or absence of TE.

Results: Twelve (18.18%) IMN patients with anti-PLA2R positivity had TE, including both venous and arterial TE. No TE occurred in the anti-PLA2R-negative group. IMN patients in the anti-PLA2R-positive group had significantly higher levels of total cholesterol and low-density lipoprotein than those in the anti-PLA2R-negative group. No significant difference was observed in the anti-PLA2R Ab titer between patients with and without TE. Patients with TE were significantly older than those without TE.

Conclusion: This study demonstrates that the positive status of anti-PLA2R Abs contributes to thrombosis formation in IMN.

Introduction: Acute kidney injury (AKI) is a common clinical syndrome associated with high morbidity and mortality. Inhibition of the methyltransferase enhancer of zeste homolog 2 (EZH2) by its inhibitor 3-deazaneplanocin A (3-DZNeP) exerts renal benefits in acute renal ischemia-reperfusion injury (IRI). However, the underlying mechanisms are not completely known. This study aimed to elucidate the pathological mechanism of EZH2 in renal IRI by combination of multi-omics analysis and expression profiling in a public clinical cohort.

Methods: In this study, C57BL/6 J mice were used to establish the AKI model, which were treated with 3-DZNeP for 24 h. Kidney samples were collected for RNA-seq analysis, which was combined with publicly available EZH2 chromatin immunoprecipitation sequencing (ChIP-seq) data of mouse embryonic stem cell for a joint analysis to identify differentially expressed genes. Several selected differentially expressed genes were verified by quantitative PCR. Finally, single-nucleus sequencing data and expression profiling in public clinical datasets were used to confirm the negative correlation of the selected genes with EZH2 expression.

Results: 3-DZNeP treatment significantly improved renal pathology and function in IRI mice. Through RNA-seq analysis combined with EZH2 ChIP-seq database, 162 differentially expressed genes were found, which might be involved in EZH2-mediated pathology in IRI kidneys. Four differential expressed genes (Scd1, Cidea, Ghr, and Kl) related to lipid metabolism or cell growth were selected based on Gene Ontology and Kyoto Encyclopedia of Genes and Genome enrichment analysis, which were validated by quantitative PCR. Data from single-nucleus RNA sequencing revealed the negative correlation of these four genes with Ezh2 expression in different subpopulations of proximal tubular cells in IRI mice in a different pattern. Finally, the negative correlation of these four genes with EZH2 expression was confirmed in patients with AKI in two clinical datasets.

Conclusions: Our study indicates that Scd1, Cidea, Ghr, and Kl are downstream genes regulated by EZH2 in AKI. Upregulation of EZH2 in AKI inhibits the expression of these four genes in a different population of proximal tubular cells to minimize normal physiological function and promote acute or chronic cell injuries following AKI.

Introduction: Upper urinary tract stones combined with parenchymal infiltrative renal pelvic cancer are challenging to detect on imaging and to evaluate the differential diagnosis.

Case presentation: The symptoms and diagnoses in three cases of parenchymal infiltrative renal pelvic cancer and upper urinary tract stones that occurred between June 2019 and June 2022 were reviewed. Primary symptoms of lumbar discomfort and hematuria were evident in all 3 patients. Preoperative computed tomography (CT) abdominal imaging revealed that all three cases had hydronephrosis along with renal stones, while the other two cases only had localized hypoenhancement of the renal parenchyma, which was only thought to be limited inflammatory changes in the renal cortex as a result of the combination of renal pelvis infection. After percutaneous nephrolithotomy or ureteroscopic lithotripsy, a combined renal pelvis tumor was discovered in all of these instances. Radical tumor surgery was later performed. One patient who had several tumor metastases passed away 6 months after surgery. A case with multiple metastases was discovered 15 months after surgery and survived with the help of the current chemotherapy. A case with a bladder tumor recurrence was discovered 16 months after surgery and had transurethral bladder tumor electrosurgery and routine bladder perfusion chemotherapy.

Conclusion: Upper urinary tract stones and parenchymal infiltrative pyel carcinoma have atypical imaging, easily confused with infectious diseases. CT or computed tomography urography (CTU) must be considered by urologists. Patients who have a CT with local renal parenchyma density should be suspected of having parenchymal invasive renal pelvis carcinoma; a needle biopsy ought to be performed; and repeat biopsies may be performed if necessary. High-risk individuals need multiple, sufficient biopsies as needed and a comprehensive intraoperative assessment of the renal pelvic mucosa.

Introduction: We aimed to evaluate the prognostic impact of renal insufficiency and fluctuation of glomerular filtration observed during hospitalization for heart failure (HF).

Methods: We followed 3,639 patients hospitalized for acute HF and assessed the mortality risk associated with moderate or severe renal insufficiency, either permanent or transient.

Results: After adjustment, severe renal failure defined as estimated glomerular filtration (eGFR) <30 mL/min indicates ≈60% increase in 5-year mortality risk. Similar risk also had patients with only transient decline of eGFR to this range. In contrast, we did not observe any apparent mortality risk attributable to mild/moderate renal insufficiency (eGFR 30-59.9 mL/min), regardless of whether it was transient or permanent.

Conclusion: Even transient severe renal failure during hospitalization indicates poor long-term prognosis of patients with manifested HF. In contrast, only moderate renal insufficiency observed during hospitalization has no additive long-term mortality impact.

Background: Cancer patients are prone to developing acute kidney disease (AKD), yet this phenomenon remains understudied compared to acute kidney injury (AKI). AKD, which often develops insidiously, can cause treatment interruptions, extended hospital stays, and increased mortality.

Summary: This perspective article explores the intricate relationship between AKD and cancer, focusing on prevalence, risk factors, implications for anticancer therapy, and long-term outcomes, including chronic kidney disease progression.

Key messages: To emphasize the importance of early detection and intervention, this work advocates for increased research and awareness among clinicians to improve patient outcomes and manage healthcare burdens associated with AKD in cancer patients.

Introduction: This study aimed to explore the correlation between the extent of fundus damage and the severity of chronic kidney disease (CKD).

Methods: We collected data from 118 CKD patients, including general information, renal function indicators, and fundoscopic examination results. The stages of CKD and degrees of fundus lesions were graded. SPSS 25.0 software facilitated the analysis of correlations using Kendall's tau-b correlation analysis and ordinal regression analysis.

Results: Statistically significant differences were observed among multiple CKD stages in the distribution of age, systolic blood pressure, diastolic blood pressure, hemoglobin, total cholesterol, homocysteine, cystatin C, serum creatinine, blood urea, eGFR, 24-h urine protein, urine microalbumin, urine microalbumin/urine creatinine, and blood β2-microglobulin, complement C3. Notably, the levels of cytokeratin 19 fragment and transforming growth factor β significantly increased in all CKD stages. Kendall's tau-b correlation analysis revealed a significant positive correlation between CKD stage and fundus lesion grade. Ordinal regression analysis indicated that sex differences, total cholesterol levels, and hemoglobin levels were significant predictors of fundus lesion risk. Compared with patients at stage 5 CKD, the risk of fundus damage is significantly lower in patients in stage 2 and stage 3, further demonstrating a positive correlation between renal function deterioration and increased risk of fundus damage.

Conclusions: Routine fundus screening and early intervention for fundus lesions are vital for assessing CKD deterioration, providing new directions for future related research.

Background: Physical exercise (PE) can regulate inflammation, cardiovascular health, sarcopenia, anaemia, and bone health in the chronic kidney disease (CKD) population. Experimental and clinical studies both help us better understand the mechanisms that underlie the beneficial effects of the exercise, especially in renal anaemia and CKD-mineral bone disorders (CKD-MBDs). Here, we summarize this evidence, exploring the biological pathways involved, locally released substances, and crosstalk between tissues, but also the shortcomings of current knowledge.

Summary: Anaemia: Both in healthy and CKD subjects, PE may mimic hypoxia, inhibiting PHDs; so hydroxylate HIF-α subunits may be translocated into the nucleus, resulting in dimerization of HIF-1α and HIF-1β, recruitment of p300 and CBP, and ultimately, binding to HREs at target genes to cause activation. However, in CKD subjects acute PE causes higher levels of lactate, leading to iron restriction by upregulating hepatic hepcidin expression, while chronic PE allows an increased lactate clearance and HIF-α and VEGFα levels, stimulating both erythropoiesis and angiogenesis.

Ckd-mbd: PE may improve bone health decreasing bone resorption and increasing bone formation throughout at least three main pathways: (a) increasing osteoprotegerin and decreasing RANKL system; (b) decreasing cytokine levels; and (c) stimulating production of myokines and adipokines.

Key messages: Future research needs to be defined to develop evidence-based exercise guidance to provide optimal benefit for CKD using exercise interventions as adjuvant therapy for CKD-related complications such as anaemia and CKD-MBD.

Introduction: The literature lacks whether metabolic alkalemia occurs in outpatients with hypercalciuric nephrolithiasis. Thus, we aim to investigate it because these patients are often treated with thiazides to reduce urinary calcium excretion. However, thiazides induce chloride losses due to the inhibition of Na-Cl cotransporter expressed in the renal distal tubule cells. Besides thiazide prescription, many of these patients are also supplemented with potassium citrate, which is an addition of alkali source in their bodies.

Methods: We collected clinical, demographic characteristics, and laboratory data from electronic medical charts of outpatients with calcium kidney stones followed in our institution from January 2013 to July 2021. We diagnosed those cases as metabolic alkalemia, in which the venous blood gas tests showed pH ≥7.46 and bicarbonate concentration >26 mEq/L. Then, we applied statistical analysis to compare distinct categories between patients with and without metabolic alkalemia.

Results: We diagnosed metabolic alkalemia in 4.3% of hypercalciuric nephrolithiasis outpatients, and we verified that thiazides had been used in all of them except in one case. Furthermore, we observed that the amount of thiazide taken daily was higher in patients with metabolic alkalemia than in those without this imbalance. Additionally, hypokalemia was present in 37% of patients who developed metabolic alkalemia. We also found lower chloride, magnesium and ionic calcium serum concentrations in patients with metabolic alkalemia than in those without an acid-base disequilibrium.

Conclusion: Despite the low prevalence of metabolic alkalemia in hypercalciuric kidney stone formers, it is important to monitor these patients due to the high incidence of hypokalemia and the potential presence of other electrolyte disorders.