Diabetic nephropathy (DN) is a common complication in diabetic patients, and the pathological mechanism has not been fully understood. PIAS2, as a counter regulator of the JAK2/STAT3 signaling pathway, may play a crucial role in DN. This study aims to investigate the expression of PIAS2 in high glucose-induced podocytes and the protective effect against podocyte cell injury.

Chronic kidney disease (CKD) is associated with elevated mortality risk. The study aimed to investigate the extent to which multiple risk factors controlled could attenuate CKD-related excess mortality.

Renal damage in Fabry disease (FD) is a consequence of pathological and progressive glycosphingolipids accumulation, which occurs in different magnitudes among FD phenotypes, but is a constant renal tissue phenomenon in all patients with renal involvement. A significant correlation between plasma Lyso-Gb3 (Gb3 analog) and disease severity, has been described but, there is lack of information from clinical studies regarding the correlation between Lyso-Gb3 and renal events in humans and, the few results have certain discrepancies. In clinical practice it is necessary to have disease-specific biomarkers, non-invasive and useful in diagnosis, prognosis and therapeutic response. Evidence relating to the prognostic value of lyso-GL3 is mixed.

Patients with chronic kidney disease (CKD) often experience symptoms consistent with orthostatic hypotension (OH); however, not much is known about OH in this population. Therefore, study analyzed OH prevalence and risk according to renal function decline.

Background Maintaining fluid balance is one of major challenges of the dialysis therapy. It includes, in particular, the management of "dry body mass". We postulated that simple measurement of subscapular skinfold thickness before and after hemodialysis could help monitor hydration status in chronic dialysis patients. Aim of the study The aim of the study was to compare the conventional methods of monitoring hydration status during hemodialysis with an assessment of skin fold thickness. Materials and Methods 50 participants (21 F, 29 M; age 60 ±15 years) were enrolled. Directly before the hemodialysis session the following parameters were measured: body composition with bioimpedance spectroscopy, skinfold thickness in subscapular area with standardized caliper and blood tests: blood count, urea, n-terminal pro B-type natriuretic peptide (nt-proBNP) and pro-adrenomedullin (pro-ADM). The procedures were repeated at the end of three consecutive hemodialysis sessions. Results The mean change of skinfold thickness in subscapular area before and after hemodialysis session was -2.2 ±1.6 mm. A significant correlation was found between the change of extracellular water volume and skinfold thickness before and after hemodialysis (r=0.33; p=0.02) and between the change of total water volume and body mass before and after hemodialysis (r=0.49; p<0.01). There was also a positive correlation between the change of skinfold thickness and systolic blood pressure before and after a hemodialysis session (R=0.36; p=0.01). Dialysis vintage correlated significantly with the changes of plasma nt-proBNP level during hemodialysis (r=0.40; p=0.02). Multivariate analysis revealed that baseline body mass, BMI, changes of systolic blood pressure determined the variability of skinfold thickness during hemodialysis. Receiver operating curve analysis revealed that BIA spectrometry was more sensitive and specific than the skinfold thickness assessment for the assessment of hydration condition. Conclusions The simple measurements of skinfold in subscapular area may approximate changes of hydration status but are inferior to BIA spectroscopy. Further research is needed to confirm the utility of this method in monitoring blood pressure control in dialysis patients.

Background Urine samples could partially reflect the renal condition and could provide possible mechanism of high-risk factor for the long-term development of chronic kidney disease caused by prematurity. Methods Urine samples were collected from preterm infants (gestational age <28 weeks) when their corrected gestational weeks reached ≥37 weeks. In addition, urine samples were collected from full term infants beyond three days after birth as the control group. The urine proteome was investigated by using LC‒MS/MS analysis, and subsequent bioinformatics analysis was performed. Differentially expressed proteins were validated using ELISA. Results A total of 2634 proteins were identified, 366 proteins were highly expressed in the preterm group, while 102 proteins were enriched in the full-term group. Based on functional analysis, proteins enriched in preterm group were implicated in structure organization, cell adhesion, and extracellular part, while proteins enriched in urine of the full-term group were implicated in the immune response. Kidney inherent cells accelerated into urine have been examined in preterm infants group. Each of the top 20 differentially expressed proteins enriched in the urine of preterm infants was used as a keyword for literature retrieval, ultimately leading to the selection and validation of CDH6 and CDH11 through ELISA. Both proteins were found to be more abundant in the urine of preterm infants than in that of full-term infants. Conclusions The present study provides differences in urine protein profiles between preterm and full-term infants and a new potential explanation for the high risk of CKD development caused by preterm birth.

Depression and cognitive declines are common and frequently co-occur among older adults with hypertension but their symptom-level relationships are poorly understood. This study explored inter-relationships between depressive symptoms and cognitive function as well as their associations with quality of life (QoL) in a national hypertension sample from China.

Introduction High sodium and low potassium intake are associated with cardiovascular disease. This meta-analysis investigates the combined effect of dietary sodium and potassium intake (Na/K-ratio), on cardiovascular outcome. Methods We systematically searched MEDLINE and EMBASE databases (1946 - 2024) for randomized controlled trials and cohort studies reporting the association between estimated dietary Na/K-ratio and cardiovascular events or mortality in adults. Two authors independently screened articles, extracted data, and assessed risk of bias (ROBINS-E tool). We pooled results using random-effects models and compared outcomes across the general population, patients with chronic kidney disease, and those with a history of cardiovascular disease. The study was registered in PROSPERO (ID: CRD42024450279). Results Twenty-four studies were included. Participants were 59±11 years old, 49±22% were men and the estimated dietary Na/K-ratio was 2.0±0.6 mmol/mmol. The risk of bias was low in 9% of the studies, high in 39% of the studies and 52% of the studies were appraised as some concerns. Higher estimated dietary Na/K-ratio was associated with a higher risk for cardiovascular events and mortality (HR 1.10 [95% CI: 1.06-1.16]), which was apparent in the general population and subjects with a history of cardiovascular disease. In patients with chronic kidney disease, only limited data was available. Conclusion Higher estimated dietary Na/K-ratio is associated with an increased incidence of cardiovascular events and mortality in the general population and patients with a cardiovascular disease history.

Chronic kidney disease worsens the prognosis of cardiovascular disease (CVD) and vice versa. This study aimed to evaluate the mortality of patients with a high CVD burden and unplanned start of maintenance hemodialysis (HD).

Abstract： Background The pathogenesis of systemic lupus erythematosus (SLE) remains complex, and studies have found that abnormal lipid metabolism may be involved in the disease. Therefore, we aim to investigate the dyslipidemia in SLE patients and analyze the relationship between lipid metabolism and the disease activity. Methods 174 patients diagnosed with SLE were enrolled in Henan Provincial People's Hospital from December 2016 to September 2022. Clinical data and laboratory indicators were collected, and SLE patients were grouped according to the levels of serum lipid. SPSS 26.0 statistical software was used for comparative analysis of SLE patients. Results The prevalence of dyslipidemia was about 92.53% (161/174), mainly with decreased HDL (125/174, 77.64%) and increased TG (86/174, 53.42%). The lipids were positively correlated with inflammatory indexes, such as WBC, NEC, SII, NLR, LMR and so on. Furthermore, the blood lipid levels were significantly correlated with SLEDAI-2K, ESR, C3, C4, BUN, Scr and 24-hour urine protein(P<0.05). With the increasing types of dyslipidemia, the value of inflammatory indicators such as WBC and SII were higher, as well as the rate of kidney involvement. This is manifested by the elevation of renal function parameters such as BUN, Scr, eGFR and 24-hour urine protein levels, while the levels of IgG, total protein and albumin decrease accordingly. The area under the curve (AUC) values of TC, TG and LDL predicting LN were 0.759, 0.713 and 0.729, which provided 69.6%, 81.4% and 63.7% sensitivity, and 76.4%, 56.9% and 73.6% specificity, respectively. With an AUC of 0.771, the combined detection of TC, TG, HDL, and LDL exhibited a greater potential for discrimination than any separate measurements. Conclusions Dyslipidemia is prevalent among SLE patients, and the levels of lipid can be informative in predicting renal involvement in SLE. It is crucial to monitor lipid levels and inflammation indexes and take lipid-lowering therapy along the discourse of SLE. Keywords：systemic lupus erythematosus, dyslipidemia, albuminuria, inflammation.

Introduction Chronic kidney disease (CKD) is an important risk factor for cardiovascular disease and mortality. However, data on the prediction of long-term adverse outcomes in advanced predialysis CKD patients is lacking. Methods We studied the factors associated with mortality and major adverse cardiovascular and cerebrovascular events (MACCE, including cardiovascular death, myocardial infarction, stroke and coronary revascularization) in a cohort of 210 patients with non-dialysis CKD stage 4-5 during a five-year follow-up. The participants underwent stress ergometry testing to study maximal exercise capacity (Wmax%), a plain lateral abdominal radiograph to study abdominal aortic calcification score (AAC) and laboratory tests including cardiac troponin T (TnT) and N-terminal pro-B-type natriuretic peptide (ProBNP). Furthermore, a dichotomous composite covariate was created and explored by combining ProBNP and Wmax% using the cut-offs determined with the Youden index. The associations between covariates of interest and study outcomes were explored using multivariable Cox proportional hazards models adjusted with age, sex, coronary artery disease (CAD) and incident kidney transplantation (KTx). Results Median age at baseline was 65 (52-73) years and eGFR 12 (10-15) ml/min/1.73 m2, 34.8 % were female and 44.8 % had diabetes. Altogether 67 (31.9 %) patients died during follow-up and 65 (31.0%) were observed with a MACCE. In separate multivariable Cox proportional hazards models adjusted for age, gender, CAD and KTx, Wmax% (HR 0.983 [95 % CI: 0.968-0.999], p=0.019), TnT (HR 1.004 [95 % CI: 1.002-1.005], p<0.001 and) and ProBNP (HR 1.036 per 1000 ng/l [95 % CI: 1.014-1.059], p=0.002 were independently associated with mortality. In similarly adjusted multivariable Cox models Wmax% (HR 0.977 [95 % CI: 0.962-0.992], p=0.003), TnT (HR 1.004 [95 % CI: 1.002-1.005], p<0.001) and ProBNP (HR 1.034 per 1000 ng/l [95 % CI: 1.010-1.058], p=0.006) were independently associated with the occurrence of MACCE during follow-up. AAC was associated with the risk of an incident MACCE (HR 1.080 [95% CI 1.028-1.135], p=0.002) but, surprisingly, not with mortality (HR 1.046 [95% CI 0.994-1.101], p=0.083). Finally, in participants with Wmax ≤50 % and ProBNP ≥1270 ng/l the risk of mortality (HR 8.760 [95 % CI: 4.730-16.222], p<0.001) and MACCE (HR 3.293 [95 % CI: 1.850-5.862], p<0.001) was significantly greater than those with Wmax>50% and/or ProBNP <1270 ng/L. Conclusion Wmax% and ProBNP separately and together as a composite risk factor may serve as important predictors of long-term all-cause mortality and MACCE in patients with CKD stage 4-5 not undergoing dialysis at baseline.

Introduction Acute kidney injury (AKI) is a prevalent issue in intensive care units (ICUs). There is a paucity of data regarding the use of blood gas and electrolyte measurements in predicting the risk of significant endpoints (kidney replacement therapy, death) in emerging, yet undiagnosed AKI. Methods Retrospective, observational, single-center study. The study documented 4 admission electrolytes (serum sodium, potassium, ionized calcium, and phosphate) and 3 admission blood gas variables (arterial pH, actual bicarbonate, pCO2). The endpoints of the study were the need for kidney replacement therapy (KRT) and death in the ICU. Results A total of 213 patients were included in the study. The ICU mortality rate was 31%, and 22.5% of all subjects required at least one individual KRT session. There were significant differences in admission serum sodium and phosphate levels between survivors and non-survivors (both lower in survivors), and in arterial pH and actual bicarbonate levels (both higher in survivors). The majority of all tested variables were identified as independent predictors of either the need for KRT or ICU death. Conclusions Integrating admission electrolytes and blood gas variables may potentially aid in identifying subsets of acute kidney injury (AKI) patients at risk of death.

Introduction Previous studies have found a relative risk of 1.6-2 for renal function deterioration with serum uric acid (UA) level increment. However, the association between the baseline urinary uric acid (UUA) level and renal function decline remains unclear, and we aimed to assess this association. Methods In this retrospective cohort-controlled study, we included patients who met the following inclusion criteria: age > 18 years, the presence of at least one UUA level in their electronic medical records (EMR), and two eGFR values. The exclusion criteria were chronic dialysis treatment before the baseline eGFR or any history of kidney transplantation. The EMR of the patients have been retrospectively screened between 31st December 2001 and 31st January 2022. The study group consisted of patients with UUA levels of ≥750 mg/day. In the control group, we included patients whose every UUA level was <750 mg/day. The primary endpoint was a composite of eGFR decline of ≥50%, eGFR <15 mL/min, dialysis initiation, or death. Secondary endpoints were as follows: eGFR decline of ≥50%, the latest eGFR <15 mL/min, or death. The endpoints were compared between the groups by Cox proportional hazards model analysis. Results We included 480 patients in the study group and 2,998 in the control group. The primary end point was observed in 30.95% and 16.25% of participants in the control and study groups, respectively; however, after it was compared between the two groups using the Cox model, there was no significant difference (HR 1.20, 95% CI: 0.96-1.51, p = 0.11). Similarly, no significant differences in the rates of secondary endpoints between the two groups were observed, except the difference between the eGFR declines >50% which was significant, as was observed by the Cox model (HR 2.22, 95% CI: 1.47-3.37, p < 0.001). Conclusion There was no significant difference in the rate of the composite endpoint between the study and control groups. Kidney function deterioration (as measured by eGFR decline of ≥50%) was significantly higher among patients with baseline hyperuricosuria (UUA ≥750 mg/day) than in those with normal uricosuria, as was observed by the Cox model. Further prospective studies are needed to clarify the role of uricosuria in renal function deterioration.

Cognitive impairment (CI) is common in patients with end-stage renal disease (ESRD), but the mechanism of uremia-associated CI is poorly recognized.

To explore bone metabolism in chronic kidney disease (CKD) and its correlation with nutritional indicators and to identify risk factors for abdominal aortic calcification (AAC).

Limited studies have explored the link between sleep duration and chronic kidney disease (CKD). However, the longitudinal alteration of sleep duration over time, known as sleep duration trajectories, have not been well explored. This gap results in an unclear understanding of the relationship between sleep duration trajectories and the risk of developing CKD, which is addressed in this study.

Cisplatin-induced acute kidney injury (Cis-AKI) is a significant cause of renal damage, characterized by tubular injury, ferroptosis, and oxidative stress. While therapeutic options for Cis-AKI remain limited, identifying novel targets to prevent kidney injury is critical. This study focuses on GALNT14, a gene associated with ferroptosis, and its potential role in mitigating Cis-AKI.

Urinary acidification is a crucial aspect of kidney tubular function that helps maintain the body's acid-base balance. The primary component of net acid excretion is ammonium (NH4+), which is formed when hydrogen ions (H+) secreted from the tubule combine with the major urinary buffer, ammonia (NH3). Consequently, both H+ and NH3 influence urine NH4+ excretion. While urine NH4+ is the standard measure of renal acid excretion, urine pH is also valuable for assessing urinary acidification, as it reflects the extent of H+ secretion from the collecting duct. Urine pH can be accurately measured using a pH meter, and urine NH4+ can be quantified through an enzymatic method adapted from plasma ammonia assays.

Alpha-blockers are considered an additional option when the major antihypertensive drug classes are insufficient in reducing blood pressure. While the impact of alpha-blockers on blood pressure control seems comparable, data evaluating their effects on renal outcomes are lacking. This systematic review and meta-analysis assess the impact on renal function from a medium to long-term perspective.

Primary aldosteronism (PA) is the predominant cause of secondary hypertension, leading to cardiovascular and renal damage. However, current epidemiology findings on the association between PA and estimated glomerular filtration rate (eGFR) remain inconsistent.

Primary hyperoxaluria type 1 (PH1) is a rare autosomal recessive disorder caused by a deficiency of the hepatic peroxisomal enzyme alanine-glyoxylate aminotransferase (AGT), which catalyses the conversion of glyoxylate to glycine, resulting in increased oxalate production. The clinical consequences of the progressive build up of oxalates include nephrocalcinosis, nephrolithiasis, chronic kidney disease and ultimately renal failure with extra-renal involvement. The diagnosis of PH1 is challenging due to the non-specific nature of its symptoms and the need for costly genetic testing. For many years, the management of PH1 was mainly supportive care. Currently, we have access to novel RNA interference (RNAi) therapeutics such as lumasiran and nedosiran, which reduce hepatic oxalate production, however, they are prohibitively expensive in most countries. The only curative treatment is liver transplantation, and in cases that progress to end-stage kidney disease (ESKD), simultaneous dual kidney and liver transplantation is usually indicated. Case presentation: We present a case of a 46-year-old woman admitted to our clinic on the eighth day post-kidney transplantation for evaluating the causes of delayed graft function (DGF). During the diagnostic work-up, primary hyperoxaluria type 1 (PH1) was diagnosed. A biopsy of the transplanted kidney also revealed microvascular inflammation (MVI). The patient was treated with fluid therapy, a restrictive diet, pyridoxine and, initially, intensive haemodialysis. Given the identification of a genetic variant of the disease that responds well to pyridoxine treatment, and considering the exceedingly high cost of lumasiran therapy, this medication was not utilized. In addition, it was decided to administer methylprednisolone pulses, plasmapheresis and immunoglobulin infusions in response to MVI. This treatment resulted in improvements in both clinical and laboratory parameters. Conclusions: PH1 is a rare cause of calcium oxalate nephrolithiasis and nephrocalcinosis and should be considered in the differential diagnosis of patients with progressive renal failure. This case highlights the importance of early diagnosis, which allows optimal supportive and/or RNAi therapy and appropriate qualification for kidney transplantation in cases of end-stage kidney disease. This is particularly important as isolated kidney transplantation (without concomitant liver transplantation) can lead to rapid loss of graft function and may ultimately prove futile.