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Oxalic acid, a toxic metabolic end product, accumulates when kidney function deteriorates. Apart from its direct tubulotoxicity, it crystallizes at concentrations above 30-40 µmol/L. High oxalic acid concentrations at transplantation might negatively influence kidney transplant function. The influence of the concentrations of oxalic acid and its precursors and residual diuresis on kidney transplant outcomes was studied. In this prospective cohort study, patients who received a kidney transplant between September 2018 and January 2022 participated. Concentrations of oxalic acid and precursors were determined in pre-transplant blood samples. Data on residual diuresis and other recipient, donor or transplant related variables were collected. Follow-up lasted until July 1st 2023. 496 patients were included, 154 were not on dialysis. Median residual diuresis was 1000 mL/day (IQR 200; 2000 mL/day). There were 230 living donor transplantations. Oxalic acid concentrations exceeded the upper normal concentration in 99% of patients, glyoxylic acid in all patients. There were 52 (10%) graft failures. As the influence of oxalic acid on the risk of graft failure censored for death was non-linear, it was categorized into two groups: ≤ 60 and > 60 μmol/L. In multivariable Cox analysis the graft failure censored for death risk was significantly influenced by residual diuresis, donor type (living versus deceased), donor age and oxalic acid. In 180 patients oxalic acid concentration shortly after transplantation was significantly lower than pre-transplant concentrations, suggesting excretion by the new graft. A better eGFR at day 7 was associated with lower oxalic acid concentration. Oxalic acid and residual diuresis did not influence patient survival. Residual diuresis and oxalic acid concentration are important and independent predictors of graft survival censored for death. These results underline the importance of pre-emptive transplantation, or optimizing the pre-transplant patients' condition regarding waste product concentrations.

Urinary extracellular vesicles (uEVs) are emerging as non‐invasive biomarkers for various kidney diseases, but it is unknown how differences in nephron mass impact uEV excretion. To address this, uEV excretion was measured before and after human kidney donor nephrectomy and rat nephrectomy. In male and female donors, uEVs were quantified in cell‐free spot and 24‐h urine samples using nanoparticle tracking analysis (NTA), EVQuant, and CD9‐time‐resolved fluorescence immunoassay. Female donors had significantly lower total kidney volume (TKV) and excreted 49% fewer uEVs than male donors. uEV excretion correlated positively with estimated glomerular filtration rate (eGFR), creatinine clearance, and TKV (R's between 0.6 and 0.7). uEV excretion rate could also be predicted from spot urines after multiplying spot uEV/creatinine by 24‐h urine creatinine. Donor nephrectomy reduced eGFR by 36% ± 10%, but the excretion of uEVs by only 16% (CD9+ uEVs ‐37%, CD9‐ uEVs no decrease). Donor nephrectomy increased the podocyte marker WT‐1 and the proximal tubule markers NHE3, NaPi‐IIa, and cubilin in uEVs two‐ to four‐fold when correcting for the nephrectomy. In rats, the changes in GFR and kidney weight correlated with the changes in uEV excretion rate (R = 0.46 and 0.60, P < 0.01). Furthermore, the estimated degree of hypertrophy matched the change in uEV excretion rate (1.4‐ to 1.5‐fold after uninephrectomy and four‐fold after 5/6th nephrectomy). Taken together, our data show that uEV excretion depends on nephron mass, and that nephrectomy reduces uEV excretion less than expected based on nephron loss due to compensatory hypertrophy. The major implication of our findings is that a measure for nephron mass or uEV excretion rate should be included when comparing uEV biomarkers between individuals.

Delayed graft function (DGF) after kidney transplantation heralds a worse prognosis. In patients with hyperoxaluria, the incidence of DGF is high. Oxalic acid is a waste product that accumulates when kidney function decreases. We hypothesize that residual diuresis and accumulated waste products influence the DGF incidence. Patients transplanted between 2018–2022 participated in the prospective cohort study. Pre-transplant concentrations of oxalic acid and its precursors were determined. Data on residual diuresis and other recipient, donor or transplant related variables were collected. 496 patients were included, 154 were not on dialysis. Oxalic acid, and glyoxylic acid, were above upper normal concentrations in 98.8%, and 100% of patients. Residual diuresis was ≤150 mL/min in 24% of patients. DGF occurred in 157 patients. Multivariable binary logistic regression analysis demonstrated a significant influence of dialysis type, recipient BMI, donor type, age, and serum creatinine on the DGF risk. Residual diuresis and glycolic acid concentration were inversely proportionally related to this risk, glyoxylic acid directly proportionally. Results in the dialysis population showed the same results, but glyoxylic acid lacked significance. In conclusion, low residual diuresis is associated with increased DGF incidence. Possibly accumulated waste products also play a role. Pre-emptive transplantation may decrease the incidence of DGF.

Metabolic acidosis unfavourably influences the nutritional status of patients with non‐dialysis dependent chronic kidney disease (CKD) including the loss of muscle mass and functionality, but the benefits of correction are uncertain. We investigated the effects of correcting metabolic acidosis on nutritional status in patients with CKD in a systematic review and meta‐analysis. A search was conducted in MEDLINE and the Cochrane Library from inception to June 2023. Study selection, bias assessment, and data extraction were independently performed by two reviewers. The Cochrane risk of bias tool was used to assess the quality of individual studies. We applied random effects meta‐analysis to obtain pooled standardized mean difference (SMD) and 95% confidence intervals (CIs). We retrieved data from 12 intervention studies including 1995 patients, with a mean age of 63.7 ± 11.7 years, a mean estimated glomerular filtration rate of 29.8 ± 8.8 mL/min per 1.73 m2, and 58% were male. Eleven studies performed an intervention with oral sodium bicarbonate compared with either placebo or with standard care and one study compared veverimer, an oral HCl‐binding polymer, with placebo. The mean change in serum bicarbonate was +3.6 mEq/L in the intervention group and +0.4 mEq/L in the control group. Correcting metabolic acidosis significantly improved muscle mass assessed by mid‐arm muscle circumference (SMD 0.35 [95% CI 0.16 to 0.54], P < 0.001) and functionality assessed with the sit‐to‐stand test (SMD −0.31 [95% CI −0.52 to 0.11], P = 0.003). We found no statistically significant effects on dietary protein intake, handgrip strength, serum albumin and prealbumin concentrations, and blood urea nitrogen. Correcting metabolic acidosis in patients with CKD improves muscle mass and physical function. Correction of metabolic acidosis should be considered as part of the nutritional care for patients with CKD.

Hemodialysis is associated with high morbidity and mortality rates as well as low quality of life. Altered nutritional status and protein-energy wasting are important indicators of these risks. Maintaining optimal nutritional status in patients with hemodialysis is a critical but sometimes overlooked aspect of care. Nutritional support strategies usually begin with dietary counseling and oral nutritional supplements. Patients may not comply with this advice or oral nutritional supplements, however , or compliance may be affected by other complications of progressive chronic kidney disease. Intradialytic parenteral nutrition (IDPN) may be a possibility in these cases, but lack of knowledge on practical aspects of IDPN delivery are seldom discussed and may represent a barrier. In this review, we, as a consensus panel of clinicians experienced with IDPN, survey existing literature and summarize our views on when to use IDPN, which patients may be best suited for IDPN, and how to effectively deliver and monitor this strategy for nutritional support. Lay Summary Hemodialysis for patients with chronic kidney disease is associated with high morbidity and mortality rates as well as low quality of life. Poor nutritional status is an important predictor of these risks, so maintaining optimal nutrition in patients on hemodialysis is a critical but sometimes overlooked aspect of care. Because many patients undergoing hemodialysis cannot maintain good nutrition through daily diet or oral nutritional supplements, intravenous delivery of nutrition during hemodialysis sessions has been proposed as another way to support nutrition over time. In this review, a consensus panel of experienced clinicians reviews the available literature and provides experience-based guidance on when to use this nutritional strategy, which patients may be best suited for this approach, practical strategies for delivery, and how to monitor patients receiving this nutrition during hemodialysis. Graphical Abstract Graphical Abstract

With expanding kidney transplantation programs, remaining hemodialysis patients are more likely to have a high comorbidity burden and may therefore be more prone to lose muscle mass. Our aim was to analyze risk factors for muscle loss in hemodialysis patients with high comorbidity. Fifty-four chronic hemodialysis patients (Charlson Comorbidity Index 9.0 ± 3.4) were followed for 20 weeks using 4-weekly measurements of lean tissue mass, intracellular water, and body cell mass (proxies for muscle mass), handgrip strength (HGS), and biochemical parameters. Mixed models were used to analyze covariate effects on LTM. LTM (−6.4 kg, interquartile range [IQR] −8.1 to −4.8), HGS (−1.9 kg, IQR −3.1 to −0.7), intracellular water (−2.11 L, IQR −2.9 to −1.4) and body cell mass (−4.30 kg, IQR −5.9 to −2.9) decreased in all patients. Conversely, adipose tissue mass increased (4.5 kg, IQR 2.7 to 6.2), resulting in no significant change in body weight (−0.5 kg, IQR −1.0 to 0.1). Independent risk factors for LTM loss over time were male sex (−0.26 kg/week, 95% CI −0.33 to −0.19), C-reactive protein above median (−0.1 kg/week, 95% CI −0.2 to −0.001), and baseline lean tissue index ≥10th percentile (−1.6 kg/week, 95% CI −2.1 to −1.0). Age, dialysis vintage, serum albumin, comorbidity index, and diabetes did not significantly affect LTM loss over time. In this cohort with high comorbidity, we found universal and prominent muscle loss, which was further accelerated by male sex and inflammation. Stable body weight may mask muscle loss because of concurrent fat gain. Our data emphasize the need to assess body composition in all hemodialysis patients and call for studies to analyze whether intervention with nutrition or exercise may curtail muscle loss in the most vulnerable hemodialysis patients.

Respiratory tract infections frequently occur in ill returned travelers, a minority of whom present with pneumonia. The most accurate and cost-effective diagnostic work-up remains an area of uncertainty. In this retrospective cohort study, the utility of routine chest radiography was evaluated. This study was performed at the Institute for Tropical Diseases in Rotterdam and included all returned travelers in the period between 2007 and 2009 that were ill with symptoms lasting less than 1 month and had chest radiography on admission. Travelers' demographic (including travel history), clinical, and laboratory data were collected on admission and evaluated for their diagnostic power to predict radiographic evidence of a pulmonary infiltrate. Fifty-three (7%) of 750 ill returned travelers had radiographic evidence of a pulmonary infiltrate. Presentation with cough (odds ratio [OR] 2.80, 95% confidence interval [CI] 1.46-5.38), or elevated C-reactive protein values (OR 1.13, 95% CI 1.09-1.17), and white blood cell count (OR 1.08, 95% CI 1.05-1.17) strongly correlated with the presence of a pulmonary infiltrate. Recursive partitioning analysis identified a subset of 384 patients presenting with both cough and fever, or C-reactive protein values in excess of 23 mg/L that would optimally benefit from chest radiography. The results of this study indicate that a more judicious use of chest radiography in the routine work-up of ill returned travelers is warranted.

High salt intake is common and contributes to poor cardiovascular health. Sustained cortisol excess also induces an adverse cardiovascular profile. Urinary cortisol excretion positively correlates with urinary sodium excretion. We hypothesised that this was due to hypothalamic-pituitary-adrenal axis activation by high salt intake. In male C57BL6/J mice, 2 weeks of high salt intake increased Crh and Pomc mRNA abundance in the hypothalamus and anterior pituitary, respectively and caused a sustained rise in plasma corticosterone. Plasma copeptin and anterior pituitary V1b receptor mRNA expression was elevated, which may contribute to basal HPA axis activation. Additionally, high salt intake amplified glucocorticoid response to restraint stress, indicative of enhanced HPA axis sensitivity. In the periphery, high salt intake reduced the binding capacity of corticosteroid-binding globulin, enhancing glucocorticoid bioavailability. Within several tissues, the expression of glucocorticoid-regenerating enzyme, 11β-hydroxysteroid dehydrogenase type 1, was increased and the glucocorticoid receptor downregulated. Overall, high salt intake increased glucocorticoid exposure in the hippocampus, anterior pituitary and liver. Chronic high salt intake amplifies basal and stress-induced glucocorticoid levels and resets glucocorticoid biology centrally, peripherally and within cells. This shows direct connectivity between salt homeostasis and HPA axis function. The cumulative effect is likely maladaptive and may contribute to the long-term health consequences of a high salt diet. Competing Interest Statement The authors have declared no competing interest.

To the Editor: Escherichia coli 0157:H7 is the causative organism of hemorrhagic colitis and is one of the agents associated with hemolytic uremic syndrome. 1 2 3 4 5 Although hamburger has been implicated as the source of E. coli 0157:H7, 1 , 3 , 6 , 7 the reservoir and mode of transmission of the agent remain unknown. We encountered sporadic cases and an outbreak of hemorrhagic colitis, and although our attempts to identify the source of the agent have been unsuccessful, the epidemiologic data we have gathered seem to indicate that humans may be a source of E. coli 0157:H7 and that person-to-person contact could be an important mode of . . .