Journal of Nephrology最新文献

Background and objectives: Crush injury, the most important trauma complication encountered in earthquake victims, occurs as a result of prolonged compression of muscle mass. Crush syndrome, resulting from crush injury, and acute kidney injury (AKI) are the most common causes of in-hospital deaths after earthquakes. The aim of this study is to convey our experience after the devastating Turkey-Syria earthquake and to identify the risk factors of crush syndrome and crush-related AKI.

Methods: Of the 1134 children admitted to the emergency department, 265 with crush injury were included the study. Demographic information, laboratory and clinical data of the patients were retrospectively analyzed.

Results: Mean age of the patients was 10.3 ± 4.9 years (134 females and 131 males). The median time spent under the rubble was 20 h. Crush syndrome developed in 135 (50.9%). Patients with crush syndrome were older and had higher body weight, respectively (p = 0.014, p = 0.044). Acute kidney injury was present in 157 (59.2%) patients. Thirty-two patients (12.1%) received kidney replacement therapy (KRT). The risk factors for the development of AKI Stage 3 were crush syndrome, abdominal trauma, and age.

Conclusion: This disaster taught us the importance of establishing in advance a national emergency disaster plan. Older pediatric earthquake victims with multiple trauma and severe crush syndrome should be closely followed-up for development of AKI and, if necessary, started on dialysis. Timely access to medical care, early fluid resuscitation, and effective use of dialysis treatment are essential.

Peritoneal dialysis (PD) catheter malfunction commonly leads to the removal of the catheter and eventually to a transfer to hemodialysis. The most common cause is intraluminal obstruction caused by blood and fibrin clots. Recommended interventions include irrigation of the catheter with heparinized saline; if this method fails, thrombolytic agents may be used. Mechanical methods such as intraluminal brushing are also utilized, typically after medical treatment fails. Here, we present a case of a patient who developed an intraluminal blood clot that persisted despite attempts with intraluminal thrombolytic drugs and intraluminal brushing. To salvage the catheter, targeted thrombolysis was performed using an endoscopic retrograde cholangiopancreatography (ERCP) guidewire to reinforce the coiled PD catheter and puncture the clots. Additionally, a Swing Tip cannula was employed for direct injection of the thrombolytic agent. These interventions successfully preserved the catheter, resolving the clot and ensuring continued functionality.

Background: Numerous studies have explored the role of kidney replacement therapy (KRT) in phosphorus (P) control among prevalent hemodialysis (HD) patients. However, whether the reduction of P achieved during KRT affects parathyroid hormone (PTH) levels is still a matter of debate.

Methods: We conducted a retrospective observational study on the prevalent HD population at the Division of Nephrology, University Hospital of Verona, from January to December 2022. We Included clinically stable adult patients undergoing HD for over 6 months, with multiple recorded visits during the follow-up. Demographic, clinical, laboratory, and medication data were collected. Time-varying variables were updated at each study visit. The primary outcome of interest was PTH levels. The absolute intra-HD change in P (intra-HD ∆P), defined as the difference between pre- and post-HD P levels, served as the main exposure. Multivariable adjusted linear mixed models were used to investigate the relationship between intra-HD ∆P and PTH levels.

Results: A total of 211 patients contributed to 904 study visits. A significant and positive relationship was observed between intra-HD ∆P and pre-HD P (β = 0.76, 95% CI 0.75, 0.78, p < 0.001) and urea reduction ratio (β = 0.38, 95% CI 0.35, 0.41; p < 0.001). An increase in intra-HD ∆P was significantly and independently associated with low PTH levels (β = - 0.16, 95% CI - 0.30, -0.03; p = 0.020).

Conclusions: The extent of intra-HD P reduction significantly correlates with low PTH levels. Strategies focused on optimizing or enhancing depurative efficiency in KRT can exert a substantial impact on managing positive phosphorus balance and secondary hyperparathyroidism. The assessment of intra-HD P reduction may play a pivotal role in the management and follow-up of secondary hyperparathyroidism in HD patients.

Background: Acute kidney injury (AKI) is a common complication of traumatic hemorrhagic shock. The risk factors for AKI after traumatic hemorrhagic shock remain unclear. The aim of this study was to investigate the risk factors for AKI after traumatic hemorrhagic shock.

Methods: This was a ten-year retrospective cohort study of patients who experienced traumatic hemorrhagic shock between January 2013 and April 2023. Patient characteristics and clinical data were recorded for 417 patients. The outcome was the occurrence of AKI, defined as a serum creatinine increase of ≥ 0.3 mg/dL (≥ 26.5 μmol/L) within 48 h, or an increase to 1.5 times the baseline, or a urine volume of < 0.5 mL/(kg h.). Risk factors for AKI were tested by logistic regression models.

Results: The incidence of AKI after traumatic hemorrhagic shock was 29.3% (122/417 patients). Multivariable analysis revealed that the independent risk factors for AKI included age (OR, 1.048; 95% CI, 1.022-1.074; p < 0.001), B-type natriuretic peptide (OR, 1.002; 95% CI, 1.000-1.004; p = 0.041), sepsis (OR, 4.536; 95% CI, 1.651-12.462; p = 0.030) and acute myocardial injury (OR, 2.745; 95% CI, 1.027-7.342; p = 0.044). Road traffic accidents (OR, 0.202; 95% CI, 0.076-0.541; p = 0.001), mean arterial pressure (OR, 0.972; 95% CI, 0.950-0.995; p = 0.017), and base excess (OR, 0.842; 95% CI, 0.764-0.929; p = 0.001) were negatively correlated with AKI. The area under the receiver operating characteristic (ROC) curve for prediction by this model was 0.85 (95% CI, 0.81-0.90).

Conclusion: The incidence of AKI after traumatic hemorrhagic shock was 29.3% in our series. Indicators of blood perfusion, sepsis and acute myocardial injury may be independent risk factors for AKI after traumatic hemorrhagic shock. Early detection and effective intervention on these risk factors could reduce the occurrence of AKI and improve outcomes.

The tubular function of the kidney is very complex and is finely regulated by many factors. These include a variety of hormonal signaling pathways which are involved in the expression, activation and regulation of renal transporters responsible for the handling of electrolytes. Glucose-lowering drugs such as insulin and incretin-based therapies, exert a well-known renal protective role in diabetic kidney disease, mainly acting at the glomerular level. In the literature, several studies have described the effect of insulin and the incretin hormones on tubular transport. Most of these studies focused on the variations in excretion and clearance of sodium but did not extensively and systematically investigate the possible variations that these hormones may induce in the tubular regulation of all the other electrolytes, urea metabolism, acid-base balance and urinary pH. While insulin action on the kidney is very well-described, the renal tubular impact of incretin-based therapies is less consistent and the results available are scarce. To our knowledge, this is the first review summarizing the effects induced on renal tubules by insulin, glucagon-like peptide-1 (GLP-1) receptor agonists and serine protease dipeptidyl peptidase-4 (DPP4) inhibitors in both healthy and diabetic human subjects. This is significant because it highlights the existence of a renal-gut and pancreas axis which also has a direct tubular effect and enables a deeper understanding of renal physiology.

Cardiorenal syndrome refers to the interrelated dysfunction of the heart or kidney resulting in a cascade of feedback mechanisms, hemodynamic, neurohormonal, and immunological and/or biochemical feedback pathways causing damage in the other organ. Cardiorenal syndrome is categorized into five clinical subtypes depending on the perceived primary precipitant of organ injury and is associated with high morbidity and mortality. Therefore, the development of tools for the earliest identification of cardiorenal syndrome in hospitalized patients is of extremely high significance to ameliorate the prognosis and outcome of these patients. There is increasing interest in identifying molecules serving as biomarkers, reflecting hemodynamic changes, heart and kidney damage and/or dysfunction and oxidative stress-induced cell damage or changes in the extracellular matrix of both the heart and kidneys. Biomarkers provide important insights into the pathophysiology of cardiorenal syndrome and are invaluable tools to predict the decrease in renal function during cardiac dysfunction and vice versa. Based on the pathophysiological mechanisms of cardiorenal syndrome, we reviewed and evaluated the available literature on serum and urinary biomarkers as predictors of kidney and/or heart injury. In addition, heart- and kidney-specific biomarkers were also evaluated based on their reference to kidney and cardiac (dys)function respectively, and whether they would provide any prediction and prognostication of cardiorenal syndrome. In this article, we discuss the current knowledge on the pathophysiology of different types of cardiorenal syndrome, examine the clinical utility of candidate biomarkers in the early diagnosis of cardiorenal syndrome, and guide treatment by evaluating the respective roles of the involved pathophysiological pathways.