Acute kidney injury: the experience of a tertiary center of Pediatric Nephrology / Insuficiência renal aguda: experiência de um centro terciário de Nefrologia Pediátrica

ABSTRACT Introduction: Acute kidney injury (AKI) is an abrupt deterioration of kidney function. The incidence of pediatric AKI is increasing worldwide, both in critically and non-critically ill settings. We aimed to characterize the presentation, etiology, evolution, and outcome of AKI in pediatric patients admitted to a tertiary care center. Methods: We performed a retrospective observational single-center study of patients aged 29 days to 17 years and 365 days admitted to our Pediatric Nephrology Unit from January 2012 to December 2021, with the diagnosis of AKI. AKI severity was categorized according to Kidney Disease Improving Global Outcomes (KDIGO) criteria. The outcomes considered were death or sequelae (proteinuria, hypertension, or changes in renal function at 3 to 6 months follow-up assessments). Results: Forty-six patients with a median age of 13.0 (3.5-15.5) years were included. About half of the patients (n = 24, 52.2%) had an identifiable risk factor for the development of AKI. Thirteen patients (28.3%) were anuric, and all of those were categorized as AKI KDIGO stage 3 (p < 0.001). Almost one quarter (n = 10, 21.7%) of patients required renal replacement therapy. Approximately 60% of patients (n = 26) had at least one sequelae, with proteinuria being the most common (n = 15, 38.5%; median (P25-75) urinary protein-to-creatinine ratio 0.30 (0.27-0.44) mg/mg), followed by reduced glomerular filtration rate (GFR) (n = 11, 27.5%; median (P25-75) GFR 75 (62-83) mL/min/1.73 m2). Conclusions: Pediatric AKI is associated with substantial morbidity, with potential for proteinuria development and renal function impairment and a relevant impact on long-term prognosis.

RESUMO Introdução: Insuficiência renal aguda (IRA) é uma deterioração abrupta da função renal. A incidência de IRA pediátrica está aumentando em todo o mundo, em ambientes críticos e não críticos. Nosso objetivo foi caracterizar apresentação, etiologia, evolução e desfechos da IRA em pacientes pediátricos internados em um centro de atendimento terciário. Métodos: Realizamos estudo retrospectivo observacional de centro único de pacientes com idade entre 29 dias a 17 anos e 365 dias internados em nossa Unidade de Nefrologia Pediátrica, de janeiro de 2012 a dezembro de 2021, com diagnóstico de IRA. A gravidade da IRA foi categorizada de acordo com os critérios do Kidney Disease Improving Global Outcomes (KDIGO). Os desfechos considerados foram óbito ou sequelas (proteinúria, hipertensão ou alterações na função renal em avaliações de acompanhamento de 3 a 6 meses). Resultados: Incluímos 46 pacientes com idade mediana de 13,0 (3,5-15,5) anos. Cerca de metade (n = 24; 52,2%) apresentou um fator de risco identificável para o desenvolvimento de IRA. Treze pacientes (28,3%) eram anúricos; todos foram classificados como IRA KDIGO 3 (p < 0,001). Quase um quarto (n = 10; 21,7%) dos pacientes necessitaram de terapia renal substitutiva. Aproximadamente 60% (n = 26) apresentou pelo menos uma sequela, sendo proteinúria a mais comum (n = 15; 38,5%; mediana (P25-75) da relação proteína/creatinina urinária 0,30 (0,27-0,44) mg/mg), seguida de taxa de filtração glomerular (TFG) reduzida (n = 11; 27,5%; mediana (P25-75) da TFG 75 (62-83) mL/min/1,73 m2). Conclusões: A IRA pediátrica está associada à morbidade substancial, com potencial para desenvolvimento de proteinúria e comprometimento da função renal e impacto relevante no prognóstico de longo prazo.

Acute kidney injury in nonagenarians: clinical characteristics and mortality / Injúria renal aguda em nonagenários: características clínicas e mortalidade

Abstract Introduction: Nonagenarians constitute a rising percentage of inpatients, with acute kidney injury (AKI) being frequent in this population. Thus, it is important to analyze the clinical characteristics of this demographic and their impact on mortality. Methods: Retrospective study of nonagenarian patients with AKI at a tertiary hospital between 2013 and 2022. Only the latest hospital admission was considered, and patients with incomplete data were excluded. A logistic regression analysis was conducted to define risk factors for mortality. A p-value < 0.05 was considered statistically significant. Results: A total of 150 patients were included, with a median age of 93.0 years (91.2-95.0), and males accounting for 42.7% of the sample. Sepsis was the most common cause of AKI (53.3%), followed by dehydration/hypovolemia (17.7%), and heart failure (17.7%). ICU admission occurred in 39.3% of patients, mechanical ventilation in 14.7%, vasopressors use in 22.7% and renal replacement therapy (RRT) in 6.7%. Death occurred in 56.7% of patients. Dehydration/hypovolemia as an etiology of AKI was associated with a lower risk of mortality (OR 0.18; 95% CI 0.04-0.77, p = 0.020). KDIGO stage 3 (OR 3.15; 95% CI 1.17-8.47, p = 0.023), ICU admission (OR 12.27; 95% CI 3.03-49.74, p < 0.001), and oliguria (OR 5.77; 95% CI 1.98-16.85, p = 0.001) were associated with mortality. Conclusion: AKI nonagenarians had a high mortality rate, with AKI KDIGO stage 3, oliguria, and ICU admission being associated with death.

Resumo Introdução: Nonagenários constituem um percentual de pacientes internados em ascensão, sendo a injúria renal aguda (IRA) frequente nesses pacientes. Sendo assim, é importante analisar as características clínicas dessa população e seu impacto na mortalidade. Métodos: Estudo retrospectivo de pacientes nonagenários com IRA entre 2013 e 2022 em um hospital terciário. Apenas o último internamento foi considerado e pacientes com dados incompletos foram excluídos. Uma análise por regressão logística foi realizada para definir fatores de risco para mortalidade. Um valor de p < 0,05 foi considerado significativo. Resultados: Foram incluídos 150 pacientes com mediana de idade 93,0 anos (91,2-95,0) e sexo masculino em 42,7%. Sepse foi a causa mais comum de IRA (53,3%), seguida de desidratação/hipovolemia (17,7%) e insuficiência cardíaca (17,7%). Admissão na UTI ocorreu em 39,3% dos pacientes, ventilação mecânica em 14,7%, uso de vasopressores em 22,7% e realização de terapia renal substitutiva (TRS) em 6,7%. Óbito ocorreu em 56,7% dos pacientes. Desidratação/hipovolemia como etiologia da IRA foi associado a menor risco de mortalidade (OR 0,18; IC 95% 0,04-0,77, p = 0,020). Estágio KDIGO 3 (OR 3,15; IC 95% 1,17-8,47, p = 0,023), admissão na UTI (OR 12,27; IC 95% 3,03-49,74, p < 0,001) e oligúria (OR 5,77; IC 95% 1,98-16,85, p = 0,001) foram associados à mortalidade. Conclusão: Nonagenários com IRA apresentaram alta mortalidade e IRA KDIGO 3, oligúria e admissão na UTI foram associadas ao óbito.

Metabolic alkalosis in cystic fibrosis: from vascular volume depletion to impaired bicarbonate excretion.

Cystic fibrosis (CF) is the most common life-threatening genetic disease in the United States and among people of European descent. Despite the widespread distribution of the cystic fibrosis transmembrane conductance regulator (CFTR) along kidney tubules, specific renal phenotypes attributable to CF have not been well documented. Recent studies have demonstrated the downregulation of the apical Cl-/HCO3 - exchanger pendrin (Slc26a4) in kidney B-intercalated cells of CF mouse models. These studies have shown that kidneys of both mice and humans with CF have an impaired ability to excrete excess HCO3 -, thus developing metabolic alkalosis when subjected to excess HCO3 - intake. The purpose of this minireview is to discuss the latest advances on the role of pendrin as a molecule with dual critical roles in acid base regulation and systemic vascular volume homeostasis, specifically in CF. Given the immense prevalence of vascular volume depletion, which is primarily precipitated via enhanced chloride loss through perspiration, we suggest that the dominant presentation of metabolic alkalosis in CF is due to the impaired function of pendrin, which plays a critical role in systemic vascular volume and acid base homeostasis.

Systemic autoinflammatory disease, IgA glomerulonephritis and renal cortical necrosis: coincidence or causation?

We present a patient with a rare systemic autoinflammatory disease (mevalonate kinase deficiency -MKD-) with the identification of two heterozygous variants (c.1129G>A and c.32C>T) in the Mevalonate Kinase gene, detected by next generation sequencing and a highly prevalent glomerulonephritis (IgA nephropathy). The patient presents clinically with a monthly recurrent periodic fever from 12 days of age, accompanied by mucocutaneous lesions (maculopapular rash in extremities, aphthous stomatitis), joint (arthralgias in ankles, wrists and knees), lymphoid (cervical lymphadenopathy, splenomegaly), gastrointestinal (diarrhea, abdominal pain) and kidney (hematuria and proteinuria) with repeated biopsies showing IgA nephropathy alternating activity with chronicity. During follow-up. The patients presented a poor therapeutic response to multiple immunosuppressive regimens used for 7 years (corticosteroids, azathioprine, mycophenolate, cyclophosphamide, rituximab and tocilizumab), and finally a good response to canakinumab. Four years after starting canakinumab, during the course of an infection due to a muscle abscess, the clinical presentation is complicated by a severe renal microvascular event (renal cortical necrosis -RCN-) with acute kidney injury and dialysis requirement. Therecurrent episodes of inflammation due to MKD could act as triggers for the reactivation of glomerulonephritis (which would explain the poor response to immunosuppressants and the rapid progression to histological chronicity) and to generate a microenvironment that predisposes the development of RCN in the face of a non-serious infection. A defect in IgA molecules has been described in MKD, a phenomenon also observed in IgA nephropathy. This raises the challenging hypothesis of a common pathogenetic link between all the patient's clinical manifestations.

Presentamos un paciente con una rara enfermedad autoinflamatoria sistémica (deficiencia de mevalonato quinasa -DMQ-) con la identificación de dos variantes heterocigotas (c.1129G>A y c.32C>T) en el gen Mevalonato Quinasa, detectadas por secuenciación masiva en paralelo y una glomerulonefritis de alta prevalencia (nefropatía por IgA). El paciente presentó un cuadro de fiebre periódica recurrente mensual desde los 12 días de vida, acompañada de lesiones mucocutáneas (rash maculopapular en extremidades, estomatitis aftosa), compromiso articular (artralgias en tobillos, muñecas y rodillas), linfoideo (linfoadenopatía cervical, esplenomegalia), gastrointestinal (diarrea, dolor abdominal) y renal (hematuria y proteinuria) con repetidas biospias mostrando nefropatía por IgA alternando actividad y cronicidad. Durante el seguimiento, tuvo una pobre respuesta terapéutica a múltiples esquemas inmunosupresores utilizados durante 7 años (corticoides, azatrioprina, micofenolato, ciclofosfamida, rituximab y tocilizumab), y buena respuesta finalmente a canakinumab. Cuatro años posteriores al inicio de canakinumab, durante el curso de una infección por un absceso muscular, el cuadro clínico se complica con un evento microvascular renal grave (necrosis cortical renal -NCR-) con fallo renal agudo y necesidad de diálisis. Los episodios recurrentes de inflamación por la DMQ podrían actuar como gatillos para la reactivación de su glomerulonefritis (lo que explicaría la escasa respuesta a inmunosupresores y la progresión rápida a cronicidad histológica) y para generar un microambiente que predisponga el desarrollo de una NCR ante una infección no grave. En la DMQ se ha descripto un defecto en las moléculas de IgA, fenómeno también observado en la nefropatía por IgA. Esto plantea la desafiante hipótesis de un vínculo patogénico común entre todas las manifestaciones clínicas del paciente.

The anti-inflammatory properties of green tea extract protect against gentamicin-induced kidney injury.

We assessed in vivo the protective effects and underlying antioxidant and anti-inflammatory properties of dry green tee extract (GTE) on glomerular and tubular kidney function and structure in an experimental model of gentamicin (GEN)-induced nephrotoxicity. Wistar rats were divided into four groups and treated daily for 10 days. The control group received distilled water; the GTE group received 20 µg/g body weight (BW) GTE by gavage; the GEN group received 100 mg/g BW GEN intraperitoneally; and the GEN+GTE group received GTE and GEN simultaneously, as described above. At the beginning and end of treatment, the serum creatinine, fractional excretion of sodium and potassium, and plasma heme oxygenase (HO)-1 levels and oxidative stress (OS) were assessed. At the end of the experiment, kidney fragments were collected for histological evaluation and immunohistochemical studies of cyclooxygenase (COX)-2 and nuclear factor (NF)kB. The levels of interleukin (IL)-1b, IL-4, IL-6, IL-10 and monocyte chemotactic protein (MCP)-1 were measured in kidney tissue. The results showed that GTE attenuated significantly kidney structural injury and prevented GEN-induced kidney functional injury (glomerular and tubular function). GTE significantly attenuated the kidney tissue increase of the proinflammatory mediators NF-kB, COX2, IL-1b and MCP-1 and significantly increased the kidney expression of the anti-inflammatory cytokines IL-6 and IL-10. However, GTE did not prevent OS increase in GEN-treated animals. In conclusion, GTE protected against GEN nephrotoxicity, likely due to direct blockade of the inflammatory cascade, which might had occurred independently of its antioxidant effect.

Factors associated with the onset of acute kidney injury following subarachnoid hemorrhage.

BACKGROUND: Acute kidney injury (AKI) is a complication often observed in critically ill patients, indicating a worsening prognosis. However, factors predicting AKI in subarachnoid hemorrhage (SAH) patients are unclear. This study aims to elucidate the predictors of AKI occurrence. METHODS: All patients with SAH admitted to the intensive care unit between 2013 and 2019 were included. Patients with very severe SAH who are unsuitable to receive aggressive treatment, those who previously received a contrast medium at another medical institution within 24 hours before admission, and those on maintenance dialysis were excluded. We retrospectively examined blood tests conducted upon admission, oral medications administered, and the total amount of contrast medium used after initiating treatment to investigate their association with AKI occurrence. RESULTS: Of the 254 SAH patients treated during the relevant period, 195 (median age 64 years, 72 males) met the inclusion/exclusion criteria and 32 patients (16.3%) developed AKI. When multivariate analysis was performed using sex, uric acid level, and hemoglobin, which obtained p < 0.01 in the univariate analysis, as variables, only uric acid level was found as an independent predictor of AKI [odds ratio, 1.501; 95% confidence interval, 1.109-2.033, p-value of 0.009]. There was no difference in the occurrence of AKI between survivors and nonsurvivors (12/163 vs. 2/32, P = 0.824). CONCLUSIONS: AKI occurred in 16.3% of the patients with SAH. Patients who developed AKI had significantly higher uric acid levels. SAH with high uric acid levels warrants attention for AKI.

Proton pump inhibitors may increase the risk of cisplatin-induced acute kidney injury in patients with nasopharyngeal carcinoma: a prospective cohort study.

Cisplatin is the most commonly used platinum-based treatment for nasopharyngeal carcinoma (NPC). However, its clinical application is limited owing to its nephrotoxicity and gastrointestinal reactions. Proton pump inhibitors (PPIs) have been reported to increase nephrotoxicity risk in previous studies. We aimed to evaluate whether PPIs increase cisplatin-induced nephrotoxicity in patients with NPC. In total, 295 patients were included in this prospective cohort study: 145 in the PPIs group and 150 in the non-PPIs group. All patients underwent cisplatin-based induction chemotherapy, followed by cisplatin-based concurrent chemoradiotherapy. The PPIs group received 40 mg of intravenous esomeprazole sodium for 7 days in each chemotherapy cycle. Chi-squared test and logistic regression analyses with odds ratios and 95% confidence intervals were applied to assess the association between PPIs and the risk of acute kidney injury (AKI). AKI incidence in the PPIs group was significantly higher than that in the non-PPIs group (P = 0.005). After adjusting for various confounders including demographic features, clinical features, and renal function indices, PPIs use was significantly associated with a higher AKI risk (odds ratio: 2.775; 95% confidence interval 1.280-6.020; P = 0.010). The incidences of acute and chronic kidney diseases were similar between both groups (P > 0.05), whereas the incidence of nausea was lower in the PPIs group than in the non-PPIs group (P = 0.029). This study has shown that PPIs use may increase the risk of cisplatin-induced acute nephrotoxicity in patients with NPC.

Machine learning-based prediction of off-pump coronary artery bypass grafting-associated acute kidney injury.

Background: The cardiac surgery-associated acute kidney injury (CSA-AKI) occurs in up to 1 out of 3 patients. Off-pump coronary artery bypass grafting (OPCABG) is one of the major cardiac surgeries leading to CSA-AKI. Early identification and timely intervention are of clinical significance for CSA-AKI. In this study, we aimed to establish a prediction model of off-pump coronary artery bypass grafting-associated acute kidney injury (OPCABG-AKI) after surgery based on machine learning methods. Methods: The preoperative and intraoperative data of 1,041 patients who underwent OPCABG in Chest Hospital, Tianjin University from June 1, 2021 to April 30, 2023 were retrospectively collected. The definition of OPCABG-AKI was based on the 2012 Kidney Disease Improving Global Outcomes (KDIGO) criteria. The baseline data and intraoperative time series data were included in the dataset, which were preprocessed separately. A total of eight machine learning models were constructed based on the baseline data: logistic regression (LR), gradient-boosting decision tree (GBDT), eXtreme gradient boosting (XGBoost), adaptive boosting (AdaBoost), random forest (RF), support vector machine (SVM), k-nearest neighbor (KNN), and decision tree (DT). The intraoperative time series data were extracted using a long short-term memory (LSTM) deep learning model. The baseline data and intraoperative features were then integrated through transfer learning and fused into each of the eight machine learning models for training. Based on the calculation of accuracy and area under the curve (AUC) of the prediction model, the best model was selected to establish the final OPCABG-AKI risk prediction model. The importance of features was calculated and ranked by DT model, to identify the main risk factors. Results: Among 701 patients included in the study, 73 patients (10.4%) developed OPCABG-AKI. The GBDT model was shown to have the best predictions, both based on baseline data only (AUC =0.739, accuracy: 0.943) as well as based on baseline and intraoperative datasets (AUC =0.861, accuracy: 0.936). The ranking of importance of features of the GBDT model showed that use of insulin aspart was the most important predictor of OPCABG-AKI, followed by use of acarbose, spironolactone, alfentanil, dezocine, levosimendan, clindamycin, history of myocardial infarction, and gender. Conclusions: A GBDT-based model showed excellent performance for the prediction of OPCABG-AKI. The fusion of preoperative and intraoperative data can improve the accuracy of predicting OPCABG-AKI.

Postoperative Acute Kidney Injury After Intraoperative Hypotension in Major Risk Procedures.

Background Reportedly prevalent, intraoperative hypotension (IOH) is linked to kidney injury and increased risk of mortality. In this study, we aimed to assess IOH incidence in high-risk non-cardiac surgery and its correlation with postoperative acute kidney injury (PO-AKI) and 30-day postoperative mortality. Methodology This retrospective cohort study included adult inpatients who underwent elective, non-cardiac, high-risk European Society of Anaesthesiology/European Society of Cardiology surgery from October to November of 2020, 2021, and 2022, excluding cardiac, intracranial, or emergency surgery. IOH was primarily defined by the 2022 Anesthesia Quality Institute. PO-AKI was defined as an increase in serum creatinine ≥0.3 mg/dL within 48 hours, the need for dialysis in dialysis-naïve patients, or the documentation of AKI in clinical records. For univariate analysis, the Mann-Whitney U test and chi-square or Fisher's exact tests were performed, as appropriate. Logistic regression was used to test risk factors for IOH in univariate analysis (p < 0.1). The significance level considered in multivariate analysis was 5%. Results Of the 197 patients included, 111 (56.3%) experienced IOH. After adjustment, surgical time >120 minutes remained associated with higher odds of IOH (odds ratio (OR) = 9.62, 95% confidence interval (CI) = 2.49-37.13), as well as combined general + locoregional (vs. general OR = 3.41, 95 CI% = 1.38-8.43, p = 0.008; vs. locoregional OR = 6.37, 95% CI = 1.48-27.47). No association was found between IOH and 30-day postoperative mortality (p = 0.565) or PO-AKI (p = 0.09). The incidence of PO-AKI was 14.9% (27 patients), being significantly associated with higher 30-day postoperative mortality (p = 0.018). Conclusions Our study highlights the high prevalence of IOH in high-risk non-cardiac surgical procedures. Its impact on PO-AKI and 30-day postoperative mortality appears less pronounced compared to the significant implications of PO-AKI, emphasizing the need for PO-AKI screening and renal protection strategies.

Urine metabolite changes after cardiac surgery predict acute kidney injury.

Background: Acute kidney injury (AKI) is a serious complication in patients undergoing cardiac surgery, with the underlying mechanism remaining elusive and a lack of specific biomarkers for cardiac surgery-associated AKI (CS-AKI). Methods: We performed an untargeted metabolomics analysis of urine samples procured from a cohort of patients with or without AKI at 6 and 24 h following cardiac surgery. Based on the differential urinary metabolites discovered, we further examined the expressions of the key metabolic enzymes that regulate these metabolites in kidney during AKI using a mouse model of ischemia-reperfusion injury (IRI) and in hypoxia-treated tubular epithelial cells (TECs). Results: The urine metabolomic profiles in AKI patients were significantly different from those in non-AKI patients, including upregulation of tryptophan metabolism- and aerobic glycolysis-related metabolites, such as l-tryptophan and d-glucose-1-phosphate, and downregulation of fatty acid oxidation (FAO) and tricarboxylic acid (TCA) cycle-related metabolites. Spearman correlation analysis showed that serum creatinine was positively correlated with urinary l-tryptophan and indole, which had high accuracy for predicting AKI. In animal experiments, we demonstrated that the expression of rate-limiting enzymes in glycolysis, such as hexokinase II (HK2), was significantly upregulated during renal IRI. However, the TCA cycle-related key enzyme citrate synthase was significantly downregulated after IRI. In vitro, hypoxia induced downregulation of citrate synthase in TECs. In addition, FAO-related gene peroxisome proliferator-activated receptor alpha (PPARα) was remarkably downregulated in kidney during renal IRI. Conclusion: This study presents urinary metabolites related to CS-AKI, indicating the rewiring of the metabolism in kidney during AKI, identifying potential AKI biomarkers.

Targeting complement dysregulation: eculizumab in scleroderma renal crisis management-a case-based review.

Systemic sclerosis (SSc) poses significant challenges in clinical management, especially when complicated by scleroderma renal crisis (SRC), a rare but life-threatening manifestation. Here, we report a 41-year-old female patient with SSc who presented with SRC and concurrent thrombotic microangiopathy. Her condition persisted despite conventional treatments such as plasma exchange and renin-angiotensin-aldosterone system blockade. In particular, treatment with eculizumab, a C5 complement inhibitor, led to a rapid improvement in platelet count, reduction in lactate dehydrogenase levels, and complete recovery of renal function. Genetic testing revealed a variant of unknown significance in the thrombomodulin (THBD) gene, which is associated with the complement system. This case highlights the complex interplay between complement dysregulation and SRC, and highlights the promising role of eculizumab in refractory cases. Further investigation of complement involvement and the efficacy of eculizumab in SRC warrants attention to improving therapeutic outcomes in this challenging condition.

Study on the application of a segmented sodium citrate solution anticoagulation strategy in critically ill patients receiving CRRT: a prospective, randomized controlled study.

BACKGROUND: To explore the feasibility and effectiveness of a segmented sodium citrate solution anticoagulation strategy in patients receiving CRRT. METHODS: A prospective, randomized controlled study was conducted. RESULTS: According to the inclusion and exclusion criteria, 80 patients were included and randomly divided into two groups. Moreover, coagulation indices, liver function indices, renal function indices, and SOFA and APACHE II scores did not significantly differ between the two groups (P > 0.05). The coagulation grade of the venous ports in the experimental group was lower than that in the control group and the two groups of filters, but the difference was not statistically significant (P = 0.337). Both sodium citrate solution infusion methods maintained a low blood calcium concentration (0.25-0.45 mmol/L) in the peripheral circulation pathway, and no patient developed hypocalcaemia (< 1.0 mmol/L). The lifespans of the extracorporeal circulation tube in the experimental group and the control group were 69.43 ± 1.49 h and 49.39 ± 2.44 h, respectively (t = 13.316, P = 0.001). CONCLUSION: The segmented citrate solution anticoagulation strategy could extend the lifespan of the extracorporeal circulation tube and improve CRRT efficacy. TRIAL REGISTRATION: The Chinese Clinical Trial Registry number is ChiCTR2200057272. Registered on March 5, 2022.

Acute kidney injury in critically ill obstetric patients: Incidence and role of neutrophil gelatinase-associated lipocalcin - A prospective observational cohort study.

Background and Aims: Data focussing on acute kidney injury (AKI) in obstetric patients admitted to the intensive care unit (ICU) are scarce and even more so regarding the role of neutrophil gelatinase-associated lipocalcin (NGAL) in detecting AKI or predicting outcomes in these patients. Hence, we aim to evaluate the incidence of AKI in obstetric ICU patients and validate the role of urinary and serum NGAL in predicting the onset of AKI and mortality. Methods: This prospective observational cohort included 45 obstetric patients admitted in ICU, excluding those with prior renal dysfunction. Serum creatinine and urine output were monitored for the occurrence of AKI during the ICU stay. The outcome of the patient (survival or death) in the ICU and hospital was recorded, and serum and urinary NGAL were determined at the time of ICU admission. Results: AKI occurred in 32 [71.1%; 95% confidence interval (CI): 55.4%, 86.8%] patients during their ICU stay. Serum NGAL showed an area under receiver operating characteristic curve (AUROCC) of 0.630 (95% CI: 0.417, 0.842) (P = 0.231) for AKI and 0.486 (95% CI: 0.295, 0.676) (P = 0.883) for ICU mortality. Urinary NGAL showed AUROC = 0.472 (95% CI: 0.285, 0.660) (P = 0.772) to predict AKI and 0.430 (95% CI: 0.268, 0.652) (P = 0.684) for ICU mortality. Conclusions: AKI is common amongst critically ill obstetric ICU patients. However, serum and urinary NGAL cannot be advocated to discriminate between patients with or without AKI or between survivors and non-survivors in critically ill obstetric patients.

Comparison of incidence of acute kidney injury after robot-assisted radical prostatectomy with that after open retropubic and extraperitoneal laparoscopic radical prostatectomies in patients with prostate cancer.

Background: We retrospectively evaluated the postoperative renal function in patients who had undergone radical prostatectomy to compare the incidences of postoperative acute kidney injury (AKI) among the patients who had undergone robot-assisted radical prostatectomy (RARP), retropubic radical prostatectomy (RRP), and extraperitoneal laparoscopic radical prostatectomy (exLRP). Materials and methods: Patients with prostate cancer who had undergone radical prostatectomy at our institution between 2008 and 2014 were included. Robot-assisted radical prostatectomy was performed using an intraperitoneal approach in a 25-degree Trendelenburg position, whereas other procedures were performed with the patient in the supine position. We evaluated the serum creatinine levels and estimated glomerular filtration rates immediately after surgery and on postoperative day 1. We evaluated the incidence of AKI after prostatectomy using the Acute Kidney Injury Network criteria of the Kidney Disease: Improving Global Outcomes guidelines. Results: A total of 150 consecutive patients were included, with each of the 3 groups (RARP, RRP, and exLRP) comprising 50 patients. Postoperative AKI was observed in 15 (30.0%), 1 (2.0%), and 3 (6.0%) patients in the RARP, RRP, and exLRP groups, respectively. Stage 1 AKI was observed in all the patients except one. The incidence of AKI in RARP group was significantly higher than that in the other groups (p < 0.001). In the RARP group, the serum creatinine level was significantly elevated immediately after the surgery; however, it returned to baseline on postoperative day 1. Surgical procedures were the only independent factor associated with AKI incidence. Conclusions: This study suggest that compared with RRP and exLRP, RARP is associated with a higher incidence of postoperative AKI, although most patients recover rapidly. Intra-abdominal pneumoperitoneum may contribute to AKI onset.

Incidence of Acute Kidney Injury Post Transcatheter Aortic Valve Implantation (TAVI): A Single-Center Experience.

INTRODUCTION: Transcatheter aortic valve implantation (TAVI) has dramatically changed the approach to treating aortic stenosis, particularly for patients unsuitable for surgical aortic valve replacement. Nevertheless, the possibility of quick deterioration of kidney function, known as acute kidney injury (AKI), post operation is considered one of the complications. OBJECTIVES: The study aimed to determine the incidence of AKI in adults post TAVI. METHODS: This retrospective cohort study focuses on patients who underwent the TAVI procedure at the King Faisal Cardiac Center at the Ministry of National Guard Health Affairs (MNGHA) in Jeddah, Saudi Arabia, from May 2016 to December 2022. Acute kidney injury post TAVI was defined based on RIFLE (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease) criteria. Chi-square tests and independent sample t-tests were used to compare clinical and demographic characteristics between patients who developed AKI with those who did not, using an alpha of 5%. RESULTS: The study involved 103 adult patients. Among them, 11 (10.7%) developed AKI post TAVI within seven days of the procedure, while 92 (89.3%) did not. Findings also revealed that patients with hyperlipidemia and a previous history of kidney diseases faced a higher risk of AKI post TAVI. Despite its valuable insights, the study has limitations due to its retrospective nature and small sample size. CONCLUSIONS: The study emphasizes the importance of identifying patients with hyperlipidemia and pre-existing kidney conditions and closely monitoring renal function. While some preventive methods did not significantly impact AKI occurrences, further research is needed to refine preventive strategies.

Machine Learning with Clinical and Intraoperative Biosignal Data for Predicting Cardiac Surgery-Associated Acute Kidney Injury.

Early identification of patients at high risk of cardiac surgery-associated acute kidney injury (CSA-AKI) is crucial for its prevention. We aimed to leverage perioperative clinical and intraoperative biosignal data to develop machine learning models that predict CSA-AKI. We introduced a novel approach for extracting relevant features from high-resolution intraoperative biosignals to reflect the patient's baseline status, the extent of unfavorable conditions encountered intraoperatively, and data variability. We developed XGBoost models from 2,003 patients across three consecutive perioperative phases using: 1) only preoperative, 2) pre- and intraoperative, and 3) pre-, intra-, and postoperative variables. The predictive performance progressively improved throughout the three consecutive perioperative phases (e.g., AUROC of 0.767 to 0.797 and 0.840), all surpassing the Thakar Score's performance. According to the SHAP method, intraoperative perfusion pressure was most important in the prediction, highlighting the importance of intraoperative patient management and the use of high-resolution biosignal data in predictive modeling to analyze hemodynamic fluctuations during surgery. Early postoperative biomarkers were also important predictors, highlighting the importance of intensified monitoring early after surgery.

Optimizing ICU Care: Machine Learning and PCA for Early Prediction of Renal Replacement Therapy Requirement.

Forecasting the need for Renal Replacement Therapy (RRT) in intensive care units (ICUs) at an early stage can enhance patient outcomes and optimize resource allocation. The study aimed to develop a model for early prediction of Renal Replacement Therapy (RRT) requirement within 24 hours of ICU admission, utilizing machine learning techniques and SHapley Additive exPlanations (SHAP). It assessed various models including Random Forest (RF), Neural Network (NN), and XGBoost, using data from 34,000 ICU admissions. XGBoost showed superior performance in terms of AUPRC, while RF performed better in AUC-ROC. Results were consistent before and after Principal Component Analysis (PCA) and feature evaluation analysis. The top 10 feature models outperformed the PCA model while using fewer inputs. These findings suggest the potential utility of the developed models in accurately predicting RRT requirement within 24 hours of ICU admission, aiding in efficient critical care delivery.

Linagliptin mitigates cisplatin-induced kidney impairment via mitophagy regulation in rats, with emphasis on SIRT-3/PGC-1α, PINK-1 and Parkin-2.

Cisplatin (CDDP) often leads to kidney impairment, limiting its effectiveness in cancer treatment. The lack of mitophagy in proximal tubules exacerbates this issue. Hence, targeting SIRT-3 and PGC1-α shows promise in mitigating CDDP-induced kidney damage. The potential renoprotective effects of linagliptin, however, remain poorly understood. This study represents the first exploration of linagliptin's impact on CDDP-induced kidney impairment in rats, emphasizing its potential role in mitophagic pathways. The experiment involved four rat groups: Group (I) received saline only, Group (II) received a single intraperitoneal injection of CDDP at 6 mg/kg. Groups (III) and (IV) received linagliptin at 6 and 10 mg/kg p.o., respectively, seven days before CDDP administration, continuing for an additional four days. Various parameters, including renal function tests, oxidative stress, TNF-α, IL-1ß, IL-6, PGC-1α, FOXO-3a, p-ERK1, and the gene expression of SIRT-3 and P62 in renal tissue, were assessed. Linagliptin improved renal function, increased antioxidant enzyme activity, and decreased IL-1ß, TNF-α, and IL-6 expression. Additionally, linagliptin significantly upregulated PGC-1α and PINK-1/Parkin-2 expression while downregulating P62 expression. Moreover, linagliptin activated FOXO-3a and SIRT-3, suggesting a potential enhancement of mitophagy. Linagliptin demonstrated a positive impact on various factors related to kidney health in the context of CDDP-induced impairment. These findings suggest a potential role for linagliptin in improving cancer treatment outcomes. Clinical trials are warranted to further investigate and validate its efficacy in a clinical setting.