Blood Urea Nitrogen In Patients Research Articles

Prognostic Value of Blood Urea Nitrogen for Short-Term Mortality in Patients with Infective Endocarditis.

Blood urea nitrogen (BUN) is a metabolic product validated to be an independent risk factor in the prognosis of several diseases. However, the prognostic value of BUN in patients with infective endocarditis (IE) remains unevaluated. A total of 1371 patients with a diagnosis of IE were included and divided into four groups according to BUN (mmol/L) at admission: < 3.5 (n = 343), 3.5-4.8 (n = 343), 4.8-6.8 (n = 341), and ≥ 6.8 (n = 344). Restricted cubic spline was used to assess the association of BUN with in-hospital mortality. Multivariate analysis was performed to identify the independent risk factors for adverse outcomes. The in-hospital mortality reached 7.4%, while the 6-month mortality was 9.8%. The restricted cubic spline plot exhibited an approximately linear relationship between BUN and in-hospital mortality. Receiver operating characteristics curve analysis showed that the optimal cut-off of BUN for predicting in-hospital death was 6.8mmol/L. Kaplan-Meier analysis showed that patients with BUN > 6.8mmol/L had a higher 6-month mortality than other groups (log rank = 97.9, P < 0.001). Multivariate analysis indicated that BUN>6.8mmol/L was an independent predictor indicator for both in-hospital [adjusted odds ratio (aOR) = 2.365, 95% confidence interval (CI) 1.292-4.328, P = 0.005] and 6-month mortality [adjusted hazard ratio (aHR) = 2.171, 95% CI 1.355-3.479, P = 0.001]. BUN is suitable for independently predicting short-term mortality in patients with IE.

Prognosis prediction performs better in patients with non-cirrhosis hepatitis B virus-related acute-on-chronic liver failure than those with cirrhosis.

The accurate prediction of the outcome of hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is impeded by population heterogeneity. The study aimed to assess the impact of underlying cirrhosis on the performance of clinical prediction models (CPMs). Using data from two multicenter, prospective cohorts of patients with HBV-ACLF, the discrimination, calibration, and clinical benefit were assessed for CPMs predicting 28-day and 90-day outcomes in patients with cirrhosis and those without, respectively. A total of 919 patients with HBV-ACLF were identified by Chinese Group on the Study of Severe Hepatitis B (COSSH) criteria, including 675 with cirrhosis and 244 without. COSSH-ACLF IIs, COSSH-ACLFs, Chronic Liver Failure-Consortium Acute-on-Chronic Liver Failure score (CLIF-C ACLFs), Tongji Prognostic Predictor Model score (TPPMs), Model for End-Stage Liver Disease score (MELDs), and MELD-Sodium score (MELD-Nas) were all strong predictors of short-term mortality in patients with HBV-ACLF. In contrast to a high model discriminative capacity in ACLF without cirrhosis, each prognostic model represents a marked decline of C-index, net reclassification index (NRI), and integrated discrimination improvement (IDI) in predicting either 28-day or 90-day prognosis of patients with cirrhosis. The hazard analysis identified largely overlapping risk factors of poor outcomes in both subgroups, while serum bilirubin was specifically associated with short-term mortality in patients with cirrhosis and blood urea nitrogen in patients without cirrhosis. A subgroup analysis in patients with cirrhosis showed a decline of discrimination of CPMS in those with ascites or infections compared to that in those without. Predicting the short-term outcome of HBV-ACLF by CPMs is optimal in patients without cirrhosis but limited in those with cirrhosis, at least partially due to the complicated ascites or infections.

Oxidized Albumin as a Mediator of Kidney Disease

Renal diseases are a global health concern, and nearly 24% of kidney disease patients are overweight or obese. Particularly, increased body mass index has been correlated with oxidative stress and urinary albumin excretion in kidney disease patients, also contributing to increased cardiovascular risk. Albumin is the main plasma protein and is able to partially cross the glomerular filtration barrier, being reabsorbed mainly by the proximal tubule through different mechanisms. However, it has been demonstrated that albumin suffers different posttranslational modifications, including oxidation, which appears to be tightly linked to kidney damage progression and is increased in obese patients. Plasma-oxidized albumin levels correlate with a decrease in estimated glomerular filtration rate and an increase in blood urea nitrogen in patients with chronic kidney disease. Moreover, oxidized albumin in kidney disease patients is independently correlated with higher plasma levels of transforming growth factor beta (TGF-β1), tumor necrosis factor (TNF-α), and interleukin (IL)-1β and IL-6. In addition, oxidized albumin exerts a direct effect on neutrophils by augmenting the levels of neutrophil gelatinase-associated lipocalin, a well-accepted biomarker for renal damage in patients and in different experimental settings. Moreover, it has been suggested that albumin oxidation occurs at early stages of chronic kidney disease, accelerating the patient requirements for dialytic treatment during disease progression. In this review, we summarize the evidence supporting the role of overweight- and obesity-induced oxidative stress as a critical factor for the progression of renal disease and cardiovascular morbimortality through albumin oxidation.

Monitoring Serum Creatinine, Blood Urea Nitrogen in Patients Brain Injury with Mannitol Therapy

Increased intracranial pressure is a further effect of brain injury due to structural damage and osmotic and water imbalances (Edema). Mannitol works in the proximal tubules and mannitol in the absorption of tubular cells by the mechanism of pinocytosis. The fluid transfer will draw fluid into the intracellular, so that the cell will be switched and broke. This phenomenon is referred to as the phenomenon of "Nephrosis Osmotic", in which mannitol administration may occur as a result of accumulation of drugs in the kidneys due to prolonged exposure to mannitol in the kidney and given dosage. The effects of osmotic diuresis occurring plus the dose and duration of mannitol administration are reported to cause renal function disorders (Scr and BUN). The aim of this study was to analyze changes in serum creatinine and BUN in patients with brain injury from before receiving mannitol therapy and during mannitol treatment. From the results of the study the number of patients who met the inclusion criteria, 32 patients. Serum creatinine, the initial average of 0.85 ± 0.17 mg / dl and the last day of the mean SCr 0.74 ± 0.30 mg / dl. While the mean BUN (Blood Urea Nitrogen) was 11.27 ± 2.75 mg / dl and the mean last day was 17.08 mg / dl ± 8.59 mg / dl. From Serum Creatinine and BUN data it can be concluded that there is no significant change.

Monitoring Serum Creatinine, Blood Urea Nitrogen in Patients Brain Injury with Mannitol Therapy

Increased intracranial pressure is a further effect of brain injury due to structural damage and osmotic and water imbalances (edema). Mannitol works in the proximal tubules and mannitol in the absorption of tubular cells by the mechanism of pinocytosis. The fluid transfer will draw fluid into the intracellular, so that the cell will be switched and broke. This phenomenon is referred to as the phenomenon of "Nephrosis Osmotic", in which mannitol administration may occur as a result of accumulation of drugs in the kidneys due to prolonged exposure to mannitol in the kidney and given dosage. The effects of osmotic diuresis occurring plus the dose and duration of mannitol administration are reported to cause renal function disorders (Scr and BUN). The aim of this study was to analyze changes in serum creatinine and BUN in patients with brain injury from before receiving mannitol therapy and during mannitol treatment. From the results of the study the number of patients who met the inclusion criteria, 32 patients. Serum creatinine, the initial average of 0.85±0.17 mg/dl and the last day of the mean SCr 0.74±0.30 mg/dl. While the mean BUN (Blood Urea Nitrogen) was 11.27±2.75 mg/dl and the mean last day was 17.08 mg/dl±8.59 mg/dl. From Serum Creatinine and BUN data it can be concluded that there is no significant change.

Expression profiles revealed potential kidney injury caused by SARS-CoV-2: a systematic analysis of ACE2 and clinical lessons learned from this discovery.

Background: Novel Coronavirus disease 2019 (COVID-19) was first detected in pneumonia patients in Wuhan, China in December 2019. Based on the current understanding, COVID-19 has become a global issue. Presumably, numerous studies have found that SARS-CoV-2 also transpires in kidney tissue with permanent viral loads. However, it is elusive as to whether SARS-CoV-2 can directly damage the kidney or induce acute renal failure. Hence, to comprehensively understand the impact of COVID-19 on kidney damage, we conducted a retrospective series of case studies to assess kidney functions. Additionally, ACE2 distribution in kidney tissue was analyzed through RNAseq data in open-access databases.Results: According to the findings from transcriptome analysis, we revealed higher ACE2 expression levels in females than males. Similar results were more noticeable in the elderly than in young adults. Furthermore, single-cell RNA sequencing data analysis showed high ACE2 expression in kidney tubule and collecting duct principal cells as well as glomerular parietal epithelial cells. On their admission, the patient's serum creatinine and blood urea nitrogen (BUN) were elevated to between 36.13% and 16.80%, respectively. The estimated glomerular filtration rate (EGFR) of < 60 ml/min per 1.73 m2 was reported in 10.92 % of the patients. Notably, at admission, increased BUN time varied linearly following the generalized additive mixed model. Thus, the hourly-increase of BUN in patients was 0.495 (95%CI: 0.263, 0.726).Conclusion: Based on clinical findings, it was ascertained that COVID-19 can damage renal function, but it seldom causes acute renal failure. Coronavirus may directly bind to ACE2-positive cells and damage kidney tissue in the analysis of scRNA-seq data in kidney tissue. Therefore, this evidence suggests that kidney tissue act as the SARS-CoV-2 infection site and the findings could provide insight into the pathophysiology of kidney damage.Methods: We systematically analyzed ACE2 expression profiles in organs based on open-access datasets for healthy individuals. Meanwhile, single-cell sequencing data for kidney samples were collected and analyzed. Assessments on kidney functions were conducted on 119 selected COVID-19 positive patients admitted from 10th February – 18th March 2020, in hospital in Wuhan City, Hubei Province. Consequently, their clinical records and laboratory findings, such as the estimated glomerular filtration rate (eGFR), Blood Urea Nitrogen (BUN), Creatinine, and Comorbidities, were collected.

Blood urea nitrogen in the prediction of in-hospital mortality of patients with acute aortic dissection.

Blood urea nitrogen (BUN) has been shown to be associated with adverse cardiovascular disease outcomes. The aim of the present study was to evaluate the prognostic role of BUN in patients with acute aortic dissection (AAD). BUN has correlation with in-hospital mortality of patients with AAD. Patients admitted to the emergency room within the first 24 h of onset of AAD were included in the study. BUN levels were measured on admission and the endpoints were mortality during hospi-talization after receiving surgical or endovascular repair. A total of 192 patients with AAD were enrolled. During hospitalization, 19 patients died and 173 patients survived. Increased levels of BUN (8.9 [7.0-9.7] vs. 6.0 [5.1-7.2] mmol/L, p < 0.001) were found in non-survivors compared with those survived. Using multivariable logistic analysis, BUN was an independent predictor of in-hospital mortality in patients with AAD (OR 1.415, 95% CI 1.016-1.971, p = 0.040). Furthermore, using receiver operating characteristic analysis, the optimal cutoff value for BUN was 6.95 mmol/L. Under this value, the area under the curve was 0.785 (95% CI 0.662-0.909, p < 0.001) and the sensitivity and specificity to predict in-hospital mortality was 78.9%, and 72.2%, respectively. Admission BUN levels were an independent predictor for in hospital mortality in pa-tients with AAD.

Factors Associated with Benign Paroxysmal Positional Vertigo: A Chinese Case-Control Study.

BackgroundBenign paroxysmal positional vertigo (BPPV) is one of the most common and most successfully treated vestibular disorders. However, there is a lack of predictive factors for BPPV in clinical practice. We aimed to explore several possible predictive factors for BPPV in the Chinese population.Material/MethodsWe enrolled 240 patients with BPPV from Beijing Chaoyang Hospital between July 2013 and July 2016. Biochemical and hematological markers were obtained along with the history of cardiovascular and cerebrovascular diseases.ResultsSerum uric acid (SUA) [279.0±84.7 vs. 331.0±82.7], hemoglobin A1C (HbA1c) [5.75±1.17 vs. 6.61±1.00], albumin [38.1±3.71 vs. 40.9±4.1], and creatinine [68.4±19.3 vs. 81.5±24.1] were significantly lower in patients with BPPV compared with controls (P<0.05). Multiple logistic regression analysis showed that lower levels of HbA1c and albumin were independently associated with BPPV (P<0.05), with odds ratio (OR) 0.680 (95% CI 0.551–0.839) and 0.338 (95% CI 0.190–0.603), respectively. However, the level of SUA was not independently related with BPPV [OR=0.999 (95% CI 0.991–1.006), P=0.713]. There were no significant differences between the parameters of systolic blood pressure, diastolic blood pressure, blood routine examination, lipid profiles, homocysteine, pre-albumin, and blood urea nitrogen in patients with BPPV vs. controls (P>0.05).ConclusionsLower levels of HbA1c and albumin were independently associated with BPPV. Although the level of SUA was lower in BPPV patients, SUA was not an independent risk factor for BPPV.

Prognostic Value of Blood Urea Nitrogen in Patients Hospitalized With Worsening Heart Failure: Insights From the Acute and Chronic Therapeutic Impact of a Vasopressin Antagonist in Chronic Heart Failure (ACTIV in CHF) Study

Hospitalization for acute decompensated heart failure (ADHF) is associated with a high postdischarge mortality and readmission rate. The association between baseline blood urea nitrogen (BUN) and clinical outcomes in patients admitted for ADHF was evaluated in a post-hoc analysis of the ACTIV in CHF trial. Patients were categorized into quartiles according to baseline BUN. Cox proportional hazards regression was used to test the association between BUN, mortality, and death or readmission within 60 days. Patients in the highest quartile (>40 mg/dL) had the highest 60-day mortality (14.3%, 9.3%, 4.0%, 0%, respectively; P < .001) and the highest rate of death or heart failure hospitalization (30.0%, 21.3% 18.4%, 8.6%; P < .001). After adjustment for covariates, BUN was a statistically significant predictor of both mortality and the composite endpoint of death or heart failure hospitalization at 60 days after hospital discharge. Serum creatinine and estimated creatinine clearance did not predict mortality after covariate adjustment. Higher baseline BUN is a powerful predictor of increased postdischarge mortality in patients hospitalized for heart failure, even in the absence of severe renal failure. Even mild to moderate elevations in baseline BUN were predictive. BUN remains an easily accessible risk stratification tool that physicians should closely monitor in the hospital setting.

Comparison of Prognostic Significance of Amino-Terminal Pro-Brain Natriuretic Peptide Versus Blood Urea Nitrogen for Predicting Events in Patients Hospitalized for Heart Failure

N-terminal pro-brain natriuretic peptide (NT-pro-BNP) and blood urea nitrogen (BUN) predict outcomes in patients with heart failure (HF). However, it is unknown whether NT-pro-BNP is a better prognostic marker than BUN in patients hospitalized with HF. Chart reviews were performed on 257 consecutively hospitalized patients with HF whose NT-pro-BNP levels were drawn at the time of admission. The ability of NT-pro-BNP and BUN to predict the primary end point (death or readmission <30 days after discharge) was determined. Seventy-three patients (28%) reached the primary end point. Patients who reached the primary end point had significantly higher NT-pro-BNP and BUN levels. On multivariate regression analysis, the predictive values of BUN and NT-pro-BNP were very similar: the hazard ratio for NT-pro-BNP greater than the median was 1.81 (p = 0.044), and the hazard ratio for BUN greater than the median was 1.83 (p = 0.039). Analysis of the associations between NT-pro-BNP, BUN, and 30-day death or readmission as end points showed that BUN is a better predictor of outcomes (hazard ratio 3.15, p = 0.012) than NT-pro-BNP (hazard ratio 1.44, p = 0.399). In conclusion, in patients admitted to hospitals with HF, BUN is at least an equal prognosticator of HF rehospitalization or death as NT-pro-BNP. BUN outperforms NT-pro-BNP in predicting mortality in patients with advanced HF. If admitting physicians are confident that the diagnosis of HF is correct, then admission NT-pro-BNP adds little to clinical management.

Room 310, 10/16/2000 9: 00 AM - 10: 30 AM (PD) Are There Clinically Significant Changes of Creatinine and Blood Urea Nitrogen in Patients with Renal Insufficiency after Low-Flow-Sevoflurane?

Room 310, 10/16/2000 9: 00 AM - 10: 30 AM (PD) Are There Clinically Significant Changes of Creatinine and Blood Urea Nitrogen in Patients with Renal Insufficiency after Low-Flow-Sevoflurane?

Atrial natriuretic hormone secretion in patients with renal failure

To study the effects of volume overload and renal failure on plasma levels of immunoreactive atrial natriuretic hormone (IR-ANH), we measured levels of this hormone in normal subjects, in patients with advanced chronic renal failure (CRF) with and without clinically evident volume overload, and in patients with end-stage renal disease (ESRD) treated with chronic hemodialysis. The levels were 13 ± 2 pmol/l in normal volunteers, 77 ± 24 pmol/lin patients with CRF without volume overload, and 219 ± 50 pmol/l in patients with CRF and clinically evident volume overload (analysis of variance, p < 0.001, α = 0.05 compared to normals). In patients with ESRD, the levels of IR-ANH were 145 ± 46 pmol/l before dialysis and decreased to 87 ± 31 after dialysis (p < 0.025). No correlation was found between the decrease in IR-ANH levels and the decrease in weight during dialysis. A significant positive correlation was found between the IR-ANH levels and blood urea nitrogen in patients with CRF (r = 0.658, p < 0.01). Volume overload appears to be the most important stimulatory factor for ANH secretion in renal failure patients but other mechanisms, especially a decrease in metabolic clearance, may also contribute to elevated plasma levels. The increased secretion of ANH in patients with renal failure may be an important adaptive response to volume overload and hypertension.

Effects of renal impairment on liver transplantation

To determine the incidence, prevalence, and prognostic value of preoperative and postoperative renal dysfunction occurring in adults undergoing orthotopic liver transplantation, the records of 102 consecutive adults who underwent orthotopic liver transplantation using cyclosporin A were reviewed. Renal dysfunction was defined arbitrarily as an increase in creatinine or blood urea nitrogen, or both, to 1.5 and 50 mg/dl, respectively, in patients previously having normal renal function or a 50% increase in either creatinine or blood urea nitrogen in patients with preexisting renal dysfunction. Twenty-six of the 102 patients had renal dysfunction before orthotopic liver transplantation. Sixty-eight of the 102 patients studied experienced an episode of renal impairment after orthotopic liver transplantation. Forty-nine of these episodes developed early, having occurred within the first 6 days. Late renal impairment occurred in 36 cases at 32 ± 6 days after orthotopic liver transplantation. Using multivariate analysis, cirrhosis of a noncholestatic nature was found to be an independent predictor of early renal impairment. Trough blood cyclosporin A levels measured by radioimmunoassay were higher in those who experienced early renal impairment or late renal impairment than in those who did not (p < 0.05). Several factors capable of adversely influencing renal function (nephrotoxic drugs, shock, and graft failure) other than cyclosporin A were present also in half of the patients who developed late renal impairment. Overall, 25 patients died. Multivariate analyses identified serious postoperative infection, graft failure, and preoperative renal dysfunction to be independent predictors of mortality.

Aggregation of red cells and plasma viscosity in renal patients treated by haemodialysis or kidney graft effect of proteins and ABO blood groups

A study of aggregation of red cells and plasma viscosity was carried out on renal patients either undergoing haemodialysis or following a cadaveric kidney transplantation. Significant differences ( P < 0.01) between successful and unsuccessful kidney grafts were observed in the dependence of the degree of aggregation of red cells on the fibrinogen level. Plasma viscosity correlated positively with blood urea nitrogen in patients on haemodialysis ( P < 0.01) but not patients having kidney graft. Very significant differences ( P < 0.001) were found between renal patients of A and O, A and B, and B and O blood groups in the dependence of red cell aggregation on the ratios of native albumin/fibrinogen, albumin/globulin, and globulin/fibrinogen.