Higher Serum Urea Concentrations Research Articles

Serum urea concentration and risk of 16 site-specific cancers, overall cancer, and cancer mortality in individuals with metabolic syndrome: a cohort study.

The relationship between serum urea concentration and cancer in patients with metabolic syndrome (MetS) remains unclear. This study aimed to investigate the association between serum urea concentration and 16 site-specific cancers, overall cancer incidence, and cancer mortality in individuals with MetS. We analysed the data of 108,284 individuals with MetS obtained from the UK Biobank. The Cox proportional hazards model was used to determine the association between serum urea concentration at recruitment and cancer. The Benjamini-Hochberg correction was used to account for multiple comparisons. Over the median follow-up period of 11.86years, 18,548 new incident cases of cancer were documented. There were inverse associations of urea concentration with overall cancer incidence, and the incidence of oesophageal and lung cancers, with respective hazard ratios (95% confidence intervals) [HR (95% CI)] for the highest (Q4) vs lowest (Q1) urea quartiles of 0.95 (0.91-0.99), 0.68 (0.50-0.92), and 0.76 (0.64-0.90). However, high serum urea concentrations increased the male prostate cancer risk (HR 1.15; 95% CI 1.02-1.30). Although the Cox model indicated a protective effect of higher urea levels against stomach (HR 0.67; 95% CI 0.45-0.98; p = 0.040; FDR 0.120) and colorectal cancer (HR 0.86; 95% CI 0.74-0.99; p = 0.048; FDR 0.123), no strong evidence of association was found after applying the Benjamin-Hochberg correction. Moreover, across the median follow-up period of 13.77years for cancer mortality outcome, 5034 cancer deaths were detected. An "L-shaped" nonlinear dose-response relationship between urea concentration and cancer mortality was discovered (p-nonlinear < 0.001), and the HR (95% CI) for urea concentration Q4 vs Q1 was 0.83 (0.77-0.91). Serum urea concentration can be considered as a valuable biomarker for evaluating cancer risk in individuals with MetS, potentially contributing to personalised cancer screening and management strategies.

Acute gastroenteritis-related acute kidney injury in a tertiary care center.

Acute gastroenteritis (AGE) can cause acute kidney injury (AKI) via hypoperfusion mechanisms. Early detection of AKI caused by AGE can significantly decrease mortality rates. In Saudi Arabia, studies investigating the association between AGE and AKI are limited; thus, we aimed to fill this knowledge gap. Analyze all cases of AGE reported in tertiary-care hospitals to assess the prevalence of AKI among AGE patients. Retrospective cohort SETTINGS: Single tertiary-care center PATIENTS AND METHODS: The study included patients treated for AGE between October 2017 and October 2022. Stool culture was used to diagnose AGE. Inclusion criteria were infective diarrhea and/ or vomiting, and availability of data (demographics, comorbidities, malignancies, length of hospital stay, vital signs at the time of diagnosis, dehydration, causative agents of diarrhea, hemodialysis status, and laboratory data. Prevalence of AKI among AGE patients and factors associated with development of AKI. 300 patients diagnosed with AGE. Of the 300 patients with AGE, 41 (13.6%) had AKI, those older than 60 years were more likely to develop AKI. The most frequent cause of AGE was Salmonella spp. (n=163, 53.3%), whereas AKI was most common in Clostridium difficile AGE patients (n=21, 51.2%). Furthermore, the most common comorbidity in the present study was malignancy, especially leukemia and lymphoma the risk of AKI was independently associated with mild dehydration, higher serum urea concentrations and low GFR values. Patients hospitalized for diarrheal disease are at an increased risk of developing AKI due to dehydration and comorbid conditions. It is crucial to keep kidney function in mind for AGE patients as this is associated with a high mortality rate and poor prognosis. The main limitation of this study was its retrospective design. Another limitation is that it is limited to a single center. None.

Mechanism of how carbamylation reduces albumin binding to FcRn contributing to increased vascular clearance.

Chronic kidney disease results in high serum urea concentrations leading to excessive protein carbamylation, primarily albumin. This is associated with increased cardiovascular disease and mortality. Multiple methods were used to address whether carbamylation alters albumin metabolism. Intravital two-photon imaging of the Munich Wistar Frömter (MWF) rat kidney and liver allowed us to characterize filtration and proximal tubule uptake and liver uptake. Microscale thermophoresis enabled quantification of cubilin (CUB7,8 domain) and FcRn binding. Finally, multiple biophysical methods including dynamic light scattering, small-angle X-ray scattering, LC-MS/MS and in silico analyses were used to identify the critical structural alterations and amino acid modifications of rat albumin. Carbamylation of albumin reduced binding to CUB7,8 and FcRn in a dose-dependent fashion. Carbamylation markedly increased vascular clearance of carbamylated rat serum albumin (cRSA) and altered distribution of cRSA in both the kidney and liver at 16 h post intravenous injection. By evaluating the time course of carbamylation and associated charge, size, shape, and binding parameters in combination with in silico analysis and mass spectrometry, the critical binding interaction impacting carbamylated albumin's reduced FcRn binding was identified as K524. Carbamylation of RSA had no effect on glomerular filtration or proximal tubule uptake. These data indicate urea-mediated time-dependent carbamylation of albumin lysine K524 resulted in reduced binding to CUB7,8 and FcRn that contribute to altered albumin transport, leading to increased vascular clearance and increased liver and endothelial tissue accumulation.

Hypervolemic hypernatremia is the most common type of hypernatremia in the intensive care unit.

A high incidence of hypervolemic hypernatremia has been described in patients recovering from acute kidney injury (AKI) in intensive care units. However, this has been limited to only a few cases. One hundred fifty adult patients recovering from AKI in the intensive care unit of a single institution during a 6-year period, who developed hypernatremia during the course of their illness, were investigated. Serum and urine electrolytes, osmolality, urea nitrogen and creatinine were measured. The weights of these patients at the time of hypernatremia development and at presentation to the hospital were also measured. Even though the hypernatremia was mild in most patients (146-160 mEq/L), the average rise in serum sodium concentration was 14.5 ± 7.1 mEq/L. Of the 34 patients who had all urinary studies available, the average urine osmolality was 436 ± 128 mmol/kg of which 172 ± 54 mmol/L was contributed by sodium, potassium and their accompanying anion. Another 204 ± 96 mmol/L was accounted for by urea and creatinine (mainly urea). Almost all the patients had hypervolemia as evidenced by the presence of edema and an average weight gain of more than 9 ± 11 kg between the time of presentation and the onset of hypernatremia despite likely having lost muscle mass from being in the intensive care unit for several days. The weight data were available in 54 patients, and only eight of these patients had lost weight at the time of the development of hypernatremia. Hypervolemic hypernatremia is by far the most common cause of hypernatremia in patients in the intensive care unit. Even though the patients are in negative fluid balance at the time of the development of the hypernatremia, earlier saline administration has caused massive volume overload despite the ongoing losses. Post-AKI diuresis in the face of inability to maximally concentrate the urine because of renal failure often leads to mainly mild elevations in serum sodium concentration. The urine solute is mainly urea because of the often high serum urea concentrations with little electrolytes being present in the urine.

The health and performance of cows fed large amounts of urea

SUMMARYFrom 6 weeks before calving to the end of lactation 2 groups of 8 cows were fed a ration incorporating a dairy nut containing 29 g/kg urea or an isocaloric isonitrogenous nut containing fish-meal and groundnut. During the 18 weeks after calving, concentrates were fed to appetite. 305-d yields of milk (7023 and 5796 kg) and lactose (345.7 and 273.4 kg) were significantly lower in the urea-fed cows (P&lt; 0·05). Intakes of dry matter, metabolizable energy and digestible crude protein were similar in both groups until 18 weeks after calving when feeding according to yield commenced, but by 6 weeks after calving the urea-fed cows lost only 5% of their immediate post-calving weight compared with 7% in the controls. There was no evidence of ammonia toxicity in the urea-fed cows. Blood glucose concentrations were similar in both groups, but higher serum urea concentrations in the urea-fed cows suggested that there was poor utilization of ingested N. A model proposed by Royet al.(1977) has been used to calculate the requirements of rumen-degradable protein and undegraded protein (UDP) of the 2 groups from their energy intakes and milk yields. Between 4 and 11 weeks post-calving, dietary requirement for UDP closely matched intake of UDP. It is concluded that UDP intake was a major factor in determining the peak milk yield. Mechanisms by which the degradability of the dietary protein might influence milk yield are discussed.