Multi-Modal Neurorehabilitation for Persisting Post-Concussion Symptoms.

Treatment of the chronic sequela that persist after a mild traumatic brain injury has been challenging with limited efficacy. The aim of this work was to report outcomes obtained from persons who met the criteria of persisting post-concussive symptoms (PPCS), utilizing a novel combination of modalities in a structured neurorehabilitation program. This work was designed as a retrospective, pre-post chart review of objective and subjective measures collected from 62 outpatients with PPCS a mean of 2.2 years post-injury, before and after a multi-modal 5-day treatment protocol. The subjective outcome measure was the 27-item modified Graded Symptom Checklist (mGSC). Objective outcome measures were motor speed/reaction time, coordination, cognitive processing, visual acuity, and vestibular function. Interventions included non-invasive neuromodulation, neuromuscular re-education exercises, gaze stabilization exercises, orthoptic exercises, cognitive training, therapeutic exercises, and single/multi-axis rotation therapy. Pre-post differences in measures were analyzed using the Wilcoxon signed-rank test, with effect size determined by the rank-biserial correlation coefficient. Pre-post treatment comparisons for the subjective mGSC overall, combined symptom measures, individual components of the mGSC, and cluster scores significantly improved for all items. Moderate strength relationships were observed for the mGSC composite score, number of symptoms, average symptom score, feeling in a "fog," "don't feel right," irritability, and physical, cognitive, and affective cluster scores. Objective symptom assessment significantly improved for trail making, processing speed, reaction time, visual acuity, and Standardized Assessment of Concussion. Patients suffering from PPCS ∼2 years after injury may have significant benefits with some moderate effect sizes from an intensive, multi-modal neurorehabilitation program.

Intrarectal Xyloglucan Administration Reduces Disease Severity in the Dextran Sodium Sulfate Model of Mouse Colitis.

BACKGROUND: The pathophysiology of inflammatory bowel diseases remains poorly understood and treatment remains suboptimal for many patients. We hypothesize that the inflammatory milieu secondarily prolongs the injury and attenuates healing. We propose primary or adjuvant therapy with biocompatible adhesives to restore a barrier to protect submucosal structures, particularly stem cells. METHODS: We used the well-described mouse dextran sodium sulfate (DSS) model of colitis resembling human ulcerative colitis to test the therapeutic efficacy of intrarectal administration of the tamarind plant-derived xyloglucan (TXG) polymer adhesive which underwent extensive analytic characterization. Mice in control, DSS-only, TXG-only, and DSS + TXG groups were studied for gross (weight, blood in stool, length of colon) and multiple histologic parameters. RESULTS: Compared to DSS-only mice, TXG prevented the weight loss, occurrence of blood in the stool and colon shortening, with all those parameters not being statistically different from treatment naïve animals. Histologically, there was dramatic and highly statistically significant reduction in the total inflammatory index and protection from goblet cell loss, cellular infiltration, crypt abscess formation, epithelial erosion, granulation tissue, epithelial hyperplasia crypt irregularity and crypt loss. The TXG purity and characterization were established by nuclear magnetic resonance, infrared spectroscopy, differential scanning calorimetry, and texture analysis. CONCLUSION: The striking attenuation of disease severity by intrarectal TXG use warrants future investigations of natural bioadhesives with well-established high safety profiles, and which could potentially be derivatized to include therapeutically active moieties for local drug delivery.

Use of the esa resistance index to guide dosing for anaemia management.

BACKGROUND: Identifying erythropoiesis-stimulating agent (ESA) resistance is important for treating reversible causes, reaching target haemoglobin levels with minimal dosing, avoiding adverse effects and reducing costs. The resistance index (RI, dose/kg weight/g haemoglobin/dl) is reportedly superior to absolute or weight-based dosing. OBJECTIVES: With the growing number of ESA classes and medications, our goal was to develop methodology to establish RI ranges in otherwise healthy haemodialysis patients as a structured approach to identify remediable causes of anaemia. DESIGN: We retrospectively studied anaemia management with darbepoetin in 100 chronic haemodialysis patients and a subgroup of 48 without identifiable conditions that impair erythropoiesis. Data included inflammatory and bone marrow conditions, medications with hematologic effects, catheter use, iron, parathyroid and dialysis measures. RESULTS: The haematologically healthy group was aged 57.1 ± 1.9 SEM years, 33% diabetic, with haemoglobin 10.4 ± 0.2 g/dl. The darbepoetin RI (DRI) values were 0.05 ± 0.01, absolute dose 38.5 ± 3.5 mcg/week and weight-based 0.50 ± 0.05 mcg/kg. Regression analyses included iron saturation, ferritin, parathyroid hormone and urea reduction ratio. DRI was superior to other dosing approaches based on the distribution of results (kurtosis) and discordance between the measures that occurred in 17% of patients at haemoglobin target. CONCLUSIONS: We demonstrate the value of determining the RI for use with expanding ESA choices, using as an example how DRI values can be established for healthy haemodialysis patients so as to guide dosing. When elevated, the RI can trigger evaluation for remediable factors causing hyporesponsiveness even when haemoglobin goals have been reached.

Improved outpatient haemodialysis adequacy using queued schedules.

BACKGROUND: Although technical advances help achieve haemodialysis adequacy, we hypothesise remediable non-therapy factors exacerbate patient dissatisfaction, non-adherence to treatment time and failure to meet dialysis goals. Scheduling inefficiencies lead to the total time in the unit far greater than actual treatment time, impacting facility efficiency and patient frustration. OBJECTIVES: We used queuing theorem principles to optimise schedules by incorporating timing and workflow for every dialysis process step to design a new schedule, rather than the whole-shift blocks at baseline. DESIGN: The goals were to: (1) craft schedules that maximised efficiency and economics from a facility perspective, and (2) minimise total time in the dialysis unit from a patient viewpoint. As dialysis units are held to a national standard of urea clearance, reduction ratios (URRs) were measured for the 3 months before and after the new scheduling was implemented. RESULTS: Dialysis staff and process parameters were measured to craft queued schedules of staggered small groups of patients instead of baseline blocks of 2 large shifts, 24 each. A total of 65 patients changed to groups of 8, with entry-to-exit at 290 minutes for four hours treatments. The URRs improved from 72.8 ± 6.9 to 75.2 ± 5.4% (p < 0.001). Before implementation, only 89% of subjects reached the URR facility compliance target of 65%, and afterwards 97% (p < 0.001). CONCLUSION: Queuing theorem principles can be successfully adopted to optimise haemodialysis scheduling. The resultant staggered timing increases facility efficiency, minimises the long wait time dissatisfier, and is associated with improved URRs with more patients reaching target clearance thresholds.

Trends in anemia care in non-dialysis-dependent chronic kidney disease (CKD) patients in the United States (2006-2015).

BACKGROUND: The objective of the study was to examine overall anemia management trends in non-dialysis patients with chronic kidney disease (CKD) from 2006 to 2015, and to evaluate the impact of Trial to Reduced Cardiovascular Events with Ananesp Therapy (TREAT)'s study results (October 2009) and the US Food and Drug Administration (FDA)'s (June 2011) safety warnings and guidelines on the use of ESA therapy in the current treatment of anemia. METHODS: A retrospective cohort analysis of anemia management in CKD patients using Truven MarketScan Commercial and Medicare Supplemental databases was conducted. Monthly rates and types of anemia treatment for post-TREAT and post-FDA safety warning periods were compared to pre-TREAT period. Anemia management included ESA, intravenous iron, and blood transfusion. A time-series analysis using Autoregressive Integrated Moving Average (ARIMA) model and a Generalized Estimating Equation (GEE) model were used. RESULTS: Between 2006 and 2015, CKD patients were increasingly less likely to be treated with ESAs, more likely to receive intravenous iron supplementation, and blood transfusions. The adjusted probabilities of prescribing ESAs were 31% (odds ratio (OR) = 0.69, 95% confidence interval (CI): 0.67-0.71) and 59% (OR = 0.41, 95% CI: 0.40, 0.42) lower in the post-TREAT and post-FDA warning periods compared to pre-TREAT period. The probability of prescribing intravenous iron was increased in the post-FDA warning period (OR = 1.11, 95% CI: 1.03-1.19) although the increase was not statistically significant in the post-TREAT period (OR = 1.03, 95% CI: 0.94-1.12). The probabilities of prescribing blood transfusion during the post-TREAT and post-FDA warning periods increased by 14% (OR = 1.14, 95% CI: 1.06-1.23) and 31% (OR = 1.31, 95% CI: 1.22-1.39), respectively. Similar trends of prescribing ESAs and iron supplementations were observed in commercially insured CKD patients but the use of blood transfusions did not increase. CONCLUSIONS: After the 2011 FDA safety warnings, the use of ESA continued to decrease while the use of iron supplementation continued to increase. The use of blood transfusions increased significantly in Medicare patients while it remained stable in commercially insured patients. Results suggest the TREAT publication had effected treatment of anemia prior to the FDA warning but the FDA warning solidified TREAT's recommendations for anemia treatment for non- dialysis dependent CKD patients.

Interventions to improve hemodialysis adequacy: protocols based on real-time monitoring of dialysate solute clearance.

BACKGROUND: The monitoring of dialysate ultraviolet (UV) absorbance is a validated technology to measure hemodialysis adequacy and allows for continuous and real-time tracking every session as opposed to the typical once-monthly assessments. Clinical care guidelines are needed to interpret the findings so as to troubleshoot problematic absorbance patterns and intervene during an individual treatment as needed. METHODS: When paired with highly structured clinical care protocols that allow autonomous nursing actions, this technology has the potential to improve treatment outcomes. These devices measure the UV absorbance of dialysate solutes to calculate and then display the delivered as well as predicted clearance for that session. Various technical factors can affect the course of dialysate absorbance, confound the device's readout of clearance results and thus lead to challenges for the dialysis unit staff to properly monitor dialysis adequacy. We analyze optimal and problematic patterns to the device's 'clearance' display (e.g. due to thrombosis of hollow fibers, inadequate access blood flow or recirculation) and provide specific interventions to ensure delivery of an adequate dialysis dose. A rigorous algorithm is presented with representative device monitor display profiles from actual hemodialysis sessions. Procedural rationale and interventions are described for each individual scenario. CONCLUSION: Real-time hemodialysate UV absorbance patterns can be used for protocol-based intradialytic interventions to optimize solute clearance.

Repurposed biological scaffolds: kidney to pancreas.

Advances in organ regeneration have been facilitated by gentle decellularization protocols that maintain distinct tissue compartments, and thereby allow seeding of blood vessels with endothelial lineages separate from populations of the parenchyma with tissue-specific cells. We hypothesized that a reconstituted vasculature could serve as a novel platform for perfusing cells derived from a different organ: thus discordance of origin between the vascular and functional cells, leading to a hybrid repurposed organ. The need for a highly vascular bed is highlighted by tissue engineering approaches that involve transplantation of just cells, as attempted for insulin production to treat human diabetes. Those pancreatic islet cells present unique challenges since large numbers are needed to allow the cell-to-cell signaling required for viability and proper function; however, increasing their number is limited by inadequate perfusion and hypoxia. As proof of principle of the repurposed organ methodology we harnessed the vasculature of a kidney scaffold while seeding the collecting system with insulin-producing cells. Pig kidneys were decellularized by sequential detergent, enzymatic and rinsing steps. Maintenance of distinct vascular and collecting system compartments was demonstrated by both fluorescent 10 micron polystyrene microspheres and cell distributions in tissue sections. Sterilized acellular scaffolds underwent seeding separately via the artery (fibroblasts or endothelioma cells) and retrograde (murine ßTC-tet cells) up the ureter. After three-day bioreactor incubation, histology confirmed separation of cells in the vasculature from those in the collecting system. ßTC-tet clusters survived in tubules, glomerular Bowman's space, demonstrated insulin immunolabeling, and thereby supported the feasibility of kidney-to-pancreas repurposing.

Postoperative hyperkalemia.

Hyperkalemia occurs frequently in hospitalized patients and is of particular concern for those who have undergone surgery, with postoperative care provided by clinicians of many disciplines. This review describes the normal physiology and how multiple perioperative factors can disrupt potassium homeostasis and lead to severe elevations in plasma potassium concentration. The pathophysiologic basis of diverse causes of hyperkalemia was used to broadly classify etiologies into those with altered potassium distribution (e.g. increased potassium release from cells or other transcellular shifts), reduced urinary excretion (e.g. reduced sodium delivery, volume depletion, and hypoaldosteronism), or an exogenous potassium load (e.g. blood transfusions). Surgical conditions of particular concern involve: rhabdomyolysis from malpositioning, trauma or medications; bariatric surgery; vascular procedures with tissue ischemia; acidosis; hypovolemia; and volume or blood product resuscitation. Certain acute conditions and chronic co-morbidities present particular risk. These include chronic kidney disease, diabetes mellitus, many outpatient preoperative medications (e.g. beta blockers, salt substitutes), and inpatient agents (e.g. succinylcholine, hyperosmolar volume expanders). Clinicians need to be aware of these pathophysiologic mechanisms for developing perioperative hyperkalemia as many of the risks can be minimized or avoided.

Life-threatening hyperkalemia in a patient with normal renal function.

With media focus on benefits from reducing sodium intake, there is increased popularity of salt substitutes, typically potassium chloride. While viewed by the public as a healthy alternative to standard table salt, less appreciated is the severe risk with certain comorbidities and medications. We report the case of an elderly female with chronically high salt substitute intake, normal renal function, diabetes, hypertension treated with angiotensin-converting enzyme inhibitor and beta blockade, who developed life-threatening hyperkalemia after a minimally invasive outpatient procedure. We describe the pathophysiology of the disruption in potassium homeostasis and emphasize the importance of dietary history and educating high-risk patients to avoid salt substitutes.

Knuckle cracking: secondary hyperparathyroidism and what your mother did not tell you.

INTRODUCTION: Secondary hyperparathyroidism in end-stage renal disease patients has protean musculoskeletal manifestations. Some of our dialysis patients spontaneously vocalized that they had lost the ability to crack their knuckles and then experienced gratifying restoration after surgical parathyroidectomy. We propose that the physiology and mechanical basis of knuckle cracking would be affected by parathyroid-related mineral and bone disorders. METHODS AND RESULTS: We surveyed all of our chronic dialysis outpatients who had undergone surgical parathyroidectomy. Thirteen (∼12% of the population) individuals were identified: eight males, age 37.7 ± 12.5 years old, dialysis duration of 10.2 ± 7.0 years and peak preoperative intact parathyroid hormone (PTH) levels of 2344 ± 900 pg/mL. Seven patients had no recollection of knuckle cracking issues, with surgery as remote as decades. Six individuals were able to provide adequate histories: four had postoperative restoration of knuckle cracking and expressed great satisfaction from the emotional relief from what appeared to be habitual knuckle cracking. Two of these patients reported rapid return of cracking, occurring in less than ∼2 weeks. CONCLUSIONS: This is the first report of loss of knuckle cracking due to hyperparathyroidism and its cure in 67% of patients, following surgical parathyroidectomy. We propose that parathyroid (e.g. calcific) changes in articular structures (tendons, ligaments) cause reduced elasticity, limited joint surface separation upon flexion, attenuation of cavitation and thus, loss of the audible crack upon vacuum collapse. The psychological 'release' from habitual knuckle cracking may be a motivator from some patients to adhere to complex parathyroid regimens or to pursue surgical intervention.

Congestive renal failure: the pathophysiology and treatment of renal venous hypertension.

Longstanding experimental evidence supports the role of renal venous hypertension in causing kidney dysfunction and "congestive renal failure." A focus has been heart failure, in which the cardiorenal syndrome may partly be due to high venous pressure, rather than traditional mechanisms involving low cardiac output. Analogous diseases are intra-abdominal hypertension and renal vein thrombosis. Proposed pathophysiologic mechanisms include reduced transglomerular pressure, elevated renal interstitial pressure, myogenic and neural reflexes, baroreceptor stimulation, activation of sympathetic nervous and renin angiotensin aldosterone systems, and enhanced proinflammatory pathways. Most clinical trials have addressed the underlying condition rather than venous hypertension per se. Interpreting the effects of therapeutic interventions on renal venous congestion are therefore problematic because of such confounders as changes in left ventricular function, cardiac output, and blood pressure. Nevertheless, there is preliminary evidence from small studies of intense medical therapy or extracorporeal ultrafiltration for heart failure that there can be changes to central venous pressure that correlate inversely with renal function, independently from the cardiac index. Larger more rigorous trials are needed to definitively establish under what circumstances conventional pharmacologic or ultrafiltration goals might best be directed toward central venous pressures rather than left ventricular or cardiac output parameters.

Ultrafiltration therapy for cardiorenal syndrome: physiologic basis and contemporary options.

BACKGROUND: Heart failure (HF) has a high readmission rate in part due to conventional and recently developed therapeutic options having suboptimal results. Extracorporeal and peritoneal ultrafiltration have been advocated as more beneficial methods for fluid removal in decompensated or refractory HF, respectively. METHODS: Traditional and emerging concepts explaining the pathophysiology of HF and the cardiorenal syndrome are reviewed. Extracorporeal and peritoneal ultrafiltration clinical trials are then discussed in terms of potential physiologic benefits, feasibility and their effects on both cardiac and renal function. RESULTS: Ultrafiltration therapy can efficiently correct volume overload in the acute setting, improve cardiac functional and quality of life parameters, and is associated with long-lasting benefits such as reduced HF-related readmissions. Although excessive fluid removal can adversely affect the kidneys, there is evidence that careful protocols can restore diuretic sensitivity and maintain stable renal function; crafting safe parameters has yet to be studied. CONCLUSION: While extracorporeal ultrafiltration is an appealing therapeutic option for patients with acute decompensated HF, determining the optimal fluid removal rate and the impact on renal function need further investigation. Peritoneal dialysis may be an appropriate alternative in the setting of chronic refractory HF, but controlled studies are needed. Further trials are warranted to determine the long-term outcomes from both ultrafiltration modalities in HF.

Mouse stem cells seeded into decellularized rat kidney scaffolds endothelialize and remodel basement membranes.

INTRODUCTION: To address transplant organ shortage, a promising strategy is to decellularize kidneys in a manner that the scaffold retains signals for seeded pluripotent precursor cells to differentiate and recapitulate native structures: matrix-to-cell signaling followed by cell-cell and cell-matrix interactions, thereby remodeling and replacing the original matrix. This would reduce scaffold antigenicity and enable xeno-allografts. RESULTS: DAPI-labeled cells in arterial vessels and glomeruli were positive for both endothelial lineage markers, BsLB4 and VEGFR2. Rat scaffold's basement membrane demonstrated immunolabeling with anti-mouse laminin ß1. Labeling intensified over time with 14 day incubations. CONCLUSION: We provide new evidence for matrix-to-cell signaling in acellular whole organ scaffolds that induces differentiation of pluripotent precursor cells to endothelial lineage. Production of mouse basement membrane supports remodeling of host (rat)-derived scaffolds and thereby warrants further investigation as a promising approach for xenotransplantation. METHODS: We previously showed that murine embryonic stem cells arterially seeded into acellular rat whole kidney scaffolds multiply and demonstrate morphologic, immunohistochemical and gene expression evidence for differentiation. Vascular cell endothelialization was now further tested by endothelial specific BsLB4 lectin and anti-VEGFR2 (Flk1) antibodies. Remodeling of the matrix basement membranes from rat to mouse ("murinization") was assessed by a monoclonal antibody specific for mouse laminin ß1 chain.

Psychoactive "bath salts" intoxication with methylenedioxypyrovalerone.

Abuse of the psychoactive "designer drug" methylenedioxypyrovalerone (MDPV) has become a serious international public health concern because of the severity of its physical and behavioral toxicities. MDPV is the primary ingredient in so-called "bath salts," labeled as such to avoid criminal prosecution and has only been classified recently as a controlled substance in the United States and some other countries. However, it remains a danger because of illegal sources, including the Internet. MDPV is a synthetic, cathinone-derivative, central nervous system stimulant and is taken to produce a cocaine- or methamphetamine-like high. Administered via oral ingestion, nasal insufflation, smoking, intravenous or intramuscular methods, or the rectum, the intoxication lasts 6 to 8 hours and has high addictive potential. Overdoses are characterized by profound toxicities, causing increased attention by emergency department and law enforcement personnel. Physical manifestations range from tachycardia, hypertension, arrhythmias, hyperthermia, sweating, rhabdomyolysis, and seizures to those as severe as stroke, cerebral edema, cardiorespiratory collapse, myocardial infarction, and death. Behavioral effects include panic attacks, anxiety, agitation, severe paranoia, hallucinations, psychosis, suicidal ideation, self-mutilation, and behavior that is aggressive, violent, and self-destructive. Treatment is principally supportive and focuses on counteracting the sympathetic overstimulation, including sedation with intravenous benzodiazepines, seizure-prevention measures, intravenous fluids, close (eg, intensive care unit) monitoring, and restraints to prevent harm to self or others. Clinical presentation is often complicated by coingestion of other psychoactive substances that may alter the treatment approach. Clinicians need to be especially vigilant in that MDPV is not detected by routine drug screens and overdoses can be life-threatening.

Predictive models for maximum recommended therapeutic dose of antiretroviral drugs.

A novel method for predicting maximum recommended therapeutic dose (MRTD) is presented using quantitative structure property relationships (QSPRs) and artificial neural networks (ANNs). MRTD data of 31 structurally diverse Antiretroviral drugs (ARVs) were collected from FDA MRTD Database or package inserts. Molecular property descriptors of each compound, that is, molecular mass, aqueous solubility, lipophilicity, biotransformation half life, oxidation half life, and biodegradation probability were calculated from their SMILES codes. A training set (n = 23) was used to construct multiple linear regression and back propagation neural network models. The models were validated using an external test set (n = 8) which demonstrated that MRTD values may be predicted with reasonable accuracy. Model predictability was described by root mean squared errors (RMSEs), Kendall's correlation coefficients (tau), P-values, and Bland Altman plots for method comparisons. MRTD was predicted by a 6-3-1 neural network model (RMSE = 13.67, tau = 0.643, P = 0.035) more accurately than by the multiple linear regression (RMSE = 27.27, tau = 0.714, P = 0.019) model. Both models illustrated a moderate correlation between aqueous solubility of antiretroviral drugs and maximum therapeutic dose. MRTD prediction may assist in the design of safer, more effective treatments for HIV infection.

Perioperative fluid balance and acute kidney injury.

BACKGROUND: Positive fluid balance (FB) has been linked to adverse clinical outcomes. We performed this study to explore the relationship between perioperative fluid balance and acute kidney injury (AKI). METHODS: The relationships between FB and AKI were explored using a prospective, observational design. Patients were divided into quartiles based on FB status in the first 24 h from initiation of surgery in order to further explore this relationship. RESULTS: One hundred adult patients undergoing cardiovascular surgery were included in the analysis. The major finding of the study was that positive FB occurred early in the intraoperative period and progressed into the postoperative period and that fluid administration was not clearly associated with any identifiable volume-sensitive event. The evolution of positive FB preceded the rise in serum creatinine. Progressive severity of positive FB was associated with increased incidence of AKI. The highest quartile FB group had a five-fold increased risk for AKI (adjusted odds ratio 4.98, 95 % confidence interval 1.38-24.10, p = 0.046) compared to the lowest quartile group, higher postoperative peak serum creatinine values (p < 0.001), surgery-related complications (p < 0.001) and intensive care unit (p < 0.001) and hospital length of stay (p = 0.048). CONCLUSIONS: Positive FB was associated with increased incidence of AKI.

Chronic kidney disease and end-stage renal disease predict higher risk of mortality in patients with primary upper gastrointestinal bleeding.

BACKGROUND: The outcome of gastrointestinal bleeding in chronic kidney disease (CKD) and end-stage renal disease (ESRD) patients is difficult to discern from the literature. Many publications are small, single-center series or are from an era prior to advanced interventional endoscopy, widespread use of proton pump inhibitors or treatment for Helicobacter pylori infections. In this study, we quantify the role of CKD and ESRD as independent predictors of mortality in patients admitted to the hospital with a principal diagnosis of primary upper gastrointestinal bleeding (UGIB). METHODS: We used the Nationwide Inpatient Sample that contains data on approximately 8 million admissions in 1,000 hospitals chosen to approximate a 20% stratified sample of all US facilities. Patients discharged with the principal diagnosis of primary UGIB, CKD or ESRD were identified through the ninth revision of the International Classification of Diseases, clinical modification (ICD-9-CM) codes. The outcome variables included frequency and in-hospital mortality of UGIB in CKD and ESRD patients as compared to non-CKD patients and were analyzed using logistic regression modeling. RESULTS: In 2007, out of a total of 398,213 admissions with a diagnosis of primary UGIB, 35,985 were in CKD, 14,983 in ESRD, and 347,245 in non-renal disease groups. The OR for primary UGIB hospitalization in CKD and ESRD was 1.30 (95% CI 1.17-1.46) and 1.84 (95% CI 1.61-2.09), respectively. The corresponding all-cause mortality OR was 1.47 (95% CI 1.21-1.78) and 3.02 (95% CI 2.23-4.1), respectively. CONCLUSION: Patients with CKD or ESRD admitted with primary UGIB have up to three times higher risk of all-cause in-hospital mortality, warranting heightened vigilance by their clinicians.