Presence Of Azotemia Research Articles

Risk factors and outcomes associated with external ventricular drain related hemorrhage

ObjectiveThe objective of this study was to determine risk factors predictive of external ventricular drain (EVD)-related hemorrhage and the association of such hemorrhages with mortality, discharge disposition, length of stay (LOS), and total cost. MethodsAfter Institutional Review Board approval, data was collected retrospectively for adult patients requiring EVD placement from 2015 to 2018 at the authors’ institution. Collected data included demographic patient information, peri-procedural factors, and relevant post-procedural measures. Computerized tomography (CT) images and associated radiologic reports were independently reviewed, identifying hemorrhages accompanying EVD placement. ResultsFrom this 487-patient sample, 85 (17.5 %) patients had hemorrhages, including asymptomatic hemorrhages identified on imaging alone. A univariable analysis of patient parameters in the overall cohort was performed to identify possible predictors of hemorrhage. Age (p = 0.002), Charlson Comorbidity Index (CCI) (p < 0.001), platelet count (p = 0.002), presence of uremia (p = 0.035), and the number of times the EVD was replaced (p < 0.001) were associated with hemorrhage in univariable models. The experience of the resident surgeon based on post-graduate year (PGY level) and the number of attempts/passes needed for EVD placement were not associated with hemorrhage risk. Significant predictor of hemorrhage confirmed in a multivariable analysis only included the number of times the EVD was replaced (OR = 2.78, adjusted p < 0.001). Outcomes between EVD-related hemorrhage versus no hemorrhage groups, including mortality, discharge disposition, LOS, and cost, were compared. EVD-related hemorrhage was found to be associated with increased mortality (OR = 3.58, adjusted p < 0.001) and decreased likelihood of discharge home (OR = 0.13, adjusted p = 0.030) in the associated multivariable regressions. ConclusionThe number of times an EVD was replaced was associated with EVD-related hemorrhage outcome. EVD-related hemorrhage is associated with increased mortality and a decreased likelihood of being discharged home.

The Longitudinal Outcome Of Canine (K9) myxomatous mitral valve disease (LOOK-Mitral registry): Baseline characteristics

IntroductionThe Longitudinal Outcome Of Canine (K9) myxomatous mitral valve disease (MMVD) registry (LOOK-Mitral registry) was established to describe the natural history and predictors of outcome in dogs affected by MMVD. This study was intended to describe the baseline characteristics of dogs in the LOOK-mitral registry. AnimalsDogs with echocardiographic evidence of MMVD were prospectively enrolled by thirteen referral centers. ResultsA total of 6102 dogs with MMVD were included. The median age was 10 years (1–19 years), and mixed breed was the most common breed (n = 1,360, 22%). Concomitant diseases were reported in 2459 dogs with chronic respiratory diseases occurring most frequently (14%), followed by the presence of azotemia (6%) and orthopedic diseases (5%). Regarding disease severity, 65% of dogs were in ACVIM Stage-B1, 15% in Stage-B2, and 20% in Stage-C. Dogs in Stage-B1 were younger (p<0.001) than dogs in other stages. Murmur intensity, heart rate during physical examination, and radiographic vertebral heart score were positively associated with the stage. Dogs in Stage-C were more likely to have tachypnea (p<0.001), dyspnea (p<0.001), cough (p<0.001), syncopal episodes (p<0.001), and tachyarrhythmias (p<0.001) compared to dogs in Stage-B1 and B2. Echocardiographic indices of left atrial and ventricular size were positively correlated with the ACVIM stage. Interestingly, 4% of dogs that weighed <20 kg had an increased normalized end-systolic left ventricle internal diameter (>1.26). ConclusionsThis study contributes to a better understanding of the clinical characteristics of dogs affected by MMVD and provides new findings that may be of clinical relevance.

Incidence and treatment of feline renal lymphoma: 27 cases.

Lymphoma is the most common feline hematopoietic malignancy. Incidence of renal lymphoma has not been reported as a subset of a large population of feline lymphoma cases. Previous studies have reported renal lymphoma as both a singular entity as well as a component of multicentric disease. The clinical presentation, diagnostic evaluation, therapy and outcomes related to renal lymphoma have not been reported since Mooney et al in 1987. This retrospective study aimed to describe the incidence of renal lymphoma, clinical signs, treatment and survival. Using a database of cats diagnosed with lymphoma between January 2008 and October 2017, cats with renal lymphoma were selected for further analysis. Cases were retrospectively staged according to Mooney et al (1987) and Gabor et al (1998). Data collected included age, clinical signs, clinicopathologic data, diagnostic imaging findings, lymphoma diagnostic method(s), treatment protocol(s) and survival time. Analyses comparing median survival based on therapy administered, renal lymphoma vs multicentric lymphoma, central nervous system involvement, presence of azotemia, anemia and International Renal Interest Society (IRIS) stage at diagnosis were performed. From a population of 740 cats with lymphoma, 27 cats had renal lymphoma (incidence, 3.6%), and 14 of those cats had multicentric lymphoma. Fewer stage IV and V cases were identified in this data set compared with Mooney et al; however, not all cats were completely staged. Median survival (range) for cats receiving corticosteroids alone compared with those receiving an L-CHOP (L-asparaginase, vincristine, cyclophosphamide, doxorubicin, prednisolone)-based protocol was 50 days (20-1027 days) in the corticosteroid group and 203 days (44-2364 days) for the L-CHOP group (P = 0.753) for cats that died secondary to lymphoma. Neither clinical stage nor other factors were predictive of survival. Prospective studies are required to determine the optimal chemotherapy protocol.

Maxillomandibular Deformity in a Canine with Fibrous Osteodystrophy Secondary to Chronic Kidney Disease

Background: Cases of renal fibrous osteodystrophy are usually associated with nutritional causes, which of renal causes are considered uncommon in dogs. This disorder is characterized by the intense proliferation of fibrous connective tissue in bones, impairing bone stiffness. The aim of this study was to report a case of fibrous osteodystrophy secondary to chronic kidney disease in a canine with a "rubber jaw" facial deformity.Case: A 4-year-old male unneutered mongrel dog weighing 5.2 kg had a history of apathy, progressive weight loss and vomiting for one month, and polyuria and polydipsia for more than three months. In addition, the owner complained about the deformed appearance in the muzzle region of the animal, which was evidenced flexibility of the same, with a displacement of the mandible and maxilla on physical examination, similar to the "rubber jaw". Blood tests revealed macrocytic anemia, elevated total plasma proteins, and lymphopenia-associated neutrophilia, as well as hyperphosphatemia (24 mg/dL), uremia (283.6 mg/dL) and increased creatinine (8.6 mg/dL), ALT (143.2 UI/L) and alkaline phosphatase (3222.2 UI/L), while calcium (8.8 mg/dL) and albumin (1.9 g/dL) were decreased. A serological test for visceral leishmaniasis was also performed, which was negative. Abdominal ultrasound imaging revealed kidneys with alterations in tissue architecture, increased thickness and complete loss of cortico-medullary relationship, while the parathyroid gland was enlarged and spindle-shaped. Cranial radiography showed marked radiopacity of the bilateral maxillary bones, with destruction of the nasal, turbinate and frontal bones, as well as loosening of the teeth and destruction of the mandibular bone matrix, characterizing an aspect of “rubber jaw”. Based on the history, history and evidence of azotemia, hyperphosphatemia and loss of facial bone density, the diagnosis of fibrous osteodystrophy secondary to chronic kidney disease associated with hyperparathyroidism was concluded.Discussion: The clinical and laboratory findings reported in the present study were similar to those described in dogs with renal fibrous osteodystrophy associated with hyperparathyroidism. In the presence of azotemia, the patient was in stage 4 of chronic kidney disease which, despite investigating the infectious etiology, which was negative, remained unknown. Along with chronic kidney disease, the observation of hyperphosphatemia associated with hypokalemia contributed to the clinical investigation, whose pathophysiological mechanisms of this disorder were discussed in this study. The organic alterations observed in the patient's imaging examination coincided with the pathophysiological processes of renal fibrous osteodystrophy. The findings of renal and parathyroid alterations on ultrasound, as well as the damage to the bone matrix, maxillomandibular deformity and loss of bone support evidenced on cranial radiography, led to the conclusion of the diagnosis of renal fibrous osteodystrophy secondary to hyperparathyroidism. Despite the recommended symptomatic therapy, the patient died within 24 hours of hospitalization, and it was not possible to perform a necropsy. This report is highlighted by the occurrence of bone deformity at the maxillary and mandibular level, as a result of renal dysfunction in a young canine, alerting to the importance of complementary exams for proper diagnosis.

Prevalence of acute kidney injury in a population of hospitalized horses.

BackgroundHospital‐acquired acute kidney injury (AKI) in humans and dogs increases morbidity and nonsurvival. Azotemia at presentation has been associated with a poor outcome in horses; however, prevalence and consequences of hospital‐acquired AKI are unreported.Hypothesis/ObjectivesTo evaluate the prevalence of AKI in hospitalized horses, risk factors associated with AKI, and the effect of AKI on short‐term survival. We hypothesized that the prevalence of AKI in horses is similar to that reported in other domestic mammalian species and would be associated with nonsurvival.AnimalsAdult horses hospitalized for >2 days from which a minimum of 2 measurements of serum creatinine concentration were available.MethodsRetrospective cohort study. Clinical records were reviewed and horses grouped according to their baseline serum creatinine concentration and change in serum creatinine concentration from baseline. The associations between signalment, diagnosis, and treatment variables, and the presence of azotemia or AKI were assessed using multinomial logistic regression. The relationship between these conditions and survival to discharge was evaluated.ResultsThree hundred twenty‐five horses were included; 4.3% (14/325) had azotemia at baseline and 14.8% (48/325) developed AKI. There were no significant associations between investigated risk factors and development of AKI. The presence of azotemia and AKI did not significantly affect survival to discharge (P = .08 and .81, respectively).Conclusions and Clinical ImportanceThe prevalence of AKI in this population of hospitalized horses is similar to that reported in dogs and humans; however, in this study population, there was less impact on morbidity and short‐term survival.

ASSOCIATIONS BETWEEN ULTRASOUND AND CLINICAL FINDINGS IN 87 CATS WITH URETHRAL OBSTRUCTION.

Urethral obstruction is a life-threatening form of feline lower urinary tract disease. Ultrasonographic risk factors for reobstruction have not been previously reported. Purposes of this retrospective cross-sectional study were to describe urinary tract ultrasound findings in cats following acute urethral obstruction and determine whether ultrasound findings were associated with reobstruction. Inclusion criteria were a physical examination and history consistent with urethral obstruction, an abdominal ultrasound including a full evaluation of the urinary system within 24 h of hospitalization, and no cystocentesis prior to ultrasound examination. Medical records for included cats were reviewed and presence of azotemia, hyperkalemia, positive urine culture, and duration of hospitalization were recorded. For medically treated cats with available outcome data, presence of reobstruction was also recorded. Ultrasound images were reviewed and urinary tract characteristics were recorded. A total of 87 cats met inclusion criteria. Common ultrasound findings for the bladder included echogenic urine sediment, bladder wall thickening, pericystic effusion, hyperechoic pericystic fat, and increased urinary echoes; and for the kidneys/ureters included pyelectasia, renomegaly, perirenal effusion, hyperechoic perirenal fat, and ureteral dilation. Six-month postdischarge outcomes were available for 61 medically treated cats and 21 of these cats had reobstruction. No findings were associated with an increased risk of reobstruction. Ultrasonographic perirenal effusion was associated with severe hyperkalemia (P = 0.009, relative risk 5.75, 95% confidence interval [1.54-21.51]). Findings supported the use of ultrasound as an adjunct for treatment planning in cats presented with urethral obstruction but not as a method for predicting risk of reobstruction.

Abstract 143: Role of Chronic Kidney Disease Promoted Caspase-1 Activation in Neointimal Hyperplasia

The major cause of vascular access failure is venous stenosis due to neointimal hyperplasia (NH) [62]. Vascular smooth muscle cells (VSMC) are critical for the development of NH lesions, as they have the ability to modulate their phenotype from “contractile” to a “synthetic” in the presence of uremia, through the regulation of sensor genes for uremia danger signals and VSMC-specific differentiation genes. Recent research indicates that Caspase-1 (casp-1) activation plays an essential role in sensing metabolic danger signal-associated molecular patterns[4] and initiating vascular inflammation. Therefore, the goal of this project is to examine the role of CKD-driven casp-1 activation in VSMC and CKD-related NH. We have established a CKD mouse model and published CKD-associated vascular remodeling. We exposed wild type and caspase-1 knockout mice to our CKD model, analyzed and quantified the NH lesion formed. We also examined in vitro and ex-vivo changes in VSMC-specific differentiation genes when exposed to uremic serum and cLDL, in the presence or absence of casp-1 inhibitor. We found that CKD serum induces with casp-1 activation and phenotypic changes in VSMCs from a “contractile” to a “synthetic” phenotype, which are reversed with casp-1 inhibition. In an ex-vivo model using relative quantification we found that VSMC contractile markers α -Actin, Calponin, SM-22, and Smoothelin gene expression of CKD mouse carotid VSMC were higher in casp-1 knockout mice when compared to wild-type (1.40, 1.28, 1.22, 1.41 respectively). Also using an in-vivo model, relative quantification of α-actin decreased from 1.0 to 0.329 when VSMCs were exposed to uremic serum and increased back to 0.588 when casp-1 inhibitor is added. The relative quantification of Calponin also decreased from 1.0 to 0.394 when exposed to uremic serum and increased back to 0.601 with caspa-1 inhibitor. We also found that casp-1 deficiency significantly reversed CKD-related vascular remodeling by reducing NH volume from 1,440,023.70 in wild-type mice to 71,069.97 μm2 in casp-1 knockouts (p-value 0.002). Our results provide a novel insight over the therapeutic potential of casp-1 inhibitors for CKD induced NH.

Retrospective evaluation of presenting temperature of urethral obstructed male cats and the association with severity of azotemia and length of hospitalization: 243 cats (2006–2009)

To evaluate whether the presenting rectal temperature and level of azotemia predicts the length of hospitalization (LOH) in a population of obstructed male cats. To describe the relationships between physical examination parameters, blood electrolytes, and azotemia in a clinical population of obstructed male cats. Retrospective clinical study. Emergency and referral specialty hospitals. Two hundred and forty-three male cats that presented with urethral obstruction between 2006 and 2009. None. No significant association between the hours of hospitalization and rectal temperature was detected (P = 0.39). Blood urea nitrogen (BUN) and creatinine (CREA) concentrations were positively correlated with LOH (P < 0.01). BUN and CREA were significantly higher (P < 0.01) for the hypothermic group compared to the normothermic group. Potassium was negatively correlated to heart rate and rectal temperature but positively correlated to BUN and CREA. No association with regard to rectal temperature and LOH could be demonstrated in this population of cats. However, the presence of azotemia in obstructed male cats appears to provide the clinician with additional information regarding the necessary LOH and eventual cost to the client.

Risk factors for cerebral edema in diabetic ketoacidosis in a developing country

To study the clinical profile and risk factors of cerebral edema in children with diabetic ketoacidosis with specific reference to fluid refractory shock. Retrospective review of medical records. Twelve-bed pediatric intensive care unit of a teaching hospital. Seventy-seven patients admitted to pediatric intensive care unit with a diagnosis of diabetic ketoacidosis over 5 yrs. Medical records were reviewed, and data with respect to patients' age, clinical features, biochemical profile (blood glucose, osmolality, electrolytes, urea, creatinine, arterial pH, PaCO(2), and HCO(3) at admission, 6-12 hrs, 24 hrs, and beyond 24 hrs), cerebral edema, presence of sepsis and shock, treatment details, and primary outcome in terms of survival or death were retrieved. Patients with and without cerebral edema were compared. Variables that were significant on univariate analysis were entered in a multiple logistic regression analysis to determine the predictors for cerebral edema. Odds ratio and 95% confidence interval were calculated using SPSS version 15. Mean age of the patients was 5.6 (standard deviation, 3.8) years. Fifty-five (71.4%) patients had new-onset diabetes mellitus. Cerebral edema was seen in 20 patients (26%). Blood glucose, serum osmolality, and CO(2) values at admission and rate of decline in glucose and osmolality during the first 12 hrs were similar in the cerebral edema and noncerebral edema groups. On multiple logistic regression analysis, fluid refractory shock (odds ratio, 7.3; 95% confidence interval, 1.3-41; p = .025) and presence of azotemia (odds ratio, 4.3; 95% confidence interval, 1.1-16; p = .034) at admission were predictors for development of cerebral edema. Mortality in cerebral edema group was 25% as compared to 3% in the noncerebral edema group. Patients with fluid refractory shock and azotemia at admission had higher odds for development of cerebral edema. Initial blood glucose, effective osmolality, or decline in glucose and osmolality had no association with cerebral edema.

Prognostic factors in radical cystectomy affecting survival.

IntroductionThe aim of the study was to evaluate the prognostic factors in radical cystectomy affecting survival.Material and methodsA total of 100 hundred patients were included in the study. Incontinent diversion was applied to 73 of these, and continent diversion to 27. Prospective and retrospective data of the patients were examined. The prognostic value for survival was evaluated for of lymph node involvement, tumor grade (low grade: grade 0-II, high grade: ≥ III or epidermoid carcinoma), tumor stage (low stage: stage pT0-2, high stage: stage ≥ 3a pT3a), presence of preoperative unilateral of bilateral hydronephrosis, presence of preoperative uremia (serum urea value: ≤ 60), and age (> 70 and ≤ 70 years of age) on survival were investigated. Kaplan-Meier survival analysis and Log-Rank statistical methods were used in the study.ResultsGrade, stage, uremia, and lymph node involvement had significant effects on survival (p values 0.0002, 0.03, 0.01, and 0.02, respectively). Presence of preoperative hydronephrosis and age had no statistically significant effects on survival (p values 0.8 and 0.2, respectively).ConclusionsTumor grade, tumor stage, preoperative uremia, and lymph node involvement are prognostic factors affecting survival. Advanced age and presence of preoperative hydronephrosis have no prognostic value for survival. The presence of uremia in the preoperative assessment of the patients is more important than hydronephrosis.

Association of Zinc Deficiency and Depression in the Patients With End-stage Renal Disease on Hemodialysis

Depression is a common psychological symptom in patients undergoing chronic hemodialysis. In the general population, low serum zinc level is associated with major depression. The current study surveys the possible relationship between the prevalence of depression and plasma level of zinc in patients on hemodialysis (HD). A total of 135 patients with end-stage renal disease (ESRD) on HD were enrolled in the study. The severity of depression was assessed using Beck Depression Inventory (BDI). Plasma zinc level was measured from fasting samples. Mean age of the patients was 52.45 (standard deviation: 15.33) years. In all, 76% of the patients had some degree of depression according to BDI scoring system (BDI >14). The mean level of plasma zinc in the depressed patients was significantly lower than the rest of the patients (67.46 ± 29.7 vs. 85.26 + 40.05). Zinc deficiency may be a reversible cause which might contribute to the increased rate of depression in HD patients. This is the first study reporting the association of zinc deficiency with the presence of depression in HD patients; therefore, these findings need further investigations.

Uremia impacts renal inflammatory cytokine gene expression in the setting of experimental acute kidney injury

Inflammatory cytokines are evoked by acute kidney injury (AKI) and may contribute to evolving renal disease. However, the impact of AKI-induced uremia on proinflammatory (e.g., TNF-alpha, MCP-1, TGF-beta1) and anti-inflammatory (e.g., IL-10) cytokine gene expression remains unknown. This study was undertaken to gain some initial insights into this issue. CD-1 mice were subjected to left renal ischemia-reperfusion (I/R) in the absence or presence of uremia (+/- right ureteral transection). TNF-alpha, MCP-1, TGF-beta1, and IL-10 mRNAs, cytokine protein levels, and RNA polymerase II (Pol II) recruitment to these genes were assessed. Renal cytokine mRNA levels were also contrasted with unilateral vs. bilateral renal parenchymal damage (I/R or ureteral obstruction). Potential effects of uremia on cytokine mRNAs in the absence of parenchymal renal damage [bilateral ureteral transection (BUTx)] were sought. Finally, the impact of simulated in vitro uremia (HK-2 tubular cells exposed to peritoneal dialysate from uremic vs. normal mice) on cytokine mRNA and microRNA profiles was assessed. Uremia blunted TNF-alpha, MCP-1, and TGF-beta1 mRNA increases in all three in vivo parenchymal acute renal failure models. These results were paralleled by reductions in cytokine protein levels and Pol II recruitment to their respective genes. Conversely, uremia increased IL-10 mRNA, both in the presence and absence (BUTx) of parenchymal renal damage. The uremic milieu also suppressed HK-2 cell proinflammatory cytokine mRNA levels and altered the expression of least 69 microRNAs (P < 0.0001). We conclude that both pro- and anti-inflammatory cytokine gene expressions are influenced by uremia, with a potential predilection toward an anti-inflammatory state. Changes in gene transcription (as reflected by Pol II recruitment), and possible posttranscriptional modifications (known to be induced by microRNAs), are likely involved.

Endothelial Progenitor Cells, Neointimal Hyperplasia, and Hemodialysis Vascular Access Dysfunction

Vascular stenosis as a result of neointimal hyperplasia is a major clinical problem that has an impact on multiple and diverse disciplines, including cardiology (coronary restenosis), cardiothoracic and vascular surgery (saphenous vein and polytetrafluoroethylene [PTFE] graft failure), neurology (carotid stenosis), nephrology (dialysis access dysfunction), and transplant medicine (chronic allograft rejection in hearts and kidneys). The traditional response to injury hypothesis on the pathogenesis of neointimal hyperplasia focuses on the migration of medial smooth muscle cells from the media into the intima.1 Recently, there has been a great deal of excitement about the role of circulating smooth muscle progenitor cells in the pathogenesis of neointimal hyperplasia. These cells have been identified in a variety of experimental models of vascular injury,2 and interventions that reduce the number of these cells can attenuate neointimal hyperplasia. In marked contrast to the deleterious effects of smooth muscle progenitor cells on neointimal hyperplasia, circulating endothelial progenitor cells (EPCs) are believed to play an important role in vascular repair and in the inhibition of neointimal hyperplasia.3 See p 12 In this issue of Circulation , Rotmans and colleagues have attempted to achieve the “holy grail” for a vascular access procedure: rapid and complete endothelialization.4 Their experiments are based on a newly developed technique that can coat the surface of stent and graft material with antibodies against CD34 (Orbus Medical Technologies). CD34 is a marker for hematopoietic stem cells, and previous research has demonstrated that coronary stents coated with anti-CD34 have a significant increase in endothelialization as early as 1 hour after deployment because of the binding of circulating CD34+ cells, which then differentiate into endothelial cells.5 Placement of anti-CD34–coated grafts in an arteriovenous model of PTFE graft stenosis by Rotmans et al resulted in almost complete endothelialization of the grafts (both …

Overview of renal bone disease: Causes of treatment failure, clinical observations, the changing pattern of bone lesions, and future therapeutic approach: Management of comorbidities in kidney disease in the 21st century: Anemia and bone disease

Divalent ions, metabolism abnormalities, and hyperparathyroid bone disease noted in patients with chronic kidney disease (CKD) develop early in the course of renal insufficiency. In the last two decades, therapy has focused mostly in treating the bone lesion as well as controlling the secondary hyperparathyroidism. However, recent large epidemiologic studies have highlighted the importance of both hyperphosphatemia and an increase in the calcium burden as major factors leading to the high mortality rate of end-stage renal disease (ESRD) patients [1–3]. Furthermore, a recent study strongly suggests the high mortality rate may be due to an increase in cardiac events [4]. In the present manuscript, the causes for the failure of the original therapeutic goals will be discussed first; the changing pattern in the bone lesions will be assessed second; and third, future therapeutic approaches will be explored, with special emphasis in early therapy and avoiding the cardiovascular abnormalities recently noted in CKD patients.

Intimal Exuberance: Veins in Jeopardy

Address reprint requests to Anupam Agarwal, M.D., Associate Professor of Medicine, Biochemistry and Molecular Biology, Box 100224, University of Florida, 1600 SW Archer Road, Gainesville, FL 32610. E-mail: .ude.lfu.cdren.psren@lawraga

The effects of dehydration on rehabilitation outcomes of elderly orthopedic patients

Mukand JA, Cai C, Zielinski A, Danish M, Berman J. The effects of dehydration on rehabilitation outcomes of elderly orthopedic patients. Arch Phys Med Rehabil 2003;84:58-61. Objective: To study the effects of dehydration, by using the indices of prerenal azotemia and orthostasis, on the rehabilitation outcomes of elderly orthopedic patients. Design: Prospective, pilot study. Setting: Regional inpatient rehabilitation center. Participants: A consecutive sample of 39 patients (29 women, 10 men), ranging in age from 58 to 94 years (mean, 78y), of whom 13 had total hip replacements, 12 had total knee replacements, and 14 had hip fractures. Interventions: Not applicable. Main Outcome Measures: Length of stay (LOS), change in the FIM[trade ] instrument score, and discharge to home. Results: The mean LOS was significantly longer in the group with prerenal azotemia (n=21, 12.9[plusmn]3.0d, t=2.49, P[lt ].01) than in the nonazotemic group (n=18, 9.4[plusmn]4.6d). LOS was also significantly longer in the orthostatic group (n=18, 13.7[plusmn]3.4d, t=2.94, P[lt ].01) than in the nonorthostatic group (n=21, 9.8[plusmn]3.9d). Two-way analysis of variance showed a statistically significant effect on LOS for both azotemia (F=8.4, P=.006) and orthostasis (F=10.5, P=.003). A statistical interaction existed (F=4.7, P=.038), but it was more pronounced in the absence of both conditions, as opposed to the presence of both. LOS for the group with both azotemia and orthostasis was 13.6[plusmn]2.7 days (n=10, F=4.7, P=.038), in contrast to 7.2[plusmn]2.8 days in the group without either condition (n=10). Of the patients who had neither azotemia nor orthostasis, 100% (n=10) went home; 80% (n=8) of patients who had both conditions went home. Logistic regression analysis, however, did not show a statistically significant correlation between discharge to home and the presence of azotemia, orthostasis, or both. Conclusion: Prerenal azotemia and orthostasis are present in a significant number of elderly orthopedic patients and have a major effect on rehabilitation outcomes. [copy ] 2003 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

The Measurement of Cytokine Production Capacity during Dialysis - a New Dynamic Method for the Evaluation of Biocompatibility?

The activation of monocytes and other immunocompetent cells during hemodialysis can be attributed to their contact with immunogenic structures such as membranes, blood lines, and endotoxins. The simple measurement of cytokines in blood cannot completely describe the whole dimension of this event. Stimulation of monocytes and other immunocompetent cells in whole blood with lipopolysaccharides (LPS) for IL-6 and phytohemagglutinine (PHA) for TNF at the start and end of dialysis may make it possible to better analyze cellular response during dialysis. Ten healthy volunteers and 10 patients suffering from chronic renal failure were tested with the commercial whole-blood stimulation assays "Dynamix"-IL-6-DIA and -TNF-alpha-DIA (Biosource Diagnostics, Ratingen, Germany). Then 24 patients undergoing hemodialysis with hemophane (n=12) and polyamide (n=12) membranes were examined before and after dialysis treatment. The unpaired Wilcoxon t- test was used for statistical analysis. Healthy volunteers and patients with chronic renal failure showed no statistical differences in concentrations of TNF-alpha and IL-6 before or after whole blood stimulation (WBS). In comparison to patients with chronic renal failure, pre-WBS concentrations of both cytokines (p<0.034) were increased in patients of each membrane group before dialysis. After whole blood stimulation, no differences were observed. At the end of dialysis treatment, the pre- and post-WBS IL-6 values were both significantly higher in the hemophane group (p=0.049 and p=0.0038, respectively) TNF-alpha concentrations were unchanged. No significant differences in the polyamide group were found between the start and end of treatment for either cytokine. A comparison of these membrane groups showed that only the pre-WBS IL-6 concentration in the hemophane group was elevated (p=0.022) after dialysis. In conclusion, the presence of uremia alone could not influence the cytokine production and release capacity. In our patients, dialysis elevated pre-WBS concentrations of TNF-alpha and IL-6, and increased IL-6 release from immunocompetent cells after whole blood stimulation in the hemophane group. The use of polyamide membranes decreased the action of monocytes and other immunocompetent cells, but could not completely prevent this phenomenon. The whole blood stimulation assays for measurement of TNF-alpha and IL-6 may represent a new, dynamic method for evaluating biocompatibility.

Changes in patterns of 24-hr heart rate variability after kidney and kidney-pancreas transplant.

Transplantation has been shown to improve cardiorespiratory reflex measures of autonomic function. However, there are limited data on how kidney or kidney-pancreas transplantation influence continuous autonomic modulation of heart rate and the clinical utility of 24-hr heart rate variability (HRV) monitoring. Ninety nondiabetic kidney and 30 diabetic kidney-pancreas transplant recipients underwent 24-hr Holter monitoring before and again at 6 and 12 months posttransplantation. Tapes were submitted for determination of HRV including interbeat variability (the proportion of adjacent R-R intervals having a difference <50 msec, the SD of all R-R intervals for the entire recording, and the SD of the averages of R-R intervals calculated over 5-min blocks for the entire recording) which is associated with vagal function, sudden death, and circadian function, respectively. Power spectral analysis quantified total neural, sympathetic, and parasympathetic modulation of the heart in ln(msec2). Nondiabetic kidney recipients showed improvement (P< or =0.05) in the SD of the averages of R-R intervals calculated over 5-min blocks (83.2 vs. 95.7 msec) and the SD of all R-R intervals (94.5 vs. 104.4 msec) by 6 months and all groups showed improvement by 12 months. Kidney-pancreas recipients also showed improved total neural (4.35 vs. 4.64) and sympathetic modulation (2.70 vs. 3.13). Kidney-pancreas recipients had significantly poorer values for each measure (P< or =0.05) at all time points. Cardiac autonomic neuropathy arises in the presence of uremia and diabetes, with severe dysfunction seen when these conditions occur concomitantly. Improvement in cardiac autonomic function follows both kidney and kidney-pancreas transplantation with more pronounced improvement in the circadian measures. Therefore, circadian measures of 24-hr HRV could be used to monitor the restoration of cardiac autonomic function.

The use of dynamic magnetic resonance imaging to evaluate orthotopic continent urinary diversion

Objectives The purpose of this study was to evaluate a dynamic magnetic resonance (MR) examination in patients after radical cystoprostatectomy with a neobladder. Methods All 12 subjects were studied with the injection of gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) and showed normal renal enhancement patterns and upper urinary tracts, except 1 patient who had mild right hydronephrosis. All neobladders were also visualized with gadolinium and 9 of 11 patients were able to void on command. There was close agreement in all cases with the MR findings and other imaging studies. Results A static and dynamic Cd-DTPA contrast medium MR did image the entire urinary system, similar to a computed tomographic scan or intravenous urogram. Renal function data, similar to a renal radioisotope scan, was obtained from the Gd-DTPA scans. A dynamic voiding study provided visualization of the lower genitourinary tract similar to a conventional voiding cystourethrogram. Conclusions We conclude that this single MR technique may provide information similar to that obtained from multiple standard imaging studies in the postoperative assessment of the radical cystectomy patient with a neobladder. It may be especially helpful in the presence of azotemia or contrast allergy.

Colonic necrosis following sodium polystyrene sulfonate (Kayexalate®)-sorbitol enema in a renal transplant patient

The authors present the case of a patient who developed near total colonic necrosis shortly after renal transplantation. The onset of symptoms was temporally related to the administration of sodium polystyrene (Kayexalate; Sanofi Winthrop Pharmaceuticals, New York, NY)-sorbitol enemas for treatment of hyperkalemia. Three similar cases have been reported in the literature. The presence of uremia and the use of sorbitol appear to be common denominators in the pathophysiology of this complication. It is suggested that Kayexalate-sorbitol enemas be avoided in renal transplant patients.