Acute on chronic liver failure (ACLF) is characterized by a high short-term mortality. Liver transplantation (LT) is a potential therapy for patients who do not improve under supportive measurements but the efficacy of LT has not been shown. The aim of this study was to investigate the feasibility of LT and to determine the postoperative outcome of patients with ACLF. All patients referred to our liver unit between 2002 and 2010 were registered in a database. The diagnosis of ACLF was made corresponding to the Asian Pacific Association for the Study of the Liver consensus. The post-LT outcome was compared with a cohort of patients with chronic liver disease transplanted for other indications during the same period. One hundred forty four out of 238 patients fulfilled the ACLF criteria. In the intention-to-treat- analysis the median transplant free survival was 48 days. Multi-organ failure was the major cause of death. Ninety-four patients (65%) were evaluated for LT, 71 (49%) could be listed and 33 patients (23%) finally underwent deceased donor LT resulting in a wait list mortality of 54%. Patients who developed infectious complications, in particular pneumonia and/or sepsis, and patients receiving renal replacement therapy or mechanical ventilation were less likely to undergo LT. The 1- and 5-year survival rates of 87% and 82% were comparable to those of the non-ACLF group. In conclusion, this study shows that LT remains the only therapeutic option in the vast majority of patients with ACLF. However, LT was feasible in only a quarter of patients with a 5-year survival rate of more than 80%. Liver Transpl, 2013. © 2013 AASLD.

Few reports are available concerning outcomes following trauma in transplanted patients. Investigating outcomes for patients in this population may yield helpful information about both immunosuppression and inflammatory responses.This was a retrospective study. The trauma registry was used to identify all patients with a history of solid-organ transplant who were admitted to the trauma center between January 2007 and June 2011. Data were stratified by age, sex, Injury Severity Score (ISS), and length of stay (LOS).During the study period, 50 patients admitted for traumatic injury also had previous organ transplants. We found that white blood cell count was significantly lower for transplanted patients (p < 0.001) and remained significantly lower at each stratification criteria. In addition, LOS was either lower or no different for transplanted patients when data were stratified. Only one patient explicitly had an injured graft (a kidney) secondary to trauma at the time of admission. This resulted in acute renal failure and a doubling of the serum creatinine. Three patients had questionable graft injuries, but graft function remained normal. Seventeen percent of patients developed acute rejection following admission for trauma.Outcomes following injury in patients with previous organ transplant are not worse than outcomes for nontransplanted patients, and transplanted organs are infrequently injured. Prospective data are needed to understand better the balance of inflammatory and anti-inflammatory mediators following acute injury in this population.Therapeutic/care management, level III.

Lymphomatoid granulomatosis is a rare lymphoproliferative disorder composed of rare-to-abundant atypical Epstein Barr virus infected B-cells admixed with numerous reactive T-cells. We report a case of a 42 year-old man presenting with fevers of unknown origin and acute renal failure. CT scan demonstrated lung opacities which progressed to numerous nodules throughout both lungs without any cavitations. Wedge lung biopsy showed nodular polymorphous mononuclear infiltrates containing scattered atypical large Epstein Barr virus positive B-cells consistent with lymphomatoid granulomatosis. The patient responded to chemotherapy, but later underwent relapse and transformation to diffuse large B-cell lymphoma. The clinical and histological features of lymphomatoid granulomatosis and differential diagnoses as related to this case are discussed.

The role of extracorporeal membrane oxygenation (ECMO) as a therapeutic strategy has been very well documented for over a decade now with consistently positive remarks. The aim of the present study was analyzing the outcome of ECMO application in our lung transplant program, especially the feasibility and safety of our ECMO approach. Therefore, we retrospectively analyzed the data of 15 patients recipients requiring ECMO support. We analyzed clinical data, complications, and survival of the lung-transplanted population that needed ECMO support at our institution from 2006-2009. During that period, 19 applications of ECMO were done on 15 adult patients with the following indications: primary graft dysfunction (10 patients), "bridge to transplantation" (five), pulmonary hypertension (three), and severe acute respiratory distress syndrome (one). At 28 days, the overall survival was 93% (14 of 15 patients) and 12 of these patients (80%) survived at least 6 months. Complications included acute renal insufficiency with temporary need of renal replacement therapy (53%), bleeding (33%), critical illness polyneuropathy (66%), and reversible thrombocytopenia (73%). Based on the evaluation of the patients in this analysis, ECMO seems to be a safe therapeutic approach in lung transplant recipients with severe respiratory failure directly after transplantation.

Heart failure is a common medical disorder in elderly people. Previous studies have shown that non-steroidal anti-inflammatory drugs (NSAIDs) were considered to be associated with congestive heart failure (CHF) due to salt and water retention. However there is limited data on NSAIDs-associated CHF in Thai population. The objective of the present study was to identify the significance of NSAIDs-related heart failure.This is a retrospective cohort study. Patient's medical records with the diagnosis of CHF between January 2008 and December 2009 were reviewed The authors divided patients with CHF into two groups according to history of NSAIDs-exposure within a one year prior to admission. Baseline characteristics were compared and Kaplan-Meier analysis was used to determine survival difference.One hundred ninety six CHF patients were included in the present study. NSAIDs-used within one year was confirmed in 47 patients (23.9%). Most of baseline characteristics were comparable for both groups. The major precipitating cause of CHF in NSAIDs-exposed group was statistically significant for acute coronary syndrome (40.4% vs. 14.8%, p-value <0.001), whereas anemia and renal failure failed to show statistical significance with p-value 0.859 and 0. 370, respectively. Overall mortality showed no difference in both groups with p-value of 0.639.Previous studies considered NSAIDs to be associated with CHF due to salt and water retention. However in the Thai population, there was an increasing incidence of acute coronary syndrome in concomitant with decompensated CHF Overall mortality in both groups was not significantly different.

Tubulointerstitial nephritis and uveitis (TINU) syndrome is a rare disorder defined by the combination of biochemical abnormalities, tubulointerstitial nephritis, and uveitis. We describe a 12-year-old female, presented with a ten-day history of fever, characterized by sudden onset and rapid spontaneous resolution in few hours, accompanied by shivering, extreme fatigue, and loss of appetite. Laboratory values were consistent with renal failure of tubular origin. Renal biopsy confirmed a tubulointerstitial nephritis, with acute tubulitis, polymorphonuclear infiltration, and microabscesses. The renal interstitium was occupied by a dense inflammatory infiltrate, consisting of lymphocytes, plasma cells, and neutrophils. Glomerular structures were preserved. Ophthalmological examination that suggested a previous asymptomatic bilateral uveitis and HLA typing (HLA-DQA1∗0101/0201 and HLA-DQB1∗0303/0503) further supported the suspect of TINU syndrome. TINU syndrome is probably an underdiagnosed disorder, responsible for many cases of idiopathic anterior uveitis in young patients, especially in those who have asymptomatic renal disease and when proper diagnostic tests are not performed at the time of presentation.

OBJECTIVES

Acute kidney injury (AKI) is one of the most frequently occurring complications after off-pump coronary artery bypass graft (OPCAB). Hyperglycaemia is a major, potentially modifiable risk factor of adverse outcome after cardiac surgery known to aggravate organ damage. The aim of this study was to address the association between intraoperative glucose concentration and postoperative AKI in patients who underwent OPCAB.

METHODS

The medical records of 880 consecutive patients were retrospectively reviewed. Patients were divided into three groups according to the time-weighted average of intraoperative glucose concentrations (<110, 110-150 and >150 mg/dl), and the incidence of AKI (increase of serum creatinine to >2.0 mg/dl and 2 × most recent preoperative value or a new requirement for dialysis) was compared. Multivariate logistic regression analysis was performed to identify independent risk factors for postoperative AKI.

RESULTS

The incidence of AKI was higher in patients with a glucose level >150 mg/dl than in patients with a glucose level = 110-150 mg/dl [8% (20 of 251) vs 3% (14 of 453), P = 0.004]. On multivariate analysis, glucose >150 mg/dl (odds ratio [OR], 2.78; 95% confidence interval [CI], 1.12-6.86, P = 0.027), coefficient of variation of glucose (OR, 1.04; 95% CI, 1.01-1.07, P = 0.027) and preoperative serum creatinine >1.4 mg/dl (OR, 8.81; 95% CI, 3.90-19.9, P < 0.001) were identified as independent risk factors for postoperative AKI.

CONCLUSIONS

Intraoperative glucose concentration >150 mg/dl and increased variability of glucose were independently associated with AKI after OPCAB. Tight intraoperative glycaemic control (<110 mg/dl) does not seem to provide additional benefit in terms of AKI.

Chronic heart failure often leads to worsening of the renal function. Mediators of this process include inflammatory and neuroendocrine factors. CCN1 (Cyr 61), a member of growth factor-inducible immediate early genes, which modulates inflammation and fibrogenesis, is excreted with urine in the early phase of acute renal injury and may be involved in the pathogenesis of the cardiorenal syndrome. The aim of the study was to evaluate CCN1 protein abundance and localization in the kidney of IL-6-deficient C57BL/6J (IL-6 KO) mice and respective wild-type (WT) animals in basal conditions and in animals with chronic heart failure twelve weeks after myocardial infarction. Age- and sex-matched mice from both strains subjected to sham operation served as controls. One group of WT animals subjected to myocardial infarction was treated with antagonist of AT1 receptor telmisartan over 12 weeks. Abundance and localization of CCN1 protein in kidney were assessed with Western blotting and immunohistochemistry, respectively. In all groups the strongest immunohistochemical reaction for CCN1 was observed in distal convoluted tubules and in smaller arteries, however, the total expression of CCN1 protein was lower in IL-6 KO mice in comparison to WT animals. The main difference in CCN1 distribution between the examined genotypes was lack of reaction in internal renal medulla and very weak reaction in proximal convoluted tubules in IL-6 KO mice. Experimental heart failure only slightly attenuated the expression of CCN1 protein in the kidney of WT mice and had no effect in IL-6 KO mice. Although, blockade of AT1 receptor did not alter CCN1 protein expression in kidneys of WT mice after myocardial infarction, it significantly changed its CCN1 distribution in the renal tubular system. (Folia Histochemica et Cytobiologica 2013, Vol. 51, No. 1, 84-91).

PURPOSE:

Hemolacria is a rare phenomenon of bloody tears caused by various ocular and systemic conditions, as well as psychological, pharmacologic, and idiopathic etiologies. Hemolacria is typically a benign process; however, serious systemic associations can exist. It is predominantly unilateral and self-limiting, but because of limited literature, its prevalence and predilection toward a specific gender, race, or age is not known.

CASE REPORT:

An 82-year-old Caucasian male presented for an emergent eye examination with an acute onset of hemolacria of the right eye (OD). Patient medical history was extensive with coronary artery disease, atrial fibrillation, lipidemia, insulin-dependent diabetes, uncontrolled hypertension, and untreated severe renal failure. Before the incident, patient medication included warfarin, 81 mg of aspirin, insulin, glipizide, and blood pressure regime with which the patient was noncompliant. The patient was forwarded to urgent care to address his stage 2 hypertension and referred for a medical evaluation, which included a complete blood count, an International Normalized Ratio, a prothrombin time, and a glycated hemoglobin.

CONCLUSIONS:

Spontaneous resolution of the hemolacria occurred within 24 hr after evaluation and restoration of blood pressure to normal range. Before follow-up, the patient died because of kidney failure. After a review of pertinent laboratory results and literature, the etiology of this patient's hemolacria could be attributed to either uncontrolled hypertension, chronic renal failure, aggressive anticoagulant therapy, and/or diabetes. An extensive literature review of documented etiologies and management is included.

In cardiorenal syndrome (CRS) type 2, chronic heart failure (HF) results in the onset or progression of chronic kidney disease (CKD). Examples of CRS type 2 (CRS2) include progressive CKD resulting from chronic HF in congenital or acquired heart disease or from repeated bouts of acute decompensated HF. Animal data and clinical studies indicate that extended periods of chronic HF result in altered renal hemodynamics followed by progressive renal pathology. Experimental and clinical data indicate that CRS2 is characterized by mild to moderate proteinuria, a progressive decline of glomerular filtration rate, and an elevated expression of renal injury biomarkers. Important pathophysiological triggers of renal disease progression include chronic increases in renal venous pressure, maladaptive activation of the renin-angiotensin-aldosterone axis and the sympathetic nervous system, as well as a chronic inflammatory state. Intrarenal oxidative stress and proinflammatory signaling precipitate structural injury, including glomerulosclerosis and tubulointerstitial fibrosis. Yet, clinical interventional trials that directly test the impact of renin-angiotensin system antagonists and β-blockers on the progression of CKD in CRS2 are lacking. Secondary analyses of trials designed to assess the impact of these agents on cardiovascular endpoints have failed to show a consistent benefit regarding renal functional parameters. In contrast, left ventricular assist device placement and cardiac resynchronization therapy in HF patients consistently improved renal function, suggesting a marked potential for reversibility in many cases of CRS2. Future research should be directed towards the evaluation of novel biomarkers to improve the diagnosis, severity grading as well as our understanding of the pathophysiology of CRS2. In addition, there is a need for interventional trials in HF patients to address long-term renal endpoints incorporating clinical information and measures of renal function as well as renal injury.