Familial Mediterranean fever (FMF) is an autosomal recessive disorder characterized by attacks of fever and diffuse abdominal pain. The primary concern with this presentation is to distinguish it from acute appendicitis promptly. Thus, we aimed to evaluate the role of neutrophil lymphocyte ratio (NLR) to leverage the differential diagnosis of acute FMF attack with histologically proven appendicitis.
Twenty-three patients with histologically confirmed acute appendicitis and 88 patients with acute attack of FMF were included in the study. NLR, C-reactive protein and other hematologic parameters were compared between the groups.
Neutrophil to lymphocyte ratio was significantly higher in patients with acute appendicitis compared to the FMF attack group (8.24 ± 6.31 vs. 4.16 ± 2.44, p = 0.007). The performance of NLR in diagnosing acute appendicitis with receiver operating characteristic analysis with a cut-off value of 4.03 were; 78% sensitivity, 62% specificity, and area under the curve 0.760 (95% confidence interval, 0.655 to 0.8655; p < 0.001).
This study showed that NLR, the simple and readily available inflammatory marker may have a useful role in distinguishing acute FMF attack from acute appendicitis.
Neutrophil-to-lymphocyte ratio; Familial Mediterranean fever attack; Acute appendicitis; Abdominal pain; Inflammation
Anti-proteinase 3; Glomerulonephritis, IGA; Antibodies, antineutrophil cytoplasmic
Hospitalizations due to heart failure are increasing steadily despite advances in medicine. Patients hospitalized for worsening heart failure have high mortality in hospital and within the months following discharge. Kidney dysfunction is associated with adverse outcomes in heart failure patients. Recent evidence suggests that both deterioration in kidney function and renal congestion are important prognostic factors in heart failure. Kidney congestion in heart failure results from low cardiac output (forward failure), tubuloglomerular feedback, increased intra-abdominal pressure or increased venous pressure. Regardless of the cause, renal congestion is associated with increased morbidity and mortality in heart failure. The impact on outcomes of renal decongestion strategies that do not compromise renal function should be explored in heart failure. These studies require novel diagnostic markers that identify early renal damage and renal congestion and allow monitoring of treatment responses in order to avoid severe worsening of renal function. In addition, there is an unmet need regarding evidence-based therapeutic management of renal congestion and worsening renal function. In the present review, we summarize the mechanisms, diagnosis, outcomes, prognostic markers and treatment options of renal congestion in heart failure.
acute kidney injury; fluid management; heart failure; hypervolemia; renal congestion
Erectile dysfunction (ED) is a frequent complaint of elderly subjects, and is closely associated with endothelial dysfunction and cardiovascular disease. Uric acid is also associated with endothelial dysfunction, oxidative stress and cardiovascular disease, raising the hypothesis that an increased serum uric acid might predict erectile dysfunction in patients who are at risk for coronary artery disease.
To evaluate the association of serum uric acid levels with presence and severity of ED in patients presenting with chest pain of presumed cardiac origin.
This is a cross-sectional study of 312 adult male patients with suspected coronary artery disease who underwent exercise stress test (EST) for workup of chest pain and completed a sexual health inventory for men (SHIM) survey form to determine the presence and severity of ED. Routine serum biochemistry (and uric acid levels) were measured. Logistic regression analysis was used to assess risk factors for ED.
Main Outcome Measures
The short version of the international index of erectile function (IIEF-5) questionnaire diagnosed ED (cutoff score ≤21). Serum Uric acid levels were determined. Patients with chest pain of suspected cardiac origin underwent an exercise stress test.
149 of 312 (47.7%) male subjects had ED by survey criteria. Patients with ED were older and had more frequent CAD, hypertension, diabetes, and impaired renal function, and also had significantly higher levels of uric acid, fibrinogen, glucose, CRP, triglycerides compared with patients without ED. Uric acid levels were associated with ED by univariate analysis (OR = 1.36, p = 0.002); however, this association was not observed in multivariate analysis adjusted for eGFR.
Subjects presenting with chest pain of presumed cardiac origin are more likely to have ED if they have elevated uric acid levels.
Uric Acid; Erectile Dysfunction; Coronary Artery Disease; Endothelial Dysfunction
Massive haematuria is a life-threatening condition, demanding immediate management of bleeding. The mortality is very high in the case of delayed management of bleeding, especially in elderly patients with concomitant comorbidity. The treatment options of haematuria are wide, and depend on underlying conditions. However, therapeutic choices are limited in the presence of massive and intractable haematuria caused by disseminated intravascular coagulation (DIC). Ankaferd blood stopper (ABS) is a novel, commercially available, haemostatic agent, which has been approved by the Ministry of Health for local use in Turkey. Here, for the first time in the literature, we report a case of diffuse intravesical bleeding stopped by intravesical use of ABS in a 72-year-old man, haemodialysis patient complicated with sepsis and DIC.
Potassium and sodium share a yin/yang relationship in the regulation of blood pressure (BP). BP is directly associated with the total body sodium and negatively correlated with the total body potassium. Epidemiologic, experimental, and clinical studies have demonstrated that potassium is a significant regulator of BP and further improves cardiovascular outcomes. Hypertensive cardiovascular damage, stroke and stroke-related death are accelerated by salt intake but could be prevented by increased dietary potassium intake. The antihypertensive effect of potassium supplementation appears to occur through several mechanisms that include regulation of vascular sensitivity to catecholamines, promotion of natriuresis, limiting plasma renin activity, and improving endothelial function. In the absence of chronic kidney disease, the combined evidence supports a diet high in potassium content serves a vasculoprotective function, especially in the setting of salt-sensitive hypertension and prehypertension.
dietary potassium; blood pressure; natriuresis; sodium chloride; renin; endothelium
Cardiovascular risk is increased in the early stages of chronic kidney disease (CKD) and also found to be ongoing in renal transplant (Rtx) patients. As a sign of atherosclerosis, increased carotid intima-media thickness (CIMT) has been widely accepted as a strong predictor of cardiovascular disease (CVD) and mortality in CKD patients. A novel markers, soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and neutrophil-to-lymphocyte ratio (NLR) were introduced as potential markers in inflammatory disorders including CKD. The role of Rtx in terms of atherogenesis is still unclear. We aimed to investigate the relationship between sTWEAK, NLR and CIMT in Rtx patients without overt CVD and to compare these results with those obtained from healthy subjects.
Cross-sectional analysis in which CIMT measurements, NLR and serum TWEAK levels were assessed in 70 Rtx patients (29 females; mean age, 40.6 ± 12.4 years) and 25 healthy subjects (13 females, mean age; 37.4±8.8 years).
sTWEAK levels were significantly decreased (p=0.01) and hs-CRP, NLR and CIMT levels of Rtx patients were significantly increased compared to healthy subjects (p<0.0001, p=0.001, p<0.0001, respectively). sTWEAK was also found to be decreased when eGFR was decreased (p=0.04 between all groups). CIMT was positively correlated with sTWEAK and NLR in Rtx patients (r=0.81, p<0.0001 and r=0.33, p=0.006, respectively). sTWEAK was also positively correlated with NLR (r=0.37, p=0.002). In the multivariate analysis only sTWEAK was found to be an independent variable of increased CIMT.
sTWEAK might have a role in the pathogenesis of ongoing atherosclerosis in Rtx patients.
sTWEAK; Neutrophil-to-lymphocyte ratio; Carotid intima-media thickness; Renal transplantation
The triggers of secondary thrombotic thrombopcytopenic purpura (TTP) include drug toxicity, radiation and high-dose chemotherapy, angioinvasive infections, surgery and acute graft versus host disease. TTP secondary to surgery have been reported in a number of cases. Most of the cases have been occurred after open heart surgery. Extensive endothelial damage is held responsible as the initiating mechanism in postoperative TTP cases. However, there is no report of secondary TTP describing development owing to ABO incompatible blood transfusion. Here, we describe a patient who developed TTP after transfusion of ABO incompatible blood during hospitalization for bypass surgery. We also propose a hypothesis which may account for the possible underlying mechanism.
ABO incompatible; blood transfusion; coronary artery bypass grafting surgery; thrombotic thrombocytopenic purpura
Brucellosis is a zoonotic infection that humans contract usually by ingestion of unpasteurized milk and milk products or by direct contact with raw infected animal products. Infection is endemic in many countries, including Turkey. Being a systemic disease, brucellosis may affect almost any part of the body. The peritoneum is a site rarely involved in brucellosis. Most peritonitis episodes involving Brucella species have been spontaneous cases reported in cirrhotic patients with ascites. To our knowledge, the literature contains only 5 cases of Brucella peritonitis related to continuous ambulatory peritoneal dialysis. Here, we report Brucella peritonitis in a continuous ambulatory peritoneal dialysis patient, and we discuss the relevant literature.
Brucellosis; CAPD; peritonitis
Background and Objectives
Cardiovascular disease is prevalent in chronic kidney disease (CKD). Uric acid is increased in subjects with CKD and has been linked with cardiovascular mortality in this population. However, no study has evaluated the relationship of uric acid with angiographically proven coronary artery disease (CAD) in this population. We therefore investigated the link between serum uric acid (SUA) levels and (i) extent of CAD assessed by the Gensini score and (ii) inflammatory parameters, including C-reactive protein (CRP) and pentraxin-3, in patients with mild-to-moderate CKD.
Material and Methods
In an unselected population of 130 patients with estimated glomerular filtration rate (eGFR) between 90 and 30 ml/min/1.73 m2, we measured SUA, serum pentraxin-3, CRP, urinary protein-to-creatinine ratio, lipid parameters and the severity of CAD as assessed by coronary angiography and quantified by the Gensini lesion severity score.
The mean serum values for SUA, pentraxin-3 and CRP in the entire study population were 5.5 ± 1.5 mg/dl, 6.4 ± 3.4 ng/ml and 3.5 ± 2.6 mg/dl, respectively. The Gensini scores significantly correlated in univariate analysis with gender (R = −0.379, p = 0.02), uric acid (R = 0.42, p = 0.001), pentraxin-3 (R = 0.54, p = 0.001), CRP (R = 0.29, p = 0.006) levels, eGFR (R = −0.33, p = 0.02), proteinuria (R = 0.21, p = 0.01), and presence of hypertension (R = 0.37, p = 0.001), but not with smoking status, diabetes mellitus, and lipid parameters. After adjustments for traditional cardiovascular risk factors, only uric acid (R = 0.21, p = 0.02) and pentraxin-3 (R = 0.28, p = 0.01) remained significant predictors of the Gensini score.
SUA and pentraxin-3 levels are independent determinants of severity of CAD in patients with mild-to-moderate CKD. We recommend a clinical trial to determine whether lowering uric acid could prevent progression of CAD in patients with CKD.
Chronic kidney disease; Coronary artery disease; Uric acid; Pentraxin-3
Atherosclerosis, endothelial dysfunction, coronary artery calcification (CAC), and left ventricular hypertrophy are the most commonly encountered risk factors in the pathogenesis of cardiovascular disease in end-stage renal disease patients. Epicardial adipose tissue (EAT) is the true visceral fat depot of the heart. The relationship between coronary artery disease and EAT has been shown in healthy subjects and patients with a high risk of coronary artery disease. In the present study, we aimed to investigate the relationship between EAT and CAC in peritoneal dialysis (PD) patients. Patients and Methods: Forty-five PD patients (18 females, 27 males, with a mean age of 50.6 ± 15 years) and 25 healthy subjects (12 females, 13 males, with a mean age of 52.4 ± 10.7 years) were enrolled in the study. EAT and CAC score (CACS) measurements were performed by a multidetector computed tomography scanner.
EAT of the PD patients was significantly higher than that of the healthy subjects (p = 0.02). When patients were divided into two subgroups (group 1: CACS ≤10, n = 20; group 2: CACS >10, n = 25), EAT was also significantly higher in group 2 patients than in group 1 patients and healthy subjects. Age and EAT were also found to be correlated with CACS ≥10.
There is a relationship between the anatomic assessment of coronary artery lesions by multidetector computed tomography and EAT in PD patients. This relationship might be attributed to increased inflammation and proinflammatory cytokines in uremic patients.
Peritoneal dialysis; Epicardial adipose tissue; Coronary artery calcification; End-stage renal disease
Purpose of review
Investigation into the underlying mechanisms of salt sensitivity has made important advances in recent years. This review examines in particular the effects of sodium and potassium on vascular function.
Sodium chloride (salt) intake promotes cutaneous lymphangiogenesis mediated through tissue macrophages and directly alters endothelial cell function, promoting increased production of transforming growth factor-β (TGF-β) and nitric oxide (NO). In the setting of endothelial dysfunction, such as occurs with aging, diminished NO production exacerbates the vascular effects of TGF-β, promoting decreased arterial compliance and hypertension. Dietary potassium intake may serve as an important countervailing influence on the effects of salt in the vasculature.
There is growing appreciation that, independently of alterations in blood pressure, dietary intake of sodium and potassium promote functional changes in the vasculature and lymphatic system. These changes may serve as compensatory changes that protect against development of salt-sensitive hypertension. While salt sensitivity cannot be ascribed exclusively to these factors, perturbation of these processes promote hypertension during high-salt intake. These studies add to the list of genetic and environmental factors that are associated with salt sensitivity, but in particular provide insight into adaptive mechanisms during high salt intake.
dietary sodium; dietary potassium; nitric oxide; TGF-β; arterial compliance
Common variable immunodeficiency (CVID) is a heterogenous group of predominantly antibody-deficiency disorders that make up the greatest proportion of patients with symptomatic primary hypogammaglobulinemia. The rare coincidence of amyloidosis and hypogammaglobulinemia has been reported previously. Contrary to the usual insidious, slowly progressive disease following hepatitis C infection, a rapidly progressive cirrhotic form can develop in hypogammaglobulinemic patients. We report a HCV-positive patient with a new onset of nephrotic syndrome and systemic amyloidosis secondary to CVID. Blood analyses showed serum creatinine of 1.8 mg/dL and serum albumin of 3.1 gm/dL; 24-h urinary protein was 11 800 mg/day. Serum immunoglobulin levels were IgG 340 mg/dL, IgM 18 mg/dL, IgA 11 mg/dL. Duodenal biopsy revealed AA-type amyloidosis with potassium permanganate and Congo red staining. After a month of antiproteinuric therapy, the proteinuria was reduced to 3350 mg/day.
calcification; constrictive pericarditis; haemodialysis; masked
abdominal aorta; hypertension; pseudocoarctation
Metabolic alkalosis is a rare occurence in hemodialysis population compared to metabolic acidosis unless some precipitating factors such as nasogastric suction, vomiting and alkali ingestion or infusion are present. When metabolic alkalosis develops, it may cause serious clinical consequences among them are sleep apnea, resistent hypertension, dysrhythmia and seizures. Here, we present a 54-year-old female hemodialysis patient who developed a severe metabolic alkalosis due to baking soda ingestion to relieve dyspepsia. She had sleep apnea, volume overload and uncontrolled hypertension due to metabolic alkalosis. Metabolic alkalosis was corrected and the patient's clinical condition was relieved with negative-bicarbonate hemodialysis
baking soda; haemodialysis; metabolic alkalosis