The predictors of catheter-related bloodstream infections in patients undergoing hemodialysis: A single center experience.

BACKGROUND: Here we aimed to investigate the predictors of catheter-related bloodstream infections (CRBSI) in patients with acute kidney injury or chronic kidney disease who required renal replacement therapy through a non-tunneled hemodialysis catheter. METHODS: A total of 111 patients who received non-tunneled hemodialysis catheters were retrospectively evaluated. Patients were divided into two groups; those who developed CRBSI and those who did not. Patient's demographic data, laboratory results at admission, information regarding catheter infections, and culture results were obtained from electronic medical records. RESULTS: The mean age of the patients was 64 ± 16 years, and 51 of them were male. CRBSI occurred in 14 patients (12.6%). Admission serum albumin level (OR: 0.119, 95% CI: 0.019-0.756, p = 0.024), admission mean platelet volume (OR: 2.207, 95% CI: 1.188-4.100, p = 0.012) and catheter duration (OR: 1.580, 95% CI: 1.210-2.064, p = 0.001) were independent predictors for the CRBSI development. ROC curve analysis demonstrated that a catheter duration of 22 days was predictive for presence of CRBSI (78% sensitivity, 76% specificity, AUC: 0.825, 95% CI: 0.724-0.925, p < 0.001). CONCLUSIONS: Prolonged catheter duration, low serum albumin, and high mean platelet volume independently predict the development of CRBSI in patients undergoing hemodialysis for acute kidney injury or chronic kidney disease.

Is Vitamin D Deficiency Associated With Metabolic Syndrome in Renal Transplant Recipients?

Renal transplantation is the gold standard method for the treatment of end-stage renal failure. The main causes of graft loss are chronic allograft dysfunction and death with functioning graft due to cardiovascular diseases. Metabolic syndrome (MetS) is common in renal transplant recipients (RTRs). Vitamin D deficiency or insufficiency is common in RTRs. Studies suggest that vitamin D deficiency or insufficiency may lead to the development of MetS apart from impairment in calcium and bone metabolism. We aimed to investigate the relationship between vitamin D deficiency and MetS in patients with renal transplantation. One hundred forty-one RTRs were included in the study. MetS prevalence was 63.8%. Mean vitamin D level was 17.2 ± 10. 2 ng/mL. Patients were divided into 2 groups according to vitamin D level. Patients with vitamin D levels below 25 ng/mL were in group 1; those above were group 2. There were no differences regarding the presence of metabolic syndrome; presence of diabetes mellitus; hypertension; systolic and diastolic blood pressure; waist circumference; glucose; creatinine; triglyceride; or HDL level between groups (P > .05). The area under curves (confidence interval [CI] 95%) of vitamin D level to predict MetS were 0.58 (0.48-0.68) (P > .05). We did not find any relationship between vitamin D level and MetS. This result may be related to the small sample size of our study. Investigation of this relationship with large study groups are needed to clearly determine this relationship.

Assessment of Mean Platelet Volume in Patients with AA Amyloidosis and AA Amyloidosis Secondary to Familial Mediterranean Fever: A Retrospective Chart - Review Study.

BACKGROUND Amyloidosis is a protein-misfolding disease characterized by the deposition of aggregated proteins in the form of abnormal fibrils that disrupt tissue structure, ultimately causing disease. Amyloidosis is very frequent in untreated familial Mediterranean fever (FMF) patients and it is the most important feature that determines the prognosis of FMF disease. The mean platelet volume (MPV) in FMF has been previously studied. However, whether MPV level in FMF patients is lower or higher compared to healthy controls remains a topic of ongoing debate. In this study, we aimed to investigate MPV values and to assess the correlation between MPV and proteinuria in patients with AA amyloidosis and AA amyloidosis secondary to familial Mediterranean fever (AA-FMF) through a retrospective chart-review. MATERIAL AND METHODS This study was carried out on 27 patients with AA amyloidosis, 36 patients with AA amyloidosis secondary to FMF (a total of 63 patients with AA), and 29 healthy controls. There was no statistically significant difference between the AA patients and the control group (p=0.06) or between the AA-FMF group and the control group in terms of MPV values (p=0.12). RESULTS We found a statistically significant negative correlation between MPV and thrombocyte count in all groups (p<0.05 for all groups), but there was no correlation between MPV and proteinuria levels in AA patients (p=0.091). CONCLUSIONS While similar results also exist, these findings are contrary to the majority of previous studies. Therefore, further controlled clinical prospective trials are necessary to address this inconsistency.

Chronic rhinosinusitis, endothelial dysfunction, and atherosclerosis.

BACKGROUND: Chronic inflammation is associated with accelerated atherosclerosis, endothelial dysfunction (ED), and cardiovascular diseases. Because chronic rhinosinusitis (CRS) is an inflammatory disease, it may be associated with the development of ED and accelerated atherosclerosis. OBJECTIVE: To investigate the relationship between CRS and carotid intima-media thickness (CIMT), flow-mediated dilation (FMD) of the brachial artery, and microalbuminuria. MATERIALS AND METHODS: This cross-sectional study included 38 patients with CRS and 29 healthy controls. In addition to measuring spot urine albumin-creatinine ratios, FMD of the brachial artery and CIMT were assessed noninvasively. RESULTS: Patients with CRS had lower FMD scores (p = 0.031), higher CIMT scores (p = 0.005), and a higher urinary albumin-creatinine ratio (p = 0.036) compared with healthy controls. In a multivariate analysis, CIMT and FMD were independently associated with the presence of CRS. However, the relationship between urinary albumin and creatinine, and the presence of CRS was no longer observed. CONCLUSIONS: CRS is associated with ED and atherosclerosis, as indicated by decreased FMD and increased CIMT in patients with CRS. Further studies are necessary to identify the exact pathophysiologic mechanisms responsible for our findings.

An unusual case of peritonitis after vaginal leak in a patient on peritoneal dialysis / Un caso infrecuente de peritonitis tras fuga vaginal en un paciente en diálisis peritoneal

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Lowering Uric Acid With Allopurinol Improves Insulin Resistance and Systemic Inflammation in Asymptomatic Hyperuricemia.

BACKGROUND: Hyperuricemia is an independent predictor of impaired fasting glucose and type 2 diabetes, but whether it has a causal role in insulin resistance remains controversial. Here we tested the hypothesis that lowering uric acid in hyperuricemic nondiabetic subjects might improve insulin resistance. METHODS: Subjects with asymptomatic hyperuricemia (n = 73) were prospectively placed on allopurinol (n = 40) or control (n = 33) for 3 months. An additional control group consisted of 48 normouricemic subjects. Serum uric acid, fasting glucose, fasting insulin, HOMA-IR (homeostatic model assessment of insulin resistance), and high-sensitivity C-reactive protein were measured at baseline and at 3 months. RESULTS: Allopurinol-treated subjects showed a reduction in serum uric acid in association with improvement in fasting blood glucose, fasting insulin, and HOMA-IR index, as well as a reduction in serum high-sensitivity C-reactive protein. The number of subjects with impaired fasting glucose significantly decreased in the allopurinol group at 3 months compared with baseline (n = 8 [20%] vs n = 30 [75%], 3 months vs baseline, P < 0.001). In the hyperuricemic control group, only glucose decreased significantly and, in the normouricemic control, no end point changed. CONCLUSIONS: Allopurinol lowers uric acid and improves insulin resistance and systemic inflammation in asymptomatic hyperuricemia. Larger clinical trials are recommended to determine if lowering uric acid can help prevent type 2 diabetes.

Retrobulbar blood flow and carotid intima-media thickness alteration may relate to subclinic atherosclerosis in patients with chronic inflammatory diseases.

OBJECTIVE: AA amyloidosis occurs in the setting of longstanding inflammation. An increased incidence of coronary artery disease (CAD) was noted in patients with chronic inflammatory disease (CID). Retrobulbar blood flow predicts future macrovascular events including CAD. Increase in carotid artery intima-media thickness is regarded as a marker for early atherosclerosis. The relationship between chronic inflammation and atherosclerosis is well known; however, the connection between amyloidosis-advanced CIDs and retrobulbar microvascular function and carotid intima-media thickness (CIMT) is unidentified. We aimed to investigate whether retrobulbar microcirculation and CIMT were impaired or not in amyloidosis-advanced CID patients compared to normal subjects. METHODS: Fourteen patients with renal AA amyloidosis and a group of healthy volunteers were included in the study. Measurement of CIMT and retrobulbar blood flow velocities was performed with ultrasound scanner and color Doppler ultrasonography. RESULTS: The CIMT of patients with renal amyloidosis was significantly thicker than that of the normal population (p < 0.001). The resistivity index of the ophthalmic artery (OA) of patients with renal amyloidosis was significantly higher than the study group (p < 0.001). CONCLUSION: This study demonstrates that accelerated atherosclerosis which can be shown by increased OA resistivity index and CIMT are found in amyloidal-related CID patients.

Renalase: Another puzzle piece between hypertension and simple renal cysts?

BACKGROUND AND AIM: Since renalase is mostly expressed in kidney tubules, simple renal cyst (SRC) originates from the kidney tubules, and both conditions are related to hypertension, it may be possible that SRC is associated with increased renalase levels. Therefore, in the current study we aimed to confirm the relation between renalase and epinephrine levels, the association between SRC and renalase levels and the association between renalase, blood pressure levels and endothelial dysfunction. MATERIALS AND METHODS: We made a cross-sectional study including 75 patients with SRC, and 51 controls were included to the study. Flow-mediated dilatation (FMD) was assessed, and serum renalase and epinephrine levels were determined. RESULTS: Patient with SRC had lower renalase, higher epinephrine and lower FMD levels when compared to patients without SRC (p < 0.05). Log renalase was correlated with log epinephrine (r = -0.302, p = 0.001) and log FMD (r = 0.642, p < 0.0001). There was no correlation between renalase and urine albumin/creatinine ratio and glomerular filtration rate. In univariate analysis, age, glomerular filtration rate, renalase and FMD were associated with the presence of SRC. Multivariate regression analysis of factors which are statistically significant in univariate analysis showed that age and renalase was associated with the presence of SRC. CONCLUSION: We have demonstrated that renalase levels were associated with the presence of SRC and endothelial dysfunction. Further research is necessary to highlight underlying mechanisms.

Hyperuricemia is associated with progression of IgA nephropathy.

BACKGROUND AND AIM: IgA nephropathy (IgAN) is one of the world's most common glomerular diseases. Hyperuricemia was recently defined as risk factor for chronic kidney disease. We aimed to investigate the impact of baseline serum uric acid levels on progression of IgAN. MATERIALS AND METHODS: A total of 93 patients with IgAN were screened. Demographic information and biochemical data were recorded. eGFR (using the CKD-EPI = Chronic Kidney Disease Epidemiology Collaboration formula) was used as renal function marker. Baseline and sixth month eGFR values were calculated. Progression of renal disease was defined as the difference between baseline eGFR and sixth month eGFR (delta eGFR). RESULTS: Mean age of the patients was 40 ± 11 years (60% were males). Baseline mean eGFR was 77.9 ± 30.2 mL/min, and baseline mean serum uric acid was 5.65 ± 1.68 mg/dL. Importantly, baseline serum uric acid levels were found to be associated with the change in eGFR (r = 0.252, p = 0.01). In multivariate analysis (adjusted R(2) = 0.171, p = 0.031), adjusting for age, gender, baseline eGFR, blood pressure, baseline albumin concentration and ACEI and/or ARB use revealed that the baseline serum uric acid levels significantly predicted the change in eGFR. CONCLUSION: Baseline serum uric acid concentration is directly proportional to the rate of decline in renal functions in patients with IgAN. Uric acid-lowering treatments may be beneficial for the prevention of progression of IgAN. However, randomized controlled studies are needed for this purpose.

Low serum pancreatic enzyme levels predict mortality and are associated with malnutrition-inflammation-atherosclerosis syndrome in patients with chronic kidney disease.

PURPOSE: Serum levels of amylase and lipase are frequently increased in patients with chronic kidney disease (CKD). Relatively low serum pancreatic enzyme levels in CKD may represent a state of pancreatic insufficiency and may contribute to protein-energy wasting (PEW). We aimed to investigate the relationships of serum pancreatic enzyme levels with PEW, inflammation, and mortality in CKD patients. METHODS: Two hundred and thirty CKD patients (male/female: 144/86; mean age, 59 ± 16 years) were enrolled. Serum total α-amylase and lipase activities were measured by enzymatic colorimetric assays. Mean follow-up time was 18 ± 10 months. Forty-seven patients (20 %) died during this period. RESULTS: Serum amylase levels were increased in 95 patients (41 %) and serum lipase levels were increased in 71 patients (30 %) out of the 230 patients. Diabetic patients had significantly lower serum amylase levels than non-diabetic ones (86 ± 46 vs. 111 ± 60 IU/L, p < 0.0001). Patients with ischemic heart disease also had significantly lower serum amylase (82 ± 37 vs. 108 ± 60 IU/L, p < 0.0001) and lipase levels (39 ± 36 vs. 57 ± 57 IU/L, p = 0.007). Serum amylase and lipase levels were directly correlated with serum creatinine (r = 0.173, p = 0.009 and r = 0.374, p < 0.0001) and albumin (r = 0.410, p < 0.0001 and 0.287, p < 0.0001), and inversely correlated with CRP (r = -0.223, p = 0.001 and r = -0.147, p = 0.027). The Kaplan-Meier analysis revealed survival advantages for both high-amylase and high-lipase groups in end-stage renal disease (ESRD) (CKD stage 5) patients (log rank, p < 0.001 and p = 0.02, respectively). In the Cox regression analysis, serum amylase was found to be an independent predictor for mortality. CONCLUSION: Serum amylase activity was found to be an independent predictor of mortality in ESRD patients. Relatively low serum pancreatic enzyme levels in CKD may be regarded as a novel component of the malnutrition-inflammation-atherosclerosis syndrome.

An unusual case of renal failure due to solitary plasmacytoma: parenchymal invasion of the kidney.

Solitary extramedullary plasmacytoma (EMP) is a rare plasma cell disorder mostly involving the upper airway; however, retroperitoneal infiltration is very rare. Kidney injury associated with EMP is exceptionally rare with only anecdotal reports. Herein we report a case of retroperitoneal EMP causing renal failure by the way of direct renal parenchymal infiltration. Renal parenchymal invasion should be considered in aggressive and refractory plasma cell dyscrasias with unexplained renal failure.

Reversible posterior leukoencephalopathy in the course of Goodpasture syndrome.

Reversible posterior leukoencephalopathy syndrome (RPLS) is characterized by headache, altered consciousness, seizures, and cortical blindness. The most frequent etiological factors are hypertension, kidney diseases, and immunosuppressive drugs such as steroids and cyclophosphamide. Herein we present a case of a 22-year-old female patient presented with alveolar hemorrhage and acute renal failure necessitating hemodialysis. In renal biopsy, necrotizing crescentic glomerulonephritis and immunofluorescence pattern compatible with Goodpasture syndrome were found. Anti-glomerular basement membrane antibody result was positive. At follow-up, respiratory failure ensued, steroid pulse treatment was started, and she was transferred to intensive care unit (ICU). In the ICU, she had visual disturbances and blindness together with seizures. Cranial magnetic resonance imaging (MRI) revealed irregular T2- and fluid-attenuated inversion recovery (FLAIR)-weighted lesions in bilateral occipital lobes. On clinical and radiological grounds, RPLS was diagnosed. With the supportive and anti-hypertensive treatment, RPLS was resolved without a sequela. Subsequent cranial MRI was totally normal. In the literature, RPLS associated with Goodpasture syndrome was reported only once. Hypertension and methylprednisolone might be the responsible etiologies in this case.

Cardiomyopathy mimicking left ventricular noncompaction in a patient with lupus nephritis.

A 37-year-old female patient was admitted with exertional dyspnea. Her serum creatinine was 2.4 mg/dL and anti-nuclear antibody was positive in a titer of 1/320. Renal biopsy revealed diffuse proliferative lupus nephritis. Echocardiography and cardiac magnetic resonance (MR) imaging showed increased apical trabeculations compatible with left ventricular noncompaction (LVNC), which is a rare genetic cardiomyopathy. The patient expressed a marked improvement in exertional dyspnea after the immune-suppressive treatment for systemic lupus erythematosus (SLE). Control echocardiography revealed a significant increase of ejection fraction. SLE may cause a kind of cardiomyopathy with high resemblance to LVNC. Discrimination of these two similar clinical entities is important because SLE-induced cardiomyopathy is potentially reversible after the immune-suppressive treatment for SLE.