Fatih Mehmet Erdur

Platelet-to-lymphocyte ratio better predicts inflammation than neutrophil-to-lymphocyte ratio in end-stage renal disease patients.

Neutrophil‐to‐lymphocyte ratio (NLR) was introduced as a potential marker to determine inflammation in end‐stage renal disease (ESRD) patients. Recently, platelet‐to‐lymphocyte ratio (PLR) and NLR were found to positively correlated with inflammatory markers including tumor necrosis factor‐α (TNF‐α) and interleukin (IL)‐6 in cardiac and noncardiac patients. Data regarding PLR and its association with inflammation are lacking in hemodialysis (HD) and peritoneal dialysis (PD) patients. Hence, we aimed to determine the relationship between PLR, NLR, and inflammation in ESRD patients. This was a cross‐sectional study involving 62 ESRD patients (29 females, 33 males; mean age, 49.6 ± 14.6 years) receiving PD or HD for ≥6 months in the Dialysis Unit of Necmettin Erbakan University. PLR, NLR, C‐reactive protein, TNF‐α, IL‐6 levels were measured. PLR, NLR, serum high sensitive C‐reactive protein, IL‐6, and TNF‐α levels were significantly higher in PD patients when compared with HD patients. ESRD patients with PLR ≥ 140 had significantly higher NLR, IL‐6, and TNF‐α levels when compared to patients with PLR < 139. In the bivariate correlation analysis, PLR was positively correlated with NLR, IL‐6, and TNF‐α in this population. When we compared the association of PLR and NLR with IL‐6 (r = 0.371, P = 0.003 vs. r = 0.263, P = 0.04, respectively) and TNF‐α (r = 0.334, P = 0.008 vs. r = 0.273, P = 0.032, respectively), PLR was found to be superior to NLR in terms of inflammation in ESRD patients. Simple calculation of PLR can predict inflammation better than NLR in ESRD patients.

The relationship between neutrophil‐to‐lymphocyte ratio and vascular calcification in end‐stage renal disease patients

Chronic inflammation was found to be correlated with coronary (CAC) and thoracic peri‐aortic calcification (TAC) in end‐stage renal disease (ESRD) patients. Neutrophil‐to‐lymphocyte ratio (NLR) was introduced as a potential marker to determine inflammation in cardiac and noncardiac disorders. Data regarding NLR and its association with TAC and CAC are lacking. We aimed to determine the relationship between NLR and vascular calcification in ESRD patients. This was a cross‐sectional study involving 56 ESRD patients (22 females, 34 males; mean age, 49.9 ± 14.2 years) receiving peritoneal dialysis or hemodialysis for ≥6 months in the Dialysis Unit of Necmettin Erbakan University. TAC and CAC scores were measured by using an electrocardiogram‐gated 64‐multidetector computed tomography. NLR was calculated as the ratio of the neutrophils and lymphocytes. There was a statistically significant correlation between NLR, TACS and CACS in ESRD patients (r = 0.43, P = 0.001 and r = 0.30, P = 0.02, respectively). The stepwise linear regression analysis revealed that age, as well as NLR were independent predictors of TACS. However, increased age was the only independent predictor of CACS according to linear regression analysis. Simple calculation of NLR can predict vascular calcification in ESRD patients.

Serum paraoxonase activity and oxidative stress in patients with adult nephrotic syndrome

OBJECTIVE It has been shown that low paraoxonase-1 (PON1) activity is associated with a risk of an early development of atherosclerosis. In the present study, we investigated serum paraoxonase, and arylesterase activities and oxidative stress in patients with adult nephrotic syndrome (NS). In addition, we examined the relationship between these measurements and atherosclerosis. METHODS Twenty-one patients with NS and 21 healthy controls were enrolled in the study. Serum basal and salt-stimulated paraoxonase activities, arylesterase activity, lipid hydroperoxide (LOOH) and total thiol (SH) levels were measured. RESULTS Serum basal and salt-stimulated paraoxonase activities, arylesterase activity and total SH levels were significantly lower in patients with NS than in controls (p<0.05, p<0.05, p<0.01 and p<0.05, respectively), whereas LOOH levels were significantly higher (p<0.05). Serum LOOH levels were significantly correlated with total-SH levels in patients with NS (r=-0.467; p<0.01). Moreover, proteinuria levels were significantly correlated with serum LOOH levels (r=0.397; p<0.01), whereas no correlation was found among serum paraoxonase activity, arylesterase activity and total-SH levels in NS patients (p>0.05). CONCLUSIONS We concluded that oxidative stress is increased, while serum PON1 activity is decreased in patients with adult NS. In addition, these results indicate that lower PON1 activity is associated with an oxidant-antioxidant imbalance that may contribute to atherosclerosis in adult patients with NS.

Fenofibrate-induced rhabdomyolysis in a patient with chronic renal failure due to nephrotic syndrome: A rare case report

OBJECTIVES Fenofibrate is a fibric acid derivative that is used alone or combination with statins in the treatment of hyperlipidemia. These drugs have potential risks, including rhabdomyolysis and acute renal failure. Despite reports of rhabdomyolysis with the use of fenofibrate alone or with statin-fibrate combinations, there have been no cases of rhabdomyolysis described when fenofibrate was used alone to treat patients with chronic renal failure owing to nephrotic syndrome. DESIGN AND METHODS We report on a 26-year-old male who presented with fenofibrate-induced rhabdomyolysis with chronic renal failure due to nephrotic syndrome. RESULTS After the discontinuation of fenofibrate, the patient was treated with intravenous fluid replacement and urine alkalization. Subsequently, his clinical and biochemical findings improved. CONCLUSIONS Before starting fenofibrate therapy, the causes of secondary hyperlipidemia, especially nephrotic syndrome, should be investigated. In the presence of chronic renal failure and hypoalbuminemia, the fenofibrate dose should be adjusted. Physicians should be aware of the potential toxicities of fenofibrate, and patients should be informed about its potential side effects.

Apoptosis, autophagy & endoplasmic reticulum stress in diabetes mellitus

The prevalence of diabetes mellitus (DM) is increasing secondary to increased consumption of food and decreased physical activity worldwide. Hyperglycaemia, insulin resistance and hypertrophy of pancreatic beta cells occur in the early phase of diabetes. However, with the progression of diabetes, dysfunction and loss of beta cells occur in both types 1 and 2 DM. Programmed cell death also named apoptosis is found to be associated with diabetes, and apoptosis of beta cells might be the main mechanism of relative insulin deficiency in DM. Autophagic cell death and apoptosis are not entirely distinct programmed cell death mechanisms and share many of the regulator proteins. These processes can occur in both physiologic and pathologic conditions including DM. Besides these two important pathways, endoplasmic reticulum (ER) also acts as a cell sensor to monitor and maintain cellular homeostasis. ER stress has been found to be associated with autophagy and apoptosis. This review was aimed to describe the interactions between apoptosis, autophagy and ER stress pathways in DM.

The Prevalence of Fabry Disease in Patients with Chronic Kidney Disease in Turkey: The TURKFAB Study.

Background/Aims: Fabry disease is a treatable cause of chronic kidney disease (CKD) characterized by a genetic deficiency of α-galactosidase A. European Renal Best Practice (ERBP) recommends screening for Fabry disease in CKD patients. However, this is based on expert opinion and there are no reports of the prevalence of Fabry disease in stage 1-5 CKD. Hence, we investigated the prevalence of Fabry disease in CKD patients not receiving renal replacement therapy. Methods: This prospective study assessed α-galactosidase activity in dried blood spots in 313 stage 1-5 CKD patients, 167 males, between ages of 18-70 years whose etiology of CKD was unknown and were not receiving renal replacement therapy. The diagnosis was confirmed by GLA gene mutation analysis. Results: Three (all males) of 313 CKD patients (0.95%) were diagnosed of Fabry disease, for a prevalence in males of 1.80%. Family screening identified 8 aditional Fabry patients with CKD. Of a total of 11 Fabry patients, 7 were male and started enzyme replacement therapy and 4 were female. The most frequent manifestations in male patients were fatigue (100%), tinnitus, vertigo, acroparesthesia, hypohidrosis, cornea verticillata and angiokeratoma (all 85%), heat intolerance (71%), and abdominal pain (57%). The most frequent manifestations in female patients were fatigue and cornea verticillata (50%), and tinnitus, vertigo and angiokeratoma (25%). Three patients had severe episodic abdominal pain attacks and proteinuria, and were misdiagnosed as familial Mediterranean fever. Conclusions: The prevalence of Fabry disease in selected CKD patients is in the range found among renal replacement therapy patients, but the disease is diagnosed at an earlier, treatable stage. These data support the ERBP recommendation to screen for Fabry disease in patients with CKD of unknown origin.

Risk factors that can affect the progression of chronic kidney disease in patients with poststreptecoccal glomerulonephritis history.

To the Editor: Recently, Hoy et al.1 suggested that patients who had a history of poststreptecoccal glomerulonephritis (PSGN) might have the tendency to develop chronic kidney disease in the following years. The study was designed as a retrospective cohort study. Of the 177 PSGN patients, 36 of them were between 10 and 19 years old, 74 of them were between 20 and 29 years old, and 70 of them were between 30 and 39 years old. According to the results of this study, there is an increased risk of albumin/creatinine ratio and decrements of glomerular filtration rate of patients who had history of PSGN. However, in the study-setting part of the article, the data about the history of PSGN patients regarding chronic diseases such as tubulointerstitial disease, vesicoureteral reflux, and hemolytic uremic syndrome (HUS), etc., which could cause microalbuminuria and increased albumin/creatinine ratio, were not detailed by the authors. Sharma et al.2 showed that chronic kidney disease is more commonly seen in patients with diarrhea-positive HUS. Acute interstitial nephritis is also associated with mild proteinuria in children.3 Therefore, the data about patients’ history should be detailed in the article, including the diseases-causing proteinuria, as an exclusion criterion. In addition, as the present study did not include a control group comprising healthy subjects to compare the results, this issue should be mentioned as a limitation of this study.

The Emerging Role of Sirtuin 1,-3 and -4 in Glucose and Lipid Metabolism and in Diabetes Mellitus

Diabetes mellitus has been accepted as an epidemic worldwide during the last two decades. Despite the diagnostic tools and therapeutic approaches, the pathophysiology of this metabolic disorder and cellular defensive mechanisms remain mysterious. The maintenance of cellular homeostasis requires well-organized network between glucose, amino acid and lipid metabolism. Sirtuins are a group of nicotinamide adenine dinucleotide dependent proteins that are involved in cellular homeostasis by their deacetylating activity. Among them, sirtuin 1,-3 and -4 have been the most extensively explored. In the present review, we aimed to discuss the role of associated sirtuins in glucose and lipid metabolism and in the pathogenesis and treatment of diabetes mellitus.

Hepatic Encephalopathy in Connection With Budd-Chiari Syndrome due to Infection With Echinococcus Multilocularis: A Case Report

Budd-Chiari syndrome (BCS) is a hepatic venous outflow block generally resulting from disorders affecting hepatic venous system. Elevated hepatic venous pressure results in portal hypertension. BCS may also cause hepatic encephalopathy. Echinococcus multilocularis is a tapeworm parasite and the natural course of the disease may affect liver parenchyma as well as hepatic venous tree. It is the most terrible parasitic disease of the liver and is easily confused with hepatic malignancies. Albendazole therapy may suppress disease progression. Alveolar echinococcosis of the liver rarely causes Budd-Chiari syndrome-related hepatic encephalopathy (HE). We report a rare case of alveolar echinococcosis-related BCS with HE, who was successfully managed by rifaximin and albendazole.