Aysun Aybal Kutlugun

Effects of lowering dialysate sodium on flow-mediated dilatation in patients with chronic kidney disease

OBJECTIVE This study examined the effects of low dialysate sodium on endothelial dysfunction (ED) as measured by flow-mediated dilatation (FMD) of brachial artery in haemodialysis (HD) patients. METHODS Thirty HD patients (17 men; mean age: 48.4 ± 17.8 years) were studied. Subjects underwent two consecutive 6-week HD periods. Dialysate sodium was 143 mEq/L in the first period (standard Na HD) and 137 mEq/L in the second period (low Na HD). After each period, we performed FMD, echocardiographic evaluation and 24-h ambulatory blood pressure monitoring (ABPM). Interdialytic weight gain (IDWG), levels of pre- and post-dialysis blood pressure (BP), and dialysis-related symptoms were monitored during the study. RESULTS Per cent FMD was significantly greater (P < 0.05) after low Na HD (9.3 ± 6.2) compared with standard Na HD (5.7 ± 6.2). IDWG was significantly lower during low Na HD (2.35 ± 0.86 kg versus 2.71 ± 0.89 kg; P < 0.001). BP control was improved during low Na HD, as assessed by ABPM (128.2/77.5 mmHg versus 132.4/80.8 mmHg). Dialysis-related symptoms were more frequent during low Na HD (P < 0.05). There was no change in left ventricular mass after reducing dialysate sodium. CONCLUSIONS Reducing dialysate sodium concentration reduced ED, and provided better control of IDWG and BP, but increased dialysis-related symptoms.

Daily Sodium Intake in Chronic Kidney Disease Patients during Nephrology Clinic Follow-Up: An Observational Study with 24-Hour Urine Sodium Measurement

Objective: To determine daily sodium intake in ‘real practice’ in a large group of chronic kidney disease (CKD) patients who were under regular follow-up in a nephrology clinic. Methods: A total of 373 consecutive outpatients with CKD stages 1–5 (not on dialysis; men: 52.3%, mean age: 51.6 ± 15.4 years) were included in the study. All patients had at least 3 or more nephrology visits and received information on reducing their sodium intake. Data for systolic and diastolic blood pressure, number of antihypertensive medications and 2 consecutive 24-hour urinary sodium levels were obtained from the patients’ medical records. Results: The mean 24-hour urinary sodium levels of 2 consecutive urine samples were 168.8 ± 70.3 and 169.3 ± 67.4 mEq/day (p > 0.05). Only 14.7% of the patients had a sodium excretion <100 mmol/day. There was no difference in daily sodium intake from stages 1 to 4, but it was significantly lower in stage 5 (126.6 ± 60.5 mEq/day, p < 0.05). No relation was found between 24-hour urinary sodium output, number of antihypertensives or thiazide use. Conclusions: This study showed that almost 85% of CKD patients under regular nephrologic care were consuming more sodium than the recommended level. More robust measures should be devised to increase patient and physician compliance with reducing sodium intake in CKD.

Elevated urinary angiotensinogen a marker of intrarenal renin angiotensin system in hypertensive renal transplant recipients: does it play a role in development of proteinuria in hypertensive renal transplant patients?

The aim of this study was to evaluate the relationship of local intrarenal renin angiotensin system (RAS) with hypertension and proteinuria in renal transplant recipients. Sixty‐nine nondiabetic renal transplant recipients (39 male, mean age: 36.3 ± 11.5 years) were included in this study. All patients were in stable condition with GFR greater than 30 ml/min/1.73 m2; (MDRD). Hypertension was defined to be present if there was a recorded diagnosis of hypertension, systolic blood pressure >130 mmHg and/or diastolic blood pressure >80 mmHg according to ambulatory blood pressure monitoring. None of the hypertensive patients were receiving RAS blockers. Spot urine samples were obtained to measure urinary angiotensinogen (AGT) using human AGT‐ELISA, urinary creatinine and protein levels. The demographic properties and laboratory findings were similar between hypertensive and normotensive transplant recipients. Urinary AGT–creatinine ratio (UAGT/UCre) was significantly higher in hypertensive patients compared with the normotensives (8.98 ± 6.89 μg/g vs. 5.48 ± 3.33 μg/g; P = 0.037). Importantly, a significantly positive correlation was found between UAGT/Ucre levels and proteinuria in hypertensive patients (P = 0.01, r = 0.405). Local intrarenal RAS probably plays an important role in the development of hypertension and proteinuria in renal transplant recipients.

A Case of Familial Glomerulopathy With Fibronectin Deposits Caused by the Y973C Mutation in Fibronectin

Glomerulopathy with fibronectin deposits is a rare hereditary kidney disease characterized by the extensive deposition of fibronectin in glomeruli, particularly in mesangial regions and subendothelial zones. Prognostically, the disease is known as slowly progressive, leading to kidney failure in most cases. We recently diagnosed glomerulopathy with fibronectin deposits in a 24-year-old man in whom proteinuria was detected incidentally. Genetic analysis of the fibronectin 1 (FN1) gene showed heterozygosity for the Y973C mutation. The same mutation was found in his elder brother, who similarly experienced proteinuria. Both patients had normal kidney function but persistent proteinuria after 30 months and 11 years of follow-up, respectively.

Lansoprazole-induced acute allergic interstitial nephritis in a renal transplant recipient: a case report

Drug-induced interstitial nephritis is one of the causes of graft dysfunction in renal transplant recipients. Although commonly implicated as a cause of drug-induced interstitial nephritis in the general population, proton pump inhibitor-induced interstitial nephritis has not yet been reported in renal transplant recipients. Trimethoprim-sulfamethoxazole is responsible for most cases of interstitial nephritis in this population. Here, we describe the first case of proton pump inhibitor-related interstitial nephritis in a renal transplant recipient.

The relation between urinary angiotensinogen and proteinuria in renal AA amyloidosis patients.

Objective: The aim of this study was to evaluate the relationship of local intrarenal renin angiotensin system (RAS) with proteinuria in patients with renal AA amyloidosis. Methods: Thirty-two patients with renal AA amyloidosis (19 male, mean age: 45 ± 13 years) and sixteen healthy controls (5 male, mean age: 32 ± 5 years) were included in this study. Spot urine samples were obtained to measure urinary angiotensinogen (AGT) using human AGT-ELISA, urinary creatinine and protein levels. Logarithmic transformations of urinary AGT-creatinine ratio log(UAGT/Ucre) and urinary protein-to-creatinine ratio (UPCR) were done to obtain the normal distributions of these parameters. Results: Log(UAGT/UCre) was significantly higher in patients compared with the controls (1.88 ± 0.92 µg/g vs. 1.25 ± 0.70 µg/g; p = 0.023). Importantly a significantly positive correlation was found between log(UAGT/Ucre) and logUPCR in patients (r = 0.595, p = 0.006). Conclusions: Urinary AGT levels are higher in renal AA amyloidosis patients than in controls. Also, there is a significant positive correlation between urinary AGT and proteinuria in renal AA amyloidosis.

AA type renal amyloidosis secondary to FMF: a long-term follow-up in two patients

Renal amyloidosis, which leads to renal failure, is the most important long-term complication of familial Mediterranean fever (FMF). Resolution of nephrotic syndrome secondary to amyloidosis in FMF following colchicine treatment has rarely been reported. We describe two patients with FMF and nephrotic syndrome. These patients were treated with colchicine 1.5 mg/day and had a complete remission of nephrotic syndrome with a stable clinical course over 30 years. To our knowledge, our patients have the longest follow-up time without proteinuria.

Living Donor Kidney Volume as a Predictor of Graft Function: Is There a Role for Proteinuria?

BACKGROUND The proposed mechanism by which nephron underdosing contributes to graft failure is hyperfiltration damage leading to proteinuria and nephron loss. We evaluated whether proteinuria had an impact on the relationship between graft size and outcome in living donor kidney transplantation. METHODS We analyzed 69 living donors and their recipients who underwent transplantation between 2003 and 2007. Transplanted kidney volumes were measured by 3-D helical computed tomography scanning. A transplant kidney volume-recipient body weight (Vol/Wt) ratio was calculated for each donor-recipient pair. The subjects were divided into tertiles according to Vol/Wt ratios: low (<2.0), medium (2.0-2.7) and high (>2.7). RESULTS Recipient glomerular filtration rate (GFR) positively correlated with Vol/Wt ratio at 6, 12, and 24 months posttransplantation (r = .49, P < .001; r = .47, P < .001; r = .42, P < .001, respectively). Mean GFR increased significantly in graded fashion from low to high Vol/Wt ratio groups at 6, 12, and 24 months posttransplantation. Proteinuria did not differ between the three groups during 24 months after transplantation. Upon multivariate analysis, donor age, recipient age, and Vol/Wt ratio showed significant impacts on graft function. CONCLUSION Vol/Wt ratio displayed a significant independent effect on graft function in living donor kidney transplantation. This close association did not appear to be related to the degree of proteinuria during 24 months.

HFE gene mutation is a risk factor for tissue iron accumulation in hemodialysis patients

Introduction: HFE gene mutations are responsible from iron overload in general population. Studies in hemodialysis patients investigated the effect of presence of HFE gene mutations on serum ferritin and transferrin saturation (TSAT) with conflicting results. However effect of HFE mutations on iron overload in hemodialysis patients was not previously extensively studied.

Postural Epigastric Pain: A Challenging Symptom for Cytomegalovirus (CMV) Gastritis

Abstract Postural epigastric pain is an uncommon symptom and is hardly acquired unless specifically asked to the patient. Here we present a cytomegalovirus (CMV) gastritis case in a renal transplant patient with postural epigastric pain. A 36-year-old male was admitted to our clinic on the 50th day of renal transplantation with postural epigastric pain. All investigations were unremarkable except biopsy-proven CMV gastritis and increased CMV viral load. The patient was free of symptom after ganciclovir treatment. Postural epigastric pain has not been described together with a clinical entity. Although not proved yet, it can be regarded as a unique symptom of CMV gastritis. Renal transplant patients presenting with postural epigastric pain which is not relieved with acid suppression should raise suspicion of CMV gastritis and this has to be confirmed by endoscopy and biopsy.