Polyomavirus Associated Nephropathy: Frequency and Graft Survival Analysis in Northeast of Iran.

BACKGROUND & OBJECTIVE: Polyomavirus-associated nephropathy (PVAN), mainly caused by the BK virus, is one of the most important infectious complications of kidney transplantation. The leading histopathologic characteristics of PVAN is viral cytopathic effects, such as nucleomegaly with smudged or clumped chromatin and intranuclear ground-glass inclusion, mostly in tubular epithelial cells. Moreover, tubular necrosis, tubulitis, interstitial inflammation, atrophy, and fibrosis have been noted. Positive immunohistochemistry (IHC) staining for SV-40 highlights the infected epithelial cells of renal tubules. METHODS: A total of 85 core needle biopsies of transplanted kidneys were evaluated histologically and were stained for SV-40 using the IHC method. In addition, a follow-up of graft failure was performed. RESULTS: Our findings revealed that the frequency of polyomavirus infection in kidney transplant patients in the Northeast of Iran is 4.7%. There was no significant correlation between PVAN and graft rejection. Although a higher rate of graft loss was observed in PVAN patients, in comparison with non-PVAN patients (25% vs. 14.8%), the difference was not statistically significant. Moreover, patients with immunohistochemically confirmed PVAN and those with histopathologic features of viral-like cytopathic effects had significantly lower graft survival in the follow-up period (42.5 vs. 196.8 months and 109.4 vs. 205.7 months, respectively). CONCLUSION: The frequency of polyomavirus infection in kidney transplant patients in the Northeast of Iran is 4.7%. There was no significant correlation between PVAN and graft rejection. Furthermore, we observed that polyomavirus infection accelerates the course of graft loss.

Impact of Propranolol on Preventing Renal Dysfunction in Patients with Cirrhosis.

BACKGROUND One of the earliest diagnostic signs of hepatorenal syndrome in patients suffering from liver cirrhosis is an increase in the renal vascular resistive index (RI). In this study, the impact of propranolol on decreasing this index and to postpone the probability of hepatorenal syndrome has been investigated. METHODS In the current research, 30 patients with liver cirrhosis with different age and sexes have been enrolled. Demographic data and complete medical history have been collected using a specific questionnaire. At first, renal artery Doppler ultrasonography was performed to determine the RI. The patients were then treated with propranolol, and under supervision, the dose of the drug was increased gradually every 3 to 5 days to reach the target of 25% decrease in resting heart rate. One month after reaching the target dose of the medicine, Doppler ultrasonography was repeated for the patients and the second RI was compared with the pretreatment ones. RESULTS According to our results after treatment with propranolol, a significant decrease of RI was observed (p < 0.01). However, there was no significant difference in the glomerular filtration rate (GFR) before and after treatment with propranolol (p = 0.290). In our study, we found that administering propranolol was associated with significant changes in RI and GFR between the patients with compensated and decompensated cirrhosis (mean change: -0.005 ± 0.017 vs. -0.058 ± 0.045; p < 0.01 for RI and -4.226 ± 17.440 vs. 13.486 ± 12.047; p < 0.01 for GFR in patients with compensated and decompensated cirrhosis, respectively). CONCLUSION Propranolol reduces renal vascular RI in patients with cirrhosis. The response rates in the patients with decompensating cirrhosis were significantly higher than the patients with compensating cirrhosis.

The relationship between serology of hepatitis E virus with liver and kidney function in kidney transplant patients.

Although hepatitis E virus (HEV) is well known to cause acute hepatitis, there are reports showing that HEV may also be responsible for progression of acute to chronic hepatitis and liver cirrhosis in patients receiving organ transplantation. In this study, we aimed to evaluate the prevalence of HEV in patients with kidney transplantation. In this study, 110 patients with kidney transplantation were recruited, and anti-HEV IgG, creatinine, alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and estimated glomerular filtration rate (eGFR) in the first, third and sixth months after renal transplantation were measured. The mean serum anti-HEV IgG titers in the study participants was 1.36 (range 0.23 to 6.3). Twenty-three patients were found to be seropositive for HEV Ab defined as anti-HEV IgG titer > 1.1. The difference in liver and renal function tests (creatinine, eGFR, AST, ALT and ALP) at different intervals was not significant between patients with HEV Ab titers higher and lower than 1.1 (p > 0.05). However, an inverse correlation was observed between HEV Ab and eGFR values in the first (p = 0.047, r = -0.21), third (p = 0.04, r = -0.20) and sixth (p = 0.04, r = -0.22) months after renal transplantation in patients with HEV Ab < 1.1 but not in the subgroup with HEV Ab > 1.1. Also, a significant correlation between age and HEV Ab levels was found in the entire study population (p = 0.001, r = 0.33). Our findings showed a high prevalence of seropositivity for anti-HEV IgG in patients receiving renal transplants. However, liver and renal functions were not found to be significantly different seropositive and seronegative patients by up to 6 months post-transplantation.

A linear relationship between serum high-sensitive C-reactive protein and hemoglobin in hemodialysis patients.

BACKGROUND: Inflammatory process in hemodialysis patients involves hematopoiesis. The aim of the study was to determine the relationship between serum C-reactive protein (CRP) as a marker of inflammation with hemoglobin in patients under hemodialysis. METHODS: Patients under maintenance hemodialysis for more than 3 months were studied. Serum high-sensitive CRP (hs-CRP) was measured by immunoturbidimetric method and hemoglobin < 11 g/dl was considered as anemia. Iron deficiency anemia was confirmed by percent transferrin saturation < 20 %. Correlation coefficient, linear regression and odds ratio (OR) were used to determine the relationship. RESULTS: A total of 73 patients aged 50 ± 16.9 years with median hemodialysis duration of 24 (3-280) months entered the study. High serum hs-CRP (> 5 mg/l) was found in 42 (57.5 %) and anemia in 32 (43.8 %) patients. High CRP was significantly associated with anemia OR = 20.8 (95 % CI 5.35-81, p = 0.001). After adjustment for age, dialysis duration, blood indices and serum albumin, the odds of anemia in the high CRP group remained at a significant level of 16.7 (95 % CI 3.7-75, p = 0.001). Hemoglobin levels conversely correlated with serum hs-CRP (r = -0.607, r (2) = 0.36, p = 0.001). In linear regression analysis for each 1 mg/l increase in serum hs-CRP, hemoglobin value increased by 12.4 % (p = 0.002). Serum iron at cutoff level of 54 µg/dl discriminated patients with and without iron deficiency anemia with sensitivity of 93.3 %, specificity of 84 % and accuracy of 90 % (AUC ± SE = 0.901 ± 0.04 (95 % CI, 0.805-0.998, p = 0.001). CONCLUSION: These findings indicate that in hemodialysis patients, the inflammatory process alters hemoglobin level in converse correlation with CRP concentration with a linear relationship pattern. Serum iron <54 µg/dl indicates iron deficiency anemia with high accuracy.

Serum triiodothyronine level as an indicator of inflammation in patients undergoing dialysis.

INTRODUCTION. It has been shown that inflammation affects thyroid function. In patients with end-stage renal disease, low plasma triiodothyronine (T3) may be an unsuspected expression of the inflammatory state of these patients. This study evaluated the correlation between T3 and high-sensitivity C-reactive protein (HSCRP) levels in patients on peritoneal dialysis (PD) and hemodialysis. MATERIALS AND METHODS. This is a cross-sectional study aiming at the correlation between T3 and HSCRP levels among 30 patients on PD, 30 patients on hemodialysis, and 20 healthy individuals. Serum levels of HSCRP, T3, thyroxine (T4), thyroid stimulating hormone, T3 resin uptake, and free T3 index (FT3I) and free T4 index (FT4I) were compared between the three groups. RESULTS. There were no significant differences between hemodialysis and PD patients in respect to T3, T4, FT3I, and FT4I. In PD and hemodialysis patients, T3 and FT3I were lower than in controls (P < .001), but there was no significant difference between PD and hemodialysis patients. T3 resin uptake and thyroid stimulating hormone differed significantly between PD and hemodialysis patients. There was a significant inverse correlation between HSCRP and T3 and FT3I among hemodialysis patients (P = .04); however, there was no such correlations in PD patients. CONCLUSIONS. The relationship between T3 and HSCRP suggests that inflammation might be involved in the low T3 syndrome in hemodialysis patients, but we did not find a significant correlation between T3 and HSCRP levels in patients on peritoneal dialysis.

Thyroid hormone changes in early kidney transplantation and its correlation with delayed graft function.

INTRODUCTION: Thyroid hormones affect kidney function and may alter with changes in kidney function, as well. We evaluated changes in serum levels of triiodothyronine (T3), thyroxin (T4), and thyroid-stimulating hormone (TSH) early after kidney transplantation and their relationship with delayed graft function (DGF). MATERIALS AND METHODS: Fifty-five consecutive kidney allograft recipients were enrolled in the study. Serum levels of T3, T4, and TSH were measured on the day before transplantation, and also on posttransplant days 1, 3, 7, 14, and 21. Results were compared between patients with a normal allograft function and those with DGF. RESULTS: The mean T3 level decreased from 110.41 +/- 49.79 ng/dL before transplantation to 80.78 +/- 51.42 ng/dL on the 1st day after transplantation (P = .04), while T4 reduction reached a significant level on the 3rd day after transplantation (8.27 +/- 3.27 microg/dL to 5.50 +/- 2.57 microg/dL, P = .004). Patients with DGF experienced a significantly greater decrease in the serum level of T3 at the end of the 1st week after transplantation compared with patients with normal kidney function (P = .02). This significant decrease in T3 continued until the end of the 2nd week. Serum levels of T4 reduced comparably in the two groups, until the end of the 1st week, when it showed a significantly more reduction in the patients with DGF (P = .04). CONCLUSION: Both T3 and T4 reduced early after kidney transplantation, and this reduction was significantly more prominent in those with DGF. This is compatible with a consequence rather than a cause of DGF, explained in the setting of sick euthyroid syndrome.