Chemerin, TNF - α and the degree of albuminuria in patients with diabetic kidney disease.

BACKGROUND: Chronic inflammation has been increasingly recognized as an essential pathogenic mechanism for the development and progression of diabetic kidney disease (DKD). Chemerin is an adipokine which has been suggested to be related to inflammation and has been correlated with the development of diabetic complications. We aimed to explore the potential links between chemerin, TNF - α, as a marker of systemic inflammation, and the level of albuminuria in patients with type 2 diabetes mellitus (T2DM). METHOD: The study included 84 patients with T2DM and 10 normoalbuminuric non-diabetic controls. Demographic, clinical and laboratory data including chemerin and TNF-α levels were collected. RESULTS: A total of 84 diabetic patients were enrolled, 32 males (38.1 %), with mean age 57.9 ± 10.7 years. They were divided into 3 groups: A1: 14 with normalbuminuria, A2: 27 with microalbuminuria, and A3: 43 with macroalbuminuria (uACR < 30, 30-300 and > 300 mg/gm respectively). Chemerin and TNF-α levels increased with the progress of albuminuria (control: 21.3 (14.7 -77), A1: 794 (683-925), A2: 1150 (962.9 - 1221.5) and A3: 1466 (1197.5 - 2002.5) ng/ml; p < 0.001) and (control: 77.9 (59 - 96.8), A1: 85.2 (71-116.3), A2: 87.3 (81 - 97.5) and A3: 99 (85.1 - 142.5) pg/ml; p = 0.009) respectively. Among the diabetics, a significant association was evident between serum chemerin and serum TNF-α (r = 0.53; p < 0.001). On linear stepwise regression analysis, chemerin was significantly associated with TNF-α and HbA1c (unstandardized ß 10.881 and 272.68 respectively, p < 0.001); and TNF-α was significantly correlated with chemerin, uACR (unstandardized ß 0.059 and 0.004 respectively, p < 0.001) and HbA1c (unstandardized ß -13.699, p = 0.014). CONCLUSION: Our findings suggest a potential role of chemerin and TNF-α in the development and progression of DKD, and thus support the role of the inflammatory pathway. Larger follow up studies are warranted to further explore the potential links between chemerin, inflammation and DKD.

Screening for BK Viremia/Viruria and the Impact of Management of BK Virus Nephropathy in Renal Transplant Recipients.

OBJECTIVES: The prevalence of BK-induced nephritis in renal transplant recipients is estimated to be 1% to 10%; the rate of graft loss within 1 year is 30% to 65%. We conducted this study to evaluate screening of BK virus in blood and/or urine among renal transplant recipients and to assess the effects of different therapeutic modalities in renal transplant recipients with BK nephropathy. MATERIALS AND METHODS: Kidney transplant recipients were screened at the time of transplant and then at 1, 2, 3, 6, 9, 12, 18, and 24 months posttransplant. Fiftynine patients were diagnosed with BK virus viremia. Patients were divided into 2 groups according to treatment: group 1 (n = 29) received an active treatment and group 2 (n = 30) received minimized immunosuppression. RESULTS: Most patients required graft biopsies to confirm diagnosis (86.2% in group 1 vs 50% in group 2; P = .03). Both groups were comparable regarding demographic data. Initial posttransplant graft function was significantly better in group 1 (P = .017); ultimately, there was no significant difference between both groups regarding graft survival (P= .51). Fifty percent of patients had biopsy-proven acute T-cell-mediated rejection before BK virus-associated nephropathy diagnosis (significantly higher in group 1). Serum creatinine levels were significantly better in group 2 at 3, 4, and 5 years after BK nephropathy (P = .001, .017, and .003, respectively). CONCLUSIONS: The prevalence of BK nephropathy in our renal transplant recipients was 5.9% with a rate of graft loss ranging from 43% to 51%. Regular screening, less intensive immunosuppressive therapy, and early intervention by reduction of immunosuppressive medications are advisable to obtain early diagnosis and to have better outcomes of BK virus-associated nephropathy with antiviral agents.

Musculoskeletal manifestations in end-stage renal disease patients on hemodialysis and relation to parathyroid dysfunction.

End-stage renal disease (ESRD) is associated with chronic kidney disease-mineral and bone disorder (CKD-MBD); including renal osteodystrophy, and biochemical changes reflecting mineral and hormonal abnormalities. CKD-MBD can lead to serious musculoskeletal manifestations with an impact on the functional status of patients. The objective is to find the frequency of the musculoskeletal manifestations in dialysis patients, to determine the impact on the functional ability of patients, and to detect the relation between parathyroid hormone (PTH) level and musculoskeletal manifestations. The sample size included 53 adult patients on hemodialysis (HD), three times weekly, divided into two groups as follows; (Group A) included 15 patients (10 males and 5 females) on HD for a year or <1 year and (Group B) included 38 patients (24 males and 14 females) on HD for >1 year. All patients were subjected to a full history and physical examination plus a comprehensive assessment of patient's disability was done with a health assessment questionnaire (HAQ)-disability index. The most common neurological manifestations are uremic polyneuropathy (43.4%) and carpal tunnel syndrome. Arthralgia is the most common musculoskeletal manifestation (83%).The most common radiological signs of SHPT is the subperiosteal resorption of the terminal phalanges (67.9%). The most common MSUS abnormalities are Achilles tendinopathy (67.9%). Osteoporosis is detected in 24.5% of patient. There are highly positive significant correlations between HAQ score and age, HD duration, serum PTH, T-score, and X-ray findings. Musculoskeletal system involvement remains a common problem which decreases the physical function of patients with ESRD.

The Long-Term Effect of Hepatitis C Virus on the Outcome of Live-Donor Kidney Transplant Recipients. A Retrospective Study.

OBJECTIVES: Hepatitis C virus infection occurs frequently among end-stage renal disease patients. Moreover, its effect on long-term patient and renal graft survival is controversial. This study was performed to assess the long-term effect of hepatitis C virus on the outcome of kidney allografts. MATERIALS AND METHODS: We retrospectively analyzed 273 hepatitis B negative renal transplant recipients who were transplanted at Mansoura Urology and Nephrology Center, for whom hepatitis C virus RNA polymerase chain reaction results were available before transplant, and followed them for at least 17 years after transplant. We compared graft and patient survival rates between viremic group (study group) and nonviremic group (control group). We also studied posttransplant hepatic function, graft performance, and incidence of posttransplant diabetes mellitus. RESULTS: Hepatitis C virus was detected in sera of 195 patients (71%). No statistically significant increased risk for graft failure (P = .29) or patient death (P = .47) was found among the groups. Hepatitis C virus viremic transplant recipients had significantly greater frequencies of biochemical chronic liver disease (P = .01). However, we did not report significant differences regarding incidence, quantity of proteinuria, biopsy-proven acute rejection, chronic allograft nephropathy, and incidence of posttransplant diabetes mellitus between the studied groups. CONCLUSIONS: Hepatitis C virus infection was shown to increase the incidence of chronic hepatitis posttransplant. However, no statistically significant adverse effect on long-term renal graft and patient survival was noted.

Renalase gene polymorphism and epinephrine level in chronic kidney disease.

Chronic kidney disease (CKD) is an important public health problem. Patients with end-stage renal disease have a significant renalase deficiency, which could be one of the mechanisms explaining high prevalence of hypertension in these patients. The aim of this study was to investigate the possible association of renalase gene (rs2296545) polymorphism with normotensive and hypertensive CKD in sampled Egyptian patients and to determine the effect of such polymorphism on epinephrine level. Renalase gene (rs2296545) polymorphism was genotyped in 178 patients with CKD (83 normotensive and 95 hypertensive nephrosclerosis) and 178 normal healthy adults using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). Epinephrine level was measured by HPLC method. We found an association of renalase (rs2296545) CC genotype and C allele with CKD. Also, the epinephrine level was significantly increased in normotensive and hypertensive nephrosclerosis patients as compared to controls. CKD patients with CC genotype showed significant high epinephrine level as compared to CG and GG genotypes.