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Background: In chronic kidney failure, a hypoxic state, infiltrating inflammatory cells play a crucial role in the progression to end-stage renal disease. No studies have evaluated the influence of hypoxia and infiltrating inflammatory cells on chronic allograft dysfunction., Methods: Renal transplant recipients who underwent renal allograft biopsy with interstitial fibrosis/tubular atrophy (IF/TA) were enrolled and renal allograft tissue sections were processed for immunohistochemical staining including hypoxia-inducible factor-1α (HIF-1α), nitrotyrosine, α-smooth muscle actin and e-cadherin. Patients with total renal tissue HIF score ≥1 were defined as positive for HIF-1α. To assess the phenotype of the infiltrating cells, dual staining of HIF-1α with CD45, CD68 and CD3 was performed. The correlation between HIF-1α score and Banff's score was analysed. Clinical parameters including renal survival among patients with or without an expression of HIF-1α were compared., Results: Out of 55 patients enrolled, 23 patients (41.8%) had an HIF-1α score ≥1 (Group B). Compared with Group A (total renal HIF score <1), Group B had a significantly higher Banff score of interstitial infiltrates (i) (P = 0.029), vascular fibrous intimal thickening (cv) (P = 0.007) and arteriolar hyaline thickening (ah) (P = 0.026). Clinically, patients with an HIF-1α score were associated with a poor graft survival. Significantly inferior allograft survival was noted in Group B. HIF scores had an adjusted hazard ratio of 3.25 (95% confidence inteval: 1.71-6.16, P = 0.0003) in allograft failure., Conclusions: We first demonstrated the expression of HIF-1α protein among infiltrating inflammatory cells in areas with IF/TA in patients with chronic allograft dysfunction.

Background: Pulmonary hypertension (PH) is an overlooked cardiovascular morbidity in patients undergoing haemodialysis. Inflammation has been demonstrated to play a significant role with certain types of PH in non-uraemic patients, but studies analysing the mechanisms in dialyzed patients with PH are rare. Hence, we investigated systemic and local inflammation biomarkers associated with PH in uraemia patients to elucidate the potential mechanism., Methods: A cross-sectional study was conducted in which 97 haemodialysis patients were initially evaluated in our hospital. Twelve inflammatory cytokines were measured using a cytometric beads assay in patients with and without PH. FE(NO) (fractional exhaled nitric oxide) was checked by a chemiluminescence analyser in patients with and without PH as well as by normal controls., Results: Thirty-nine eligible patients were enrolled. Compared to patients without PH (group A), patients with PH (group B) had significantly higher serum levels of hs-CRP, IL-1beta, TNF-alpha and IL-6. FE(NO) was also measured. Though the pre-dialysis FE(NO) levels were elevated in both groups; group B patients had significantly higher pre-dialysis FE(NO) levels than group A patients (39.9 +/- 16.7 versus 31.8 +/- 10.3, P = 0.045). The post-dialysis FE(NO) levels returned to normal in group A while the remaining were significantly higher in group B (30.3 +/- 10.3 versus 20.1 +/- 10.9, P = 0.003)., Conclusions: Our study revealed that dialyzed patients with PH had a significantly higher level of airway FE(NO) as well as serum levels of acute phase reactive protein and cytokines, including IL-1beta, TNF-alpha and IL-6. A chronic inflammation might play an important role in the pathogenesis of PH in patients undergoing haemodialysis.

Background: Hypokalaemia is a relatively common complication in uraemic patients undergoing continuous ambulatory peritoneal dialysis (CAPD). The hazards of hypokalaemia are multiple and have been correlated with patient morbidity and mortality. Whether it is associated with increased risk of peritonitis remains to be addressed., Methods: We retrospectively analysed our CAPD patients who had complicating peritonitis in a 2-year period. The influence of hypokalaemia on the clinical features of peritonitis was assessed. From September 2003 to August 2005, 140 unselected patients undergoing CAPD treatment and followed up in our hospital were recruited for the study. Hypokalaemia was defined as a serum potassium level <3.5 mmol/l. The impact of hypokalaemia on several clinical parameters, including the nutrition status, dialysis adequacy, occurrence of peritonitis and the etiologic pathogens, was analysed., Results: During the study period, 462 determinations (23.6%) were below quantity

Objective: We have previously demonstrated that hypokalaemia is a risk factor for enteric peritonitis in CAPD patients. The underlying mechanism is unclear, and there have been no similar reports. We hypothesized that hypokalaemia may result in dysmotility of the intestinal tract and in turn cause bacterial overgrowth and subclinical translocation of enteral bacteria., Methods: Uraemic patients undergoing CAPD in our hospital were enrolled in the study. Hypokalaemia was defined as a serum potassium (K) level < or = 3.5 mEq/L despite treatment for 1 month. A breath hydrogen test (BHT) was performed to detect if intestinal bacterial overgrowth was present. Blood samples were also collected for the study of inflammatory cytokines, including interleukin 1 (IL1), IL2, IL6, IL8, TNF-alpha and gamma-IFN., Results: A total of 68 patients were recruited. Hypokalaemia was present in 18 cases (26.5%, group 1), while 50 cases (group 2) had normal serum K levels. A higher prevalence of abnormal BHT was found in group 1 (27.8%), compared with group 2 (8.0%, P = 0.048). There was a trend towards a higher prevalence of abnormal BHT in diabetes mellitus (DM) patients with hypokalaemia (80.0%) compared with normal kalaemia (22.2%, P = 0.09), while no similar trends were found in non-DM hypokalaemic patients (7.7 versus 4.9%). When comparisons were made among different subgroups, patients with DM and hypokalaemia had a significantly higher prevalence of abnormal BHT compared to non-DM, normokalaemic patients (P < 0.0004) and non-DM, hypokalaemic patients (P = 0.008). Multivariate logistic regression analysis revealed that DM was an independent risk factor for abnormal BHT (odds ratio: 12.39, 95% CI: 2.25-68.20, P = 0.004). There was no significant difference in serum albumin, Kt/V, weekly creatinine clearance, pattern of peritoneal equilibrium test, C-reactive protein and various inflammatory cytokines between the two groups., Conclusion: CAPD patients with hypokalaemia may have intestinal bacterial overgrowth. While both DM and hypokalaemia might contribute to this abnormality, only DM appeared to be the independent risk factor.

Acquired Bartter-like syndrome, albeit rare, has not been reported to be associated with sarcoidosis. We describe the case of a 32-year-old male patient who presented with progressive muscular weakness of both lower extremities. Profound hypokalaemia associated with renal (K(+)) wasting, bilateral nephrocalcinosis and high plasma renin activity resembled Bartter's syndrome (BS). Both mediastinal lymph node and renal biopsy demonstrated sarcoidosis with non-caseating granuloma. Genetic testing responsible for hereditary BS or Gitelman's syndrome (GS) was negative. Hypokalaemia was well controlled with the administration of spironolactone with oral steroids and KCl. Early recognition and prompt treatment of sarcoidosis-associated Bartter-like syndrome avoids unnecessary complications.

Background: Idiopathic membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome in adults, and 25% of MN patients proceed to end-stage renal disease. Plasminogen activator inhibitor type 1 (PAI-1) activity plays an important role in renal fibrosis. The objective of this study was to clarify the relationship between PAI-1 gene polymorphisms and the progression of MN-associated pathologies., Methods: We recruited a cohort of 104 biopsy-diagnosed MN patients and 142 healthy subjects that served as controls. Genotyping of PAI-1 gene polymorphisms was performed using allele-specific polymerase chain reaction methods. We then analysed associations between PAI-1 gene 4G/5G polymorphisms and clinical manifestations and progression of MN., Results: The genotype distribution had no effect on the development of MN. The last measured creatinine clearance in MN patients having the 4G/4G genotype was significantly lower than in patients having the 4G/5G or 5G/5G genotypes (43.6 +/- 33.6, 55.8 +/- 44.3 and 73.3 +/- 29.8 ml/min, respectively, P = 0.008). Coronary artery diseases were more prevalent in patients having the 4G5G (14/32%) and 4G4G genotypes (4/11%) than in those having the 5G5G genotype (1/5%, P = 0.008). Peripheral vascular events were more prevalent in patients having the 4G5G (18/41%) and 4G4G (6/16%) genotypes than in those having the 5G5G genotype (3/14%, P = 0.021). Disease progression occurred more frequently in patients having the 4G4G (20/53%) and 4G5G (25/57%) genotypes compared with those having the 5G5G genotype (5/23%, P = 0.026)., Conclusions: The presence of the 4G allele was associated with renal deterioration and increased cardiovascular as well as other vascular events in MN patients. These findings should prompt specific considerations for the treatment of MN in patients having the 4G4G genotype.

Background: The most popular method for estimating post-haemodialysis BUN is the low blood flow technique. The low blood flow technique with a blood flow of 50 ml/min for 3 min may encompass the first two phases of post-haemodialysis urea rebound by access and cardiopulmonary recirculations. Some patients may have risk of clotting in extracorporeal circuit while slowing blood flow. Therefore we proposed another simpler sampling technique for measuring post-haemodialysis BUN(C2)., Methods: In the present study, 28 long-term haemodialysis patients were divided into two groups. In group 1 (n = 15), C2 sample (C2-50) was collected immediately after blood flow was slowed down to 50 ml/min for another 3 min. Then blood flow was reset to 300 ml/min. Finally, C2 sample (C2B) was obtained from arterial port at the end of bypassing dialysate for another 3 min. In group 2 (n = 13), C2 sample (C2B) was obtained from arterial port at the end of bypassing dialysate for 3 min with a blood flow of 250 ml/min. Then dialysate was reset to original flow rate and C2 sample (C2-50) was collected soon after blood flow was slowed down to 50 ml/min for another 3 min. In the meantime, recirculation rate was also checked., Results: The above two groups have similar results and there are no significant differences of post-haemodialysis BUN and calculated Kt/V between low blood flow technique and bypassing dialysate technique., Conclusion: The bypassing dialysate technique is another simpler and practical technique for the routine estimation of post-haemodialysis BUN.