Ultrafiltration for decompensated heart failure: renal implications.

The negative prognostic impact of worsening renal function in patients with decompensated heart failure has been widely recognised. As diuretics are thought to contribute to deterioration of kidney function in this setting, attempts have been made to either spare or suppress the diuretic-related pathophysiological mechanisms involved in this phenomenon. In this regard, extracorporeal ultrafiltration represents a novel therapy for patients with heart failure, lacking the adverse impacts of diuretics on kidney function (eg, activation of tubuloglomerular feedback). Consequently, besides its other positive clinical outcomes, there has been much hope for ultrafiltration therapy to play a protective role against negative effects of diuretics in patients with decompensated heart failure. However, the potential biological advantage has not been confirmed by clinical studies; currently available data from recent clinical trials have so far failed to demonstrate such expected positive results possibly due to counterbalance of the potential negative effects and other not well-known mechanisms. This paper briefly reviews the relevant pathophysiological mechanisms as well as existing evidence in this area and emphasises on the need for further studies specifically designed to explore the impact of ultrafiltration on kidney function in patients with decompensated heart failure.

Immunosuppression reduction for BK virus nephropathy: a case for caution.

BK virus nephropathy (BKVN) is increasingly recognized as a major cause of renal allograft failure. Recent reports demonstrate that prompt reduction of immunosuppression upon detection of persistent viremia can be associated with resolution of viremia, with minimal risk of acute rejection (AR). However, these experiences in general have occurred in centers with low baseline risks of AR. It is possible that a finer balance between overimmunosuppression and the risk of AR may exist in centers that routinely transplant patients with higher risk of AR. Thus the risk/benefit of this strategy may be altered in these centers. We report a case of antibody-mediated rejection that followed reduction of immunosuppression for BKVN diagnosed more than 3 months after the onset of viremia. This rejection episode resulted in a greater decrease in graft function than the initial BKVN episode. Issues relevant to the management of these patients are discussed, including the need for improved immune monitoring assays to determine more accurately the balance between infection and rejection.

Impact of malnutrition-inflammation on the association between homocysteine and mortality.

Whether high total serum homocysteine levels (tHcy) contribute to increase mortality or offer a survival advantage in chronic hemodialysis patients remains controversial. We conducted a prospective study to determine the impact of tHcy on survival in this population with special respect to chronic inflammation-malnutrition state (CIMS). In this prospective study, 459 hemodialysis patients from 10 dialysis centers located in two regions of France were included. A number of baseline parameters were measured including tHcy and markers of CIMS. Over a mean follow-up period of 54 months, 219 deaths (47.7%) occurred, of which 114 (52%) were of cardiovascular (CV) origin. tHcy of equal to or greater than 30 micromol/l was associated with a higher risk of all-cause mortality in patients without CIMS (hazard ratio (HR): 1.55 (confidence interval (CI): 1.12-4.72)), but not in overall dialysis population or those with CIMS. When only CV mortality was considered, tHcy of equal to or greater than 30 micromol/l was associated with a higher risk in patients without (CIMS HR: 1.91 (CI: 1.23-3.23)), but not in those with CIMS. Hyperhomocysteinemia is a strong risk factor for all-cause and CV mortality in hemodialysis patients who do not present CIMS. This association might be masked in patients with CIMS.

One-year post-transplant weight gain is a risk factor for graft loss.

Metabolic syndrome (MS) and obesity participate in the pathogenesis of kidney disease. We explored the impact of MS and post-transplant weight gain on graft survival. Two hundred ninety-two renal transplant recipients (RTRs) were included in the study. Various parameters (e.g. anthropometric, biological) were measured at the time of transplantation as well as 1 year post-transplant. The proportion of patients with overweight or obesity significantly increased during the first year post-transplant (p = 0.04). Mean weight gain was 2.7 +/- 5.8 kg. Thirty patients (10.3%) lost their graft during follow-up. In multivariate analysis, patients with an increase in body mass index (BMI) of more than 5% at 1 year post-transplant had an increased risk of graft loss with (HR: 2.82 [95% CI: 1.11-7.44], p = 0.015) or without death censoring (HR: 2.31 [95% CI: 1.06-5.04], p = 0.035). Low creatinine clearance (HR: 4.72 [95% CI: 1.63-13.69], p = 0.004), high urinary protein excretion (HR: 3.21 [95% CI: 1.27-8.18], p = 0.014) and delayed graft function (DGF) (HR: 2.621 [95% CI: 1.07-6.39], p = 0.036) were also independent risk factors for graft loss. MS did not independently predict graft loss, partly due to significant interactions with low-grade inflammation. We conclude that post-transplant weight gain significantly reduces graft survival.

Cytomegalovirus-associated bleeding diathesis in renal transplant recipients.

Cytomegalovirus (CMV) infection is reported to be capable of modifying endothelial surface with subsequent increased risk of thromboembolic complications. Nevertheless, there are only sparse reports on its role in the development of bleeding diathesis. Here we report two renal transplant recipients who manifested severe coagulation disorders associated with acute CMV infection. Antiviral therapy was followed by consistent correction of coagulation abnormalities.

Cutaneous Alternaria infection in renal transplant recipients: a report of two cases with an unusual mode of transmission.

We report two cases of cutaneous alternariosis in renal transplant recipients. The diagnosis was made by mycologic and histologic examination. The patients were treated with itraconazole. In one patient who had undergone surgical resection of the cutaneous lesion along with antifungal treatment, the follow-up period was uneventful with no signs of recurrence. In the other patient, surgical excision of the lesion was not performed prior to antifungal therapy. The lesion disappeared following treatment but local recurrence was observed 1.5 years later with an unfavorable evolution despite administration of the second course of therapy. Resection of the lesion and prolongation of the treatment resulted in a satisfactory course with no signs of local recurrence over a follow-up period of 4.5 years. Interestingly, both of the patients had a previous history of a mild traumatic event with a stretcher in our outpatient clinic where the follow-up visits were made. A vast mycologic survey was then made in our department, which disclosed that some of the stretchers were contaminated by the fungi and could have potentially served as the reservoirs and vectors for the transmission of the fungus.

Renal transplantation and polyomavirus infection: recent clinical facts and controversies.

Although many articles have been published on polyomavirus-induced pathologies in transplant recipients, our knowledge regarding their clinical aspects remains relatively limited. In fact, the number of questions and controversies on the subject seems even to be increasing as new publications continue to appear. This article presents some of these controversies through a brief review of recent clinical facts about the three polyomaviruses that infect humans--JC virus, simian virus 40, and BK virus--as they relate to renal transplantation.